# Contents {#contents .TOC-Heading .unnumbered} [1. INTRODUCTION [5](#introduction)](#introduction) [NEED OF THE STUDY [9](#need-of-the-study)](#need-of-the-study) [RESEARCH GAP [10](#research-gap)](#research-gap) [**2.** RESEARCH QUESTION [12](#research-question)](#research-question) [**3.** **HYPOTHESIS** [12](#hypothesis)](#hypothesis) [Null Hypothesis (H0) [12](#null-hypothesis-h0)](#null-hypothesis-h0) [Alternate Hypothesis (H1) [12](#alternate-hypothesis-h1)](#alternate-hypothesis-h1) [**4.** **AIMS AND OBJECTIVES** [13](#aims-and-objectives)](#aims-and-objectives) [Aim: [13](#aim)](#aim) [Objectives: [13](#objectives)](#objectives) [Primary Objectives [13](#primary-objectives)](#primary-objectives) [Secondary Objectives [13](#secondary-objectives)](#secondary-objectives) [**5.** **REVIEW OF LITERATURE** [14](#review-of-literature)](#review-of-literature) [AYURVEDIC REVIEW [14](#ayurvedic-review)](#ayurvedic-review) [EVOLUTION OF NETRA: [14](#evolution-of-netra)](#evolution-of-netra) [CONTRIBUTION OF *TRIDOSHAS* IN THE EVOLUTION OF EYE [15](#contribution-of-tridoshas-in-the-evolution-of-eye)](#contribution-of-tridoshas-in-the-evolution-of-eye) [CONCEPT OF *PATALAS* IN *AYURVEDA*: [16](#concept-of-patalas-in-ayurveda)](#concept-of-patalas-in-ayurveda) [ETYMOLOGICAL DERIVATION AND MEANING OF PATALA: [16](#etymological-derivation-and-meaning-of-patala)](#etymological-derivation-and-meaning-of-patala) [THICKNESS OF EACH *PATALA*:^11^ [17](#thickness-of-each-patala11)](#thickness-of-each-patala11) [FIRST PATALA (BAHYA PATALA): [17](#first-patala-bahya-patala)](#first-patala-bahya-patala) [Clinical features of 3rd patala timira are very much similar to the cortical part opacity of lens. Relative inner position of the lens cortex to 2nd patala i.e. uveal tract and retina, its medas like properties and the symptoms arising due to its pathology are similar to the cortex of the lens which can be taken as 3rd patala. [19](#clinical-features-of-3rd-patala-timira-are-very-much-similar-to-the-cortical-part-opacity-of-lens.-relative-inner-position-of-the-lens-cortex-to-2nd-patala-i.e.-uveal-tract-and-retina-its-medas-like-properties-and-the-symptoms-arising-due-to-its-pathology-are-similar-to-the-cortex-of-the-lens-which-can-be-taken-as-3rd-patala.)](#clinical-features-of-3rd-patala-timira-are-very-much-similar-to-the-cortical-part-opacity-of-lens.-relative-inner-position-of-the-lens-cortex-to-2nd-patala-i.e.-uveal-tract-and-retina-its-medas-like-properties-and-the-symptoms-arising-due-to-its-pathology-are-similar-to-the-cortex-of-the-lens-which-can-be-taken-as-3rd-patala.) [FOURTH PATALA: [19](#fourth-patala)](#fourth-patala) [CLINICAL FEATURES OF FOURTH *PATALA TIMIRA^18^*: [19](#clinical-features-of-fourth-patala-timira18)](#clinical-features-of-fourth-patala-timira18) [DESCRIPTION OF *DRISHTI*: [20](#description-of-drishti)](#description-of-drishti) [ETYMOLOGY: [20](#etymology)](#etymology) [DRISHTI: - ANATOMICAL ASPECTS: [21](#drishti---anatomical-aspects)](#drishti---anatomical-aspects) [*DRISHTI* :- PHYSIOLOGICAL ASPECTS [21](#drishti---physiological-aspects)](#drishti---physiological-aspects) [CONCEPT OF *DRISHTI* IN MODERN VIEW [22](#concept-of-drishti-in-modern-view)](#concept-of-drishti-in-modern-view) [PHYSIOLOGY OF CHAKSHURENDRIYA - (VISION) [23](#physiology-of-chakshurendriya---vision)](#physiology-of-chakshurendriya---vision) [ROLE OF TRIDOSHA IN VISION [24](#role-of-tridosha-in-vision)](#role-of-tridosha-in-vision) [UNDERSTANDING PRAMEHAJANYA TIMIRA [25](#understanding-pramehajanya-timira)](#understanding-pramehajanya-timira) [*TIMIRA* AS *PRAMEHA UPADRAVA* [25](#timira-as-prameha-upadrava)](#timira-as-prameha-upadrava) [WHAT MAKES *PRAMEHA* A *MAHAGADA*? [25](#what-makes-prameha-a-mahagada)](#what-makes-prameha-a-mahagada) [ETYMOLOGY OF *TIMIRA*: [26](#etymology-of-timira)](#etymology-of-timira) [SPECIFIC CAUSES OF *TIMIRA* -- [28](#specific-causes-of-timira)](#specific-causes-of-timira) [*SAMPRAPTHI* -- [28](#samprapthi)](#samprapthi) [PURVA RUPA OF *TIMIRA* [29](#purva-rupa-of-timira)](#purva-rupa-of-timira) [RUPA OF *TIMIRA* [29](#rupa-of-timira)](#rupa-of-timira) [ACCORDING TO *DOSHA* INVOLVEMENT- - - - - [29](#according-to-dosha-involvement---------)](#according-to-dosha-involvement---------) [ROOPA: ^61^ [29](#roopa-61)](#roopa-61) [UNDERSTANDING PRAMEHAJANYA TIMIRA VIA NIDANAPANCHAKAS [30](#understanding-pramehajanya-timira-via-nidanapanchakas)](#understanding-pramehajanya-timira-via-nidanapanchakas) [SAMPRAPTI OF *PRAMEHAJANYA* *TIMIRA* [32](#samprapti-of-pramehajanya-timira)](#samprapti-of-pramehajanya-timira) [*CHIKITSA* [36](#chikitsa)](#chikitsa) [MANAGEMENT PRINCIPLES FOR *PRAMEHAJANYA TIMIRA* [37](#management-principles-for-pramehajanya-timira)](#management-principles-for-pramehajanya-timira) [GENERAL STAGEWISE TREATMENT PROTOCOLS IN DIABETIC RETINOPATHY. [38](#general-stagewise-treatment-protocols-in-diabetic-retinopathy.)](#general-stagewise-treatment-protocols-in-diabetic-retinopathy.) [PATHYA-APATHYA AHARA: [39](#pathya-apathya-ahara)](#pathya-apathya-ahara) [VIHARA: [39](#vihara)](#vihara) [**2.1.** Role of *Raktapitta* In Manifestation Of Diabetic Retinopathy [43](#role-of-raktapitta-in-manifestation-of-diabetic-retinopathy)](#role-of-raktapitta-in-manifestation-of-diabetic-retinopathy) [• B. *Raktavritta vata*: Etiologies explained in *vidhisonitiya adhyaya* of *Charak Sutrasthan* are responsible for quantitative increase of *Rakta dhatu*, which impedes the movement of *Vata dosha* hence normal circulation is hampered and stagnation takes place leading to *Sanga* of *Raktavaha srotas*. Symptoms of *Rakatvritavata* are: *Twakmamsa antarajadaha* and *Raktayukta shotha mandala^11^* This type of symptoms can be correlated with general neuropathy; *Raktayukta shotha mandala* can be correlated with splinter haemorrhages and IRMA as retinal edema. Most of the etiological factors responsible for *Raktaja vyadhi* have similarity with *madhumeha* and *prameha* etiological factors. *Akshiragam*, *Tamasyatidarshanam* and *Raktapitta* are described as *Raktaja vyadhi* in *Charak samhita*. These can be correlated with vision defects in diabetics due to microvascular complications. In diabetic retinopathy though initially *Raktakshya* and ischemia occur but later on blood circulation increases, which lead to haemorrhages and exudative features. Treatment of *Raktavritta vata* should be done as per *Vataraktachikitsa^12^* to normalize the movement of obstructed Vata dosha. [46](#_Toc229853425)](#_Toc229853425) [• B. [47](#b.)](#b.) [• C. [47](#c.)](#c.) [• D. [47](#d.)](#d.) [**3.** Visual symptoms of *timir* and diabetic retinopathy [50](#visual-symptoms-of-timir-and-diabetic-retinopathy)](#visual-symptoms-of-timir-and-diabetic-retinopathy) [**MODERN REVIEW OF LITERATURE-** [54](#modern-review-of-literature-)](#modern-review-of-literature-) [Anatomy and Physiology of Retina [54](#anatomy-and-physiology-of-retina)](#anatomy-and-physiology-of-retina) [MICROSCOPIC STRUCTURE OF RETINA:^2^ [55](#microscopic-structure-of-retina2)](#microscopic-structure-of-retina2) [VISUAL PATHWAY [58](#visual-pathway)](#visual-pathway) [RETINAL CIRCULATION^4^ [59](#retinal-circulation4)](#retinal-circulation4) [HISTORICAL REVIEW OF DIABETIC RETINOPATHY5 [62](#historical-review-of-diabetic-retinopathy5)](#historical-review-of-diabetic-retinopathy5) [DISEASE DEFINITION [63](#disease-definition)](#disease-definition) [ETIOPATHOGENESIS [63](#etiopathogenesis)](#etiopathogenesis) [PATHOGENESIS7 [65](#pathogenesis7)](#pathogenesis7) [HEMODYNAMIC ALTERATIONS. [68](#hemodynamic-alterations.)](#hemodynamic-alterations.) [A) PARACRINE FACTORS [70](#paracrine-factors)](#paracrine-factors) [PRO-ANGIOGENIC FACTORS [70](#_Toc229853441)](#_Toc229853441) [CLASSIFICATION^8^ [71](#classification8)](#classification8) [PRESENTING COMPLAINTS9 [77](#presenting-complaints9)](#presenting-complaints9) [CLINICAL HISTORY [77](#clinical-history)](#clinical-history) [EXAMINATION [78](#examination)](#examination) [MANAGEMENT11 [84](#management11)](#management11) [RECENT ADVANCES IN RETINOPATHY MANAGEMENT12 1) SELECTIVE RETINAL THERAPY [92](#recent-advances-in-retinopathy-management12-1-selective-retinal-therapy)](#recent-advances-in-retinopathy-management12-1-selective-retinal-therapy) [2)PASCAL(PATTERNED SCANNING LASER ) PHOTOCOAGULATOR [92](#pascalpatterned-scanning-laser-photocoagulator)](#pascalpatterned-scanning-laser-photocoagulator) [**Physicochemical Parameters of Vasa** [101](#_Toc229853449)](#_Toc229853449) [(*Justiciaadhatoda*L.,DriedLeaf) **(As per Ayurvedic Pharmacopoeia of India)** [101](#_Toc229853450)](#_Toc229853450) [**Thin Layer Chromatography (TLC) for Identification of Vasa** [101](#_Toc229853451)](#_Toc229853451) [**(As per Ayurvedic Pharmacopoeia of India)** [102](#_Toc229853452)](#_Toc229853452) [**TLC Fingerprint Profile of Vasa Leaf** [102](#_Toc229853453)](#_Toc229853453) [After development and derivatization, the TLC plate shows the following characteristic spots: [102](#_Toc229853454)](#_Toc229853454) [**Marker Compounds for Standardization of Vasa** [102](#_Toc229853455)](#_Toc229853455) [**Mode of Action of Vasa in Netra Rogas** [102](#_Toc229853456)](#_Toc229853456) [**Physicochemical Parameters of Shunthi** [105](#_Toc229853457)](#_Toc229853457) [**Thin Layer Chromatography (TLC) for Identification of Shunthi** [106](#_Toc229853458)](#_Toc229853458) [*(As per Ayurvedic Pharmacopoeia of India)* [106](#_Toc229853459)](#_Toc229853459) [**TLC Fingerprint Profile of Shunthi Rhizome** [106](#_Toc229853460)](#_Toc229853460) [**Marker Compounds for Standardization of Shunthi** [107](#_Toc229853461)](#_Toc229853461) [**Mode of Action Shunthi In Netra Rogas** [107](#_Toc229853462)](#_Toc229853462) [Shunthi possesses ***Katu Rasa*, *Ushna Virya***, and ***Laghu--Snigdha Guna***, making it effective in ocular disorders associated with *Kapha* and *Vata* vitiation. Its *Deepana--Pachana* and *Amapachana* actions help in clearing *Ama* and improving microcirculation in ocular tissues, thereby reducing heaviness, stickiness, and discharge of the eyes. The *Shothahara* and mild *Vedanasthapana* properties aid in alleviating inflammation, pain, and discomfort. The presence of bioactive constituents such as gingerols and shogaols contributes to anti-inflammatory, antioxidant, and antimicrobial activities, supporting its role in conditions like *Kaphaja Abhishyanda*, *Netra Shopha*, *Netra Shoola*, and early inflammatory eye disorders. Thus, Shunthi helps restore ocular clarity and supports the maintenance of visual function. [107](#_Toc229853463)](#_Toc229853463) [**Physicochemical Parameters of Guduchi (*Tinospora cordifolia*) Stem** [110](#_Toc229853464)](#_Toc229853464) [**(As per API)** [110](#_Toc229853465)](#_Toc229853465) [**Table 2: TLC Conditions for Identification of Guduchi (As per API)** [110](#_Toc229853466)](#_Toc229853466) [**Table 3: TLC Fingerprint Profile of Guduchi Stem** [110](#_Toc229853467)](#_Toc229853467) [**Table 4: Marker Compounds Used for Standardization of Guduchi** [111](#_Toc229853468)](#_Toc229853468) [Guduchi possesses ***Tikta--Kashaya** **Rasa***, ***Ushna Virya*,** and ***Madhura Vipaka***, making it highly beneficial in ocular disorders involving *Pitta* and *Rakta* vitiation along with *Ama*. Its potent *Tridoshahara* nature, especially *Pitta--Rakta Shamaka*, helps in alleviating burning sensation, redness, and inflammatory changes in the eyes. The *Rasayana* and *Balya* properties of Guduchi promote nourishment and rejuvenation of ocular tissues, enhancing local immunity and resistance to recurrent eye diseases. Its *Shothahara*, *Dahaprashamana*, and *Raktaprasadana* actions contribute to the reduction of edema, congestion, and irritation. The presence of bioactive compounds such as tinosporaside, cordifolioside, and berberine imparts anti-inflammatory, antioxidant, and immunomodulatory effects, making it useful in conditions like *Pittaja Abhishyanda*, *Raktaja Netra Rogas*, *Netra Daha*, and chronic inflammatory eye disorders. Thus, Guduchi supports ocular healing, tissue vitality, and long-term visual health. [111](#_Toc229853469)](#_Toc229853469) [**Physicochemical Parameters of Daruharidra** [114](#_Toc229853470)](#_Toc229853470) [*(BerberisaristataDC.,DriedStem)* *(As per Ayurvedic Pharmacopoeia of India)* [114](#_Toc229853471)](#_Toc229853471) [**Thin Layer Chromatography (TLC) for Identification of Daruharidra** [115](#_Toc229853472)](#_Toc229853472) [**TLC Fingerprint Profile of Daruharidra Stem** [115](#_Toc229853473)](#_Toc229853473) [**Marker Compounds for Standardization of Daruharidra** [115](#_Toc229853474)](#_Toc229853474) [**05. RAKTA CHANDAN** [116](#_Toc229853475)](#_Toc229853475) [**Table No.: Description of Rakta Chandan** [117](#_Toc229853476)](#_Toc229853476) [Physicochemical Parameters of Rakta Chandan [119](#_Toc229853477)](#_Toc229853477) [Thin Layer Chromatography (TLC) for Identification of Rakta Chandan [120](#_Toc229853478)](#_Toc229853478) [TLC Fingerprint Profile of Rakta Chandan [120](#_Toc229853479)](#_Toc229853479) [Marker Compounds for Standardization of Rakta Chandan [120](#_Toc229853480)](#_Toc229853480) [Mode of Action of Rakta Chandan in Netra Rogas [120](#_Toc229853481)](#_Toc229853481) [**06. CHITRAKA** [121](#_Toc229853482)](#_Toc229853482) [**Table No.: Properties & Action of Chitraka** [122](#_Toc229853483)](#_Toc229853483) [**Physicochemical Parameters of Chitraka** [123](#_Toc229853484)](#_Toc229853484) [**Thin Layer Chromatography (TLC) for Identification of Chitraka** [123](#_Toc229853485)](#_Toc229853485) [*(As per Ayurvedic Pharmacopoeia of India)* [124](#_Toc229853486)](#_Toc229853486) [**TLC Fingerprint Profile of Chitraka** [124](#_Toc229853487)](#_Toc229853487) [**Marker Compounds for Standardization of Chitraka** [124](#_Toc229853488)](#_Toc229853488) [**Mode of Action of Chitraka** [124](#_Toc229853489)](#_Toc229853489) [07. **BHUNIMBA (CHIRAYTA)KIRATTIKTA** [125](#_Toc229853490)](#_Toc229853490) [**Physicochemical Parameters of Chirayta /kirattikta** [127](#_Toc229853491)](#_Toc229853491) [**Thin Layer Chromatography (TLC) for Identification of Chirayta/kirattikta** [128](#_Toc229853492)](#_Toc229853492) [**TLC Fingerprint Profile of Chirayta** [128](#_Toc229853493)](#_Toc229853493) [**Mode of Action of Chirayta in Netra Rogas** [129](#_Toc229853494)](#_Toc229853494) [**08. NIMBA TWAK** [129](#_Toc229853495)](#_Toc229853495) [**Physicochemical Parameters of Nimba Twak** [132](#_Toc229853496)](#_Toc229853496) [**Thin Layer Chromatography (TLC) for Identification of Nimba Twak** [132](#_Toc229853497)](#_Toc229853497) [**TLC Fingerprint Profile of Nimba Twak** [133](#_Toc229853498)](#_Toc229853498) [**Marker Compounds for Standardization of Nimba Twak** [133](#_Toc229853499)](#_Toc229853499) [**Mode of Action of Nimba Twak in Netra Rogas** [133](#_Toc229853500)](#_Toc229853500) [**Physicochemical Parameters of Kutaki** [136](#_Toc229853501)](#_Toc229853501) [**Thin Layer Chromatography (TLC) for Identification of Kutaki** [137](#_Toc229853502)](#_Toc229853502) [**TLC Fingerprint Profile of Kutaki** [137](#_Toc229853503)](#_Toc229853503) [**Marker Compounds for Standardization of Kutaki** [137](#_Toc229853504)](#_Toc229853504) [**Mode of Action of Kutaki in Netra Rogas** [138](#_Toc229853505)](#_Toc229853505) [**Physicochemical Parameters of Patola (Patol)** [141](#_Toc229853506)](#_Toc229853506) [**TrichosanthesdioicaRoxb.** **As per Ayurvedic Pharmacopoeia of India (API)** [141](#_Toc229853507)](#_Toc229853507) [**Thin Layer Chromatography (TLC) for Identification of Patola** [141](#_Toc229853508)](#_Toc229853508) [**TLC Fingerprint Profile of Patola Leaf** [142](#_Toc229853509)](#_Toc229853509) [After development and derivatization, the TLC plate shows the following characteristic spots: [142](#_Toc229853510)](#_Toc229853510) [**Marker Compounds for Standardization of Patola** [142](#_Toc229853511)](#_Toc229853511) [**Mode of Action of Patola in Netra Rogas** [142](#_Toc229853512)](#_Toc229853512) [**Physicochemical Parameters of Haritaki** [146](#_Toc229853513)](#_Toc229853513) [**Thin Layer Chromatography (TLC) for Identification of Haritaki** [146](#_Toc229853514)](#_Toc229853514) [**TLC Fingerprint Profile of Haritaki Fruit Pericarp** [147](#_Toc229853515)](#_Toc229853515) [After development and derivatization, the TLC plate shows the following characteristic spots: [147](#_Toc229853516)](#_Toc229853516) [**Marker Compounds for Standardization of Haritaki** [147](#_Toc229853517)](#_Toc229853517) [**Physicochemical Parameters of Vibhitaki** [150](#_Toc229853518)](#_Toc229853518) [*(TerminaliabelliricaRoxb.,DriedFruitPericarp)* *(As per Ayurvedic Pharmacopoeia of India)* [150](#_Toc229853519)](#_Toc229853519) [**Thin Layer Chromatography (TLC) for Identification of Vibhitaki** [150](#_Toc229853520)](#_Toc229853520) [**TLC Fingerprint Profile of Bibhitaka Fruit Pericarp** [151](#_Toc229853521)](#_Toc229853521) [**Marker Compounds for Standardization of Vibhitaki** [151](#_Toc229853522)](#_Toc229853522) [**Thin Layer Chromatography (TLC) for Identification of Amalaki** [155](#_Toc229853523)](#_Toc229853523) [*(As per Ayurvedic Pharmacopoeia of India)* [155](#_Toc229853524)](#_Toc229853524) [**TLC Fingerprint Profile of Amalaki Fruit** [156](#_Toc229853525)](#_Toc229853525) [**Marker Compounds for Standardization of Amalaki** [156](#_Toc229853526)](#_Toc229853526) [Properties & Action of *nagarmotha* [158](#properties-action-of-nagarmotha)](#properties-action-of-nagarmotha) [**Physicochemical Parameters of Nagarmotha** [160](#_Toc229853528)](#_Toc229853528) [**Thin Layer Chromatography (TLC) for Identification of Nagarmotha** [160](#_Toc229853529)](#_Toc229853529) [**TLC Fingerprint Profile of Nagarmotha Rhizome** [161](#_Toc229853530)](#_Toc229853530) [**Marker Compounds for Standardization of Nagarmotha** [161](#_Toc229853531)](#_Toc229853531) [**Table No.: Properties & Action of Yava** [163](#_Toc229853532)](#_Toc229853532) [**Mode of Action of Yava in Netra Rogas** [164](#_Toc229853533)](#_Toc229853533) [Charaka- *Chardinigrahana, Trishnanigrahan* [165](#charaka--chardinigrahana-trishnanigrahan)](#charaka--chardinigrahana-trishnanigrahan) [Sushruta- *Pippalyadi* [165](#sushruta--pippalyadi)](#sushruta--pippalyadi) [Bhavaprakasha Nighantu- *Guduchyadi Varga* [165](#bhavaprakasha-nighantu--guduchyadi-varga)](#bhavaprakasha-nighantu--guduchyadi-varga) [**Indrayava (Holarrhena pubescens Wall. / Holarrhena antidysenterica)** [167](#_Toc229853537)](#_Toc229853537) [*(DriedStem/Bark) (As per Ayurvedic Pharmacopoeia of India)* [167](#_Toc229853538)](#_Toc229853538) [**Physicochemical Parameters** [167](#_Toc229853539)](#_Toc229853539) [**Thin Layer Chromatography (TLC) for Identification** [167](#_Toc229853540)](#_Toc229853540) [**TLC Fingerprint Profile** [167](#_Toc229853541)](#_Toc229853541) [**17. KUTAJ TWAK** [168](#_Toc229853542)](#_Toc229853542) [**Physicochemical Parameters of Kutaj Twak** [170](#_Toc229853543)](#_Toc229853543) [**Thin Layer Chromatography (TLC) for Identification of Kutaj Twak** [171](#_Toc229853544)](#_Toc229853544) [**TLC Fingerprint Profile of Kutaj Twak** [171](#_Toc229853545)](#_Toc229853545) [After development and derivatization, the TLC plate shows the following characteristic spots: [172](#_Toc229853546)](#_Toc229853546) [**Marker Compounds for Standardization of Kutaj Twak** [172](#_Toc229853547)](#_Toc229853547) [**Mode of Action of *Kutaj Twak* in Netra Rogas** [172](#_Toc229853548)](#_Toc229853548) [Role of Vāsādi Kwātha (Conceptual Basis) [172](#role-of-vāsādi-kwātha-conceptual-basis)](#role-of-vāsādi-kwātha-conceptual-basis) [Expected actions: [173](#expected-actions)](#expected-actions) [Pathya-Apathya (Diet & Lifestyle) [202](#pathya-apathya-diet-lifestyle)](#pathya-apathya-diet-lifestyle) [Pathya: [202](#pathya)](#pathya) [Apathya: [202](#apathya)](#apathya) [Demographic and Clinical Observations [211](#demographic-and-clinical-observations)](#demographic-and-clinical-observations) [Age-wise Distribution [212](#age-wise-distribution)](#age-wise-distribution) [Gender-wise Distribution [213](#gender-wise-distribution)](#gender-wise-distribution) [Religion-wise Distribution [214](#religion-wise-distribution)](#religion-wise-distribution) [Prakruti-wise Distribution [214](#prakruti-wise-distribution)](#prakruti-wise-distribution) [Associated Hypertension Distribution [215](#associated-hypertension-distribution)](#associated-hypertension-distribution) [Addiction-wise Distribution [216](#addiction-wise-distribution)](#addiction-wise-distribution) [Duration of Diabetes Mellitus [216](#duration-of-diabetes-mellitus)](#duration-of-diabetes-mellitus) [Occupation-wise Distribution [217](#occupation-wise-distribution)](#occupation-wise-distribution) [Education-wise Distribution [218](#education-wise-distribution)](#education-wise-distribution) [Socioeconomic Status Distribution [218](#socioeconomic-status-distribution)](#socioeconomic-status-distribution) [Diet-wise Distribution [219](#diet-wise-distribution)](#diet-wise-distribution) [Total Cholesterol (TC) Levels [220](#total-cholesterol-tc-levels)](#total-cholesterol-tc-levels) [LDL Levels [221](#ldl-levels)](#ldl-levels) [Triglyceride Levels [222](#triglyceride-levels)](#triglyceride-levels) [Blood Urea Findings [222](#blood-urea-findings)](#blood-urea-findings) [Serum Creatinine Findings [223](#serum-creatinine-findings)](#serum-creatinine-findings) [Overall Interpretation of Demographic Data [223](#overall-interpretation-of-demographic-data)](#overall-interpretation-of-demographic-data) [Improvement in FBS (Fasting Blood Sugar) [224](#improvement-in-fbs-fasting-blood-sugar)](#improvement-in-fbs-fasting-blood-sugar) [FBS [224](#fbs)](#fbs) [Difference at 3 Months [224](#difference-at-3-months)](#difference-at-3-months) [Observation [224](#observation)](#observation) [Improvement in PMBS (Post Meal Blood Sugar) [225](#improvement-in-pmbs-post-meal-blood-sugar)](#improvement-in-pmbs-post-meal-blood-sugar) [PMBS [225](#pmbs)](#pmbs) [Difference [226](#difference)](#difference) [Observation [226](#observation-1)](#observation-1) [Improvement in HbA1c Levels [227](#improvement-in-hba1c-levels)](#improvement-in-hba1c-levels) [HbA1c [227](#hba1c)](#hba1c) [Difference [227](#difference-1)](#difference-1) [Observation [227](#observation-2)](#observation-2) [Minimal improvement observed. [227](#minimal-improvement-observed.)](#minimal-improvement-observed.) [Interpretation [227](#interpretation)](#interpretation) [Anterior Chamber Findings [228](#anterior-chamber-findings)](#anterior-chamber-findings) [Condition of Lens [229](#condition-of-lens)](#condition-of-lens) [Complaints of Patients of Timir [230](#complaints-of-patients-of-timir)](#complaints-of-patients-of-timir) [BCVA Distant Vision Interpretation [231](#bcva-distant-vision-interpretation)](#bcva-distant-vision-interpretation) [1. Distant Vision BCVA [231](#distant-vision-bcva)](#distant-vision-bcva) [Right Eye [231](#right-eye)](#right-eye) [Baseline [231](#baseline)](#baseline) [After Treatment [232](#after-treatment)](#after-treatment) [Difference at 3 Months [232](#difference-at-3-months-1)](#difference-at-3-months-1) [Observation [232](#observation-3)](#observation-3) [Left Eye [232](#left-eye)](#left-eye) [Difference at 3 Months [232](#difference-at-3-months-2)](#difference-at-3-months-2) [Observation [232](#observation-4)](#observation-4) [1. Distant Vision BCVA [232](#distant-vision-bcva-1)](#distant-vision-bcva-1) [Right Eye [232](#right-eye-1)](#right-eye-1) [Left Eye [233](#left-eye-1)](#left-eye-1) [Interpretation [233](#interpretation-1)](#interpretation-1) [BCVA Near Vision Interpretation [234](#bcva-near-vision-interpretation)](#bcva-near-vision-interpretation) [. Near Vision BCVA (N Notation) [234](#near-vision-bcva-n-notation)](#near-vision-bcva-n-notation) [Right Eye [234](#right-eye-2)](#right-eye-2) [Difference at 3 Months [234](#difference-at-3-months-3)](#difference-at-3-months-3) [Observation [234](#observation-5)](#observation-5) [Left Eye [235](#left-eye-2)](#left-eye-2) [Difference at 3 Months [235](#difference-at-3-months-4)](#difference-at-3-months-4) [Observation [235](#observation-6)](#observation-6) [Right Eye [235](#right-eye-3)](#right-eye-3) [Left Eye [235](#left-eye-3)](#left-eye-3) [Interpretation [235](#interpretation-2)](#interpretation-2) [Improvement in NPDR Grades [236](#improvement-in-npdr-grades)](#improvement-in-npdr-grades) [.Grades of NPDR [236](#grades-of-npdr)](#grades-of-npdr) [Right Eye [236](#right-eye-4)](#right-eye-4) [Difference at 3 Months [237](#difference-at-3-months-5)](#difference-at-3-months-5) [Observation [237](#observation-7)](#observation-7) [Left Eye [237](#left-eye-4)](#left-eye-4) [Difference at 3 Months [237](#difference-at-3-months-6)](#difference-at-3-months-6) [Observation [237](#observation-8)](#observation-8) [Interpretation [238](#interpretation-3)](#interpretation-3) [Retinal pathological changes of NPDR reduced significantly after treatment [238](#retinal-pathological-changes-of-npdr-reduced-significantly-after-treatment)](#retinal-pathological-changes-of-npdr-reduced-significantly-after-treatment) [Patalgata Timir Grades [238](#patalgata-timir-grades)](#patalgata-timir-grades) [. Patal Involvement [238](#patal-involvement)](#patal-involvement) [Right Eye [238](#right-eye-5)](#right-eye-5) [Difference [239](#difference-2)](#difference-2) [Observation [239](#observation-9)](#observation-9) [Left Eye [239](#left-eye-5)](#left-eye-5) [Difference [239](#difference-3)](#difference-3) [Observation [239](#observation-10)](#observation-10) [. Patal Involvement [240](#patal-involvement-1)](#patal-involvement-1) [Both Eyes [240](#both-eyes)](#both-eyes) [All comparisons were highly significant (p\<0.001). [240](#all-comparisons-were-highly-significant-p0.001.)](#all-comparisons-were-highly-significant-p0.001.) [Interpretation [240](#interpretation-4)](#interpretation-4) [Timir Subjective Symptoms Score (TSSS) [241](#timir-subjective-symptoms-score-tsss)](#timir-subjective-symptoms-score-tsss) [Right Eye [241](#right-eye-6)](#right-eye-6) [Right Eye [241](#right-eye-7)](#right-eye-7) [Difference [241](#difference-4)](#difference-4) [Observation [242](#observation-11)](#observation-11) [Left Eye [242](#left-eye-6)](#left-eye-6) [Difference [242](#difference-5)](#difference-5) [Observation [242](#observation-12)](#observation-12) [8.Timir Subjective Symptom Score (TSSS) [242](#timir-subjective-symptom-score-tsss)](#timir-subjective-symptom-score-tsss) [Both Eyes [242](#both-eyes-1)](#both-eyes-1) [Foveal Reflex Interpretation [243](#foveal-reflex-interpretation)](#foveal-reflex-interpretation) [Difference [244](#difference-6)](#difference-6) [Left Eye [244](#left-eye-7)](#left-eye-7) [Difference [244](#difference-7)](#difference-7) [Both Eyes [244](#both-eyes-2)](#both-eyes-2) [Findings [244](#findings)](#findings) [Observation [244](#observation-13)](#observation-13) [5. Foveal Reflex [244](#foveal-reflex)](#foveal-reflex) [Interpretation [245](#interpretation-5)](#interpretation-5) [Amsler Grid Findings [245](#amsler-grid-findings)](#amsler-grid-findings) [Right Eye [246](#right-eye-8)](#right-eye-8) [Difference at 3 Months [246](#difference-at-3-months-7)](#difference-at-3-months-7) [Observation [246](#observation-14)](#observation-14) [Left Eye [246](#left-eye-8)](#left-eye-8) [Difference at 3 Months [246](#difference-at-3-months-8)](#difference-at-3-months-8) [Observation [246](#observation-15)](#observation-15) [Interpretation [247](#interpretation-6)](#interpretation-6) [Two Point Discrimination Test [247](#two-point-discrimination-test)](#two-point-discrimination-test) [Right Eye [247](#right-eye-9)](#right-eye-9) [Difference at 3 Months [248](#difference-at-3-months-9)](#difference-at-3-months-9) [Observation [248](#observation-16)](#observation-16) [Left Eye [248](#left-eye-9)](#left-eye-9) [Difference at 3 Months [248](#difference-at-3-months-10)](#difference-at-3-months-10) [Observation [248](#observation-17)](#observation-17) [Interpretation [249](#interpretation-7)](#interpretation-7) [Photostress Test Interpretation [250](#photostress-test-interpretation)](#photostress-test-interpretation) [Photo Stress Recovery Time (PSRT) [250](#photo-stress-recovery-time-psrt)](#photo-stress-recovery-time-psrt) [Right Eye [250](#right-eye-10)](#right-eye-10) [Difference at 3 Months [250](#difference-at-3-months-11)](#difference-at-3-months-11) [Observation [250](#observation-18)](#observation-18) [Left Eye [250](#left-eye-10)](#left-eye-10) [Difference at 3 Months [250](#difference-at-3-months-12)](#difference-at-3-months-12) [Observation [251](#observation-19)](#observation-19) [Both Eyes [251](#both-eyes-3)](#both-eyes-3) [Interpretation [251](#interpretation-8)](#interpretation-8) [Overall Observation [251](#overall-observation)](#overall-observation) [Final Result [251](#final-result)](#final-result) [Parameters Showing Maximum Relief in Group A [252](#parameters-showing-maximum-relief-in-group-a)](#parameters-showing-maximum-relief-in-group-a) [Overall Comparative Interpretation [252](#overall-comparative-interpretation)](#overall-comparative-interpretation) [Overall Statistical Summary [253](#overall-statistical-summary)](#overall-statistical-summary) [Highly Significant Improvements [253](#highly-significant-improvements)](#highly-significant-improvements) [Mild/Moderate Improvement [253](#mildmoderate-improvement)](#mildmoderate-improvement) [No Significant Change [253](#no-significant-change)](#no-significant-change) [Final Statistical Summary for Thesis [254](#final-statistical-summary-for-thesis)](#final-statistical-summary-for-thesis) [Meaning of Statistical Terms [256](#meaning-of-statistical-terms)](#meaning-of-statistical-terms) [**DISCUSSION** [275](#discussion)](#discussion) [Discussion on Distant Vision BCVA [275](#discussion-on-distant-vision-bcva)](#discussion-on-distant-vision-bcva) [Statistical Findings [275](#statistical-findings)](#statistical-findings) [Percentage Relief [275](#percentage-relief)](#percentage-relief) [Interpretation [275](#interpretation-9)](#interpretation-9) [**DISCUSSION (Near Vision)** [276](#_Toc229853696)](#_Toc229853696) [**DISCUSSION (Pinhole Vision)** [277](#_Toc229853697)](#_Toc229853697) [**DISCUSSION (Two-Point Discrimination)** [278](#_Toc229853698)](#_Toc229853698) [**Discussion on photostress test** [280](#_Toc229853699)](#_Toc229853699) [**Discussion on foveal reflex** [280](#_Toc229853700)](#_Toc229853700) [**Correlation with Other Parameters** [281](#_Toc229853701)](#_Toc229853701) [**Discussion on grades of timir** [282](#_Toc229853702)](#_Toc229853702) [**Correlation with Modern Parameters** [282](#_Toc229853703)](#_Toc229853703) [**Discussion on patal involvemet** [282](#_Toc229853704)](#_Toc229853704) [**Correlation with Modern Findings** [283](#_Toc229853705)](#_Toc229853705) [**Discussion on timir subjective symptom score** [283](#_Toc229853706)](#_Toc229853706) [**Correlation with Objective Parameters** [284](#_Toc229853707)](#_Toc229853707) [**DISCUSSION overall** [284](#_Toc229853708)](#_Toc229853708) [**🔹 1. Subjective Improvement** [284](#_Toc229853709)](#_Toc229853709) [**2. Functional Visual Recovery** [284](#_Toc229853710)](#_Toc229853710) [**3. Structural (Fundus) Changes** [285](#_Toc229853711)](#_Toc229853711) [**4. NPDR Grade Regression** [285](#_Toc229853712)](#_Toc229853712) [**5. Timir Grading Improvement** [285](#_Toc229853713)](#_Toc229853713) [**6. Patal-wise Lakshan Improvement** [285](#_Toc229853714)](#_Toc229853714) [**7. Mode of Action** [286](#_Toc229853715)](#_Toc229853715) [1 Detailed Summary [287](#detailed-summary)](#detailed-summary) [Introduction [287](#introduction-1)](#introduction-1) [Aim of the Study [288](#aim-of-the-study)](#aim-of-the-study) [Objectives of the Study [288](#objectives-of-the-study)](#objectives-of-the-study) [Study Design [288](#study-design)](#study-design) [Observations and Results [289](#observations-and-results)](#observations-and-results) [1. Distant Vision BCVA [289](#distant-vision-bcva-2)](#distant-vision-bcva-2) [Percentage Relief [289](#percentage-relief-1)](#percentage-relief-1) [Statistical Significance [289](#statistical-significance)](#statistical-significance) [Summary [289](#summary)](#summary) [2. Near Vision BCVA [289](#near-vision-bcva)](#near-vision-bcva) [Percentage Relief [289](#percentage-relief-2)](#percentage-relief-2) [Statistical Findings [290](#statistical-findings-1)](#statistical-findings-1) [Summary [290](#summary-1)](#summary-1) [3. Amsler Grid [290](#amsler-grid)](#amsler-grid) [Percentage Relief [290](#percentage-relief-3)](#percentage-relief-3) [Statistical Findings [290](#statistical-findings-2)](#statistical-findings-2) [Summary [290](#summary-2)](#summary-2) [4. Two-Point Discrimination Test [290](#two-point-discrimination-test-1)](#two-point-discrimination-test-1) [Percentage Relief [291](#percentage-relief-4)](#percentage-relief-4) [Statistical Findings [291](#statistical-findings-3)](#statistical-findings-3) [Summary [291](#summary-3)](#summary-3) [5. Foveal Reflex [291](#foveal-reflex-1)](#foveal-reflex-1) [Percentage Relief [291](#percentage-relief-5)](#percentage-relief-5) [Summary [291](#summary-4)](#summary-4) [6. Grades of NPDR [291](#grades-of-npdr-1)](#grades-of-npdr-1) [Percentage Relief [292](#percentage-relief-6)](#percentage-relief-6) [Statistical Findings [292](#statistical-findings-4)](#statistical-findings-4) [Summary [292](#summary-5)](#summary-5) [7. Photo Stress Recovery Time (PSRT) [292](#photo-stress-recovery-time-psrt-1)](#photo-stress-recovery-time-psrt-1) [Percentage Relief [292](#percentage-relief-7)](#percentage-relief-7) [Statistical Findings [292](#statistical-findings-5)](#statistical-findings-5) [Summary [293](#summary-6)](#summary-6) [8. Timir Subjective Symptom Score (TSSS) [293](#timir-subjective-symptom-score-tsss-1)](#timir-subjective-symptom-score-tsss-1) [Percentage Relief [293](#percentage-relief-8)](#percentage-relief-8) [Statistical Findings [293](#statistical-findings-6)](#statistical-findings-6) [Summary [293](#summary-7)](#summary-7) [9. Patal Involvement [293](#patal-involvement-2)](#patal-involvement-2) [Percentage Relief [293](#percentage-relief-9)](#percentage-relief-9) [Statistical Findings [294](#statistical-findings-7)](#statistical-findings-7) [Summary [294](#summary-8)](#summary-8) [10. Intraocular Pressure (IOP) [294](#intraocular-pressure-iop)](#intraocular-pressure-iop) [Summary [294](#summary-9)](#summary-9) [11. Laboratory Parameters [294](#laboratory-parameters)](#laboratory-parameters) [FBS [294](#fbs-1)](#fbs-1) [PMBS [294](#pmbs-1)](#pmbs-1) [HbA1c [294](#hba1c-1)](#hba1c-1) [Summary [295](#summary-10)](#summary-10) [Overall Findings [295](#overall-findings)](#overall-findings) [Probable Mode of Action [295](#probable-mode-of-action)](#probable-mode-of-action) [Final Summary [296](#final-summary)](#final-summary) [**Overall Conclusion** [299](#_Toc229853767)](#_Toc229853767) [Detailed Conclusion [300](#detailed-conclusion)](#detailed-conclusion) [Conclusion Based on Visual Parameters [300](#conclusion-based-on-visual-parameters)](#conclusion-based-on-visual-parameters) [Distant Vision BCVA [300](#distant-vision-bcva-3)](#distant-vision-bcva-3) [Percentage Relief [300](#percentage-relief-10)](#percentage-relief-10) [Interpretation [300](#interpretation-10)](#interpretation-10) [Near Vision BCVA [300](#near-vision-bcva-1)](#near-vision-bcva-1) [Percentage Relief [301](#percentage-relief-11)](#percentage-relief-11) [Interpretation [301](#interpretation-11)](#interpretation-11) [Conclusion Based on Retinal Functional Tests [301](#conclusion-based-on-retinal-functional-tests)](#conclusion-based-on-retinal-functional-tests) [Amsler Grid [301](#amsler-grid-1)](#amsler-grid-1) [Percentage Relief [301](#percentage-relief-12)](#percentage-relief-12) [Interpretation [301](#interpretation-12)](#interpretation-12) [Two-Point Discrimination Test [301](#two-point-discrimination-test-2)](#two-point-discrimination-test-2) [Percentage Relief [302](#percentage-relief-13)](#percentage-relief-13) [Interpretation [302](#interpretation-13)](#interpretation-13) [Foveal Reflex [302](#foveal-reflex-2)](#foveal-reflex-2) [Percentage Relief [302](#percentage-relief-14)](#percentage-relief-14) [Interpretation [302](#interpretation-14)](#interpretation-14) [Conclusion Based on NPDR Grading [302](#conclusion-based-on-npdr-grading)](#conclusion-based-on-npdr-grading) [Percentage Relief [303](#percentage-relief-15)](#percentage-relief-15) [Interpretation [303](#interpretation-15)](#interpretation-15) [Conclusion Based on Photo Stress Recovery Time (PSRT) [303](#conclusion-based-on-photo-stress-recovery-time-psrt)](#conclusion-based-on-photo-stress-recovery-time-psrt) [Percentage Relief [303](#percentage-relief-16)](#percentage-relief-16) [Interpretation [303](#interpretation-16)](#interpretation-16) [Conclusion Based on Timir Subjective Symptom Score (TSSS) [304](#conclusion-based-on-timir-subjective-symptom-score-tsss)](#conclusion-based-on-timir-subjective-symptom-score-tsss) [Percentage Relief [304](#percentage-relief-17)](#percentage-relief-17) [Interpretation [304](#interpretation-17)](#interpretation-17) [Conclusion Based on Patal Involvement [304](#conclusion-based-on-patal-involvement)](#conclusion-based-on-patal-involvement) [Percentage Relief [304](#percentage-relief-18)](#percentage-relief-18) [Interpretation [305](#interpretation-18)](#interpretation-18) [Conclusion Based on Laboratory Parameters [305](#conclusion-based-on-laboratory-parameters)](#conclusion-based-on-laboratory-parameters) [FBS [305](#fbs-2)](#fbs-2) [Percentage Relief [305](#percentage-relief-19)](#percentage-relief-19) [Interpretation [305](#interpretation-19)](#interpretation-19) [PMBS and HbA1c [305](#pmbs-and-hba1c)](#pmbs-and-hba1c) [Interpretation [305](#interpretation-20)](#interpretation-20) [Conclusion Regarding Safety [306](#conclusion-regarding-safety)](#conclusion-regarding-safety) [Intraocular Pressure (IOP) [306](#intraocular-pressure-iop-1)](#intraocular-pressure-iop-1) [Interpretation [306](#interpretation-21)](#interpretation-21) [Overall Therapeutic Conclusion [306](#overall-therapeutic-conclusion)](#overall-therapeutic-conclusion) [Final Conclusion [307](#final-conclusion)](#final-conclusion) [**(Timir Lakshana)** [327](#_Toc229853809)](#_Toc229853809) **DRAFT THESIS** **Ph.D. (Ayurved)** **SHALAKYA TANTRA (2010-2011)** **MAHARASHTRA UNIVERSITY OF HEALTH SCIENCES NASHIK** **DETAILS OF THESIS** **1. Permanent Registration number:** **2710100055** **2. Name of the Candidate:** **DR. SHUBHANGI R. LOHAKARE** **3. Name of Faculty:** AYURVED **4. Name of the College/Institute:** Government Ayurved College Nagpur **5. Name of the Guide/ Research Supervisor:** Dr. Ashok P. Vaijwade **6. Name of the Co-Guide:** Not Applicable **7. Name of Examination:** **DOCTOR OF PHILOSOPHY (PH.D.)** **8. Name of Subject/ Specialty:** **SHALAKYA TANTRA** **9. Title of the Thesis-Effect of Vasadi Kwath in the management of Timir w.s.r. To Diabetic Retinopathy- A Clinical Study** **10. Admission Year (Academic Year**)**:** 2010-11 **11. Completion Year (Academic Year):** 2025-26 ----------------------------------------------------------------------- **NAME OF THE UNIVERSITY** **MAHARASHTRA UNIVERSITY OF HEALTH SCIENCES NASHIK** --------------------------- ------------------------------------------- **NAME OF COURSE** **Ph.D. (Ayurved)** **NAME OF THE SUBJECT** **SHALAKYA TANTRA** **ADMISSION YEAR** **2010-11** **SUBMISSION YEAR** **2025-26** **TOPIC OF THESIS** **Effect of Vasadi Kwath in the management of Timir w.s.r. To Diabetic Retinopathy- A Clinical Study** ----------------------------------------------------------------------- : : SHOWING *PANCHABHAUTIKA* CONTRIBUTION IN THE EVOLUTION OF EYE **\ ** **INDEX** +-----------------+-------------------------------------+-------------+ | > **Sr. No.** | > **Chapter Name** | > **Page | | | | > No.** | +=================+=====================================+=============+ | 1. | > **Introduction** | > **1-8** | +-----------------+-------------------------------------+-------------+ | 2. | > **Research Question** | > **9-10** | +-----------------+-------------------------------------+-------------+ | 3. | > **Hypothesis** | > **11-12** | +-----------------+-------------------------------------+-------------+ | 4. | > **Aim and Objectives** | > **13** | +-----------------+-------------------------------------+-------------+ | 5. | > **Review of Literature** | > **14-96** | +-----------------+-------------------------------------+-------------+ | | A. **Drug review** | > | | | | **97-190** | +-----------------+-------------------------------------+-------------+ | | B. **Previous work done** | > **191** | +-----------------+-------------------------------------+-------------+ | 6. | > **Material and Methodology** | > | | | | **192-204** | +-----------------+-------------------------------------+-------------+ | 7. | > **Observation and Results** | > | | | | **205-267** | +-----------------+-------------------------------------+-------------+ | 8. | > **Discussion** | > | | | | **268-279** | +-----------------+-------------------------------------+-------------+ | 9. | > **Conclusion** | > | | | | **279-284** | +-----------------+-------------------------------------+-------------+ | 10. | > **Summary** | > | | | | **280-289** | +-----------------+-------------------------------------+-------------+ | 11. | > **Annexures** | > | | | | **290-300** | +-----------------+-------------------------------------+-------------+ | | A. **Bibliography** | > | | | | **301-303** | +-----------------+-------------------------------------+-------------+ | | B. **Abbreviations** | > | | | | **304-309** | +-----------------+-------------------------------------+-------------+ | | C. **Case Record Form** | > | | | | **310-322** | +-----------------+-------------------------------------+-------------+ | | D. **Analysis Report** | > **321** | +-----------------+-------------------------------------+-------------+ | | E. **Master Chart** | > | | | | **322-335** | +-----------------+-------------------------------------+-------------+ | | F. **CTRI Registration** | > | | | | **336-338** | +-----------------+-------------------------------------+-------------+ | | G. **References** | > | | | | **339-350** | +-----------------+-------------------------------------+-------------+ # INTRODUCTION # {#section .unnumbered} Ayurveda is an ancient science of life that aims for healthy body and healthy mind. Principles of ayurvda leads to healthy life. It not only deals with treating the diseased but also to keep the healthy person fit. Ayurveda has its origin from vedas which were developed during the formation of world by lord Brahma. Ayurved is termed as Upved and its description is found in Atharvaveda, one among the four vedas. Ayurved is called ashtang ayurved consisting of eight branches, among them Shalakya Tantra is the branch which deals with diseases of urdhwang sharir so Vagbhat called it urdhwang chikitsa. Some others have called Shalakya Tantra as uttamnga chikitsa. Uttamanga consist of diseases of eyes, ears, nose, throat and shira. Eye is given utmost importance among the five senses. With the eyes given as precious gift of god as good vision is important for social and intellectual development of human being. Vagbhatacharya in Ashtang Hriday Samhita, Uttar sthan has given prime importance for protection of eyes, because as long as there is desire of living all efforts should be taken to protect eyes, because a blind man cannot distinguish day and night. Every thing in the world is useless without eyes even if he is a wealthy person. With eyes the world appears colourful and without eyes it appears black. So protection of eyes is the responsibility of every individual. Sedentary Lifestyle, faulty food habits, stress, urbanisation, genetic predisposition, environmental pollution , industrial and occupational hazards these leads to various systemic diseases and diabetes mellitus is one among them. This metabolic disorder leads to sight threatening vascular complication called diabetic retinopathy which causes gradual progressive diminution of vision. This complication is preventable if diagnosed and managed early and meticulously. If it is left undiagnosed it leads to loss of vision. According to Ayurveda, Drishti patal dushti by doshas leads to drishtigata rogas which cause loss of vision. Among drishtigata roga Timir vyadhi lakshanas are like diminution of vision, monocromatic vision disorders, perception of shape, size of the objects is disturbed, there is failure to see near and far objects, field defects, day and night blindness, complete loss of vision may also occur. Timir is Sadhya vyadhi when doshas are limited upto 1^st^ and 2^nd^ patal and becomes yapya when doshas reach 3^rd^ patal, and becomes asadhya when reaches the 4^th^ patal. Pujyapada muni in his book Netra prakashika has described timir as updrava of meha. Diabetes mellitus has emerged as a major global health burden, with its microvascular complications due to chronicity significantly affecting quality of life. Among these, Diabetic Retinopathy (DR) remains one of the leading causes of preventable blindness worldwide. The early stage, Non-Proliferative Diabetic Retinopathy (NPDR), is characterized by microaneurysms, retinal hemorrhages, hard exudates, and capillary non-perfusion, ultimately leading to visual impairment if not managed timely. From an Ayurvedic perspective, visual disturbances resembling DR can be correlated with Timir, having symptoms Avyakta Darshana (blurred vision), Durdarsha, Vihwala Darshana, and progressive visual impairment a progressive disorder of vision described under *Drishtigata Rogas.* The pathogenesis involves Rasavaha and Raktavaha srotodushti, which closely parallels the microangiopathic changes seen in diabetic retinopathy. The increasing prevalence of DR, along with limitations of current modern treatments---such as high cost, invasiveness (laser, injections), intravitreal anti VEGFS, corticosteroids, vitrectomy and lack of reversal in early pathology---necessitates exploration of safe, cost-effective, and holistic alternatives. Although present-day management including laser photocoagulation, intravitreal anti-VEGF injections, corticosteroids, and vitrectomy has improved visual prognosis, these interventions are expensive, invasive, stage-dependent, and mainly target advanced pathology rather than early neuro-retinal dysfunction. Moreover, they do not completely prevent disease progression and may be associated with recurrence and adverse effects. Hence, there is a growing demand for safer, economical, and holistic therapeutic approaches capable of preventing progression and improving retinal function. Symptomatology of diabetic retinopathy resembles to madhumehjanya timir especially with Tritiya patalgata timir. vitiated doshas primarily vata pitta and rasavaha and raktavaha strotodushti in madhumeha The pathogenesis involves impaired nourishment of ocular tissues, Srotodushti, Dhatukshaya, and disturbance in Alochaka Pitta. The chronicity of hyperglycemia causing vascular leakage, oxidative stress, ischemia, and neuronal degeneration parallels the Ayurvedic concepts of Dhatupaka, Srotorodha, and Rakta Dushti. are responsible for manifestation of timir. According to sushruta, vitiated doshas in madhumeha reach urdhwabhag via siras and cause timir. Ayurveda states if Pradhan vyadhi is treated properly then updravas get treated automatically. so to treat madhmehjanya timir, Vasadi kwath described by Acharya Sharangdhar for treating sarvakshi rogas which contains drugs which are laghu ruksha guna, tikta kashay rasa, katu vipak, ushna virya, these properties are required for samprapti vighatana of madhumeh and its complications. Ayurveda emphasizes preventive, promotive, and curative approaches through Rasayana, Chakshushya, Raktaprasadana, and Tridoshahara therapies. Among the various formulations described in Ayurvedic literature, Vasadi Kwath possesses properties such as Chakshushya (beneficial for eyes), Pittashamaka, Raktashodhaka, Rasayana, anti-inflammatory, antioxidant, and microcirculatory enhancing actions. The ingredients of Vasadi Kwath are believed to act at multiple levels by improving retinal perfusion, reducing oxidative stress, stabilizing capillary permeability, and nourishing ocular tissues. From a contemporary scientific perspective, many herbal components used in the formulation possess flavonoids, phenolic compounds, and bioactive phytochemicals with proven antioxidant, anti-inflammatory, neuroprotective, and vasoprotective effects. The multidimensional pharmacological actions of Vasadi Kwath suggest its potential role in arresting disease progression, improving visual functions, reducing retinal changes, and enhancing quality of life in patients suffering from Timira with special reference to diabetic retinopathy. Thus Tritiya patalgata timir (diabetic retinopathy) is a complication of madhumeh (diabetes), is treated with vasadi kwath which is the study drug. Vāsādi Kwātha, a classical Ayurvedic formulation, possesses properties like: - Pitta-shamana - Rakta-prasadana - Anti-inflammatory (Shothahara) - Microcirculatory improvement These pharmacodynamic actions suggest a potential role in: - Reducing retinal hemorrhages - Improving capillary integrity - Preventing disease progression Despite its theoretical benefits, systematic clinical evaluation of Vāsādi Kwātha in Timira WSR to Diabetic Retinopathy remains underexplored, thereby justifying the present study. Therefore, the present study entitled **"Effect of Vasadi Kwath in Timira with special reference to Diabetic Retinopathy"** is undertaken to scientifically evaluate the therapeutic efficacy of Vasadi Kwath on subjective and objective parameters of diabetic retinopathy through Ayurvedic and modern ophthalmological perspectives. # NEED OF THE STUDY {#need-of-the-study .unnumbered} Diabetic retinopathy is currently one of the foremost causes of irreversible visual impairment among the working-age population worldwide. The incidence of diabetes is increasing alarmingly, particularly in developing countries like India, making retinal complications a growing socioeconomic burden. Early stages of diabetic retinopathy often remain asymptomatic, and by the time visual symptoms appear, significant retinal damage may already have occurred. Despite advances in modern ophthalmic treatment modalities, several limitations still exist: 1. Present therapies are mainly focused on advanced retinal pathology rather than early functional impairment. 2. Laser photocoagulation and intravitreal injections are invasive, costly, and require repeated interventions. 3. Existing treatments may slow progression but often fail to restore retinal health completely. 4. Long-term management places psychological and financial stress on patients. 5. Modern medicine has limited preventive and regenerative approaches for retinal neurovascular degeneration. Ayurveda offers a holistic understanding of disease involving systemic metabolism, microcirculation, tissue nourishment, and visual function. Timira, described in classical texts, exhibits remarkable similarity with the clinical features of diabetic retinopathy. Ayurvedic management aims not only at symptomatic relief but also at correction of underlying Dosha imbalance, enhancement of tissue nutrition, and prevention of disease progression. Vasadi Kwath is traditionally indicated in ocular disorders and possesses Chakshushya, Rasayana, Pittahara, and Raktaprasadana properties. However, despite its classical importance, scientific clinical evaluation of Vasadi Kwath in diabetic retinopathy remains limited. There is a paucity of evidence-based Ayurvedic clinical studies assessing its efficacy using both Ayurvedic and modern ophthalmological parameters such as visual acuity, fundus findings, hemorrhages, exudates, photostress recovery time, contrast sensitivity, and subjective symptoms of Timira. Hence, the present study becomes necessary for the following reasons: - To explore an effective, safe, economical, and non-invasive Ayurvedic intervention for diabetic retinopathy. - To evaluate the role of Vasadi Kwath in improving visual function and retinal health. - To establish scientific evidence for Ayurvedic management of Timira with special reference to diabetic retinopathy with vasadi kwath. - To correlate classical Ayurvedic concepts with modern retinal pathology. - To assess whether early Ayurvedic intervention can delay progression of retinal complications in diabetic patients. - To contribute evidence-based data for integrative ophthalmology and Ayurvedic research. - To improve quality of life and reduce visual disability among diabetic patients. Thus, the study holds significant clinical, academic, and social importance in bridging classical Ayurvedic wisdom with modern ophthalmic science for the management of diabetic retinopathy. ## **RESEARCH GAP** {#research-gap .unnumbered} Although several studies have been conducted on diabetic retinopathy and ayurvedic management of timir, very limited scientific clinical research is available regarding the effect of vasadi kwath in timir wsr to DR. Most previous studies focused either on subjective visual symptoms or only on glycemic control, while comprehensive evaluation of both ophthalmological and ayurvedic parameters has rarely been performed. Very few studies have assessed -- NPDR grading changes, BCVA distant and near vision, amsler grid findings, photostress recovery test, two point discrimination test, foveal reflex changes, patalgat timir involvement, timir subjective symptom score alongwith biochemical parameters. There is insufficient clinical evidence regarding role of vasadi kwath in improving retinal function, visual acuity and early retinal pathological changes in diabetic retinopathy. Lack of standardized grading and Ayurvedic scoring integration. As well as Minimal studies correlating: Fundus changes, ayurvedic samprapti, clinical outcomes Hence the present study has been undertaken to evaluate the effect of vasadi kwath on timir wsr to DR through detailed subjective, objective, ophthalmological and biochemical assessment parameters to provide scientific validation for its therapeutic utility. ## {#section-1 .unnumbered} ## {#section-2 .unnumbered} ## {#section-3 .unnumbered} ## {#section-4 .unnumbered} ## {#section-5 .unnumbered} ## {#section-6 .unnumbered} ## {#section-7 .unnumbered} # RESEARCH QUESTION In patients of Timira corresponding to non-proliferative diabetic retinopathy (NPDR), does Vasadi Kwath improve visual symptoms and retinal status compared to antioxidant capsules? Does vasadi kwath produce significant theraupetic improvement in timir w.s.r to diabetic retinopathy when assessed through subjective and objective ophthalmological parameters than antioxidant capsules? # **HYPOTHESIS** ### Null Hypothesis (H0) {#null-hypothesis-h0 .unnumbered} Vasadi Kwath does not produce statistically significant improvement than antioxidant in visual acuity, Timira symptoms, or retinal parameters in patients of Timira w.s.r. to diabetic retinopathy. ### Alternate Hypothesis (H1) {#alternate-hypothesis-h1 .unnumbered} Vasadi Kwath produces statistically significant improvement than antioxidants in visual acuity, Timira symptoms, and retinal parameters in patients of Timira w.s.r. to diabetic retinopathy. # **AIMS AND OBJECTIVES** ## Aim: {#aim .unnumbered} To evaluate the clinical and therapeutic efficacy and safety of Vasadi Kwath in the management of Timira with special reference to Diabetic Retinopathy. ## Objectives: {#objectives .unnumbered} ## Primary Objectives {#primary-objectives .unnumbered} 1. To assess the effect of Vasadi Kwath on **visual acuity**(BCVA) in patients of timir.(Diabetic retinopathy) 2. To assess the effect of Vasadi Kwath on **Ayurvedic Timira subjective symptom score**. 3. To assess the effect of Vasadi Kwath on **retinal changes in NPDR- microaneurysms, haemorrhages, hard exudates.** ### Secondary Objectives {#secondary-objectives .unnumbered} 1. To evaluate change in **fundus grading** (ICDR/ETDRS-based NPDR severity)-Before and after treatment 2. To evaluate change in **DME status** (clinical grading). 3. To evaluate change in **near vision, metamorphopsia and color vision**. 4. To observe change in **glycemic control markers** (FBS, PPBS, HbA1c). 5. To assess **safety/tolerability** and adverse events and impact on quality of life of patients. 6. To analyze any reduction in progression of retinal changes associated with Diabetic Retinopathy 7. To correlate ayurvedic samprapti of timir with microvascular pathology of NPDR. # **REVIEW OF LITERATURE** ## AYURVEDIC REVIEW {#ayurvedic-review .unnumbered} *Shalakyatantra* is the only branch in which more or less a peculiar organ is selected and studied. Also, *Urdhwajatru desha* i.e. Supraclavicular region is the abode of vital areas (*shiromarma*). All the sense organs except skin, have their specific location in *urdhwanga* and the sensual faculties of all five sense organs are rooted in the Shira-- Head. Hence comes the importance of protecting *SHIRAS* as a whole for well-being. Though this include all organs above neck, more specification is given to eyes eg. *netravisharadah salakinah*. 19 chapters of *Shalakya* literature are on *Netra chikitsa. Chakshu* is regarded as the most superior and prime *indriya* and everywhere it has been protected from non-congenial factors. (eg. during *swedanakarmas*).^1^ One should always perform efforts to keep eyes healthy because the whole universe will turn useless for a blind even if he is having plenty of wealth.^2^ # EVOLUTION OF NETRA: {#evolution-of-netra .unnumbered} The evolution of all sense organs occurs in the 3rd month of intrauterine life and completes at about 7th month.^3^ PANCHABHAUTIK CONCEPT IN THE EVOLUTION: The eye is mainly built up of 5 elements of the universe -- the *Bhutas*. Its different portions are contributed by specific *Bhutas*. . +------------------------------------+---------------------------------+ | **Part** | > ***Mahabhuta*** | +====================================+=================================+ | Muscular portion | *Prithvi* | +------------------------------------+---------------------------------+ | White portion | *Jala* | +------------------------------------+---------------------------------+ | Red portion | > *Teja* | +------------------------------------+---------------------------------+ | Black portion | *Vayu* | +------------------------------------+---------------------------------+ | Tear channels | *Akasha* | +------------------------------------+---------------------------------+ : :SANDHIS OF NETRA # CONTRIBUTION OF *TRIDOSHAS* IN THE EVOLUTION OF EYE {#contribution-of-tridoshas-in-the-evolution-of-eye .unnumbered} +----------------+---------------------+------------------------------+ | PART | > DOSHA/DHATU | > CONTRIBUTING SOURCE | +================+=====================+==============================+ | *1.K | > *Rakthaja* | > *Matruja* | | rishnamandala* | | | +----------------+---------------------+------------------------------+ | *2 | *Kaphaja* | > *Pitruja* | | .Suklamandala* | | | +----------------+---------------------+------------------------------+ | 3.*D | > \- | > Both | | rishtimandala* | | | +----------------+---------------------+------------------------------+ : : > NETRA RACHANA SHARIRA: In accordance to the three coats/layers of eyeball in modern anatomy, the description of eye in Ayurveda consists of *Mandalas, Sandhis* and *Patalas* which are 5, 6 and 6 respectively.^6^ i. ***MANDALA*:** The word *Mandala* is generally used for circular structures or areas in the eye. The five *Mandalas* are as follows -- The size of the *Drishti Mandala* is equal to the cotyledon of *Masura^7^* and is a hollow structure. Such structures which have its position inner to *Krishana Mandala* seems to be pupillary area which is circular in shape. > Table : NETRA RACHANA SHARIRA: +---------------------+------------------------------------------------+---+ | ***MANDALAS*** | > **ANATOMICAL ASPECT** | | +=====================+================================================+===+ | 1\. *Pakshma | Eye Lashes When Eye Is Open | | | Mandala* | | | +---------------------+------------------------------------------------+---+ | 2\. Vartmamandala | Upper And Lower Eye Lids. | | +---------------------+------------------------------------------------+---+ | 3\. Shweta Mandala | Scleral And Conjunctival Part Of The Outer | | | | Fibrous Coat. | | +---------------------+------------------------------------------------+---+ | 4\. Krishnamandala | Cornea And Iris. | | +---------------------+------------------------------------------------+---+ | 5\. Drishti Mandala | Pupillary Area Or Circle. | | +---------------------+------------------------------------------------+---+ ii. **SANDHIS:** Junctional lines of different mandalas in relation to the eye have been considered as *sandhis*. These are six in number^8^ i.e. +--------------------------+-------------------------------------------+ | ***SANDHIS*** | > **ANATOMICAL ASPECT** | +==========================+===========================================+ | 1\. *Pakshma Vartma | The Lid Margin | | Sandhi* | | +--------------------------+-------------------------------------------+ | *2. Vartma Shukla | Fornixes Of The Eyeball | | Sandhi* | | +--------------------------+-------------------------------------------+ | *3. Shukla Krishna | Sclero-Corneal Junction | | Sandhi* | | +--------------------------+-------------------------------------------+ | *4. Krishna Drishti | Central Free Margins Of The Iris, Which | | Sandhi* | Rests On The Anterior Capsule Of The | | | Lens. | +--------------------------+-------------------------------------------+ | *5.Kaneenika Sandhi* | Inner Canthus. Lacrimal Passage Is | | | Situated. | +--------------------------+-------------------------------------------+ | *6. Apanga Sandhi* | Near The Tail Of Eyebrows | +--------------------------+-------------------------------------------+ # CONCEPT OF *PATALAS* IN *AYURVEDA*: {#concept-of-patalas-in-ayurveda .unnumbered} *Patala* is a unique concept told by *Sushruta Samhita* in *Netrashareera* and it is very important in understanding *Drishtigata* *Rogas* especially *Timira*. This is still a confusing subject among *Ayurvedic* fraternities and many of them have interpreted this in their own way. Here an attempt is made to clarify this subject in special context to the study subject. Relative position of each *patala*, constituting factors, similarity and the clinical picture due to pathology of *patala* on comparative modern grounds is being discussed here. # ETYMOLOGICAL DERIVATION AND MEANING OF PATALA: {#etymological-derivation-and-meaning-of-patala .unnumbered} *Pat + Klach pratyay* means layer, veil, covering chest, basket or enclosing/ surrounding skin, membrane especially of the eyes, A film over the eyes.^9^ Only six *patalas* are there in the eye. Among the total six *patalas* two are *vartma patalas* (upper and lower) and four others^10^. # THICKNESS OF EACH *PATALA*:^11^ {#thickness-of-each-patala11 .unnumbered} The thickness of each *patala* is 1/5th of the *drishti* RELATIVE POSITION OF EACH *PATALA*: First *Patala* among 4 *Patalas* in *netra* is known as *Bahya* or outer, this means that other 3 are relatively inner to the former. The disease *Timira* vitiates the first *Patala* follows the second, third and fourth.^12^ Therefore the first *patala* is the outermost and then the successive ones. # FIRST PATALA (BAHYA PATALA): {#first-patala-bahya-patala .unnumbered} > It is the outermost among 4 *patalas* and covers the *drishti mandala* > (Pupil). > > First *patala* is constituted by *Teja* and *Jala* *mahabhutas* > whereas *Dalhana* opines that this *patala* is constituted by *Rakta*. > *Vagbhata* has described *doshik* / *srotas* constitution of eye by > virtue of which *raktavaha strotas* forms the black part of the > *netra*. i.e. corneal part and *kaphavaha strotas* constitutes the > *shweta* mandala i.e. scleral part13. It is the known fact that > *rakta* represents the *teja* and *kapha* represents *jala mahabhuta* > in human body. > > The only clinical feature of first *patala* pathology is blurred / > indistinct vision14 which becomes clear sometimes without any reason > i.e. low-grade refractive error which can be corrected by > accommodation. SECOND PATALA: It is constituted by *mamsa* (muscles) having *kandaras* (tendon like properties) giving attachment. Also, it should have nutritive as well as contraction and relaxation properties. Structures to inner *patala* having such properties are uveal tract. > Clinical features of 2nd *patala* can be grouped as follows15- i. More dimness of vision. ii. Floaters in the visual field. iii. Scotoma or blind areas in visual field giving rise to field defects iv. Accommodation anomalies and increasing hypermetropia. v. Metamorphopsia, micropsia. vi. Diplopia etc. > The iris and ciliary body are the most sensitive tissues of the > eyeball and develops inflammatory reactions following innumerable > exogenous causes i.e. iridocyclitis. Inflammatory vitreous opacities > result from inflammatory process in the posterior uveal tract or > retina, which results, into floaters in front of the eye. The other > symptoms like metamorphopsia, micropsia, diplopia etc. May be due to > retinal pathologies like AMD, Macular scar, CSR, ERM etc. Thus > morphological, physiological and pathological characters of 2nd Patala > are alike that of uveal tract and retina. THIRD PATALA: This part of the eye inner to second *patala* and is subsisting in *medas*. > Clinical features of 3rd *patalagata* timira:^16^ - Pupillary leukocoria. - Gradual loss of vision. - Details of even big objects are not visible. - Visual field defects according to location of doshas. - Diplopia, triplopia and polyopia. > The part of the eye inner to the uveal tract, which is very much > related to *drishti* (pupil and vision), is particularly lens. The > cortical part of the lens is also having *meda* like i.e. viscous, > lipo-proteinaceous and whitish in color. # Clinical features of 3rd patala timira are very much similar to the cortical part opacity of lens. Relative inner position of the lens cortex to 2nd patala i.e. uveal tract and retina, its medas like properties and the symptoms arising due to its pathology are similar to the cortex of the lens which can be taken as 3rd patala. {#clinical-features-of-3rd-patala-timira-are-very-much-similar-to-the-cortical-part-opacity-of-lens.-relative-inner-position-of-the-lens-cortex-to-2nd-patala-i.e.-uveal-tract-and-retina-its-medas-like-properties-and-the-symptoms-arising-due-to-its-pathology-are-similar-to-the-cortex-of-the-lens-which-can-be-taken-as-3rd-patala. .unnumbered} # FOURTH PATALA: {#fourth-patala .unnumbered} > Innermost *patala* is 4th *patala*. It is constituted by asthi^17^ > hard tissue, which is supportive in function. # CLINICAL FEATURES OF FOURTH *PATALA TIMIRA^18^*: {#clinical-features-of-fourth-patala-timira18 .unnumbered} - Loss of vision. - Drishti mandala is covered by vitiated doshas. - Perception of bright illuminations unless there is some gross pathology in the *netra*. Inner to 3rd *patala* i.e. cortical part of the lens, the hard and supportive structure is lens nucleus, which give support to the new-formed lens fibers. The clinical features of 4th *patala timira* i.e. complete loss of vision -- *Linganasha* occurs in complete opacity of the lens i.e. mature cataract in which nearly complete loss of vision occurs. In advanced cataract also, perception and projection of light is always maintained. # DESCRIPTION OF *DRISHTI*: {#description-of-drishti .unnumbered} > *Pramehajanya* Timira is a *drishtigata roga*. It is quite essential > to know what the word *drishti* means. The word *drishti* has been > used in different meanings in Ayurvedic classics. # ETYMOLOGY: {#etymology .unnumbered} > A. *DRISH + Ktin karane* - means source or tool with which one > sees^19^. B. *Drish bhav + Ktin* means seeing, viewing, intellect^20^. > > C. A theory^21^ > > Drishti in Ayurvedic literature is used as an organ of vision -\'eye\' > (anatomical structure) which is particularly related with vision > process (central part of cornea, pupillary aperture) as well as the outcome of its function. (physiological entity) Thus *Drishti* is having amphisitomous meaning. # DRISHTI: - ANATOMICAL ASPECTS: {#drishti---anatomical-aspects .unnumbered} (i) DRISHTIM: a. *NetraDrishti* should be covered while doing *swedan* and *agnikarma* on lids > .^22^ a b. *Mandala* (Part of *Netra*). Size of *drishti mandala* is specified in proportion to *krishna mandala*. ^22b^ i. *DRISTIGATA ROGA VIGYANEEYAM* = *Dalhana* is of the opinion that by the word *drishti*, one should consider the mandala in which it subsists .^23^ ii. *DRISHTISAMEEPA* = central part of *krishnamandala* (cornea) Prognosis of *vranashukla*/ *vranashukra* (corneal ulcer) is not good if it is *drishti sameepa* > i.e. near the central part of the cornea^24^. iii. *DRISHTI PRASADA* = Netra *golaka* (eye ball) *Drishtiprasadaka* measures should be employed in ocular traumatic conditions where eyeball is having inflammations etc^25^. iv. *DRISHTI BHAGA = Chakshurendriya Adhishtana .* v. *DRISHTYANTARA* = Distance between two *drishtimandala* (inter pupillary distance is narrated) .^26^ vi. *DRISHTI KLEDA* = Lubricating fluid of the eyeball. vii. *DRISHTI VISHARADA* = Ocular expert. # *DRISHTI* :- PHYSIOLOGICAL ASPECTS {#drishti---physiological-aspects .unnumbered} > *DRISHTI KRISHATHAH* = Dimness of vision - *Kshudha vega dharanat* > ^27.^ (ii)*DRISHTI HANANA* = Loss of vision-prognosis of *adhimantha* > .^28^ > > *DRISHTIBALA* = *Drishti* *samarthyam* - Result of *mukhlepa* .^29^ > > (iv)*DRISHTI* *VIBHRAMA* = *Drika* *bhrama-Savisha* *Anjana > Lakshana*.^30^ (v)*DRISHTI* *VISHA* = Some immortal Snakes eg. > *Vasuki* has poison in its vision .^31^ > > (vi)*DRISHTI PRADA VARTI* = Drug which provide *drishti* to blinds > > (vii)DRISHTI = Perception. Bad prognostic symptoms of one's life when > the perception of senses is not proper . On the above discussion it can be said that *Drishti* in Ayurvedic literature have amphistomous meaning i.e. structural and functional entity # CONCEPT OF *DRISHTI* IN MODERN VIEW {#concept-of-drishti-in-modern-view .unnumbered} Different Ayurveda experts have their different opinion regarding which part of eye should be taken as *Drishti*. They are compiled below- 1. *Drishti* as Pupil: The concept of *Drishti* by *Sushrutha Samhita^32^* is little different and all his description points to pupil. \-- *Masura* *dala* *matra* (shape of a splitted red lentil) \-- Prasada of *panchamahaboota* (essence of five elements) \-- *Bahya* *patalashritha* (depending on outer *patala*) \-- *Khadyota* *visphulingabha* (Sparkle like glow worm) \-- Constantly irrigated by the cold aqueous. \-- *Vivarakritim* and *sheeta* *satmya*. \-- *Drishti* *pramana* 1/7th of *Krishna mandala* in Uttaratantra^33^ (when pupil is dilated), 1/9th of *Taraka* (*Krishna mandala*) in *Sutrasthana*.^34^ ( pupil is constricted). But *Drishtigatha rogas* cannot be explained by considering *drishti* as pupil. 2. *Drishti* as Lens: Even though *Timira*-*Kacha*-*Linganasha* can be explained by considering as lens, but many of the symptoms of these conditions also seen in retinal diseases and also some of the *drishtigatha rogas* namely, *Pitta vidagdha* and *Kapha vidagdha drishti* cannot be explained by considering *drishti* as lens. *3.Drishti* as Vision: While explaining *Adhimantha* it has been told that blindness will occur within 7 days in *Kaphaja*, within 5 days in *Rakthaja adhimantha* etc., and in this condition, *Drishti* indicates Vision.35 4\. *Drishti* as Retina: In *Drishtigatha* *Rogas*, *Pitta vidagdha drishti*, *Kapha vidagdha drishti, Nakulandhya, Gambirika, Sanimitta linganasha, Animitta linganasha* etc. clearly points out that *Drishti* can be considered as Retina. Hence, we have seen that the physiological aspect of *drishti (drishti* *karma*) is concerned with visual outcome. This function has been attributed mainly to *Alochakapitta* in our classics and its location is told to be behind iris (*antah tarakayoh sthithah*)^36^ as per our classics. This is nothing but posterior segment of eye (retina; specifically rods and cones) where initiation of vision starts with photochemical reactions. Considering all the points, it may be concluded that eye as a whole and the structures directly involved in the process of vision i.e structures of visual axis including retina and visual pathway can be taken under the term *Drishti*. Here in *Pramehajanya* Timira (BDR), the structure directly involved is the retinal part of Drishti and hence the detailed anatomy of the concerned structure will be discussed with the help of modern anatomical knowledge in the coming session. # PHYSIOLOGY OF CHAKSHURENDRIYA - (VISION) {#physiology-of-chakshurendriya---vision .unnumbered} Visual perception, like all other sensory phenomena, is dependent upon the state of mind and soul. *Sushruta* relates the theory of common origin (*tulya* *yoni*) a basis of sensory perception.^37^ It is believed that light, which illuminates the object, and the eye which receives these objects, both are derivatives of *tejamahabhuta*, hence they perceive only the *rupa* of the object not the other character like sound etc.^38^. As corollary to the same, he declares *Surya* (sun) as the *Adhidaiva* and *drishya* as *adibhuta* for *chakshu*, which is *Adhyatma*. The theory of *panchpanchaka* depicts the phenomenon of sensory perception by enumerating the five important factors, which take part in this process. They are *indriya, indriya dravya, indriya artha, indriya adhishthana & indriya buddhi*. ^39^ *Rupa (indriya artha)* will be travelling in the media of *jyoti (indriya dravya*) towards the *netras* (*indriya adhishthana*). Impulses from both these *netras* are collected at *chakshu* (*Indriya*) which is one in number. Further it will be assisted by mana and analysed at the level of *chakshu buddhi* (*indriya buddhi*) to give actual knowledge of the subject to the *atma. Acharya* *Charaka* has described this process as the conjuncture of soul, mind and the sense organ with the objects. *Kashyapa* classifies senses into *Sannikrishta Indriyas* and *Viprakrishta* *Indriyas^41^*. Eyes and Ears are the *Viprakrishta Indriyas*, where in object need not directly fall on the senses. Eye has developed sufficient skills to perceive the object from a sufficiently large distance. # {#section-8 .unnumbered} # ROLE OF TRIDOSHA IN VISION {#role-of-tridosha-in-vision .unnumbered} *Vata* is responsible for *Pravartana* (stimulation, activation) of the *Indriya* whereas *Pitta* performs *Alochana* (perception) of the *Indriya Artha. Kapha* bestows *Sthairya* (stability) to the Indriya *Adhisthana* by providing *Tarpana*. Further, the subtypes of *Doshas* like *Prana Vayu* and *Vyana Vayu* are specifically held responsible for *Vata Karmas* (Ocular movements and conduction of visual potentials), *Alochaka Pitta* for *Darshana* and *Tarpaka Kapha* for *Akshi* *Tarpana*. In the visual process, eye is the Indriya and external object is the *Indriyartha*. In order to get a clear image of the external object, there should be *Indriyartha Sannikarsha, Roopalochana* and *Jnanotpatti*. In the first step, the externally situated object is conducted into the eye in the form of light rays. Conduction is the function of *Vata*. As the refractive media are *Kapha* predominant, normal consistency of *Kapha* is absolutely necessary for the normal process of refraction. In the next stage, the analysis of the object is performed. The *Dosha*, which functions in presence of light, is *Alochaka Pitta* hence all the changes that take place in the retina after the convergence of light rays are due to the action of *Alochaka Pitta*. Here, mind is considered as the basement factor for the function of *Alochaka Pitta*. For *Jnanotpatti* to occur, the visual impulse formed is to be converted to actual visual sense. According to Bhela, *Alochaka* *Pitta* is having two functional fractions namely *Chakshurvaisheshika Alochaka* *Pitta* and *Buddhirvaisheshika Alochaka* *Pitta*.^43^ The first one acts at the level of retina while the later acts on occipital cortex. The *Buddhirvaisheshika* *Alochaka* *Pitta* receives impulses sent by the *Chakshurvaisheshika Alochaka* *Pitta* and gives determination and confirmation; and this confirmed knowledge is known as *Pratyakshajnana*. This conduction of visual impulses is carried out by *Pranavayu*. # UNDERSTANDING PRAMEHAJANYA TIMIRA {#understanding-pramehajanya-timira .unnumbered} There is no direct reference regarding the ophthalmic complications of Diabetes in our classics apart from *Netraprakashika* which has highlighted Timira as a complication of Prameha. Hence, we can analyse it as an *anuktha* vyadhi taking into consideration; the vitiated *Doshas ,Dushyas* and other *vyadhi ghatakas.* # *TIMIRA* AS *PRAMEHA UPADRAVA* {#timira-as-prameha-upadrava .unnumbered} In our classics it has not been told that Timira may be an *upadrava* of *Prameha*. Instead the only term related to eyes described in *pittaja prameha upadrava* is *peeta netrata* by *Vagbhata* which requires further clarification. However, it was Poojya Pada *Mahamuni*, one of the luminaries of *Ayurveda* from South India in his work ―*Netra Prakashika*" who clearly mentioned that *prameha* can cause *netra vikaras*. Unfortunately, no further details regarding the disease are available in his book. Hence for a better understanding of *prameha* related ophthalmopathies, it is essential to know the root pathogenesis of *Prameha* and how it leads to multi system involvements. # WHAT MAKES *PRAMEHA* A *MAHAGADA*? {#what-makes-prameha-a-mahagada .unnumbered} *Prameha* is considered as a *Maharoga* due to its *Anushangi* (no cure/continuing nature) nature, multiple dhatu involvement, inherited nature, deep rootedness etc. It is one of its kind where the prodromal symptoms persist even after the manifestation of clinical symptoms and in its complication stage. This may form an important connecting link between *Prameha* and *Timiran*; so also, with Diabetic Retinopathy. It has Subahupadravas ie complications affecting vital structures in the body viz. *Marmas. Siras* is the prime *marma* and when it affects, there must have its affection in eyes also; which are located in the former. *Timira*: *Timira* comprises all ocular diseases in which there is a gradual diminution of vision and whose grave end result is blindness. The clinical features described for *timira* are having broad applications and can be used to explain a number of ophthalmic problems ranging from refractive errors, posterior segment pathologies like retinal degenerations and even systemic ophthalmopathies like diabetic and hypertensive retinopathies. Hence an attempt has been made to understand the etiopathology of *timira* in the context of Diabetic retinopathy. # ETYMOLOGY OF *TIMIRA*: {#etymology-of-timira .unnumbered} *Vyutpatti*: The word Timira has been derived from the root word ‗*timi* with ‗*unadi* suffix ‗*Kirach*' to form the complete word *Timira*. The word *timi* has got the following meanings -- - Timi means loss of light perception.^44^ - Timi means increase of watery substances in the eye.^45^ In *Amarkosha*, the meaning of *timira* is darkness.^46^ In *Halayudha kosha*, *timira* means darkness whose enemy is sun.^47^ From this etymological derivation it is clear that *timira* 'means loss of light perception or darkness or blindness but this stage is last in *timira roga*. Thus, the nomenclature of this disease is made on the basis of its grave sequalae which follows if left untreated. ETIOLOGY OF *TIMIRA*: Etiological factors in general mentioned for all eye diseases are also considered as the causes of *timira*. This disease has been mentioned as a symptom or sequalae of some diseases in *Ayurvedic* texts. Thus, *timira roga* varies from symptom to a full-established disease. Acharya Charaka has broadly classified the causes as misuse, overuse and disuse of the senses and has regarded as ―Volitional transgression ^49^. He has specified *timira* as one among the complications of *Grahani roga*. 50 The unctuous nasal medication causes dimness of vision (*Timira*) in the case of persons greatly afflicted with fever or grief and also in those addicted to wine. *Vagbhata* has termed the causes of eye diseases as *achakshushya* or unhealthy food and activities affecting the eyes. He has confined the initiation of pathology to pitta dosha.51 Acharya Harita dictates the intake of *ushna, atikshara* and *katu* food items, injury, looking at fine objects as the causative factor of eye diseases .^52^ In Bhela Samhita, constipation and suppression of natural urges have been considered as the factors responsible for timira .^53^ In *Netra Prakashika, Pujyapada* *Muni* has considered excessive or deficient oil bath, working with shaking hand, witch craft, drug addiction, heavy weight lifting, looking at illuminous objects like sun, gems, gold or hot iron etc. as the factors responsible for eye diseases. He has also mentioned *granthi* and *meharoga* as causes of eye diseases.^54^ *Dalhana* has mentioned *avak* and *uchrita shira shayana* i.e, sleeping with the head at a too low or too higher level, *ritu* *viparyaya, jvaropatapa* as some of the causes of eye diseases. 55 # SPECIFIC CAUSES OF *TIMIRA* -- {#specific-causes-of-timira .unnumbered} 1. *Prathisyaya*(Rhinosinusitis)- *Andhya* (blindness) and severe eye diseases (may be *timira*) results as a complication of *pratishyaya* .56 2. Excessive bloodletting- Excessive blood loss results in blurring of vision and errors of refraction .^57^ 3. Injury to vital parts- Trauma to *avarta* and *apang marma* may lead to loss of vision either complete or partial.^58^ # *SAMPRAPTHI* -- {#samprapthi .unnumbered} The pathological events of *timira* begin with the increment of doshas at their respective sites. In reference to *samprapti* of *timira*, Sushruta Samhita has clearly stated that when doshas gets excessively vitiated internally, pervades the *siras* (vessels) and gets lodged in the first *patala* of *drishti*, the patient sees all the objects as blurred. *Dalhana* opines that the word ‗*Sira*' denotes here ‗*Rupavaha Sira'* and *drishti* indicates inner part of the *drishti*. The lodgment of doshas in *patalas* further prevents the functional capacity of *patalas* and lead to *avyakta* *darshana* or blurred vision. If *nidana sevana* continues, then the involvement of second and third *patalas* which lead to further deterioration of drishti; whereas in 4th *patala* affliction terminates into *linganasha* or loss of vision. From this it can be inferred that *siras* and *srotases* (vasculature and other channels of circulation) are mostly involved in progression of ophthalmopathies. Charaka states that when humors get provoked in the seats of the sense organs, they cause either the impairment or the irritation of the senses concerned .59 In context to *Pramehajanya Timira ,samanya netra roga samprapti* as mentioned by *Vagbhata* holds attention. He has emphasized Pitta vitiation producing etiological factors specific for ocular pathologies which are circulated via *siras*. *Siras* may refer to ocular vasculature --because as such; eye is the prime *indriya* which is *tejomaya* (*agneya*) and is actively in functional state. It requires continuous supply of nutrients and O2 for its proper functioning. # {#section-9 .unnumbered} # PURVA RUPA OF *TIMIRA* {#purva-rupa-of-timira .unnumbered} No specific prodromal symptoms have been mentioned for *Timira*. However, *Samanya* *poorvaroopa* of *netraroga^60^* i.e. Dirtiness, congestion, lacrimation, itching, stickiness, heaviness, burning sensation, pricking pain, redness etc. Can be considered. There may be feeling as if the cavity of the eye lids is full of painful bristles, impairment in vision or function of the eyes as compared with what they were before. As soon as the above features are seen, the intelligent clinician should regard that (eye) to have become afflicted with doshas. # RUPA OF *TIMIRA* {#rupa-of-timira .unnumbered} 1. According to involvement of Patalas. 2. According to vitiation of *Doshas* # ACCORDING TO *DOSHA* INVOLVEMENT- - - - - {#according-to-dosha-involvement--------- .unnumbered} Dominance of the particular *dosha* in the pathogenesis of *timira* also cast particular symptom complex in this disease. The symptoms according to predominant dosha are as follows -- # ROOPA: ^61^ {#roopa-61 .unnumbered} *Vataja timira* visualizes objects in abnormal or distorted way as if they are moving, hazy, black colored, views false images like spider web, hairs, flies etc. *Pittaja Timira*: like false flashes of sun, glow worm, rainbow and lightening. He views bluish and blackish colors as variegated as the feathers of a pea-cock. # {#section-10 .unnumbered} *Kaphaja Timira*: chamara or white clouds. The patient can see objects which are not excessively small, visualizes moving clouds in a cloudless sky. All still objects appear as if inundated in water. *Raktaja* *Timira*: views all objects to be of variegated colors such as dark greenish, grayish or blackish and smoky all around. *Sannipataja Timira* - In *timira* due to vitiation of all doshas together, the person views, all objects as of variegated colours, scattered (spread out images) and as having double or manifold images all around. All objects appear to possess less or more than normal parts of else as luminous. *Parimlayi Timira* -Pitta, when associated with *tejas* of *shonita*, produces the *timira* called *parimalayi*. The patient sees the landscape as yellow and visualizes as if the sun is rising. All trees appear to be interspersed with glow worms and flashes of light. # UNDERSTANDING PRAMEHAJANYA TIMIRA VIA NIDANAPANCHAKAS {#understanding-pramehajanya-timira-via-nidanapanchakas .unnumbered} - NIDANA > *[Prameha hetu kapha krit cha sarvam...^62^ chakshu. tasya viseshat > sleshmano bhayam ^63^]{.mark}* *Prameha* is to be considered as a *viprakrishta nidana* for Timira and hence all the *prameha* producing factors may also come to play in *Timira*. Among all the factors vitiated kapha dosha is to be given importance due to its influence in *pramehanidana* and its involvement in causing diseases in otherwise *agneya netra*. This indicates that qualitatively or quantitatively vitiated *kapha* can alter the normal physiology of *chakshu* and may produce visual disturbances. Common etiological factors of *prameha* and *timira*: There are some common etiological factor for *Prameha* and *Timira* which are *guru*, *snigdha* and *vidahi* in properties and are likely to increase accumulation of *kledata* in the body. *Kleda* means a state of moistness or humidity. It is formed from dietetic factors (anna rasa) later getting into circulation. In a *dravadhatu* (tissues of liquid consistency) it may indicate its altered consistency or viscous nature. Accumulation of *kleda* in the body is the prime vitiating factor for *prameha*. The pathology is similar in eyes when the accumulated *kleda* producing *abhishyanda* of *rupavahi* *srotases* there by leading to *netra rogas* ranging from a transient blurred vision to total loss of vision. Hence *achakshushya* factors by a *prameha rogi* leads to a rapid initiation of *Timira* *samprapthi* as compared to a healthy individual. Here an attempt has been made to connect both diseases in the light of *Nidanadi* *Pancha* *Roga* *pareeksha* Techniques. Some of the *nidana* of *prameha* are similar with *netra roga nidana* and most importantly the *Prameha* *Nidana* has many *achakshusya* factors. Among the *Purvarupas* of *Prameha, Maladhikya* of body or *Kayacchidra* (bodily openings) ie. excessive accumulation of unwanted products, *Upadeha* of *netra^69^* and *chikkanata* of body (sliminess)deserves special mentioning. This denotes that *Malasanchaya* in bodily fluids specially in *rasa* and *raktha* constitutes initiation of *Prameha* which is same as in the case with *Netra* *rogas* where accumulated doshas circulates via *urdhwanga siras* so as to produce diseases. Thus in a diabetic patient who is already in a kha *vaigunya avastha* ie morbid *doshic* status, the chances of *drishti rogas* ie. Visual disturbances are in its maximum. Thus it is obvious that the same non congenial factors that produced *Prameha* can also lead to Timira as one among the complications in due course if necessary interventions are not done so as to prevent its progression/reverse its pathogenesis. # {#section-11 .unnumbered} # SAMPRAPTI OF *PRAMEHAJANYA* *TIMIRA* {#samprapti-of-pramehajanya-timira .unnumbered} Before manifested as a full-fledged disease, certain series of pathological events took place which are grouped under *Sampriti*. The normal route of disease initiation in general is as follows70. *Vitiated doshas* *dhatus* *malas* *malayanas* *Upatapa/upaghata* of the concerned *asaya* structural or functional loss. These morbid doshas are circulated via *srotases* by *vyana vayu* which lodges doshas in sites of *srotovaigunya* (sites of structural imbalance). *Srotas* corresponds to all channels of circulation irrespective of the material circulated through it because filling, circulation and perfusion are all attributed to *srotases*. *Srotas* is the channel of circulation for *parinamitha* *dhatu*.ie..*rasa* to *raktha*,*mamsa* and so on.it carries both *malarupi* and *prasada rupi* *dhatus* and gives nutrition to corresponding *sthula* *dhatus* which constitutes organs 71 . *Sroto* *vaigunya* refers to the existence of a co-morbid state in the body that may aggravate or initiate the disease processes. *Kleda* plays an important part in *prameha samprapti* which is mostly formed due to *kleda* from *ahararasa. Kleda* in the body (in dhatus and their channels) is of *guru, snigdha,manda,hima* and *slakshna* properties)Accumulation of *kleda* alters structural and functional integrity of dhatus *adhya* dhatus rasa and *raktha* leads to *abhishyanda*,the basic pathology of *sarva netra rogas*. Kapha is main dosha involved in *samprapti* of Prameha. When kapha gets vitiated due to *nidana* *sevana*, it affects many *dushyas* in the body like *meda, rakta, shukra, ambu*, *vasa, lasika, majja, rasa, oja* and *mamsa* which all are *drava dhatus*. *Kapha dushita rakta* leads to *kledata* in *rakta.* Also *dhamani prathichayatwa* is a *nanatmaja vikara* of kapha that may correspond with narrowing of vasculature due to atheromatous deposition. This results in *malasanchayatva* -- kapha as a mala- or in other words; accumulation of metabolic bye-products which is later clinically visible as exudates in fundus findings. After *dosha dushya sammurchhana*, when *prameha* remains untreated it can lead to *Madhumeha* which further lead to *daurbalya* of *rasayanis* (lymphatic channels, blood vessels and microcapillaries) in the whole body affecting various organs. *Rasayani* *daurbalya* has been detailed by *Acharya Dalhana* while commenting on *Prameha pidaka chikitsa*. It is said that in the *poorvaroopa avastha* of *vyadhi*, treatment should be *apatarpana*, *vanaspatikashaya* and *vasta mutra*. If this treatment is not followed, then there is increased *maadhurya* in mutra, *sweda* and *sleshma* which leads to development of *roopa avastha* i.e *Prameha vyadhi*. In this stage of *vyadhi, ubhaya* *samshodhana* should be done. If it is not performed, the doshas vitiate more and cause dushti of Mamsa and Rakta dhatus, due to which shopha and other complications of *Prameha*^72^ like *Prameha pidika* occur. While interpreting this, *Dalhanacharya* has given a beautiful description regarding how the pathogenesis gets aggravated to further stages in the absence of any intervention. From the initial stages if *nidana* seva is continued, it causes *madhurya* to *dravadhatus*. This may be regarded as increased glucose level in blood causing glycosylation of vascular membrane protein finally leading to loss of structural integrity. This may hamper autoregulation of retinal arterioles due to vasoconstrictory effect by atheromatous deposition against vasodialatory effect as stated by metabolic theory of autoregulation. Chronic hyperglycemia may also cause pericyte functional loss, increased thickening of Basement membrane and increased formation of advanced glycation end products (AGEs) all leading to reduced blood flow and altered permeability. At this stage, whole body purification is indicated especially *virechana* which causes *dravadhatu soshana* and mala *nirharana*. Lack of proper intervention in this stage produces *shopha* or accumulation of metabolic bye-products and exudates (*rakta* and *mamsa* vitiation), which indicates deeper tissue involvement. From this stage onwards, *Vranachikitsa* especially the first 11 *upakramas* to be followed. This indicates that from an edema type of *samprapti*, it will get turned to *vruna* or micro ulcers which is nothing but hemorrhages and following Neo-vascularisation. This picture is seen in the pre and proliferative stages of DR. Thus the entire sequence of pathological events in Diabetic Retinopathy seems to be similar as explained in our texts also. The DR pathology involves both microvascular occlusion and leakage type. The occlusion type which is due to pericyte loss, endothelial cell damage etc. leading to retinal hypoxia and ischemia resulting in AV shunts, neovascularisation and ultimately haemorrhages may be correlated to a *dhatukshayajanya samprapti* constituting *Pandu* and *Raktapitta* in near future. On the other hand, leakage due to breakdown of BRB causing altered permeability leading to edema, microaneurysms and accumulation of Hard exudates may be related to *malasanchaya* and srotorodha type of pathogenesis finally ending to a Pandu-Shopha spectrum. Thus as mentioned in our texts, there can be two types of *sampraptis* for *prameha* as well *tadjanya* timira viz *avarodhajanya* and *kshayajanya* If the DR pathology is analyzed properly in ayurvedic perspectives it possesses all the four features of *srotho vaigunya* i.e., *Atipravritti*, *Sanga*, *Siragranthi* and *Vimarga gamana.* Sanga is manifested by the retinal vessels occlusion, *Siragranthi* is nothing other than development of microaneurysms, Vimargagamana is the retinal haemorrhages and *Atipravritti* can be correlated to the Neovascularization where new vessels are formed. *Samprapti Ghatakas*: *Dosha\-- Tridosha* with *Raktha. Pitta-Kapha pradhana* *Dushya \-- Rasa, rakta, mamsa, meda, majja, lasika, vasa, oja* *Agni \-- Jataragni dusti* leading to *Rasa-Raktha-Medoagni dushti* Ama \-- Jataragni and Dhatwagni mandyajanya *Srothus* \-- *Rasavaha-Raktavaha-Mamsavaha-Medovaha-Udakavaha* *Srothodusti Prakara* \-- *Sanga, Siragranthi, Vimargagamana, Atipravritti Udbhava sthana \-- Amashaya* *Sanchara sthana \-- Rasayan*i (Microvasculature) *Vyakta sthana \-- Drishti (*Retina) *Roga marga \-- Madhyama* *Roga* *marga* as *Shiras* is *pradhana marma*. *PRAMEHAJANYA TIMIRA* viz --a --viz DIABETIC RETINOPATHY. 1. The term *Timira* means excess accumulation of *kledata*. DR is also characterised by excess accumulation of *kledata* in *rasayanis* & is manifested in fundus in the form of exudates. 2. Blurring of vision may be the only presenting symptom of DR, the *Timira* also gives the same meaning. *Timira* with different dosha predominance can be compared to different stages of DR. +-------------------------------------+--------------------------------+ | ***TIMIRA LAKSHANA*** | **DR SYMPTOMS** | +=====================================+================================+ | *1.Vyaviddamiva pasyati^73^* | 1\. Hazy, spotty, blurry | | | vision in NPDR & | | | | | | PDR. | +-------------------------------------+--------------------------------+ | *2.Jalanike | 2\. Spider web appearance | | shanmashakanRashminchopekshite^74^* | caused by floaters in (PDR | | | with VH). | +-------------------------------------+--------------------------------+ | *3.Aditya khadyotha pasyati ^75^* | 3\. Flashes of light(in PDR) | +-------------------------------------+--------------------------------+ | *4.Pasyed sukshmapytyrthaha* | 4\. Difficulty in reading or | | | seeing close | | | | | | up.(in DR with CSME) | +-------------------------------------+--------------------------------+ | *5.Dhoomadhoomranichekshathe...* | 5\. Blackish and smoky vision. | +-------------------------------------+--------------------------------+ | *6.Raktani tamansi | 6\. Erythropsia.(DR with VH) | | vividhani...chekshate..* | | +-------------------------------------+--------------------------------+ Hence Diabetic Retinopathy can be compared to *Timira* involving *Dwitiya* and *Tritiya Patalas*. *SADHYA-ASADHYATA* *Pramehajanya* *Timira* is easily curable when the *Doshas* are limited to first and second *Patala*; As it gets the stage of chronicity, becomes *Yapya* by the *dushti* of third *Patala*. Timira attains the incurability when the *Doshas* reach fourth *Patala* where in surgical intervention is advocated as in case of *Kaphaja Linganasha*. DR being an *upadrava* of *Prameha*; is *Yapya* for *chikitsa*. Similarly *Timira* with its *ashraya* *sthana* in *Dwitiya Patala* (Early stages of DR) becomes *sadhya* for *chikitsa* provided along with *Timira* management, if *Prameha* is also treated. If timira takes *ashraya* in Tritiya *Patala* (Advanced stages of DR) becomes *Yapya* for chikitsa. # *CHIKITSA* {#chikitsa .unnumbered} Management of *Timira* can be broadly classified into two ways- 1. Prophylactic 2. Curative -- a) Local b) Systemic ```{=html} ``` 1. Prophylactic measures: One who takes regularly old ghee, *triphala*, *shatavari*, patola, mudga, amalaka and barley should not be afraid of severe *timira*. Simply *payasa* made of *shatavari* or amalaka or barley boiled with plentiful decoction of *triphala* and added with profuse quality of ghee alleviates timira.^76^ Also advocating various measures told in daily regimens to protect Urdhwajatru *srotases* --viz Anjana, Nasya, Abhyanga, Karnapoorana etc. prevents the occurrence of *Timira* and related disorders. 2\. Curative *^77^* Systemic: *Shodhana chikitsa- Virechana* is said to be ideal for *anulomana* of *doshas* Specially *vitiated pitta*, as eye is the site of *Alochaka Pitta dosha*. Local: local measures include *tarpana, putapaka, seka, ascyotana and anjana*. Samanya chikitsa of Timira ^80^ In the six diseases which are palliable, blood-letting should be performed by vene puncture; the patient should also be purgated with old ghee processed with purgative drugs. Oleation, blood-letting purgation, nasal medication, application of collyrium, *murdha* *basti*, *basti kriya, tarpana, lepa* or application of paste and *seka*, administered many times suitable to the doshas is the general treatment of *timira*.79 *Sushrutha Samhita* says generally all disorders of eye produced by *abhishyanda* & its causes and as such it should be treated quickly. Hence general line of management of *Abhisyanda* can also be incorporated in treatment of *Timira*.80 # MANAGEMENT PRINCIPLES FOR *PRAMEHAJANYA TIMIRA* {#management-principles-for-pramehajanya-timira .unnumbered} Analysis of *samprapthi* of DR on ayurvedic concepts, clearly explains the need for *samprapthi* *vighatana* at various levels to manage DR. Complications of DM originate with specific cellular responses to their environment. The cellular environment is determined by serum factors modified by glucose levels, which are abnormal in DM. The cells involved are those that make up the microvasculature; these are the capillary endothelial cell and the associated pericytes. Other factors like increased cholesterol, anaemia etc. also have their role in disease causing and progression. Hence along with *Prameha samprapthi vighatana* *chikitsa*, incorporation of *Kapha-Pittaja* *Timira* line of management in different stages will help in reversing the retinopathy. Based on *samprapthi*, BDR can be managed by exploring the following treatment principles--- 1. *Pramehahara* (reducing blood sugar level + other features of diabetes mellitus.) 2. *Kledahara* (removing the viscosity and stickiness of blood and its components) 3. *Raktavahasrothodustiharana --raktaprasadana* (improving blood quality) 4. *Rakta*-*Pittahara* (reducing leakage from channels and healing hemorrhages) 5. *Vatanulomana* (maintaining the normal circulatory flow) 6. *Pandu-Sophahara* .(reversing ischemia and oedema) 7. *Rasayanachikitsa*. (rejuvenation of tissues) Hyperglycemic control is the initial and prime step; even though it won't prevent DR occurrence, but delays its onset, progression and conversion to proliferative stage and edema. # GENERAL STAGEWISE TREATMENT PROTOCOLS IN DIABETIC RETINOPATHY. {#general-stagewise-treatment-protocols-in-diabetic-retinopathy. .unnumbered} *Acharya Vagbhata* says to treat the Timira after properly analysing the involvement of the *Dosha-Dushyas* In the Initial stages of DR (Background Retinopathy)---*Shodhana, Pathya, Shamanoushada, Ropana chikitsa, Anjana, Takradhara* and *lepa, Drishti bala nasya* with *Bhringaraja swarasa* mixed with *tilataila* or *akshataila* in iron vessel. In acute haemorrhagic condition (NPDR) *--- Stambhana, Ropana chikitsa, sirodhara , sirolepa, Talam, Bidalaka, Aschotana, Seka, Shamanoushada and abhisyanda chikitsa*. In the third stage (PDR) --- *Tridoshashamaka, Ropana chikitsa, Rasayana chikitsa, Anjana, Tarpana, Shamanoushada.* # PATHYA-APATHYA AHARA: {#pathya-apathya-ahara .unnumbered} Pathya81: *Purana ghrita, triphala, shatavari, patola, mudga, amalaki, yava, lohita shali,* whole grains like *yava* and *godhuma,* Cooked vegetables of jivanti, sunishannaka, tanduleeya, vastuka, chilli, mulaka, meat of birds and wild animals, karkotaka, karavella, vartaka, karira, shigru, tarkari. *Yogaratnakara* adds-^82^ *peya, vilepi, tiktha and laghu ahara, shalitandula, godhuma, saindhava, goghritha, gopaya, sitha, kshoudra, draksha, kustumburu, surana, naveena mocha, matsyakshi, punarnava* to the above. (Y.R.N.R. Chi sl.1-4 p.395) *Apathya*: *Masha, aranala, katuthaila, patra shaka, matsya, dadhi, phanita, vesavara, pinyaka (oil cake), virudhaka* (sprouts), *ambupana*, *madhukapushpa*, *sura*(alcohol), *ajangalamamsa*, *tambula*, food and drinks which are *amla, lavana, vidahi, teekshna, katu, ushna* and *guru.* # VIHARA: {#vihara .unnumbered} *Pathya*: *Manaso nivritti* (withdrawing the mind from objects of senses.), *padabhyanga, sita jala prakshalana* etc*.,* *Apathya*: *Krodha, shoka, maithuna, vata, vinmutra, nidra, vami, vegavarodha, sukshmekshana (looking at minute objects), snana, atapa, prajalpana (excessive talking), chardana.* (*AOUSHADA*) MEDICATION: *Pathya: Anjana, nasya, padapuja* (anointing, using foot wear etc), *rudhirasriti* (bloodletting), *vishuddhi* (purificatory therapies).84 *Yogaratnakara adds- aschyotana, langhana, sveda, pratisarana, prapoorana, shastrakriya*, and *lepa* to the above. > **Pathology Of Diabetic Retinopathy --Pramehjanya Timir.** > > Diabetes mellitus has in recent times, gained importance as one of the > most common, > [non](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/non-communicable-disease) > [communicable > disease,](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/non-communicable-disease) > which contributes to death and disability worldwide. Diabetes affects > almost all aspects of intermediary metabolism and is also associated > with accelerated ageing of the cardiovascular system. Hence diabetes > is best defined as a metabolic cum vascular syndrome of multiple > etiologies characterized by chronic > [hyperglycemia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hyperglycemia) > with disturbances of carbohydrate, fat and protein metabolism > resulting from defects in insulin secretion, insulin action or both, > leading to changes in both small blood vessels (microangiopathy) and > large blood vessels (macroangiopathy) and which is often associated > with long term damage, leading to malfunction and failure of various > organs like eyes, kidneys, heart, nerves and blood vessels^1^. > > [Diabetic > retinopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-retinopathy) > is a chronic progressive, potentially sight-threatening disease of the > retinal microvasculature associated with prolonged hyperglycemia and > other conditions linked to diabetes mellitus such as hypertension, > [hyperlipidemia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hyperlipidemia) > and > [proteinuria](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/proteinuria) > etc.^2^ Almost all the patients with [Type I > diabetes](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/insulin-dependent-diabetes-mellitus) > develop > [retinopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/retinopathy) > in about 15 years. In those with [Type II > diabetes,](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/non-insulin-dependent-diabetes-mellitus) > the risk of DR increases with the duration of diabetes, accompanying > hypertension and smoking. Diabetics have a 20--25 times greater risk > of blindness as compared to the normal population^3^. As far as the > working class or industrial areas are concerned Diabetic Retinopathy > is 2nd leading cause of blindness in working age group (\<55 years > old) in industrialized countries^4^. > > Diabetic Retinopathy (DR) is one of the major complications of > diabetes mellitus. It is a leading cause of blindness in developed as > well as developing countries. According to VISION 2020 (Working > together to eliminate avoidable blindness) up to 80% of the world\'s > blindness is avoidable. Avoidable blindness is defined as blindness > which can be either treated or prevented by known, cost-effective > means. Although there are many other causes of [vision > impairment](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/visual-impairment), > VISION 2020 seeks to address the main causes of avoidable blindness, > in order to have the greatest possible impact on vision loss > worldwide. Diabetic retinopathy is one among the target diseases for > VISION 2020^5^. > > The prevalence of DR, [proliferative diabetic > retinopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/proliferative-diabetic-retinopathy) > (PDR), [diabetic > macular](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-macular-edema) > [edema](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-macular-edema) > (DME), and VTDR (Vision threatening Diabetic retinopathy) among > individuals with diabetes is 34.6%, 7.0%, 6.8%, and 10.2%, > respectively. Estimate shows that the number of people with DR will > grow from 126.6 million in 2011 to 191.0 million by 2030, and the > number of people with VTDR will increase from 37.3 million to 56.3 > million, if no urgent action is taken^6^. > > Innovative alternative therapies and comprehensive approaches are > needed to reduce the risk of vision loss by prompt diagnosis and early > treatment of Vision Threatening DR (VTDR). > > After viewing the magnitude of the problem of the disease, a > comprehensive and thorough analysis of all the important literature of > both modern and Ayurveda was done and online sources are searched to > establish a probable etiopathogenesis of the disease on Ayurvedic > prospective. Though there are no direct references are available > regarding *Madhumeha/Prameha janya Timir*, enough evidences are > available in all leading treaties of Ayurveda, which substantiate that > *Timir* can be a complication of *Madhumeha*. In this review study > many aspects of basic concepts of Ayurveda were analyzed to find out > the probable etiology and pathogenesis of Diabetic retinopathy with > probable correlation of different stages of the disease with different > types of *Timir* described in Ayurvedic literature. 2. ***Samprapti* (pathogenesis) of diabetic retinopathy** # Role of *Raktapitta* In Manifestation Of Diabetic Retinopathy > Diabetic > [retinopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/retinopathy) > basically a *Dristipatalagata roga* is mainly attributed to *Sira > srotasabhisyandam* and *raktavaha sroto dusti* due to a variety of > *Achakshyushya ahara* and *vihara karanas* especially in *Prameha* > patients. In order to understand the *samprapti* of [diabetic > retinopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-retinopathy) > in Ayurveda, general *samprapti* of [eye > disease](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/eye-disease) > must be considered. *Nidana* of endogenic eye diseases are mainly > *Achakshyushya* factors which vitiates *Pitta*. The vitiated *Pitta* > in turn vitiates the *Pitta vaha srothas*. Due to interconnection of > *Pitta* and *Rakta*, which shares *Ashrya Ashrayee bhava,* the > *raktavaha srotas* is also gets vitiated due to *Pitta* vitiation. As > the *nidana* factors are *Achakshyushya*, the vitiated *pitta* and > *rakta* have an affinity towards penetrating the eyes. Hence the > vitiated *dosha* move towards the eyes through *Jatroordhwa srotas* > and finally gets confined to the eyes, there is a stage when the > *Sirasrothas* are deeply involved which is known as *Sira > abhisyanda*^7^. The whole pathology of diabetic retinopathy which > starts with *stroto dusti of Raktavaha strotas* manifested as > [microangiopathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/microangiopathy) > in the form of *Attipravriti, Sanga* and *Granthi* as > [haemorrhages,](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/bleeding) > exudates and venous beading in diabetic retinopathy respectively. > > In this context of *Siroabhisyandam* in eye diseases the *Ashraya > sthana* is *Strotas*, affected *dhatu* is *Rakta* and vitiated *dosha* > is *Pitta*. *Prameha* brings out changes in the *dristipatalam* which > greatly affects vision. In the initial stage, the etiological factors > promote *utklesha* in the vessels which causes changes in the > permeability of the vessels > > especially of head region which is the basic pathologic change for the > development of eye diseases. If the stage of *Sira abhisyanda* > continues it spreads to *netrasrotas* and the same vascular changes > takes place in the vessels of eye, because *Achaksyushya* factors > always have affinity towards the > [ophthalmic](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/agents-acting-on-the-eye) > tissues. In the stage of *netraabhisyandam*, if there is further > vitiation of *Pitta dosha*, the condition further aggravates and will > be confined to *Dristipatalam*. > > Few predisposing factors also influence the development of eye disease > associated with prameha. These include- 1. *Pittaprakritti* of the > patient. 2. Hereditary factors 3. Pitta Kapha predominant season, > foods and psychological stress factors like *krodha, shoka* etc., > which contribute towards vitiation of *Pitta*. Vitiated *Pitta* > reaches and amalgamated with *Rakta dhatu* due to similar properties. > All these factors altogether promote prominent changes in the vessels > of *Dristipatalm*. The texture of the vessels is damaged and hence the > permeability increases. This results in leakage and hemorrhages from > the blood vessels. The blood oozes out like sweat. This again > correlates with pathogenesis of *Rakttapitta*, specially quoted by > *Charaka*. Due to lack of circulation there is localized > [hypoxia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hypoxia) > which results in development of new vessels. As these vessels are > fragile they > [bleed](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/ciclonicate) > easily. Exudates formation, > [neovascularization](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/neovascularization-pathology) > and proliferation of the tissues which leads to degenerative changes > in the retina. In this context *Urdhwaga Raktapitta* can be correlated > with Diabetic Retinopathy, as the seat of *Urdhwag Raktapitta* are all > the seven natural openings of the head. And in eye, as the vessels are > minute and due to *achakshyushya* factors the vessels of > *dristipatala* or retina are affected mostly. 1. ***Avaranajanya*, *Dhatukshyajanya Timir* and diabetic retinopahy** According to *Vagbhata*, *Madhumeha* is chronic progressive stage of *Prameha* and of two types: *Avaranajanya* and *Dhatukshyajanya*^8^. *Madhumeha* is *Vataja* type of *prameha* and *Vata* can be aggravated by two ways i.e. *Avarana* and *Kshaya*^9^. *Avritta vatajanya madhumeha* is *krichhrasadhya* and *dhatukshyajanya madhumeha* is *asadhya* (incurable). As per charak "*prameha anusanginam*" means diabetes is concomitant in nature. Thus diabetes remains always present with its complications. Due to both *avarana* and *dhatukshya* all the ten *dushyas* goes into state of depletion and produce symptoms according to the seat of that particular *dhatu*. In the case of Diabetic retinopathy main affected *dhatu* is *Rakta dhatu*, though all the *dhatus* gets affected and *srotas* affected are *Raktvaha*, *mamsavaha* and *medovahasrotas* mostly. 1. Avarana ```{=html} ``` A. ***Pranavritta vyana***: *Pranavayu* acts like a controller. It is responsible for *Adana karma*. Sense organs perceive their objects with the help of *Pranavayu*. *Vyanavayu* is responsible for gati or conduction. Hence *vyanavayu* plays a significance role in *Rasavikshepana*. Conduction is not only related to cardiac cycle but all types of neural conduction should be considered. Whenever the controller *Pranavayu* will restrict the gati of conducting *vyanavayu*, the *Indriya* will not be able to perceive its *vishaya*. It may happen in one *Indriya* (homonymous) or in all *indriyas* (heteronymous) together. If it happens in all indriyas it can be compared with the vegetative stage or deep coma. *Rasa-Rakta vikshepana* (blood circulation) is function of *vyanavayu*. In case of diabetic retinopathy vascular disorder may arise due to *Pranavritta vyana*. This initially causes [retinal](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/retina-ischemia) [ischemia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/retina-ischemia) and followed with successive cascade of retinopathic changes like neovascularisation, cotton wool spots and intra retinal microvascular abnormalities (IRMA). Early break down of blood retinal barrier (BRB), hard exudates formation and [macular](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/macular-edema) [edema](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/macular-edema) are other symptoms to follow. Symptoms of *Pranavritta vyana* are *Sarva indriya shunyata*, *smriti kshaya* and *bala kshaya* and the treatment is *Urdwa Jatrugata cikitsa^10^* can be employed to relieve the [signs and symptoms](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/physical-disease-by-body-function) of Diabetic Retinopathy. ## B. *Raktavritta vata*: Etiologies explained in *vidhisonitiya adhyaya* of *Charak Sutrasthan* are responsible for quantitative increase of *Rakta dhatu*, which impedes the movement of *Vata dosha* hence normal circulation is hampered and stagnation takes place leading to *Sanga* of *Raktavaha srotas*. Symptoms of *Rakatvritavata* are: *Twakmamsa antarajadaha* and *Raktayukta shotha mandala^11^* This type of symptoms can be correlated with general [neuropathy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/neuropathy); *Raktayukta shotha mandala* can be correlated with splinter haemorrhages and IRMA as [retinal edema.](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/retina-edema) Most of the etiological factors responsible for *Raktaja vyadhi* have similarity with *madhumeha* and *prameha* etiological factors. *Akshiragam*, *Tamasyatidarshanam* and *Raktapitta* are described as *Raktaja vyadhi* in *Charak samhita*. These can be correlated with [vision defects](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/visual-impairment) in diabetics due to microvascular complications. In diabetic retinopathy though initially *Raktakshya* and [ischemia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/ischemia) occur but later on blood circulation increases, which lead to haemorrhages and exudative features. Treatment of *Raktavritta vata* should be done as per *Vataraktachikitsa^12^* to normalize the movement of obstructed Vata dosha. - And *Charak* has mentioned *Basti* as the best treatment for *Vatarakta^13^* Thus *Basti* (therapeutic enema) treatment can be administered in this type of pathological symptoms of Diabetic Retinopathy. 1. Dhatukshaya A. ***Shirasaithilya***^14^ is one of the major signs of *raktakshaya* as per Sushruta. Loss of pericytes and formation of [microaneurysms](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/microaneurysm) are earliest signs of Diabetic Retinopathy. These can be correlated with *Sirasaithilya* due to *Raktakshaya*. First *Patala* consists of *rasa* and *rakta dhatu*, so manifestation of the disease is in the form of microaneurysms and less severe in nature, which are very similar to background Diabetic retinopathy or mild NPDR and symptoms of 1st *Patalagata Timir* appears in this stage. If *Raktakshaya* persists for long time, it may lead to hypoxia related neovascularization in Diabetic retina. ## B. ***Dhamanisaithilya^14^*** is one of the features of *mamsakshaya*. This can be correlated with endothelial cell loss due to improper apoptosis and loss of capillaries, leads to early break down of blood retinal barriers and signs like dot/blot or flame shape hemorrhages appear in this stage. As 2nd *patala* consists of *sookshma rupi* [mamsa](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/amsacrine) *dhatu*, symptoms of 2nd *patalagata timir* seen in this stage. This stage may be correlated with mild NPDR or moderate NPDR depending upon the extent and severity of affected *dhatu*. ## C. > ***Sandhishunyata^14^*** is another feature of *medakshaya*, which may > be correlated with junctional cell protein loss or cell adhesion > defects and break down of BRB. Appearances of macular edema and > exudates formation are prominent signs in this stage. 3rd *patala* > consists of *Meda dhatu* and when *dhatu kshaya* reaches the 3rd > patala symptoms of 3rd *patalagata timir* appears. On severity point > of view this stage may be correlated with Moderate NPDR based on the > extent of dhatu affected. 4th *patala* of *dristipatal* is > *asthyasrita* in nature and loss of *asthi* and *majja dhatu* leads to > symptoms of 4th *patalagata timir*. ## D. > ***Timiradarshana*** is one of the symptoms of *majjakshaya^15^* and > thus leads to Vata kshaya. Depletion of marrow tissue leads to > decrease in blood cells formation and results in hypoxic condition of > retinal neurons. [Axonal > degeneration](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/nerve-fiber-degeneration) > of retinal nerve fibers occur due to *Vata kshaya*, which may be > correlated with hypoxia and this hypoxic axonal degeneration leads to formation of cotton wool spots or soft exudates in severe NPDR stages of Diabetic retina. In latent stages when *Sukradhatu* gets affected signs of paleness of retina and [optic](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/optic-nerve-atrophy) [atrophy](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/optic-nerve-atrophy) appears as *Panduta* is one of the features of *sukrakshaya^16^* In this stage the disease becomes incurable and this proves the hereditary and [genetic predisposition](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/genetic-predisposition) nature of diabetic retinopathy. > When *Avarana samprapti* is continued for longer period, it will > attain *dhatu kshaya avasta* and *dhatukshayaja samprapti* will > continue in further stages of disease process. Again due to > *Dhatwagnimandya* improperly formed *Rasa dhatu* in inadequate form is > released, which leads to successive *Anulomajanya Dhatu kshaya*. Here > *Dhatu kshaya* indicates the *sookshma/poshak dhatu* not the > *sthoolarupidhatu*. Four internal patalas of eye are based on > functional part of *sookshma* and *asthayeedhatus*. The manifestations > of the diseases depend on th affected dosa, dhatu and srotas. These > *sookshmarupi dhatus* of *Dristipatala* in eyes gets affected easily > by the vitiated *doshas* due to either *Avarana* or *dhatukshyajanya > samprapti* alone or by combination of both. 1. ***Ama dosha* and diabetic retinopathy** *Agnimandya* at the gastric level (*Jatharagni*) and at the tissue level is well established in *Prameha* and *Madhumeha* in Ayurveda. And in *Raktaja vyadhi*, *Agnisada* is another feature according to Charak^17^ and *Rakta* is one of the *dushya* in *madhumeha*. *Dhatwagnimandya* leads to accumulation of *Ama* at the tissue level. This can be correlated with generation of [reactive oxygen species](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/reactive-oxygen-metabolite) (ROS), activation of [polyol](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/polyol) pathway and accumulation of [Advanced Glycation End products](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/advanced-glycation-end-product) (ages), which are the main pathways of development of retinopathy in diabetics. Both *Charak* and *Sharangadhar* have mentioned very profoundly about *Dhatumalas* and all these can be corroborated to *dhatwagnimandya* related *malavriddhi*. In the context of *dhatusneha parmpara* in *Grahanichikitsa*, *Charak* has described the *Prasadabhaga*, which nourishes the successive *dhatu* and *Kittabhaga*, which nourishes the three humors of the body *Vata*, *Pitta* and *Kapha*. But in *Dhatwagimandya* state, the quantities of *Malarupi dosha* are increased and create the pathological features inside the body. *Mala* of *Rasa dhatu* and *Rakta dhatu* are *Kapha* and *Pitta* respectively^18^ (This *malarupi pitta* can create Diabetic Retinopathy pathology in the presence of *pitta* predisposing factors in retina. > ***2.4 Ojas kshaya* and diabetic retinopathy-** *Madhumeha* is also > known as *Ojameha*. The vitiated dosha obstructed the path of Vata and > vata carried the *Ojas* to the basti and causes *madhumeha^19^*. > According to *Chakrapani apara Oja kshaya* occurs in *madhumeha* and > the seat of Apara Oja are ten *Mahamula dhamanis*. Loss of *Oja* leads > to loss of *dhamanis* as per *ashrayaashrayeesambandha*. This can be > correlated with loss of capillaries and thus due to *Ojakshyaya* > abnormal apoptosis can enhance, leads to loss of capillaries and > basement membrane thickening. Among the functions of Oja are *bahya* > and *avyantara karana* (indriya) *karma*, means motor and sensory > functions. Sushruta also mentioned *abhighata*, *shoka* (grief), > *kshaya* (*dhatukshya*), *kopa* (anger) as causes of *Ojas kshaya^20^* > . In case of diabetes along with *dhatu kshaya*, psychological stress > is another factor which plays important role in *oja kshaya*. Loss or > diminution of sensory functions including visual loss which are > prominent features *oja kshaya*. > > ***2.4-Prameha* and diabetic retinopathy** > > Among 20 *pramehas*, 19 pramehas except *Madhumeha* are almost having > renal and urinary pathology. Main pathological features of *prameha* > are: *Prabuta avilamutrata* means increase in quantity of turbid urine > in patients with prameha. > [Proteinuria](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/proteinuria) > can be correlated with *pravuta avilamutrata* ^21^. As in long run; > *prameha* is converted to *madhumeha* stage, this nephropathy signs > are mostly associated with chronic cases of diabetes. Proteinuria > leads to > [hypoalbuminemia](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/hypoalbuminemia) > and this decreases serum osmolarity ^22^, which again leads to salt > and water retention in extracellular space of retina. This may be > another cause of [diabetic > macular](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-macular-edema) > [edema](https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/diabetic-macular-edema) > and retinal edema in general. # Visual symptoms of *timir* and diabetic retinopathy > Diabetic Retinopathy can be compared to *Timira* involving all the > four *patalas*. Patalas are described on the basis of functional > composition of *dhtaus* of *dristi*. The symptoms of vision are > manifested when the vitiated *dosha* afflicting the concerned *dhatu* > in *dristi patalas*. All the three *dosha* in single or in combination > can affect one or more *patalas* of *dristipatala* (Retina) **Shatkriyakala in Diabetic Retinopathy** **1. Sanchaya Avastha (Stage of Accumulation)** In the initial stage, continuous indulgence in Madhura ahara (excess sweet food), sedentary lifestyle, obesity, stress, and improper dietary habits lead to accumulation of Kapha and Meda. Along with this, Pitta and Vata also begin to get vitiated gradually. Due to Agnimandya and deranged metabolism, subtle changes occur in Rakta dhatu and microvasculature. Clinically, patients may remain asymptomatic or complain of mild blurring of vision, eye heaviness, fatigue, dryness of eyes, or occasional headache. **2. Prakopa Avastha (Stage of Aggravation)** Persistent hyperglycemia aggravates the vitiated doshas, especially Kapha and Pitta. Rakta dushti becomes more prominent and causes impairment of retinal microcirculation. Increased vascular permeability and endothelial dysfunction start developing. Symptoms such as intermittent blurring of vision, eye strain, burning sensation in eyes, excessive lacrimation, and difficulty in focusing may appear. At this stage, retinal damage is still minimal and reversible with proper intervention. **3. Prasara Avastha (Stage of Spread)** The aggravated doshas spread through Raktavaha srotas and localize in the delicate retinal vessels. Vata facilitates the movement of vitiated Pitta and Kapha towards ocular tissues. Microaneurysms, capillary leakage, retinal edema, and ischemic changes begin to occur. Patients may experience fluctuating vision, floaters, diminished night vision, and occasional visual distortion. This stage represents the spreading pathology affecting retinal circulation. **4. Sthanasamshraya Avastha (Stage of Localization)** The vitiated doshas localize in the weak and susceptible retinal tissues (Drishti mandala). Due to Khavaigunya in retinal microvasculature caused by chronic diabetes, structural retinal damage becomes established. Capillary basement membrane thickening, hemorrhages, exudates, and retinal edema may be seen. Clinically, patients complain of persistent blurred vision, difficulty in reading, dark spots before eyes, and impaired color perception. This stage corresponds to early non-proliferative diabetic retinopathy. **5. Vyakti Avastha (Stage of Manifestation)** At this stage, diabetic retinopathy becomes clinically evident with characteristic retinal manifestations. There is significant Rakta and Pitta dushti leading to hemorrhages, cotton wool spots, macular edema, and retinal ischemia. Vision becomes markedly affected. Patients may complain of severe blurring of vision, floaters, flashes of light, or partial loss of vision. Ophthalmoscopic examination confirms diabetic retinopathy. **6. Bheda Avastha (Stage of Complication/Differentiation)** This is the advanced stage where complications develop due to chronic retinal ischemia and neovascularization. It corresponds to proliferative diabetic retinopathy and advanced diabetic eye disease. Vitreous hemorrhage, retinal detachment, neovascular glaucoma, and irreversible blindness may occur. Severe degeneration of retinal tissue and permanent visual impairment are seen if untreated. Correlation with Modern Medicine **Shatkriyakala Stage - Diabetic Retinopathy Changes** Sanchaya - Metabolic imbalance, insulin resistance, microvascular susceptibility Prakopa - Retinal endothelial dysfunction and vascular permeability Prasara - Spread of retinal microvascular damage and edema Sthanasamshraya - Localization in retinal vessels with NPDR changes Vyakti - Clinically manifest diabetic retinopathy Bheda - Proliferative diabetic retinopathy and complications **Etiological Factors:** (Improper diet, sedentary lifestyle, obesity, chronic hyperglycemia) ↓ 1\. Sanchaya Avastha (Accumulation Stage) • Kapha, Meda accumulation • Agnimandya and metabolic imbalance • Mild visual fatigue / asymptomatic stage ↓ 2\. Prakopa Avastha (Aggravation Stage) • Aggravation of Kapha-Pitta dosha • Rakta dushti and endothelial dysfunction • Intermittent blurring, burning sensation ↓ 3\. Prasara Avastha (Spread Stage) • Spread through Raktavaha srotas • Retinal microvascular damage begins • Floaters, fluctuating vision, retinal edema ↓ 4\. Sthanasamshraya Avastha (Localization Stage) • Localization in retinal microvasculature • Microaneurysms, hemorrhages, exudates • Persistent blurred vision ↓ 5\. Vyakti Avastha (Manifestation Stage) • Clinically evident diabetic retinopathy • Cotton wool spots, macular edema • Severe blurring of vision ↓ 6\. Bheda Avastha (Complication Stage) • Proliferative diabetic retinopathy • Vitreous hemorrhage, retinal detachment • Irreversible vision loss/blindness # **MODERN REVIEW OF LITERATURE-** {#modern-review-of-literature- .unnumbered} # Anatomy and Physiology of Retina {#anatomy-and-physiology-of-retina .unnumbered} Retina, the inner most tunic of the eyeball, is a thin, delicate and transparent membrane. The term retina (Latin; rete = net) in the most comprehensive sense includes all structures derived from the optic vesicle namely, \_ Sensory layers of the retina. \_ Pigmented epithelium of the retina, \_ Epithelial lining of the ciliary body and the iris. Embryology of Sensory Retina1 The retina develops from a diverticulum of the forebrain (proencephalon). Optic vesicles develop which then invaginate to form a double walled bowl, the optic cup. The outer wall becomes the pigment epithelium, and the inner wall later differentiates into the nine layers of the retina. The retina remains linked to the forebrain throughout life through a structure known as the retino-hypothalamic tract. Retina extends from the optic disc to the Ora serrata. Grossly it is divided into two distinct regions: Posterior pole and peripheral retina separated by the so-called retinal equator. Retinal equator is an imaginary line which is considered to lie in line with the exit of the four-vena vorticose. Posterior pole refers to the area of the retina posterior to the retinal equator. The posterior pole of the retina includes two distinct areas: the optic disc and macula lutea. It is best examined by slit-lamp indirect biomicroscope using +78D and +90D lens and direct ophthalmoscopy. Optic disc. It is a pink colored, well-defined circular area of 1.5-mm diameter. At the optic disc all the retinal layers terminate except the nerve fibres, which pass through the lamina cribrosa to run into the optic nerve. The central retinal artery and vein emerge through the centre of this cup. Macula lutea. It is also called the yellow spot. It is comparatively deeper red than the surrounding fundus and is situated at the posterior pole temporal to the optic disc. It is about 5.5 mm in diameter. Fovea centralis is the central depressed part of the macula. It is about 1.5 mm in diameter and is the most sensitive part of the retina. In its centre is a shining pit called foveola (0.35-mm diameter) which is about 2-disc diameters (3 mm) away from the temporal margin of the disc and about 1 mm below the horizontal meridian. An area about 0.8 mm in diameter (including foveola and some surrounding area) does not contain any retinal capillaries and is called Foveal Avascular zone (FAZ) surrounded by the para and perifoveal areas. Peripheral retina refers to the area bounded posteriorly by the retinal equator and anteriorly by the ora serrata. Ora serrata. It is the serrated peripheral margin where the retina ends. Here the retina is firmly attached both to the vitreous and the choroid. # MICROSCOPIC STRUCTURE OF RETINA:^2^ {#microscopic-structure-of-retina2 .unnumbered} Retina consists of 3 types of cells and their synapses arranged (from without inward) in the following ten layers. 1. Pigment epithelium. It is the outermost layer of retina consisting of a single layer of cells containing pigment. It is firmly adherent to the underlying basal lamina (Bruch's membrane) of the choroid. It plays an important role in photoreceptor renewal and recycling of vitamin A. It also maintains integrity of sub-retinal space by forming outer blood retinal barrier. 2. Layer of rods and cones. Rods and cones are the end organs of vision and are also known as photoreceptors. Layer of rods and cones contains only the outer segments of photoreceptor cells arranged in a palisade manner. There are about 120 million rods and 6.5 million cones. Rods contain a photosensitive substance visual purple (rhodopsin) and subserve the peripheral vision and vision of low illumination (scotopic vision). Cones also contain a photosensitive substance and are primarily responsible for highly discriminatory central vision (photopic vision) and color vision. 3. External limiting membrane. It is a fenestrated membrane, through which pass the processes of the rods and cones. 4. Outer nuclear layer. It consists of nuclei of the rods and cones. 5. Outer plexiform layer. It consists of connections of rod spherules and cone pedicles with the dendrites of bipolar cells and horizontal cells. 6. Inner nuclear layer. It mainly consists of cell bodies of bipolar cells. It also contains cell bodies of horizontal amacrine and Muller's cells and capillaries of central artery of retina. The bipolar cells constitute the first order neurons. 7. Inner plexiform layer. It essentially consists of connections between the axons of bipolar cells dendrites of the ganglion cells, and processes of amacrine cells. 8. Ganglion cell layer. It mainly contains the cell bodies of ganglion cells (the second order neurons of visual pathway. There are two types of ganglion cells. The midget ganglion cells are present in the macular region and the dendrite of each such cell synapses with the axon of single bipolar cell. Polysynaptic ganglion cells lie predominantly in peripheral retina and each such cell may synapse with up to a hundred bipolar cells. 9.Nerve fibre layer (stratum opticum) consists of axons of the ganglion cells, which pass through the lamina cribrosa to form the optic nerve for distribution and arrangement of retinal nerve fibres. 10\. Internal limiting membrane. It is the innermost layer and separates the retina from vitreous. It is formed by the union of terminal expansions of the Muller's fibres, and is essentially a basement membrane. Structure of fovea centralis: In this area, there are no rods, cones are tightly packed and other layers of retina are very thin. Its central part (foveola) largely consists of cones and their nuclei covered by a thin internal limiting membrane. All other retinal layers are absent in this region. Functional divisions of retina Functionally retina can be divided into temporal retina and nasal retina by a line drawn vertically through the centre of fovea. The distinct layering pattern of the retina reflects the arrangement of neural, glial, and vascular cells that enables the retina to convert and process photic energy into neuronal electrical signals that ultimately reach the occipital visual cortex of the brain. # VISUAL PATHWAY {#visual-pathway .unnumbered} The entire pathway consists of the photoreceptor cell and three neurons. The photoreceptor cells (rods and cones) are located in the outermost layer of the retina. The outer segments of the rods and cones initially convert the light signal to electrical energy. The outer nuclear layer contains the cell bodies with nuclei of the photoreceptor cells. In the outer plexiform layer, axons of the photoreceptor cells synapse with the dendrites of the first neuron (the bipolar cell) and with the processes of the integrating neuronal cells, the horizontal cells. The bipolar cells, whose nuclei form the bulk of the inner nuclear layer, synapse in the inner plexiform layer with the dendrites of the second neurons, the ganglion cells. In this layer there are also synapses with amacrine cells, which resemble horizontal cells in that they provide cross wiring within the retinal layer. The ganglion cells extend their axons as the innermost retinal layer, the nerve fiber layer, through the optic nerve to the lateral geniculate body, where they synapse with the third neuron, and the cells of the lateral geniculate body, which extend their axons through the optic radiations to the occipital cortex. After light passes through the lens system of the eye and then through the vitreous humor, it enters the retina from the inside; that is, it passes first through the ganglion cells and then through the plexiform and nuclear layers before it finally reaches the layer of rods and cones located all the way on the outer edge of the retina. This distance is a thickness of several hundred micrometers; visual acuity is decreased by this passage through such nonhomogeneous tissue. However, in the central foveal region of the retina, as discussed subsequently, the inside layers are pulled aside to decrease this loss of acuity. The fovea is a minute area in the center of the retina, occupying a total area of a little more than 1 square mm; it is especially capable of acute and detailed vision. The central fovea, only 0.3 millimeters in diameter, is composed almost entirely of cones; these cones have a special structure that aids their detection of detail in the visual image. That is, the foveal cones have especially long and slender bodies, in contradistinction to the much fatter cones located more peripherally in the retina. Also, in the foveal region, the blood vessels, ganglion cells, inner nuclear layer of cells, and plexiform layers are all displaced to one side rather than resting directly on top of the cones. This allows light to pass unimpeded to the cones. # RETINAL CIRCULATION^4^ {#retinal-circulation4 .unnumbered} The retina has the highest metabolic demands of any tissue in the body The outer segments of the photoreceptors are the most metabolically active layer of the retina. Because of the high metabolic activity of the retina, the ability to regulate blood flow is an essential feature of the mammalian retina. The conflicting requirements of sufficient blood supply and minimal interference with the light path to the photoreceptors have been met by the evolution of two vascular supplies -- inherent intra-retinal vessels supply the inner two-thirds of the retina, while the choroidal circulation supplies the photoreceptors in the outer one-third of the retina. Further, in the retinas of primates, an avascular region at the fovea further facilitates high acuity vision. VASCULAR SUPPLY OF THE RETINA The human retinal vasculature is comprised of the central retinal artery, which enters the optic disc through the lamina cribrosa, where it branches into four principal intra-retinal arteries Whilst termed retinal arteries, even the central retinal artery is only of a caliber of an arteriole and if accurate terminology is used, only retinal arterioles exist, not arteries. Retinal arterioles, due to the higher oxygen content of the blood they carry, are typically surrounded by a capillary-free zone. Retinal capillaries are organized in an interconnecting two-layer network. In the mammalian retina, the vasculature in the nerve fiber and ganglion cell layers is known as the inner (or superficial) plexus, while the inner nuclear and outer plexiform layers receive blood from the deeper plexus located at the junction between them. Fine structure of retinal vessels in the human, the walls of the largest arterioles, near the optic disc, are comprised of five to seven layers of smooth muscle cells (tunica media). Smooth muscle actin filaments extend circumferentially around the retinal arterioles. In retinal arterioles, the smooth muscle cells are orientated both circularly and longitudinally, each being surrounded by a basal lamina that contains an increasing amount of collagen toward the acellular adventitia (the tunica externa). Endothelial cells (part of the tunica interna) are orientated longitudinally along the axis of the vessel and share their basement membrane with adjacent smooth muscle cells and pericytes. This basement membrane is composed of collagen IV, fibronectin, laminin, matrix metalloproteinases (MMPs-2, MMPs-9) and serine proteinase urokinase (UPA) and acts as an important regulatory matrix for the passage and sequestration of vasoactive agents and pro-survival growth factors. The retinal microvasculature is characterized by a uniquely high density of pericytes, substantially greater than that of human choriocapillaris. Retinal micro vessels are not-fenestrated and possess tight junctional complexes between the endothelial cells on their luminal aspect. The tight junctions represent the structural component of the inner blood-retinal barrier. The superficial retinal vasculature is ensheathed by both astrocytes and Müller cells, whilst the deep vascular plexus is ensheathed solely by Müller glia. VASCULAR SUPPLY OF THE CHOROID: The choroidal circulation is derived primarily from the long and short ciliary arteries with some contribution from the anterior ciliary arteries. Histologically, the choroid is divided into five layers. Starting from the retinal side, these include Bruch\'s membrane, three vascular layers (the choriocapillaris, Sattler\'s layer and Haller\'s layer) and the suprachoroidal. Haller\'s layer includes large arteries and veins, while Sattler\'s layer is composed of medium and small arterioles that feed the capillary network of the choriocapillaris and venules. The choroidal arteries arise from the long and short posterior ciliary arteries and branches of Circle of Zinn (around the optic disc). The choriocapillaris is a highly anastomosed network of capillaries (with little or no basement membrane material), forming a dense capillary network opposed to Bruch\'s membrane. In contrast to the retina, choroidal micro vessels are fenestrated and is under neurogenic control. Sympathetic innervation includes noradrenergic and neuropeptide fibers whereas the parasympathetic nerves are primarily cholinergic. The angiogenic process of retinal vasculature development is regulated by oxygen levels within the retina. In response to 'physiological hypoxia' caused by the onset of neuronal activity (increased metabolic activity in maturing retinal neurons and photoreceptors), astrocytes and Müller cells respond by secreting vascular endothelial growth factor (VEGF165), inducing formation of superficial and deep layers of retinal vessels, respectively. Pericytes have also been suggested to express VEGF inducing the formation of retinal blood vessels in normal development. Astrocytes in the retina might have highly divergent roles during developmental, physiological angiogenesis, and ischemia-driven, pathological neovascularization. The retinal veins. These follow the pattern of the retinal arteries. The central retinal vein drains into the cavernous sinus directly or through the superior ophthalmic vein. The only place where the retinal system anastomosis with ciliary system is in the region of lamina cribrosa. REGULATION OF RETINAL CIRCULATION: Auto regulation is that property of vascular bed which permits constant or nearly constant blood flow over a wide range of variations in perfusion pressure, blood gases and intraocular pressure. The normal retinal hemodynamic response to increase in perfusion pressure is an increase in vascular resistance. This behavior, termed the myogenic response, is intrinsic to smooth muscle cells, and independent of metabolic and hormonal influences. MECHANISM OF FUNCTIONAL HYPEREMIA: In retinal vasculature, any increase in metabolism which accompany neuronal activity would lower O2 and glucose levels and produce vasoactive metabolites. These metabolites would elicit vasodilation and increased blood flow, which, in turn, would restore O2 and glucose levels. When production of these metabolites is blocked, this functional hyperemia is substantially reduced, indicating that these factors play an important role in mediating functional hyperemia. Investigations of functional hyperemia in the brain suggest that arterioles, rather than capillaries, are the primary site of blood flow regulation. The pericytes may also contribute to active regulation of blood flow in the retina. They constrict in response to angiotensin II, norepinephrine, GABA antagonists and ATP. In turn, vasoactive molecules such as vasoactive intestinal peptide (VIP), pituitary adenylate cyclase activating peptide and NO donors relax retinal pericytes. Hence it is concluded that the metabolic needs of the eye are supplied by two separate vascular systems, the retinal and the choroidal vasculature, having very different hemodynamic properties. # HISTORICAL REVIEW OF DIABETIC RETINOPATHY5 {#historical-review-of-diabetic-retinopathy5 .unnumbered} Diabetic macular changes in the form of yellowish spots and extravasations that permeated part or the whole thickness of the retina were observed for the first time by Eduard Jaeger in 1856 with the help of a newly developed direct ophthalmoscope. Albrecht von Graefe openly claimed that there was no proof of a causal relationship between diabetes and retinal complications. It was only in 1872 that Edward Nettleship published his seminar paper \"On oedema or cystic disease of the retina\" providing the first histopathological proof of \"cystoid degeneration of the macula\" in patients with diabetes. In 1876, Wilhelm Manz described the proliferative changes occurring in diabetic retinopathy. In the early years of the 20th century, the debate continued whether macular changes were directly related to diabetes or whether they were due to hypertension and arteriosclerosis. It was not until the second half of the century that the work of Arthur James Ballantyne in Glasgow provided more evidence that suggested that diabetic retinopathy represents a unique vasculopathy. # DISEASE DEFINITION {#disease-definition .unnumbered} Diabetes Mellitus, in long course results in generalized macrovascular and microvascular complications of which the latter have been directly linked to glycemic control than the former. It mainly affects the kidneys, eyes and peripheral nerves. Diabetic retinopathy is a disorder of the retina that eventually develops to some degree in nearly all patients with long-standing diabetes mellitus. While defects in neurosensory function have been demonstrated in patients with diabetes mellitus prior to the onset of vascular lesions, the earliest visible clinical manifestations of retinopathy include microaneurysms and hemorrhages. Diabetic retinopathy is a complication of diabetes that affects the blood vessels of the retina. Growth of new blood vessels, known as proliferative retinopathy, may lead to blindness through hemorrhage and scarring. A deterioration of retinal blood vessels causing loss of blood vessels and leakage into the retina is known as maculopathy and leads to visual impairment and may progress to blindness. # ETIOPATHOGENESIS {#etiopathogenesis .unnumbered} Diabetic retinopathy is an ocular microangiopathy affecting small caliber retinal vessels i.e.pre-capillary arterioles, capillaries and venules eventually resulting in either (1) microvascular occlusion that causes hypoxia and development of new vessels or (2) microvascular leakage resulting in macular edema. Vascular alterations can progress to retinal capillary nonperfusion, resulting in a clinical picture characterized by increased numbers of hemorrhages, venous abnormalities, and intraretinal microvascular abnormalities (IRMA). A later stage includes closure of arterioles and venules and proliferation of new vessels on the disc, retina, iris, and filtration angle. Increased Vaso permeability results in retinal thickening (edema) during the course of diabetic retinopathy. Visual loss results mainly from macular edema, macular capillary nonperfusion, vitreous hemorrhage, and distortion or traction detachment of the retina. Risk factors associated with occurrence of DR are:^6^ 1. Duration of diabetes is the most important determining non-modifiable factor. Roughly 27 percent of patients develop DR within 5-10 years, 71-90 percent after 10 years and 95 percent within 20- 30 years of onset of the disease. For the risk, duration of DM after the onset of puberty is the important factor rather than in childhood age. 2. Type of Diabetes. It is seen in both the types; maximum prevalence with type 1. 3. Sex. Incidence is more in females than males. 4. Poor metabolic control is less important, but is nevertheless relevant to the development and progression of DR. 5. Heredity. Transmitted as a recessive trait without sex linkage. The effect of heredity is more on the proliferative retinopathy. 6. Pregnancy may accelerate the changes of diabetic retinopathy. 7. Hypertension, when associated, may also accentuate the changes of diabetic retinopathy leading to rapid progression. A patient with DM along with HTN is 3 times more likely to develop diffuse Diabetic macular edema. A reduction of 10 mm Hg systolic pressure may reduce retinopathy chances by 11% 8. Anemia -- Diabetic patients with Hb less than 12 mg/dl are having twice the risk for retinopathy and in known cases it is about 5 times. (eophta.com) 9. Hyperlipidemia --High levels of S. Cholesterol, HDL and TGs are not so significant in predicting the severity of retinopathy in Type I and II DM. are associated with fast development of hard exudates and also adversely affects the progression after LASER therapy in patients having CSME. 10. Addictions like smoking, Alcohol etc. and obesity 11. Nephropathy-renal disease evidenced by proteinuria, raised blood urea, creatinine and nitrogen levels can be a predictor of retinopathy. Similarly, a previously stable DR rapidly progressing needs Renal evaluation. # PATHOGENESIS7 {#pathogenesis7 .unnumbered} Essentially, it is a microangiopathy affecting retinal precapillary arterioles, capillaries and venules . The inciting factor that initiates the cascade and results in the structural changes is Hyperglycemia, which through a combination of factors including biochemical, hemodynamic and paracrine factors produces structural changes in the minute blood vessels. The speculative pathogenesis is depicted below. These are factors that interferes with glucose transfer causing increased intracellular glucose level. Depicting DR pathogenesis > Oxidate stress > > o2 free radicals damages endothelial cells > > protein kinase C activation mediates action of VEGF > > Increased polyol pathway > > flux basement memebrane thickening > non-enzymatic glycosylation & AGE production > > Endothelial apoptosis and VEGF production > > Biochemoical alterations # HEMODYNAMIC ALTERATIONS. {#hemodynamic-alterations. .unnumbered} Alterations in retinal capillaries are the hallmark of diabetic retinopathy and include multiple occlusions due to increased leukocyte entrapment increased permeability of the vessel wall with focal leakage occurring primarily at the location between the deep retinal capillary net and the ascending venules and, in the proliferative form, growth of newly-formed vessels (neovascularization). Retinal circulatory changes precede over clinical diabetic retinopathy and include a reduction in the functional hyperemia response, the response to hypertoxic challenge, and changes in basal blood flow. Since glucose plasma levels are a determinant of retinal blood flow acute and/or chronic hyperglycemia may also contribute to contradictory findings concerning retinal blood flow during different stages of diabetes and diabetic retinopathy. Although clinically observed microvascular changes are the hallmark used to classify diabetic retinopathy, there are also significant neuronal and glial changes that occur early during the development of the disease. Changes in the electroretinogram (ERG), a measure of neuronal function in the retina, occur in early stages of diabetic retinopathy. There is a reduction in the amplitude of the ERG a- and b-waves. The loss of pericytes in retinal micro vessels is one of the earliest morphological changes that takes place in diabetic retinopathy. Pericyte loss is associated with development of microaneurysms and shunt vessel formation in the diabetic retina. Increased blood glucose concentrations could contribute to pericyte loss. Another early histopathological sign of diabetic retinopathy of relevance to pericyte function is the thickening of the basement membrane resulting from increased synthesis of collagen IV, fibronectin, and laminin and/or reduced degradation by catabolic enzymes.Modification of vascular basement membrane may reduce bioavailability of pro-survival factors for retinal pericytes and inhibitors of angiogenesis in the eye, i.e. PDGF .In general, the physiological consequences of compromised two-way communication between endothelial cells and pericytes manifest themselves as a loss of functional integrity of the capillary unit; The major vascular pathologic events may be concised as follows. - Thickening of capillary basement membrane - Capillary endothelial cell damage - Changes in RBCs (Decreased ability to release O2, increased whole blood viscosity and adhesiveness to endothelial cells & formation of large aggregates) - Increased stickiness & fragility of platelets, decreased thromboxane and prostacyclin.  Increased leukocyte adhesion causing endothelial cell injury, VEGF release and opening of tight junctions. - Loss of capillary pericytes - Microvascular occlusion - Retinal ischemia - Capillary leakage - Microaneurysms - Haemorrhages - Retinal oedema - Hard exudates - Arteriovenous shunts - (Intraretinal microvascular abnormalities --- IRMA) Neovascularisation # PARACRINE FACTORS These refers to a plethora of growth factors implicated in the pathogenesis of Diabetic Retinopathy. Pathological abnormal vascularization in diabetic patients results due to an imbalance between the positive regulators /pro-angiogenic and negative regulators /anti-angiogenic factors. It has been found that the levels of positive factors are elevated in the vitreous of diabetic patients with proliferative changes. # PRO-ANGIOGENIC FACTORS {#pro-angiogenic-factors .unnumbered} VEGF, PDGF, HGF, Erythropoetin, Leptin, Angiogenin, Insulin growth factors 1,2 ICAM I, Endothelin I, Angiopoietin I, Angiotensin 2, IL-6,IL-8,TNF-alpha,beta I ANTI-ANGIOGENIC FACTORS Endostatin, Angiostatin, Genistein, Platelet factor 4, Pigment Epithelium Derived Factor, Thrombospondin I # {#section-12 .unnumbered} # CLASSIFICATION^8^ {#classification8 .unnumbered} Diabetic retinopathy has been presently classified as follows: I. Non-proliferative/Background Diabetic Retinopathy (NPDR/BDR) \_ Mild NPDR > \_ Moderate NPDR > > \_ Severe NPDR \_ Very severe NPDR II. Proliferative diabetic retinopathy (PDR) III. Diabetic maculopathy IV\. Advanced diabetic eye disease (ADED) > Non-proliferative diabetic retinopathy (NPDR)- > > It is characterized by Intra retinal abnormalities. Ophthalmoscopic > features of NPDR include: - Microaneurysms in the macular area (the earliest detectable lesion). - Retinal hemorrhages both deep (dot and blot hemorrhages) and superficial hemorrhage's (flame-shaped). - Hard exudates-yellowish-white waxy-looking patches are arranged in clumps or in circinate pattern. These are commonly seen in the macular area. - Retinal oedema characterized by retinal thickening. - Cotton-wool spots (if \> 8, there is high risk of developing PDR). - Venous abnormalities, beading, looping and dilatation. - Intraretinal microvascular abnormalities (IRMA). - Dark-blot hemorrhage's representing hemorrhagic retinal infarcts. On the basis of severity of the above findings the NPDR has been further classified (ETDRS) as under: 1. Mild NPDR - At least one microaneurysm or intraretinal hemorrhage. Hard/soft exudates may or may not be present. 2. Moderate NPDR - Moderate microaneurysms/intraretinal hemorrhage. - Early mild IRMA. - Hard/soft exudates, venous beading or IRMA's may also be present. 3. Severe NPDR. Any one of the following (4-2-1Rule): - Four quadrants of severe microaneurysms/intraretinal hemorrhages. • Two quadrants of venous beading. - One quadrant of IRMA changes. 4. Very severe NPDR. Any two of the following (4-2-1 Rule): - Four quadrants of severe microaneurysms/intraretinal hemorrhages. - Two quadrants of venous beading. - One quadrant of IRMA changes ```{=html} ``` II. Proliferative diabetic retinopathy (PDR) > Proliferative diabetic retinopathy develops in more than 50 percent of > cases after about 25 years of the onset of disease. Therefore, it is > more common in patients with juvenile onset diabetes. The hallmark of > PDR is the occurrence of neovascularization over the changes of very > severe non-proliferative diabetic retinopathy. It is characterized by > proliferation of new vessels from the capillaries, in the form of > neovascularization at the optic disc (NVD) and/or elsewhere (NVE) in > the fundus, usually along the course of the major temporal retinal > vessels. These new vessels may proliferate in the plane of retina or > spread into the vitreous as vascular fronds. Later on condensation of > connective tissue around the new vessels results in formation of > fibrovascular epiretinal membrane. Vitreous detachment and vitreous > hemorrhage may occur in this stage. > > Types: On the basis of high risk characteristics (HRCs) described by diabetic retinopathy study (DRS) group, the PDR can be further classified as below: 1. PDR without HRCs (Early PDR), and 2. PDR with HRCs (Advanced PDR). High risk characteristics (HRC) of PDR are as follows- - NVD 1/4 to 1/3 of disc area with or without vitreous haemorrhage (VH) or pre-retinal haemorrhage (PRH) - NVD \< 1/4disc area with VH or PRH - NVE \> ½ disc area with VH or PRH ```{=html} ``` III. Diabetic maculopathy > Changes in macular region need special mention, due to their effect on > vision. These changes may be associated with non-proliferative > diabetic retinopathy (NPDR) or proliferative diabetic retinopathy > (PDR). The diabetic macular edema occurs due to increased permeability > of the retinal capillaries due to disruption of cell junctions, loss > of endothelial cell layer integrity due to cell destruction and > increased transcellular transport through the endothelium. It is > termed as clinically significant macular edema (CSME) if one of the > following three criteria are present on slit-lamp examination with 90D > lens: - Thickening of the retina at or within 500 micron of the centre of the fovea. - Hard exudate at or within 500 micron of the centre of fovea associated with adjacent retinal thickening. - Development of a zone of retinal thickening one disc diameter or larger in size, at least a part of which is within one disc diameter of the foveal centre. > Clinico-angiographically diabetic maculopathy can be classified into > four types: 1. Focal exudative maculopathy. It is characterised by microaneurysms, haemorrhages, macular oedema and hard exudates which are usually arranged in a circinate pattern. Fluorescein angiography reveals focal leakage with adequate macular perfusion. 2. Diffuse exudative maculopathy. It is characterised by diffuse retinal oedema and thickening throughout the posterior pole, with relatively few hard exudates. Fluorescein angiography reveals diffuse leakage at the posterior pole. 3\. Ischaemic maculopathy. It occurs due to microvascular blockage. Clinically it is characterised by marked visual loss with microaneurysms, haemorrhages, mild or no macular oedema and a few hard exudates. Fluorescein angiography shows areas of non-perfusion which in early cases are in the form of enlargement of foveal avascular zone (FAZ), later on areas of capillary dropouts are seen and in advanced cases precapillary arterioles are blocked. > 4\. Mixed maculopathy. In it combined features of ischaemic and > exudative maculopathy are present. IV. Advanced diabetic eye disease It is the end result of uncontrolled proliferative diabetic retinopathy. It is marked by complications such as: - Persistent vitreous haemorrhage, - Tractional retinal detachment and - Neovascular glaucoma. DIAGNOSIS > The initial examination for a patient with diabetes mellitus includes > all features of the comprehensive adult medical eye evaluation, with > particular attention to those aspects relevant to diabetic > retinopathy. # PRESENTING COMPLAINTS9 {#presenting-complaints9 .unnumbered} > Early BDR will not affect vision and this is often a matter of > challenge for the physician and the ophthalmologist to convince the > patient for early screening and initiation of the treatment concerned. > Diabetic patients may present with the following symptoms :- i) Blurred vision --Hyperglycemia altered shape, refractive index and flexibility of lens, refractive error, distorting ability to focus blurring and frequent changes in presbyopic glasses. ii) Cloudy vision -- due to edematous retina or cataract. iii) Double vision --damage to neural control over EOM. iv) Floaters in visual field -- due to vitreous degeneration that takes place comparatively earlier in DM. v) Curtain like shadows -- due to RD or bleeding from retina into vitreous. vi) Flashes of light-due to odema causing separation of retinal pigmentary epithelium from neurosensory layers or pre-retinal hemorrhages. vii) Delayed dark adaptation --due to compromised nutrition to rods and retinal hypoperfusion due to edema. # CLINICAL HISTORY {#clinical-history .unnumbered} > An initial history should consider the following elements: - Duration of diabetes - Past glycemic control (haemoglobin A1c) Reduction of HbA1c level by 10% reduces risk of DR by 35%. - Medications - Medical history (e.g., obesity, renal disease, systemic hypertension, serum lipid levels, pregnancy) - Ocular history (e.g., trauma, ocular injections, surgery, including laser treatment and refractive surgery) # EXAMINATION {#examination .unnumbered} > The initial examination should include the following elements: - Visual acuity - Slit-lamp biomicroscopy - Intraocular pressure - Gonioscopy when indicated - Dilated funduscopy including stereoscopic examination of the posterior pole • Examination of the peripheral retina and vitreous > Slit-lamp biomicroscopy with accessory lenses is the recommended > method to evaluate retinopathy in the posterior pole and mid > peripheral retina. The examination of the peripheral retina is best > performed with indirect ophthalmoscopy or with slit lamp > biomicroscopy, combined with a contact lens. > > Because treatment is effective in reducing the risk of visual loss, > detailed examination is indicated to assess for the following features > that often lead to visual impairment: - Presence of macular edema - Optic nerve head neovascularization and/or neovascularization elsewhere - Signs of severe NPDR (extensive retinal hemorrhages/microaneurysms, venous beading, and IRMA) - Vitreous or preretinal hemorrhage. EXAMINATION SCHEDULE10 > Type 1 (Diabetes Onset Usually Before Age 30 Years) > > Many studies of patients with type 1 diabetes have reported a direct > relationship between the prevalence and severity of retinopathy and > the duration of diabetes. Among patients with type 1 diabetes, > substantial retinopathy may become apparent as early as 6 to 7 years > after onset of the disease. Ophthalmic examinations should be > performed beginning 3 to 5 years after the diagnosis of type 1 > diabetes. > > Type 2 (Diabetes Onset Usually at Age 30 Years or Older) > > The time of onset of type 2 diabetes is often difficult to determine > and may precede the diagnosis by a number of years. Up to 3% of > patients whose diabetes is first diagnosed at age 30 or later will > have CSME or high-risk characteristics at the time of the initial > diagnosis of diabetes. About 30% of patients will have some > manifestation of diabetic retinopathy at diagnosis. Therefore, the > patient should be referred for ophthalmologic examination at the time > of diagnosis of Diabetes Mellitus. > > Table-11: Showing Recommended Eye Examination Schedule For Patients > With Diabetes Mellitus +----------------------+-----------------------+-----------------------+ | **Diabetes Type** | > **Recommended Time | > **Recommended | | | > of First | > Follow up\*** | | | > Examination** | | +======================+=======================+=======================+ | Type 1 | > 3-5 years after | > Yearly | | | > diagnosis | | +----------------------+-----------------------+-----------------------+ | > Type 2 | > At time of | > Yearly | | | > diagnosis | | +----------------------+-----------------------+-----------------------+ | Prior to pregnancy | > Prior to conception | > No retinopathy to | | (type 1 or type 2) | > and early in the | > mild or moderate | | | > first trimester | > NPDR: every 3 12 | | | | > months. Severe NPDR | | | | > | | | | > or worse: every | | | | > 1--3 months. | +----------------------+-----------------------+-----------------------+ > Diabetes Associated with Pregnancy > > Diabetic retinopathy can worsen during pregnancy because of the > pregnancy itself or changes in metabolic control. Pregnant women > having diabetes should be counselled on the risk of development and/or > progression of diabetic retinopathy, and should be told to make every > attempt to lower their blood glucose levels to as near normal as > possible for their own health and the health of the fetus. Women who > develop gestational diabetes do not require an eye examination during > pregnancy, because such individuals are not at increased risk for > diabetic retinopathy during pregnancy. ANCILLARY TESTS # {#section-13 .unnumbered} > If used appropriately, a number of tests ancillary to the clinical > examination may enhance patient care. The most common tests include > the following: • Color fundus photography - Fluorescein angiography - Ultrasonography - Optical coherence tomography Color Fundus Photography > Fundus photography is a more reproducible technique than a clinical > examination for detecting diabetic retinopathy in clinical research > studies. However, clinical examination is often superior for detecting > retinal thickening associated with macular edema and may be better at > identifying fine-calibre NVD or NVE. Fundus photography may be useful > for documenting substantial progression of disease and response to > treatment. > > Fluroscein Angiography > > Fluroscein angiography is a clinically valuable test for selected > patients with diabetic retinopathy and is commonly used as a guide for > treating CSME and as a means of evaluating the cause(s) of unexplained > decreased visual acuity (see Table 5). Angiography can identify > macular capillary nonperfusion or sources of capillary leakage > resulting in macular edema as possible explanations for visual loss. > > Fluroscein angiography is not routinely indicated as a part of the > examination of patients with diabetes. It is not needed to diagnose > CSME or PDR, both of which are diagnosed by means of the clinical > examination. > > An ophthalmologist who orders fluorescein angiography must be aware of > the potential risks associated with the procedure- severe medical > complications, including death (about 1/200,000 patients). Each > angiography facility should have in place an emergency plan and a > clear protocol to minimize the risks and to manage any complications. > Although detrimental effects of fluorescein dye on the fetus have not > been documented, fluorescein dye does cross the placenta into the > fetal circulation. > > Ultrasonography > > Ultrasonography is a valuable test to detect retinal detachment in > diabetic eyes with opaque media (most commonly due to cataract or > vitreous hemorrhage). > > Optical Coherence Tomography > > Optical coherence tomography provides high-resolution (10 microns) > imaging of the vitreoretinal interface, retina, and subretinal space. > OCT can be useful for quantifying retinal thickness, monitoring > macular edema, measure changes in volume and thickness of macula, and > identifying vitreomacular traction in selected patients with diabetic > macular edema. However, optical coherence tomography measures of > retinal thickness correlate poorly with visual acuity. It is important > in defining indications for surgery in presence of vitreo-retinal > traction, determining > > prognosis and quantifying the response of the therapies like LASER, > medication or surgery. # MANAGEMENT11 {#management11 .unnumbered} > Goals for Retinopathy management - > > Stage -1(Routine screening for Diabetes in all above 40 years)-to > prevent or delay ocular complications. > > Stage II (BDR stage)-To prevent formation of new microaneurysms, to > check bleeding, resolve edema and to prevent /delay proliferative > stage. > > Stage III(PDR)-To resolve active hemorrhages and edema, prevent > vitreous or retinal detachment, to protect from irreversible visual > loss. I. Screening for diabetic retinopathy. To prevent visual loss occurring from diabetic retinopathy a periodic follow-up is very important for a timely intervention. The recommendations for periodic fundus examination are as follows: - Every year, till there is no diabetic retinopathy or there is mild NPDR. - Every 6 months, in moderate NPDR. - Every 3 months, in severe NPDR. - Every 2 months, in PDR with no high risk characteristic. - II\. Medical treatment. Besides laser and surgery to the eyes (as indicated and described below), the medical treatment also plays an essential role. Medical treatment for diabetic retinopathy can be discussed as: ```{=html} ``` 1. Control of systemic risk factors is known to influence the occurrence, progression and effect of laser treatment on DR. The systemic risk factors which need attention are. a. Strict metabolic control of blood sugar, b. Lipid & weight reduction by restricted diet c. Control Hypertension d. Quit smoking e. Control of associated anaemia, f. Control of associated hypoproteinemia 2. Role of pharmacological modulation. Pharmacological inhibition of certain biochemical pathways involved in the pathogenesis of retinal changes in diabetes is being evaluated These include: - Protein kinase C (PKC) inhibitors, - Vascular endothelial growth factors (VEGF) inhibitors like Ranibizumab > 0.5 mg (leucentis), Bevacizumab1.25 mg (Avastin) etc. - Aldose reductase and ACE inhibitors, and - Antioxidants such as vitamin E 3. Role of intravitreal steroids in reducing diabetic macular oedema is also being stressed recently by following modes of administration: - Flucinolone acetonide intravitreal implant and - Intravitreal injection of triamcinolone (IV TA 100 mcg or 400 mcg) This reduces macular edema; but has to be repeated as its effects lasts for 3 months. main side effects are glaucoma,cataract and endophthalmitis. I. Photocoagulation. It remains the mainstay in the treatment of diabetic retinopathy and maculopathy. Either argon or diode laser can be used. The > protocol of laser application is different for macula and rest of the > retina as follows: I. Macular photocoagulation. Macula is treated by laser only if there is clinically significant macular oedema (CSME). Laser treatment is contraindicated in ischaemic diabetic maculopathy. In patients with PDR associated with CSME, macular photo-coagulation should be considered first i.e., before PRP since the latter may worsen macular oedema. Macular photocoagulation includes two techniques: i. Focal treatment with argon laser is carried out for all lesions (microaneurysms, IRMA or short capillary segments) 500-3000 microns from the centre of the macula, believed to be leaking and causing CSME. Spot size of 100-200 μm of 0.1 sec. duration is used. ii. Grid treatment. Grid pattern laser burns are applied in the macular area for diffuse diabetic macular oedema. II. . Panretinal photocoagulation (PRP) or scatter laser consists of 1200-1600 spots, each 500 μm in size and 0.1 sec. duration. Laser burns are applied 2-3 disc areas from the centre of the macula extending peripherally to the equator. In PRP temporal quadrant of retina is first coagulated. PRP produces destruction of ischaemic retina which is responsible for the production of vasoformative factors. > Indications for PRP are: - PDR with HRCs, - Neovascularization of iris (NVI), - Severe NPDR associated with: - Poor compliance for follow up, - Before cataract surgery/YAG capsulotomy, - Renal failure, - One-eyed patient - Pregnancy I. Surgical treatment. > It is required in advanced cases of PDR. Pars plana vitrectomy is > indicated for dense persistent vitreous haemorrhage, tractional > retinal detachment, and epiretinal membranes. > > Management recommendations for patients with diabetes are summarized > in Table and are described according to the severity of retinopathy in > the following pages. > > Table-12 : Showing Management Recommendations For Patients of DR. +--------------+--------+-------+-------------+----------+----------+ | Severity of | Pr | Foll | > | > Flu | > Focal | | Retinopathy | esence | ow-up | Panretinal | orescein | > and/or | | | of | in | > Pho | > A | > | | | CSME\* | M | tocoagulati | ngiograp | > Grid | | | | onths | > | > hy | > Laser† | | | | | > on | | | | | | | > (Scatter) | | | | | | | > Laser | | | +==============+========+=======+=============+==========+==========+ | 1\. Normal | No | 12 | > No | > No | > No | | or | | | | | | | | | | | | | | minimal NPDR | | | | | | +--------------+--------+-------+-------------+----------+----------+ | 2.Mild to | No | 6-12 | > No | > No | > No | | moderate | | | > | > | > | | | Yes | 2-4 | > No | > | > | | NPDR | | | | Usually | Usually | +--------------+--------+-------+-------------+----------+----------+ | 3\. Severe | No | 2-4 | > Sometimes | > Rarely | > No | | NPDR | | | > | > | > | | | Yes | 2-4 | > Sometimes | > | > | | | | | | Usually | Usually | +--------------+--------+-------+-------------+----------+----------+ | 4\. Non-high | No | 2-4 | > Sometimes | > Rarely | > No | | risk PDR | | | > | > | > | | | Yes | 2-4 | > Sometimes | > | > | | | | | | Usually | Usually | +--------------+--------+-------+-------------+----------+----------+ | 5.High-risk | No | 2-4 | > Usually | > Rarely | > No | | PDR | | | > | > | > | | | Yes | 2-4 | > Usually | > | > | | | | | | Usually | Usually | +--------------+--------+-------+-------------+----------+----------+ | 6\. | No | 2-4 | > No | > No | > | | | | | > | > | Usually | | Inac | Yes | 2-4 | > No | > | > | | tive/involut | | | | Usually | > | | ed PDR | | | | | Usually | +--------------+--------+-------+-------------+----------+----------+ > \* Exceptions include hypertension or fluid retention associated with > heart failure, renal failure, pregnancy, or any other causes that may > aggravate macular edema. Deferral of photocoagulation for a brief > period of medical treatment may be considered in these cases.111 Also, > deferral of CSME treatment is an option when the center of the macula > is not involved, visual acuity is excellent, close follow-up is > possible, and the patient understands the risks. > > Adjunctive treatments that may be considered include intravitreal > corticosteroids or anti-vascular endothelial growth factor agents > (off-label use). > > Deferring focal photocoagulation for CSME is an option when the center > of the macula is not involved, visual acuity is excellent, close > follow-up is possible, and the patient understands the risks. However, > initiation of treatment with focal photocoagulation should also be > considered because although treatment with focal photocoagulation is > less likely to improve the vision, it is more likely to stabilize the > current visual acuity. Treatment of lesions close to the foveal > avascular zone may result in damage to central vision and with time, > such laser scars may expand and cause further vision deterioration. > Closer follow-up may be necessary for macular edema that is not > clinically significant. > > Panretinal photocoagulation surgery may be considered as patients > approach high risk PDR. The benefit of early panretinal > photocoagulation at the severe nonproliferative or worse stage of > retinopathy is greater in patients with type 2 diabetes than in those > with type 1. Treatment should be considered for patients with severe > NPDR and type 2 diabetes. Other factors, such as poor compliance with > follow-up, impending cataract extraction or pregnancy, and status of > the fellow eye will help in determining the timing of the panretinal > photocoagulation. > > It is preferable to perform focal photocoagulation first, prior to > panretinal photocoagulation, to minimize panretinal photocoagulation > laser--induced exacerbation of the macular edema. > > Table-13: Showing Side Effects and Complications of Treatment For > Diabetic Retinopathy. +----------------------------------+-----------------------------------+ | Treatment | > Side Effects/Complications | +==================================+===================================+ | Focal laser photocoagulation for | > 1.Initial decrease in central | | diabetic macular edema | > vision | | | > | | | > 2\. Para central scotomas if | | | > large laser burns have been | | | > placed close to the fovea. | | | > | | | > 3.Permanent central scotoma | | | > from inadvertent foveal burns | | | > | | | > 4.post application lesion | | | > enlargement. 5.sub-retinal | | | > fibrosis | | | > | | | > 6.choroidal | | | > neo-vascularisation. | +----------------------------------+-----------------------------------+ | Panretinal photocoagulation | 1. Central vision loss from | | (scatter) for severe NPDR or PDR | macular edema | | | | | | 2. Peripheral visual field | | | constrictions with poor dark | | | adaptation | | | | | | 3. Vitreous hemorrhage | | | neovascularization is present | | | | | | 4. Loss of accommodation | +----------------------------------+-----------------------------------+ | Vitrectomy | 1. Recurrent vitreous hemorrhage | | | | | | 2. Retinal detachment | | | | | | 3. Rubeosis iridis | | | | | | 4. Severe visual loss | | | | | | 5. Microbial endophthalmitis | | | 6.Cataract | +----------------------------------+-----------------------------------+ | Intravitreal corticosteroid | 1. Cataract progression | | injections | | | | 2. Elevated intraocular pressure | | | | | | 3. Infectious endophthalmitis 4. | | | Transient reactions | | | | | | > 5.Possible medication | +----------------------------------+-----------------------------------+ # RECENT ADVANCES IN RETINOPATHY MANAGEMENT12 1) SELECTIVE RETINAL THERAPY {#recent-advances-in-retinopathy-management12-1-selective-retinal-therapy .unnumbered} > It is a retinal phototherapy which do not cause severe permanent > damage. It is a selective treatment of the retinal pigment epithelium > by decreasing laser pulse duration (in microseconds)which can > selectively destroy RPE without damaging retina . Due to heat > confinement, micro and nano second laser pulses can produce explosive > vaporization of melanosomes, resulting in selective damage to RPE, > sparing photoreceptors and inner retina. Subsequent RPE proliferation > and migration restores RPE continuity. # 2)PASCAL(PATTERNED SCANNING LASER ) PHOTOCOAGULATOR {#pascalpatterned-scanning-laser-photocoagulator .unnumbered} > It is an integrated semi-automatic pattern scan laser photocoagulation > system designed to treat ocular diseases using a single shot or > pre-determined pattern array. The shorter pulse durations require less > total energy to produce burns ,there is > > less spreading, less choroidal heating and uniform energy > distribution. The burns are smaller and homogenous with less inner > retinal injury, and potentially less field loss and better clinical > outcomes. It enhances patient comfort, easy to use and is having > advanced precision due to even pattern of burns. > > Other Ocular Complications of DM:13 > > It is to be understood that not only retinal vasculature; but also > other ocular components are affected due to diabetes. Therefore it is > the responsibility of the ophthalmologist to identify other > pathognomic features also as early as possible.This may include : I) Corneal abnormalities a. Corneal sensitivity is decreased in proportion to both the duration of disease and the severity of the retinopathy b. Diabetics are more likely to have corneal abrasions than those without the disease, because adhesion between the basement membrane of the corneal epithelium and the stroma is not as firm as that found in normal corneas. Hyperglycemia and the aldose reductase pathway probably play a major role in epithelial abnormalities, because aldose reductase inhibitors accelerate healing of corneal abrasions. II) Glaucoma: Neovascularization of the iris usually is seen only in diabetics who have proliferative diabetic retinopathy (PDR). NVI may lead to posterior anterior synechiae and raised IOP leading to neo-vascular glaucoma. Panretinal photocoagulation (PRP) not only has protective value against NVI, it also is an effective treatment against established NVI. III) Cataract: The risk of cataract is 2-4 times greater in diabetics than in nondiabetics and may be 15-25 times greater in diabetics under 40 years old. Senile cataract develops early and rapidly in diabetics. It is believed to be due to glycation, carbamylation of crystallins and increased oxidative damage. Usually it is of sub capsular variety resembling a snow storm- 'Snow flake' cataract. > Complications of Cataract surgery in Diabetic patients: 1) Anterior segment: a. The most dreaded anterior complication is neovascularization of the iris. b. Pupillary block, c. Posterior synechiae, d. Pigmented precipitates on the implant, and Severe iritis. 2)Posterior segment: 1. a\) Chronic cystoid macular edema -14 times more common in diabetics than in non-diabetics. 2. b\) Proliferative retinopathy, 3. c)Vitreous hemorrhage, and 4. d)Tractional retinal detachment. ```{=html} ``` IV) Optic Neuropathy ```{=html} ``` i) Many diabetic patients without retinopathy have subclinical optic neuropathy. In addition, they often have anterior ischemic optic neuropathy identical to that seen in non-diabetics. ii) Diabetics are also susceptible to diabetic papillopathy which is characterized by acute disc edema without the pale swelling of anterior ischemic optic neuropathy. It is bilateral in one half of cases and may not show an afferent pupillary defect. > 3.Cranial Neuropathy: Extraocular muscle palsies may occur in > diabetics secondary to neuropathy involving the third, fourth, or > sixth cranial nerves. > > MECHANISM: Localized demyelinization of the nerve secondary to focal > ischemia. Pain may or may not be experienced, and not infrequently an > extraocular muscle palsy may be the initial clue to a latent diabetic > condition. Recovery of extra ocular muscle function in diabetic > cranial nerve neuropathy generally takes place in 1-3 months. > > When the third nerve is involved, pupillary function is usually > normal. Pupillary sparing in diabetic third nerve palsy is an > important diagnostic feature, distinguishing it from other causes of > oculomotor involvement such as intracranial tumor or aneurysm. **[Drug review- Ayurveda]{.underline}** **[Vasadi kwath]{.underline}** *Vasadikwatha (Maha)* is a classical polyherbal decoction described in sharangdhara samhita madhyam khanda in kwath kalpana dwitiya adhyay. It is also described in *Bṛihadyogatarangiṇī* and *Bṛihadnighaṇṭu Ratnākara (ta 131)* under ***Netra-roga Adhikara as mahavasadi kwath***. Refrence of vasadikwath is also found in yogtarangini (ta 71). The formulation is indicated in **sarva *akṣhi-roga*** (all eye disorders) along with **vaisvarya** (hoarseness of voice), ***pinasa*** (chronic rhinitis), ***Shvasa*** (dyspnoea/asthma), and **urakṣhata** (injury or ulcerative conditions of the chest). Here the analysis of the formulation on the basis of ***Dravya-guṇa, Dosha-karma***, and ***Saṃprapti-vighaṭana***, is done, highlighting its multidimensional therapeutic utility in netra rogas. Netra-rogas (eye diseases) are predominantly caused by ***Pitta and Rakta duṣhṭi***, often associated with ***Kapha saṅga*** and ***ama***. Classical Ayurvedic texts advocate the use of ***tikta-kaṣhaya rasa*-pradhana formulations** possessing chakṣuṣya, raktaśhodhana, and śhothahara properties. *Vāsādikwātha (Mahā)*, described in Sharangdhara Samhita, *Bṛihadyogatarangiṇi* and *Bṛihannighaṇṭu Ratnakara*, is indicated in ***sarva Akshi roga.*** --------------------------------------------------------------------------------------------------- **Sr. **Dravya** **Rasa** **Veerya** **Vipak** **doshaghnata** **Dhatu karya** No.** ------- -------------- ------------ ------------ ----------- ----------------- -------------------- 1 Vasa T. K. Ks. Shita Katu Pitta kapha Raktaprasadan, stambhan 2 Sunthi k\. Ushna Madhur Kapha Vata Saam dosha pachan, kledanashan 3 Guduchi T. K. Ks Ushna Madhur Tridosha Rasayan , raktaprasadan 4 Darvi T.K. Ushna Katu Kapha, Kled nashan 5 Raktachandan T. Shita Katu Pitta, kapha Raktaprasadan 6 Chitrak k\. Ushna Katu Vata kapha Agnidipan 7 Kirattikta T. K. Shita Katu Pitta, kapha Vranashodhan 8 Nimba T. Shita Katu Kapha Pitta Raktagat kled shoshan 9 Kutki T. Shita Katu Kapha pitta Pittavirechan 10 Patol T. Ushna Madhur Pitta kapha Raktaprsadan virechan 11 Haritaki M.A.K.T.Ks Ushna Madhur tridoshaghna Kledshoshan virechan, netrya 12 Vibhitaki Ks. Shita Katu Kapha pitta Same as haritaki 13 Amalaki A. Ks M. Shita Madhur tridodhaghna Netrya. Rasayan 14 Musta T, K ,Ks Shita Katu Kapha Pitta Pachan, klednashan 15 Kutaj K, T, Ks Shita Katu Kapha pitta, Stambhan --------------------------------------------------------------------------------------------------- -------------------------------------------------------------------------- 16 yava M,Ks Shita katu Kaph pitta Chakshushya , dipan pachan ------ ----------- ------- ------- ------- ---------- -------------------- 17 kalingaka T,Ks Shita katu Kapha Agnidipan , vran pitta ropan -------------------------------------------------------------------------- K- Katu, Ks- Kashay, M- Madhur, A- Amla, T- Tikta ***01.* VASA** ![Gachwala Vasaka (Justicia adhatoda) Live plant \| Malabar nut \| Vasa \| Adhatoda Medicinal Herb \| Medicinal Plant Live with Pot](media/image1.jpeg){width="3.158333333333333in" height="2.3666666666666667in"} **Fig. No.: Vasa** +----------------------+-----------------------------------------------+ | **Botanical Name** | *Justicia adhatoda/ Adhatoda Vasica Nees* | +======================+===============================================+ | **Family** | Acanthaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Vasaka, Adusa | | | > | | | > **English --** Malabar Nut, Adhatoda | | | > | | | > **Marathi --** Adulasa | | | > | | | > **Gujarati --** Aradusi | | | > | | | > **Kannada --** Adusoge | | | > | | | > **Bengali --** Basak | | | > | | | > **Tamil --** Adathodai | | | > | | | > **Telugu --** Addasaramu | | | | | | **Malayalam-** Adalodakam | +----------------------+-----------------------------------------------+ | **Synonyms** | Vasa, Vasaka, Simhasya, Vrishavalli, | | | Atarushaka | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | **Charaka Samhita-** Kasahara, Raktapittahara | | Categorization** | | | | **Sushruta Samhita-** Vasaadi Gana | | | | | | **Ashtanga Hridaya-** Kasahara, | | | Raktapittahara | | | | | | **Bhavaprakasha Nighantu** - Guduchyadi Varga | +======================+===============================================+ | **Botanical | An evergreen, perennial shrub about 1--2.5 m | | Description** | in height. Leaves opposite, | | | elliptic-lanceolate, 10--15 cm long, dark | | | green above and pale beneath. Flowers white | | | with purple markings, arranged in dense | | | axillary spikes. The plant emits a | | | characteristic odor when crushed. | +----------------------+-----------------------------------------------+ | **Distribution** | Widely distributed throughout India up to | | | 1300 m altitude, commonly found in plains, | | | sub-Himalayan tracts, and cultivated in | | | gardens. | +----------------------+-----------------------------------------------+ **Properties & Action Of *VASA *** ----------------------------------------------------------------------- *Rasa* *Tikta, Kashaya* ------------------------ ---------------------------------------------- *Guna* *Laghu, Ruksha* *Virya* *Sheeta* *Vipaka* *Katu* *Doshakarma* *Pittakapha Shamaka* *Rogaghnakarma* *Raktapittahara, Shothahara, Chakshushya, Vranaropana, Kandughna, prameha* ----------------------------------------------------------------------- +-------------------------+--------------------------------------------+ | **Chemical | Vasicine, Vasicinone, Adhatodine, | | Constituents** | Essential oils, Flavonoids, Alkaloids, | | | Tannins | +=========================+============================================+ | **Therapeutic Uses** | Raktapitta, Kasa, Shwasa, **Netraroga**, | | | timir, Vrana, Pradara, Jvara, Kushtha | +-------------------------+--------------------------------------------+ | **Part Used** | Patra (Leaf), Mula | +-------------------------+--------------------------------------------+ | **Dosage** | > **Swarasa:** 10--20 ml (Ref. API) | | | > | | | > **Kwatha:** 50--100 ml | | | > | | | > **Churna:** 2--3 g | +-------------------------+--------------------------------------------+ []{#_Toc229853449 .anchor}**Physicochemical Parameters of Vasa** []{#_Toc229853450 .anchor}(*Justiciaadhatoda*L.,DriedLeaf)\ **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed/Reported No.** Values** ------- ----------------------- ------------------- --------------------- 1 Total Ash (% w/w) Not more than 18.0 9.875 per cent per cent 2 Acid-insoluble Ash (% Not more than 3.0 0.905 per cent w/w) per cent 3 Water-soluble Not less than 20.0 19.376 per cent Extractive (% w/w) per cent 4 Alcohol-soluble Not less than 10.0 20.368 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 Not more than 10.0 6 per cent °C (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per per cent cent ------------------------------------------------------------------------- []{#_Toc229853451 .anchor}**Thin Layer Chromatography (TLC) for Identification of Vasa** []{#_Toc229853452 .anchor}**(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** ------- ----------------- ---------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Vasa leaf 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Dragendorff's reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853453 .anchor}**TLC Fingerprint Profile of Vasa Leaf** []{#_Toc229853454 .anchor}After development and derivatization, the TLC plate shows the following characteristic spots: ----------------------------------------------------------------------- **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ -------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.55 -- 0.65 Major prominent spot 4 0.70 -- 0.80 Characteristic marker spot corresponding to vasicine ----------------------------------------------------------------------- []{#_Toc229853455 .anchor}**Marker Compounds for Standardization of Vasa** ----------------------------------------------------------------------- **Sl. **Marker **API / Reported Requirement** No.** Compound** ------- ------------------ -------------------------------------------- 1 Vasicine Not less than 0.5 per cent w/w ----------------------------------------------------------------------- []{#_Toc229853456 .anchor}**Mode of Action of Vasa in Netra Rogas** Vasa possesses **Tikta--Kashaya Rasa**, **Sheeta Virya**, and **Raktapittahara** properties, making it highly effective in ocular disorders associated with **Pitta and Rakta vitiation**. Its **Shothahara** and **Chakshushya** actions help in reducing inflammation, redness, and burning sensation of the eyes. The presence of alkaloids like **vasicine** contributes to anti-inflammatory and antimicrobial activity, aiding in conditions such as **Abhishyanda, Netra Daha, Raktaja Netra Rogas**, and **Vrana of ocular tissues**. Thus, Vasa promotes ocular tissue healing and maintains visual health. ***02. AUSADHA (SHUNTHI)*** > ![](media/image2.png){width="4.958333333333333in" height="2.8in"} ***Fig. No : Aushadha (Shunthi)*** **Table No. 17: Description of *Aushadha (Shunthi)*** +------------------------+---------------------------------------------+ | **Botanical Name** | Zingiber Officinale(Roxb.) | +========================+=============================================+ | **Family** | Zingiberaceae | +------------------------+---------------------------------------------+ | **Vernacular Names** | > **Hindi --** Sonth | | | > | | | > **English --** Ginger root, Ginger | | | > | | | > **Marathi --** Sunth | | | > | | | > **Gujarati --** Sunth, Sundh, Suntha | | | > | | | > **Kannada --** Shunthi | | | > | | | > **Bengali --** Suntha, Sunthi | | | > | | | > **Tamil --** Sukku, Chukku | | | > | | | > **Telugu --** Sonthi, Sunti | | | | | | **Malayalam-** Chukku | +------------------------+---------------------------------------------+ | **Synonyms** | *Vishva, Nagara, Vishva, Vishvabheshaja, | | | Katubhadra, Mahoushadha, Shrngavera, | | | Ushana* | +------------------------+---------------------------------------------+ +-------------------------+--------------------------------------------+ | **Classical | ***Charak Samhita-** Triptighna, | | Categorization** | Arshoghna, Dipaniya, Shulaprashamana, | | | Trishnanigrahana.* | | | | | | ***Sushruta Samhita-** Pippalyadi, | | | Trikatu.* | | | | | | ***AshtangaHridya:** Vachadi* | | | | | | ***Bhava PrakashaNighantu**: | | | Haritakyadivarga,* | +=========================+============================================+ | **Botanical | > An erect perennial herb with aromatic | | Description** | > rhizome. | | | > | | | > **Stem**- erect, leafy, 15-150 cm tall. | | | > | | | > **Leave**s- subsessile, | | | > linear-lanceolate or lanceolate, | | | > acuminate, glabrous, 10-30 cm long. | | | > | | | > **Flowers**- shoot upto 12 cm long, | | | > clothed with sheaths; bracts 2-5 cm x 2 | | | > cm, light green; corolla tube light | | | > yellow, lip orbicular, dull purple with | | | > creamy blotches. | | | | | | Flowering and fruiting during | | | July-September. | +-------------------------+--------------------------------------------+ | **Distribution** | Cultivated almost throughout India**.** | +-------------------------+--------------------------------------------+ **Table No.18: Properties & Action of*Ausadha (Shunthi)* --** ----------------------------------------------------------------------- ***Rasa*** *Katu* -------------------------- -------------------------------------------- ***Guna*** *Laghu, Snigdha* ***Virya*** *Ushna* ***Vipaka*** *Madhura* ***Doshakarma*** *Kaphavatashamaka* ***Rogaghnakarma*** *Deepana, Pachana, Shwasa, Kasa, Shoola, Anulomana, Aamadoshahara, Kanthya, Shothahara, Hridya, Vrishya* ----------------------------------------------------------------------- +-------------------------+--------------------------------------------+ | **Chemical | Essential oil, Gingerol, Shogaol, Resinous | | Constituents** | matter, starch | +=========================+============================================+ | **Therapeutic Uses** | *Aamavata, Udararoga, Pandu, Aadhmana, | | | Agnimandhya* | +-------------------------+--------------------------------------------+ | **Part Used** | Kanda (Rhizome) | +-------------------------+--------------------------------------------+ | **Dosage** | *Churna* - 1-2 gm(Ref.-A.P.I.) | | | | | | *Churna-* 250mg --1gm (Ref.-B.P.N.) | +-------------------------+--------------------------------------------+ []{#_Toc229853457 .anchor}**Physicochemical Parameters of Shunthi** *(ZingiberofficinaleRoscoe,DriedRhizome)*\ *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 6.0 5.455 per cent per cent 2 Acid-insoluble Ash (% Not more than 1.5 0.47 per cent w/w) per cent 3 Water-soluble Extractive Not less than 10.0 13.768 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 4.0 5.528 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 7 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853458 .anchor}**Thin Layer Chromatography (TLC) for Identification of Shunthi** []{#_Toc229853459 .anchor}*(As per Ayurvedic Pharmacopoeia of India)* ----------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** -------- ---------------------- --------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate (93 : 7) 3 Test Solution Alcoholic extract of Shunthi rhizome 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Vanillin--Sulphuric acid reagent ----------------------------------------------------------------------- []{#_Toc229853460 .anchor}**TLC Fingerprint Profile of Shunthi Rhizome** After development and derivatization with vanillin--sulphuric acid reagent, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ --------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Characteristic marker spot corresponding to gingerols ------------------------------------------------------------------------ []{#_Toc229853461 .anchor}**Marker Compounds for Standardization of Shunthi** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 6-Gingerol Not less than 1.0 per cent w/w 2 Total Gingerols Not less than 1.5 per cent w/w ------------------------------------------------------------------------ []{#_Toc229853462 .anchor}**Mode of Action Shunthi In Netra Rogas** []{#_Toc229853463 .anchor}Shunthi possesses ***Katu Rasa*, *Ushna Virya***, and ***Laghu--Snigdha Guna***, making it effective in ocular disorders associated with *Kapha* and *Vata* vitiation. Its *Deepana--Pachana* and *Amapachana* actions help in clearing *Ama* and improving microcirculation in ocular tissues, thereby reducing heaviness, stickiness, and discharge of the eyes. The *Shothahara* and mild *Vedanasthapana* properties aid in alleviating inflammation, pain, and discomfort. The presence of bioactive constituents such as gingerols and shogaols contributes to anti-inflammatory, antioxidant, and antimicrobial activities, supporting its role in conditions like *Kaphaja Abhishyanda*, *Netra Shopha*, *Netra Shoola*, and early inflammatory eye disorders. Thus, Shunthi helps restore ocular clarity and supports the maintenance of visual function. ***03. Amrita (Guduchi)*** > ![](media/image3.png){width="3.658333333333333in" > height="2.4833333333333334in"} ***Fig. No.: Amrita / Guduchi*** > **Table No. 43: Description of *Amrita / Guduchi *** +---------------------+------------------------------------------------+ | **Botanical Name** | Tinospora Cordifolia(Willd.) | +=====================+================================================+ | **Family** | Menispermaceae | +---------------------+------------------------------------------------+ | **Vernacular | > **Hindi --** Giloe, Gurcha | | Names** | > | | | > **English --** Tinospora | | | > | | | > **Marathi --** Gulvel | | | > | | | > **Gujarati --** Galac, Garo | | | > | | | > **Kannada --** Amrutaballi | | | > | | | > **Bengali --** Gulancha | | | > | | | > **Tamil --** Seendal, Seendilkodi | | | > | | | > **Telugu --**Thippateega | | | | | | **Malayalam-** Chittamrutu | +---------------------+------------------------------------------------+ | **Synonyms** | *Amrita,Amritavalli, Madhuparni, Chinna, | | | Chinneruha, Vatsadani, Vayastha, Soma, | | | Tantrika, Kundali, Devanirmita, Vishalya, | | | Rasayani, Somavalli, Mandali, Jivanti, | | | Chakralakshanika* | +---------------------+------------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita-** Sandhaniya, Truptighna, | | Categorization** | Trushnanigrahana, Stanyashodhana, Snehopaga, | | | Dahaprashamana, Prajasthapana, Vayasthapana, | | | Tiktaskandha, Madhuraskandha* | | | | | | ***Sushruta Samhita-** Guduchyadivarga, | | | Patoladivarga, Aaragvadhadivarga, | | | Kakolyadivarga, Shyamadivarga, | | | Vallipanchamula* | | | | | | ***Ashtangahridya:** Guduchyadivarga, | | | Patoladivarga, Aaragvadhadivarga, | | | Shyamadivarga, Padamkadivarg* | | | | | | ***Bhava Prakashanighantu**: Guduchyadivarga* | +======================+===============================================+ | **Botanical | It is a Large Climber with Succulent, Corky | | Description** | And Grooved. | | | | | | **Stems-** Branches Possess Slender Pendulous | | | Fleshy Roots. | | | | | | **Leaves** -Membranous, Glabrous, 5-10 Cm | | | Long, Cordate, Petiole 2.5-7 Cm Long. | | | | | | **Flowers**- In Racemes of About 5 Cm; | | | Axillary, Terminal or From the Old Wood, Pale | | | Yellowish White In Colour. | | | | | | **Fruits**- Carpels, Dorsally Convex, | | | Ventrally Flat, Size of A Large Pea. | +----------------------+-----------------------------------------------+ | **Distribution** | Distributed Throughout Tropical India And | | | Also In Myanmar And Sri Lanka. | +----------------------+-----------------------------------------------+ **Table No. : Properties & Action Of *Amrita / Guduchi*** ----------------------------------------------------------------------- *Rasa* *Katu, Tikta, Kashaya* ----------------------- ----------------------------------------------- *Guna* *Laghu* *Virya* *Ushna* *Vipaka* *Madhura* *Doshakarma* *Tridoshashamaka* *Rogaghnakarma* *Rasayana, Balya, Daha, Raktashodhana, Krimighna, Vishaghna*etc*.* ----------------------------------------------------------------------- +-----------------------+----------------------------------------------+ | **Chemical | Giloin, Giloinin, Gilosterol, Berberine | | Constituents** | | +=======================+==============================================+ | **Therapeutic Uses** | *Kushtha, Vatarakta, Jvara, Pandu, Kamla**, | | | Prameha*** | +-----------------------+----------------------------------------------+ | **Part Used** | Kanda | +-----------------------+----------------------------------------------+ | **Dosage** | Churna- 1-3gm (Ref.-B.P.N.), 3-6gm | | | (Ref.-Api) | | | | | | Kwath- 40-80 Ml (Ref.-B.P.N.), | +-----------------------+----------------------------------------------+ []{#_Toc229853464 .anchor}**Physicochemical Parameters of Guduchi (*Tinospora cordifolia*) Stem** []{#_Toc229853465 .anchor}**(As per API)** ------------------------------------------------------------------------ **Sl. **Parameter** **API **Reported No.** Specification** Values** ------- ------------------------------ ----------------- --------------- 1 Total Ash (% w/w) Not more than 9.535 percent 16.0 2 Acid-Insoluble Ash (% w/w) Not more than 3.0 0.16 percent 3 Water-Soluble Extractive (% Not less than 15.56 percent w/w) 11.0 4 Alcohol-Soluble Extractive (% Not less than 3.0 4.472 w/w) 5 Loss on Drying at 105 °C (% Not more than 6 percent w/w) 10.0 6 Foreign Matter (% w/w) Not more than 2.0 ≤ 2.0 ------------------------------------------------------------------------ []{#_Toc229853466 .anchor}**Table 2: TLC Conditions for Identification of Guduchi (As per API)** ----------------------------------------------------------------------- **Sl. **Parameter** **Specification** No.** ------- ------------------- ------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ 2 Mobile Phase Chloroform : Methanol (9 : 1) 3 Sample Alcoholic extract of Guduchi stem 4 Application Volume 5 -- 10 µL 5 Detection UV 254 nm and 366 nm 6 Derivatizing Agent Anisaldehyde--Sulphuric acid reagent ----------------------------------------------------------------------- []{#_Toc229853467 .anchor}**Table 3: TLC Fingerprint Profile of Guduchi Stem** ----------------------------------------------------------------------- **Sl. **Rf Value **Nature of Spot** No.** (Approx.)** ------- ------------------- ------------------------------------------- 1 0.30 -- 0.35 Minor spot 2 0.55 -- 0.65 Distinct spot 3 0.72 -- 0.80 Major prominent spot 4 0.88 -- 0.93 Characteristic marker spot ----------------------------------------------------------------------- []{#_Toc229853468 .anchor}**Table 4: Marker Compounds Used for Standardization of Guduchi** ----------------------------------------------------------------------- **Sl. **Marker Compound** **Reported Assay Value** No.** ------- ------------------- ------------------------------------------- 1 Cordifolioside-A ≥ 0.02% w/w 2 Tinosporaside 0.03 -- 0.04% w/w ----------------------------------------------------------------------- **Mode of Action *Guduchi* In Netra Rogas** []{#_Toc229853469 .anchor}Guduchi possesses ***Tikta--Kashaya** **Rasa***, ***Ushna Virya*,** and ***Madhura Vipaka***, making it highly beneficial in ocular disorders involving *Pitta* and *Rakta* vitiation along with *Ama*. Its potent *Tridoshahara* nature, especially *Pitta--Rakta Shamaka*, helps in alleviating burning sensation, redness, and inflammatory changes in the eyes. The *Rasayana* and *Balya* properties of Guduchi promote nourishment and rejuvenation of ocular tissues, enhancing local immunity and resistance to recurrent eye diseases. Its *Shothahara*, *Dahaprashamana*, and *Raktaprasadana* actions contribute to the reduction of edema, congestion, and irritation. The presence of bioactive compounds such as tinosporaside, cordifolioside, and berberine imparts anti-inflammatory, antioxidant, and immunomodulatory effects, making it useful in conditions like *Pittaja Abhishyanda*, *Raktaja Netra Rogas*, *Netra Daha*, and chronic inflammatory eye disorders. Thus, Guduchi supports ocular healing, tissue vitality, and long-term visual health. ***04. DARUHARIDRA*** > ![](media/image4.jpeg){width="2.557638888888889in" > height="1.9848490813648294in"} ***Fig. No.: Daruharidra*** > **Table No. 41: Description of *Daruharidra*** +----------------------+-----------------------------------------------+ | **Botanical Name** | Berberis aristate DC. | +======================+===============================================+ | **Family** | Berberidaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Daruhaldi, Darhald | | | > | | | > **English --** Indian Barberry | | | > | | | > **Marathi --** Daruhalad, Talimkhana | | | > | | | > **Gujarati --** Daruharidra, Daruhuladur | | | > | | | > **Kannada --** Maradarishana, | | | > Maradarishina, Daruhaladi | | | > | | | > **Bengali --** Daruharidra | | | > | | | > **Tamil --** Gangeti, Varatiumanjal | | | > | | | > **Telugu --**Manupasupu | | | | | | **Malayalam-** Maramannal, Maramanjal | +----------------------+-----------------------------------------------+ | **Synonyms** | *Darvi, Pitadaru, Katankateri, Pachampacha, | | | Parjani, Kaliyak, Kaleyak, Pitadru, Haridru, | | | Pitak* | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | ***CharakSamhita-**Lekhaniya Kandughna, | | Categorization** | Arshoghna,Tiktaskandha* | | | | | | ***Sushruta Samhita-** Haridradi, Mustadi, | | | Lakshadi,* | | | | | | ***AshtangaHridya:** Haridradi, Mustadi, | | | Shirovirechana* | | | | | | ***Bhava PrakashaNighantu**: | | | HaritakyadiVarga* | +======================+===============================================+ +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Botanical | A large deciduous shrub, 1.8-3.6m high. Twigs | | Description** | whitish or pale yellowish brown, deeply | | | furrowed, rough. | | | | | | **Leaves-**3.8-10 by 1.5-3.3 cm, obovate or | | | elliptic, entire or spinous-toothed, base | | | gradually narrowed, dark green above, pale | | | be-neath. Petiole 0-4 mm. Inflorescence a | | | simple drooping raceme, 2.5-7.5 cm. long. | | | densely-flowered. | | | | | | **Fruit** 7-10 mm. long, ovoid, blue-black, | | | distinct style. | +======================+===============================================+ | **Distribution** | It grows in Himalayan region, between 6000 to | | | 10500 ft. high. Also grows in the hills of | | | Nilgiris in South India. | +----------------------+-----------------------------------------------+ **Table No. 42: Properties & Action of *Daruharidra*** ----------------------------------------------------------------------- ***Rasa*** *Tikta* ----------------------- ----------------------------------------------- ***Guna*** *Ruksha* ***Virya*** *Ushna* ***Vipaka*** *Katu* ***Doshakarma*** *Kaphapittashamaka* ***Rogaghnakarma*** *Varnashodhana, Vranaropana, Varnya, Rasayana, Shothahara, Vednasthapana, Raktashodhaka etc.* ----------------------------------------------------------------------- +----------------------+-----------------------------------------------+ | **Chemical | Berberine, Oxyacanthine, Berbamine, | | Constituents** | Palmatine, Jatrorrhizine, Columbamine, | | | Berberrubine, Hydrastine | +======================+===============================================+ | **Therapeutic Uses** | *Kandu, Medoroga, Mukharoga, Vrana, | | | Karnaroga, **Netraroga**, **Meha,** | | | Urustambha* etc. | +----------------------+-----------------------------------------------+ | **Part Used** | Mula, Kanda, Phala | +----------------------+-----------------------------------------------+ | **Dosage** | Kwath- 5-10 ml (Ref.-API), | | | | | | Churna -- 2-3 gm (Ref.-B.P.N.) | +----------------------+-----------------------------------------------+ []{#_Toc229853470 .anchor}**Physicochemical Parameters of Daruharidra** []{#_Toc229853471 .anchor}*(BerberisaristataDC.,DriedStem)*\ *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 7.0 2.73 per cent per cent 2 Acid-insoluble Ash (% Not more than 1.5 0.53 per cent w/w) per cent 3 Water-soluble Extractive Not less than 10 .0 8.312 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 8.0 7.342 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 8 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853472 .anchor}**Thin Layer Chromatography (TLC) for Identification of Daruharidra** *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** ------- ----------------- ---------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Chloroform : Methanol (9 : 1) 3 Test Solution Alcoholic extract of Daruharidra stem 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Dragendorff's reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853473 .anchor}**TLC Fingerprint Profile of Daruharidra Stem** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ --------------------------------------------- 1 0.25 -- 0.35 Minor spot 2 0.45 -- 0.55 Distinct spot 3 0.65 -- 0.75 Major prominent spot 4 0.80 -- 0.90 Characteristic marker spot corresponding to berberine ------------------------------------------------------------------------ []{#_Toc229853474 .anchor}**Marker Compounds for Standardization of Daruharidra** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Berberine Not less than 2.0 per cent w/w ------------------------------------------------------------------------ **Mode of Action of Daruharidra in Netra Rogas** Daruharidra possesses ***Tikta--Kashaya Rasa***, ***Ushna Virya***, and ***Katu Vipaka***, making it highly effective in ocular disorders associated with *Pitta*, *Kapha*, and *Rakta* vitiation, particularly in infective and inflammatory conditions. Its potent *Raktashodhaka*, *Kaphahara*, and *Lekhana* properties help in reducing ocular discharge, congestion, and turbidity. The *Shothahara* and *Vrana Ropana* actions aid in alleviating inflammation and promoting healing of ocular tissues. Daruharidra is well known for its *Chakshushya* and *Krimighna* effects, making it useful in bacterial and infective eye disorders. The presence of bioactive alkaloids such as berberine and palmatine contributes to strong antimicrobial, anti-inflammatory, and antioxidant activities, supporting its role in conditions like *Abhishyanda*, *Netra Srava*, *Netra Shopha*, *Raktaja Netra Rogas*, and ocular ulcers. Thus, Daruharidra helps purify ocular tissues, control infection, and maintain ocular clarity and visual health. []{#_Toc229853475 .anchor}**05. RAKTA CHANDAN** ![https://m.media-amazon.com/images/I/31Fccv0mJvL.jpg](media/image5.jpeg){width="3.4924245406824146in" height="2.2194444444444446in"} **Fig. No.: Rakta Chandan** []{#_Toc229853476 .anchor}**Table No.: Description of Rakta Chandan** +--------------------------------------------------------------+-------+ | +---------------+----------------------------------------+ | | | | Botanical | *Pterocarpus* *santalinus* L.f. | | | | | Name | | | | | +===============+========================================+ | | | | Family | Fabaceae | | | | +---------------+----------------------------------------+ | | | | Vernacular | > Hindi -- Rakta Chandan, Lal Chandan | | | | | Names | > | | | | | | > English--RedSandalwood\ | | | | | | > Marathi--TambadaChandan\ | | | | | | > Gujarati -- Ratanjali | | | | | | > | | | | | | > Kannada -- Rakta chandana | | | | | | > | | | | | | > Bengali -- Rakta Chandan | | | | | | > | | | | | | > Tamil -- Sivappu Sandanam | | | | | | > | | | | | | > Telugu -- Erra Chandanam | | | | | | > | | | | | | > Malayalam- Rakta Chandanam | | | | +---------------+----------------------------------------+ | | | | Synonyms | Raktachandana, Raktasara, Raktanga, | | | | | | Tilaparna | | | | +---------------+----------------------------------------+ | | | | Classical | *Charak Samhita-* Daha Prashamana, | | | | | C | Varnya | | | | | ategorization | | | | | | | *Sushruta Samhita-* Haridradi Gana | | | | | | | | | | | | *AshtangaHridya-* Daha Prashamana | | | | | | | | | | | | *Bhava PrakashaNighantu-* Chandanadi | | | | | | Varga | | | | +---------------+----------------------------------------+ | | | | Botanical | A medium-sized deciduous tree, 8--12 m | | | | | Description | in height. The heartwood is dark red | | | | | | to reddish-brown, hard, heavy, and | | | | | | aromatic. Leaves are alternate, ovate; | | | | | | flowers yellow arranged in axillary | | | | | | racemes. The heartwood is the | | | | | | medicinally useful part. | | | | +---------------+----------------------------------------+ | | | | Distribution | Endemic to South India, mainly Andhra | | | | | | Pradesh (Eastern Ghats); also | | | | | | cultivated in parts of Karnataka and | | | | | | Tamil Nadu. | | | | +---------------+----------------------------------------+ | | | | | | Table No. 24: Properties & Action of rakta chandan | | | | | | --------------------------------------------------------- | | | *Rasa* Tikta, Madhura | | | --------------------- ----------------------------------- | | | *Guna* Laghu, Ruksha | | | | | | *Virya* Sheeta | | | | | | *Vipaka* Katu | | | | | | *Doshakarma* Pittakapha Shamaka | | | | | | *Rogaghnakarma* Daha Prashamana, Raktaprasadana, | | | Varnya, Shothahara, Chakshushya | | | --------------------------------------------------------- | | | | | | +-------------------+------------------------------------+ | | | | Chemical | Santalin A & B, Pterocarpin, | | | | | Constituents | Isopterocarpin, Savinin, Tannins, | | | | | | Flavonoids, Phenolic compounds | | | | +===================+====================================+ | | | | Therapeutic Uses | Daha, Raktapitta, Kushtha, | | | | | | Mukhadushika, Vrana, Netraroga, | | | | | | Twakvikara | | | | +-------------------+------------------------------------+ | | | | Part Used | Kanda / Heartwood | | | | +-------------------+------------------------------------+ | | | | Dosage | > Churna: 1--3 g (Ref. B.P.N.) | | | | | | > | | | | | | > Lepa: As required (external use) | | | | +-------------------+------------------------------------+ | | | | | | []{#_Toc229853477 .anchor}Physicochemical Parameters of | | | Rakta Chandan | | | | | | (*Pterocarpussantalinus*L.f.,DriedHeartwood)\ | | | (As per Ayurvedic Pharmacopoeia of India) | | | | | | ---------------------------------------------------------- | | | Sl. Parameter API Requirement Observed / | | | No. Reported Values | | | ----- ------------------- ---------------- --------------- | | | 1 Total Ash (% w/w) Not more than 2.74 per cent | | | 5.0 per cent | | | | | | 2 Acid-insoluble Ash Not more than 0.25 per cent | | | (% w/w) 1.0 per cent | | | | | | 3 Water-soluble Not less than 1.672 per cent | | | Extractive (% w/w) 8.0 per cent | | | | | | 4 Alcohol-soluble Not less than 4.634 per cent | | | Extractive (% w/w) 10.0 per cent | | | | | | 5 Loss on Drying at Not more than 6 per cent | | | 105 °C (% w/w) 10.0 per cent | | | | | | 6 Foreign Matter (% Not more than Not more than | | | w/w) 2.0 per cent 2.0 per cent | | | ---------------------------------------------------------- | | | | | | []{#_Toc229853478 .anchor}Thin Layer Chromatography (TLC) | | | for Identification of Rakta Chandan | | | | | | (As per Ayurvedic Pharmacopoeia of India) | | | | | | ---------------------------------------------------------- | | | Sl. Parameter API Specification | | | No. | | | ------ ---------------- ---------------------------------- | | | 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate | | | | | | 2 Mobile Phase Toluene : Ethyl acetate (7 : 3) | | | | | | 3 Test Solution Alcoholic extract of Rakta Chandan | | | heartwood | | | | | | 4 Application 5 -- 10 µL | | | Volume | | | | | | 5 Detection Under UV light at 254 nm and 366 | | | nm | | | | | | 6 Derivatizing Anisaldehyde--Sulphuric acid | | | Reagent reagent | | | ---------------------------------------------------------- | | | | | | []{#_Toc229853479 .anchor}TLC Fingerprint Profile of Rakta | | | Chandan | | | | | | After development and derivatization, the TLC plate shows | | | the following characteristic spots: | | | | | | ---------------------------------------------------------- | | | Sl. Rf Value Description of Spot | | | No. (Approx.) | | | ------ -------------- ------------------------------------ | | | 1 0.25 -- 0.35 Minor spot | | | | | | 2 0.45 -- 0.55 Distinct spot | | | | | | 3 0.60 -- 0.70 Major prominent spot | | | | | | 4 0.75 -- 0.85 Characteristic marker spot | | | corresponding to santalin | | | ---------------------------------------------------------- | | | | | | []{#_Toc229853480 .anchor}Marker Compounds for | | | Standardization of Rakta Chandan | | | | | | ---------------------------------------------------------- | | | Sl. No. Marker Compound API / Reported Requirement | | | -------- ------------------- ----------------------------- | | | 1 Santalin (A & B) Not less than 1.0 per cent | | | w/w | | | | | | ---------------------------------------------------------- | | | | | | []{#_Toc229853481 .anchor}Mode of Action of Rakta Chandan in | | | Netra Rogas | | | | | | Rakta Chandan, due to its *Sheeta Virya, Tikta--Madhura | | | Rasa*, and Pittashamaka properties, is highly effective in | | | ocular disorders caused by *Pitta and Rakta dushti.* Its | | | *Daha-prashamana* and *Shothahara* actions relieve burning | | | sensation, redness, and inflammation of the eyes. The | | | *Raktaprasadana* and *Chakshushya* properties help purify | | | ocular blood supply and promote visual comfort. | | | Phytoconstituents such as santalin and flavonoids exhibit | | | antioxidant and anti-inflammatory activities, making Rakta | | | Chandan useful in *Netra Daha, Abhishyanda, Raktaja* *Netra | | | Rogas*, and inflammatory eye conditions. Thus, it plays a | | | significant role in soothing and maintaining ocular health. | | +==============================================================+=======+ +--------------------------------------------------------------+-------+ []{#_Toc229853482 .anchor}**06. CHITRAKA** ![Plumbago Indica (Chitrakmool) at ₹ 330/kg \| Jaipur \| ID: 2854978031462](media/image6.jpeg){width="4.083333333333333in" height="2.316666666666667in"} **Fig. No.:** Chitraka **Table No.:** Description of Chitraka +------------------+---------------------------------------------------+ | **Botanical | *Plumbago zeylanica* Linn. | | Name** | | +==================+===================================================+ | **Family** | Plumbaginaceae | +------------------+---------------------------------------------------+ | **Vernacular | > **Hindi --** Chitrak, Chita | | Names** | > | | | > **English--**Leadwort,WhiteLeadwort\ | | | > **Marathi--**Chitrak\ | | | > **Gujarati --Chitro, chitra** | | | > | | | > **Kannada --** Chitramula | | | > | | | > **Bengali --** Chita | | | > | | | > **Tamil --** Chittiramoolam | | | > | | | > **Telugu --** Chitrakamu | | | > | | | > **Malayalam-** Chitrakam | +------------------+---------------------------------------------------+ | **Synonyms** | Agni, Dahana, Jvalana, Deepana, Vyala | +------------------+---------------------------------------------------+ | **Classical | ***Charak Samhita**-* Deepaniya, Bhedaniya | | Categorization** | | | | ***Sushruta Samhita**-* Arkadi Gana | | | | | | ***AshtangaHridya**-* Deepaniya | | | | | | ***Bhava PrakashaNighantu**-* Haritakyadi Varga | +------------------+---------------------------------------------------+ | **Botanical | A perennial subshrub, 30--90 cm in height. Roots | | Description** | are thick, cylindrical, brownish externally and | | | yellowish internally. Leaves are simple, | | | ovate-oblong. Flowers are white, arranged in | | | terminal spikes. The root is the medicinally | | | useful part. | +------------------+---------------------------------------------------+ | **Distribution** | Widely distributed throughout India, especially | | | in tropical and subtropical regions; grows in | | | dry, sandy soils. | +------------------+---------------------------------------------------+ []{#_Toc229853483 .anchor}**Table No.: Properties & Action of Chitraka** ----------------------------------------------------------------------- **Rasa** Katu ------------------- --------------------------------------------------- **Guna** Laghu, Ruksha, Tikshna **Virya** Ushna **Vipaka** Katu **Doshakarma** Kapha--Vata Shamaka **Rogaghnakarma** Deepana, Pachana, Bhedana, Lekhana, Shothahara ----------------------------------------------------------------------- +----------------------+-----------------------------------------------+ | **Chemical | Plumbagin, Chitranone, Plumbagic acid, | | Constituents** | Sitosterol, Flavonoids, Tannins. | +======================+===============================================+ | **Therapeutic Uses** | Agnimandya, Grahani, Arsha, Gulma, Udara, | | | Amavata, Kushtha, Shotha | +----------------------+-----------------------------------------------+ | **Part Used** | Mula (Root) | +----------------------+-----------------------------------------------+ | **Dosage** | - **Churna**: 125--250 mg | | | | | | - **Kwatha**:20--40ml\ | | | (Ref.: API / B.P.N.) | +----------------------+-----------------------------------------------+ []{#_Toc229853484 .anchor}**Physicochemical Parameters of Chitraka** (*Plumbagozeylanica*L.,DriedRoot)\ *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------ **Sl. **Parameter** **API **Observed / Reported No.** Requirement** Values** ------- ------------------------- ---------------- --------------------- 1 Total Ash (% w/w) Not more than 4.614 % 6.0% 2 Acid-insoluble Ash (% Not more than 2.391% w/w) 1.5% 3 Water-soluble Extractive Not less than 14.824 % (% w/w) 7.0% 4 Alcohol-soluble Not less than 6.932% Extractive (% w/w) 9.0% 5 Loss on Drying at 105 °C Not more than 7 % (% w/w) 10.0% 6 Foreign Matter (% w/w) Not more than Not more than 2.0% 2.0% ------------------------------------------------------------------------ []{#_Toc229853485 .anchor}**Thin Layer Chromatography (TLC) for Identification of Chitraka** []{#_Toc229853486 .anchor}*(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** --------- ----------------------- -------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate (8 : 2) 3 Test Solution Alcoholic extract of Chitraka root 4 Application Volume 5 -- 10 µL 5 Detection UV light at 254 nm and 366 nm 6 Derivatizing Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853487 .anchor}**TLC Fingerprint Profile of Chitraka** ----------------------------------------------------------------------- **Sl. **Rf Value **Description of Spot** No.** (Approx.)** -------- --------------------- ---------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Marker spot corresponding to plumbagin ----------------------------------------------------------------------- []{#_Toc229853488 .anchor}**Marker Compounds for Standardization of Chitraka** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Plumbagin Not less than 0.5% w/w ------------------------------------------------------------------------ []{#_Toc229853489 .anchor}**Mode of Action of Chitraka** Chitraka, owing to its ***Ushna Virya**, **Katu Rasa***, and ***Tikshna Guna***, acts as a potent ***Deepana--Pachana drug***, enhancing Jatharagni and removing Ama. Its Kapha--Vata shamaka and Lekhana properties help in reducing obstruction of channels and breaking down pathological accumulations. The active constituent **plumbagin** exhibits digestive stimulant, anti-inflammatory, antimicrobial, and carminative activities. Thus, Chitraka is highly effective in disorders like Agnimandya, Grahani, Arsha, Gulma, and Amavata by restoring metabolic balance and promoting proper digestion and absorption. []{#_Toc229853490 .anchor}07. **BHUNIMBA (CHIRAYTA)KIRATTIKTA** ![](media/image7.jpeg){width="3.675in" height="2.4583333333333335in"} **Fig. No.: Bhunimba (Chirayta**)**kirattikta** +----------------------+-----------------------------------------------+ | **Botanical Name** | *Swertia chirayita* (Roxb.) Buch-Ham. ex C.B. | | | Clarke | +======================+===============================================+ | **Family** | Gentianaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Chirayta, Kirayat | | | > | | | > **English --** Chiretta, Indian Gentian | | | > | | | > **Marathi --** Chirayata, kaduchitayata | | | > | | | > **Gujarati --** Kariyatu | | | > | | | > **Kannada --** Chirata | | | > | | | > **Bengali --** chirata | | | > | | | > **Tamil --** Nilavembu | | | > | | | > **Telugu --** Nilavembu | | | | | | **Malayalam-** Kiriyattu | +----------------------+-----------------------------------------------+ | **Synonyms** | Kirata, Kiratikta, Bhunimba, Anaryatikta | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita-*** Tikta Skandha, | | Categorization** | Jvaraghna | | | | | | ***Sushruta Samhita-*** Aragvadhadi Gana | | | | | | ***Ashtanga Hridya-*** Tikta Skandha | | | | | | ***Bhava Prakasha Nighantu**-* Guduchyadi | | | Varga | +======================+===============================================+ +----------------------+-----------------------------------------------+ ----------------------------------------------------------------------- **Botanical An erect annual or biennial herb, 0.6--1.5 m Description** high. Stem slender, cylindrical, branched. Leaves opposite, sessile, ovate-lanceolate, 5--10 cm long. Flowers greenish-yellow with purple streaks, arranged in terminal panicles. Fruits are small capsules containing numerous seeds. ----------------------- ----------------------------------------------- **Distribution** Native to the temperate Himalayas at altitudes of **4000--9000 ft**, found in regions of **Himachal Pradesh, Uttarakhand, Sikkim, and Nepal**. ----------------------------------------------------------------------- **Table No. 42: Properties & Action of Chirayta/Kirattikta** ----------------------------------------------------------------------- ***Rasa*** Tikta ------------------------ ---------------------------------------------- ***Guna*** Laghu, Ruksha ***Virya*** Sheeta ***Vipaka*** Katu ***Doshakarma*** Pittakapha Shamaka ***Rogaghnakarma*** Jvaraghna, Raktashodhaka, **Chakshushya,** Kandughna, Shothahara. ----------------------------------------------------------------------- +----------------------+-----------------------------------------------+ | **Chemical | Swertiamarin, Amarogentin, Mangiferin, | | Constituents** | Swerchirin, Gentianine, Oleanolic acid, | | | Flavonoids | +======================+===============================================+ | **Therapeutic Uses** | Jvara, Kandu, Kushtha, Raktapitta, | | | **Prameha**, **Netraroga,** Yakritvikara. | +----------------------+-----------------------------------------------+ | **Part Used** | Panchanga (Whole plant) | +----------------------+-----------------------------------------------+ | **Dosage** | > **Kwatha:** 50--100 ml (Ref. API) | | | > | | | > **Churna:** 1--3 g (Ref. B.P.N.) | +----------------------+-----------------------------------------------+ []{#_Toc229853491 .anchor}**Physicochemical Parameters of Chirayta /kirattikta** (*Swertia chirayita*, Dried Whole Plant)\ **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 10.0 5.76 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 0.115 per cent w/w) per cent 3 Water-soluble Extractive Not less than 15.0 14.664 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 10.0 11.456 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 6 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853492 .anchor}**Thin Layer Chromatography (TLC) for Identification of Chirayta/kirattikta** **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** -------- -------------------- ------------------------------------------ 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Chirayta 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853493 .anchor}**TLC Fingerprint Profile of Chirayta** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ----------------- ---------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.55 -- 0.65 Major prominent spot 4 0.70 -- 0.80 Characteristic marker spot corresponding to swertiamarin ------------------------------------------------------------------------ []{#_Toc229853494 .anchor}**Mode of Action of Chirayta in Netra Rogas** Chirayta, owing to its ***Tikta Rasa**, **Sheeta Virya***, and ***Pittakapha Shamaka*** properties, is highly beneficial in ocular disorders caused by **Pitta and Rakta vitiation**. Its **Raktashodhaka** and **Shothahara** actions help reduce inflammation, burning sensation, redness, and discharge in conditions such as ***Abhishyanda, Netra Daha, Raktaja Netra Rogas***, and ***Pittaja Netrabhishyanda**.* The presence of bitter glycosides like ***swertiamarin*** and ***amarogentin*** imparts anti-inflammatory, antioxidant, and antimicrobial activities, promoting ocular tissue cleansing and strengthening vision. Thus, Chirayta acts as a ***Chakshushya and Netra-prasadaka drug**,* supporting ocular health. []{#_Toc229853495 .anchor}**08. NIMBA TWAK** ![Neem tree bark has the potential to treat coronaviruses - Earth.com](media/image8.jpeg){width="3.5166666666666666in" height="2.341666666666667in"} **Fig. No.: Nimba Twak** +----------------------+-----------------------------------------------+ | **Botanical Name** | *Azadirachta indica A.juss.syn | | | meliaazadirachta Linn* | +======================+===============================================+ | **Family** | Meliaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Neem, Nimb | | | > | | | > **English --** Neem, Indian Lilac, margosa | | | > tree | | | > | | | > **Marathi --** Kadunimb | | | > | | | > **Gujarati --** Limdo | | | > | | | > **Kannada --** Bevu | | | > | | | > **Bengali --** Nim | | | > | | | > **Tamil --** Vembu | | | > | | | > **Telugu --** Vepa | | | > | | | > **Malayalam-** Aryaveppu | +----------------------+-----------------------------------------------+ | **Synonyms** | Nimba, Arishta, Pichumarda, Sarvatobhadra, | | | Hingu Nimba | +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita**- Tikta Skandha, | | Categorization** | Kandughna, Krimighna* | | | | | | ***Sushruta Samhita**- Aragvadhadi Gana* | | | | | | ***AshtangaHridya**- Tikta Skandha* | | | | | | ***Bhava Prakasha Nighantu**-* *Guduchyadi | | | Varga* | +----------------------+-----------------------------------------------+ | **Botanical | A large evergreen tree attaining a height of | | Description** | 12--18 m. Bark (twak) is grey to dark brown, | | | rough, fissured, and exfoliating in irregular | | | scales. Leaves are imparipinnate with | | | serrated leaflets. Flowers white, fragrant; | | | fruits drupaceous, yellow when ripe | +----------------------+-----------------------------------------------+ | **Distribution** | Widely distributed throughout India, commonly | | | found in tropical and subtropical regions, | | | plains, roadsides, and cultivated areas. | +----------------------+-----------------------------------------------+ **Table No. 24: Properties & Action of *nimb*** ----------------------------------------------------------------------- ***Rasa*** *Tikta, Kashaya* ------------------------ ---------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Sheeta* ***Vipaka*** *Katu* ***Doshakarma*** *Pittakapha Shamaka* ***Rogaghnakarma*** *Kandughna, Krimighna, Raktashodhaka, Shothahara, **Chakshushya.*** ----------------------------------------------------------------------- +-----------------------+----------------------------------------------+ | **Chemical | Nimbin, Nimbidin, Azadirachtin, Salannin, | | Constituents** | Gedunin, Tannins, Flavonoids. | +=======================+==============================================+ | **Therapeutic Uses** | *Kandu, Kushtha, Vrana, **Raktapitta,** | | | Krimi, **Netraroga,** **Prameha*** | +-----------------------+----------------------------------------------+ | **Part Used** | *Twak* (Bark) | +-----------------------+----------------------------------------------+ | **Dosage** | **Kwatha:** 50--100 ml (Ref. API) | | | | | | **Churna:** 3--5 g (Ref. B.P.N.) | +-----------------------+----------------------------------------------+ []{#_Toc229853496 .anchor}**Physicochemical Parameters of Nimba Twak** (*Azadirachta indica* A. Juss., Dried Bark)\ **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 10.0 5.24 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 0.245 per cent w/w) per cent 3 Water-soluble Extractive Not less than 12.0 34.234 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 6.0 12.623 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 6 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853497 .anchor}**Thin Layer Chromatography (TLC) for Identification of Nimba Twak** **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** -------- -------------------- ------------------------------------------ 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Nimba twak 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853498 .anchor}**TLC Fingerprint Profile of Nimba Twak** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ---------------- ----------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.55 -- 0.65 Major prominent spot 4 0.70 -- 0.80 Characteristic marker spot corresponding to nimbin / azadirachtin ------------------------------------------------------------------------ []{#_Toc229853499 .anchor}**Marker Compounds for Standardization of Nimba Twak** ------------------------------------------------------------------------ **Sl. **Marker **API / Reported Requirement** No.** Compound** ------- --------------- ------------------------------------------------ 1 Nimbin Not less than 0.4 per cent w/w 2 Azadirachtin Not less than 0.2 per cent w/w ------------------------------------------------------------------------ []{#_Toc229853500 .anchor}**Mode of Action of Nimba Twak in Netra Rogas** Nimba Twak, due to its ***Tikta--Kashaya Rasa***, ***Sheeta Virya***, and ***Pittakapha Shamaka*** properties, is highly effective in ocular disorders involving ***Pitta* and *Rakta* vitiation**. Its ***Raktashodhaka**, **Shothahara***, and ***Krimighna*** actions help alleviate inflammation, itching, discharge, and microbial involvement in conditions such as ***Abhishyanda, Kandu Yukta Netra* *Rogas, Netra Daha***, and ***Raktaja Netrabhishyanda***. The presence of bioactive compounds like **nimbin and azadirachtin** provides antimicrobial, anti-inflammatory, and antioxidant effects, promoting ocular tissue purification and healing. Thus, Nimba Twak acts as a potent ***Chakshushya* and *Netra-shodhaka* drug**, supporting ocular health and vision. **09. KUTAKI** ![Backtobasics Kutki - Kutki Root - Katuki Jadd - Kutaki Roots - Picrorhiza Kurroa - Pure & Natural (400)](media/image9.jpeg){width="3.091666666666667in" height="2.2083333333333335in"} **Fig. No.: Kutaki** +----------------------+-----------------------------------------------+ | **Botanical Name** | *Picrorhiza kurroa* Royle ex Benth. | +======================+===============================================+ | **Family** | Plantaginaceae *(earlier Scrophulariaceae)* | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Kutaki, Katuki | | | > | | | > **English --** Picrorhiza, Kutki | | | > | | | > **Marathi --** Kutaki | | | > | | | > **Gujarati --** Katuki, katu | | | > | | | > **Kannada --** Katuka rohini | | | > | | | > **Bengali --** Kutki | | | > | | | > **Tamil --** Katuki | | | > | | | > **Telugu --** Katuka | | | > | | | > **Malayalam-** Katuki, katuk rohini | +----------------------+-----------------------------------------------+ | **Synonyms** | Katuki, Tikta, Rohini, Matsyakshi | +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita**-* Bhedaniya, Tikta | | Categorization** | Skandha | | | | | | ***Sushruta Samhita**-* Aragvadhadi Gana | | | | | | ***Ashtanga Hridya**-* Bhedaniya | | | | | | ***Bhava PrakashaNighantu**-* Guduchyadi | | | Varga | +----------------------+-----------------------------------------------+ | **Botanical | A small perennial herb with creeping | | Description** | rhizomes. Leaves are radical, ovate, | | | serrated. Flowers bluish-purple arranged in | | | terminal spikes. Rhizome is long, | | | cylindrical, bitter in taste, and medicinally | | | important | +----------------------+-----------------------------------------------+ | **Distribution** | Found in **Himalayan regions** at altitudes | | | of **9000--15000 ft**, particularly in | | | **Jammu & Kashmir, Himachal Pradesh, | | | Uttarakhand, and Sikkim**. | +----------------------+-----------------------------------------------+ **Table No. 24: Properties & Action of Kutaki** ----------------------------------------------------------------------- ***Rasa*** Tikta,katu ------------------------ ---------------------------------------------- ***Guna*** Laghu, Ruksha ***Virya*** Sheeta/ushna? ***Vipaka*** Katu ***Doshakarma*** Pittakapha Shamaka ***Rogaghnakarma*** Bhedana, Raktashodhaka, Shothahara, **Chakshushya,** Yakrituttejaka ----------------------------------------------------------------------- +-----------------------+----------------------------------------------+ | **Chemical | Picroside I, Picroside II, Kutkoside, | | Constituents** | Apocynin, Vanillic acid, Cucurbitacins. | +=======================+==============================================+ | **Therapeutic Uses** | Kamala, Jvara, Kushtha, **Raktapitta, | | | Prameha**, Yakritvikara, **Netraroga** | +-----------------------+----------------------------------------------+ | **Part Used** | Mula / Rhizome | +-----------------------+----------------------------------------------+ | **Dosage** | **Churna:** 500 mg -- 1 g | | | | | | **Kwatha:**20--40ml\ | | | *(Ref.: API / B.P.N.)* | +-----------------------+----------------------------------------------+ []{#_Toc229853501 .anchor}**Physicochemical Parameters of Kutaki** (*Picrorhizakurroa*,DriedRhizome)\ **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 6.0 5.46 per cent per cent 2 Acid-insoluble Ash (% Not more than 1.0 0.825 per cent w/w) per cent 3 Water-soluble Extractive Not less than 20.0 33.70 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 10.0 23.744 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 6 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853502 .anchor}**Thin Layer Chromatography (TLC) for Identification of Kutaki** **(As per Ayurvedic Pharmacopoeia of India)** ----------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** -------- --------------------- ---------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Chloroform : Methanol : Water (6 : 4 : 1) 3 Test Solution Alcoholic extract of Kutaki rhizome 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Anisaldehyde--Sulphuric acid reagent ----------------------------------------------------------------------- []{#_Toc229853503 .anchor}**TLC Fingerprint Profile of Kutaki** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ --------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.55 -- 0.65 Major prominent spot 4 0.70 -- 0.80 Characteristic marker spot corresponding to picroside ------------------------------------------------------------------------ []{#_Toc229853504 .anchor}**Marker Compounds for Standardization of Kutaki** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** --------- -------------------------- ----------------------------------- 1 Picroside-I & II (total) Not less than 4.0 per cent w/w ------------------------------------------------------------------------ []{#_Toc229853505 .anchor}**Mode of Action of Kutaki in Netra Rogas** Kutaki, endowed with **Tikta Rasa**, **Sheeta Virya**, and **Pittakapha Shamaka** properties, is highly beneficial in ocular disorders arising from **Pitta and Rakta dushti**. Its **Raktashodhaka** and **Yakrit-uttejaka** actions help in systemic detoxification, indirectly improving ocular health by correcting **Rakta and Pitta imbalance**. Kutaki's **Shothahara** and **Chakshushya** properties aid in reducing inflammation, redness, and burning sensation in conditions such as **Raktaja Netra Rogas, Abhishyanda, Netra Daha**, and **Pittaja ocular disorders**. The presence of **picrosides** contributes to anti-inflammatory, antioxidant, and hepatoprotective effects, thereby supporting ocular tissue nourishment and vision. **10. PATOL** ![](media/image10.jpeg){width="3.725in" height="2.25in"} ***Fig. No. : Patol*** **Table No. 23: Description of *Patol*** +----------------------+-----------------------------------------------+ | **Botanical Name** | Trichosanthes dioica | +======================+===============================================+ | **Family** | Cucurbitaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Parval, Parvar, Paror, Parora | | | > | | | > **English --** Pointed Gourd | | | > | | | > **Marathi --** Parval | | | > | | | > **Gujarati --** Patol | | | > | | | > **Kannada --** Padval | | | > | | | > **Bengali --** Patol, Palta | | | > | | | > **Tamil --** Pudalai | | | > | | | > **Telugu --** Potal | | | > | | | > **Malayalam-**Patolam | +----------------------+-----------------------------------------------+ | **Synonyms** | *Kulaka, Tikt, Panduk, Karkashacchad, | | | Rajiphala, Panduphala, Rajeya, Amritaphala, | | | Bijagarbha, Prateek, Kushthaha, Kasabhanjan* | +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita**- Truptighna, | | Categorization** | Trushnanigrahana.* | | | | | | ***Sushruta Samhita**- Patoladi, | | | Aaragvadhadi* | | | | | | ***AshtangaHridya**: Patoladi, Aaragvadhadi* | | | | | | ***Bhava PrakashaNighantu**: Shakavarga,* | +----------------------+-----------------------------------------------+ | **Botanical | > Climber with wooly stem having tendrils. | | Description** | > | | | > **Leaves-** 7.5 x 5 cm., ovate-oblong, | | | > cordate, acute, rough on both surfaces. | | | > | | | > **Flowers**- dioecious. Male flowers not | | | > racemed. Calyx-tube 4.5 cm. Anthers free. | | | > | | | > **Fruit-** 5-9 cm, oblong or nearly | | | > spherical, smooth, orange-red when ripe | | | > seeds helf-ellipsoid, compressed. | +----------------------+-----------------------------------------------+ | **Distribution** | Throughout the plains of north India, | | | extending to Assam and Bengal. | +----------------------+-----------------------------------------------+ **Table No. 24: Properties & Action of *Patol *** ---------------------------------------------------------------------------- ***Rasa*** *Tikta* ----------------------- ---------------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Ushna* ***Vipaka*** *Katu* ***Doshakarma*** *Tridoshashamaka(*Root*-Rechana,*Stem-*Kaphahara,* Leaf *-- Pittahara,* Fruits*- Tridoshahara)* ***Rogaghnakarma*** *Pachaka, Viryavardhaka, Agnidipaka, Kasaghna, Jvarghna, Krimighna* ---------------------------------------------------------------------------- +----------------------+-----------------------------------------------+ | **Chemical | Saponin, Bitter principles, small amount of | | Constituents** | essential oil, traces of tannin | +======================+===============================================+ | **Therapeutic Uses** | In *pittapradhana* roga, *patol* is used for | | | *virechana karma,* | | | | | | The patra is useful as *deepana, pachana, | | | balya.* | +----------------------+-----------------------------------------------+ | **Part Used** | Panchaga | +----------------------+-----------------------------------------------+ | **Dosage** | *Svarasa-* 10-20 ml, | | | | | | *Kwatha* -- 50- 100ml | +----------------------+-----------------------------------------------+ []{#_Toc229853506 .anchor}**Physicochemical Parameters of Patola (Patol)** []{#_Toc229853507 .anchor}**TrichosanthesdioicaRoxb.**\ **As per Ayurvedic Pharmacopoeia of India (API)** ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 15.0 9.215 per cent per cent 2 Acid-insoluble Ash (% Not more than 3.0 1.939 per cent w/w) per cent 3 Water-soluble Extractive Not less than 15.0 18.0 -- 28.0 per (% w/w) per cent cent 4 Alcohol-soluble Not less than 10.0 24.04 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 6 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853508 .anchor}**Thin Layer Chromatography (TLC) for Identification of Patola** **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** -------- -------------------- ------------------------------------------ 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Patola leaf 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853509 .anchor}**TLC Fingerprint Profile of Patola Leaf** []{#_Toc229853510 .anchor}After development and derivatization, the TLC plate shows the following characteristic spots: -------------------------------------------------------------------------- **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ ----------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.55 -- 0.65 Major prominent spot 4 0.70 -- 0.80 Characteristic marker spot corresponding to triterpenoids / flavonoids -------------------------------------------------------------------------- []{#_Toc229853511 .anchor}**Marker Compounds for Standardization of Patola** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** --------- ---------------------------- --------------------------------- 1 Cucurbitacin B (reported) Not less than 0.1 per cent w/w 2 Total bitter principles Not less than 1.0 per cent w/w ------------------------------------------------------------------------ []{#_Toc229853512 .anchor}**Mode of Action of Patola in Netra Rogas** Patola possesses *Tikta Rasa*, *Laghu--Ruksha Guna*, *Ushna Virya*, and *Katu Vipaka*, making it highly effective in ocular disorders arising from *Pitta* and *Kapha* vitiation, particularly those involving inflammatory, infective, and toxic pathology. Its potent *Pittashamana* and *Raktaprasadana* properties help in alleviating burning sensation, redness, excessive discharge, and irritation of the eyes. The *Shothahara* and *Dahaprashamana* actions contribute to the reduction of ocular inflammation, swelling, and discomfort. Patola is well known for its *Krimighna*, *Vishaghna*, and *Kandughna* properties, indicating strong antimicrobial, detoxifying, and anti-allergic effects, which are especially beneficial in infective and allergic eye conditions. Its *Lekhana* and *Srotoshodhana* actions help in clearing obstructed channels and reducing excessive secretions in the ocular tissues. The presence of bioactive constituents such as cucurbitacins and flavonoids imparts anti-inflammatory, antimicrobial, and antioxidant activities, supporting its therapeutic role in conditions like *Pittaja Abhishyanda*, *Kaphaja Abhishyanda*, *Netra Kandu*, *Netra Daha*, and *Raktaja Netra Rogas*. Thus, Patola aids in detoxifying ocular tissues, controlling inflammation and infection, and restoring clarity, comfort, and overall ocular health. ![](media/image11.jpeg){width="3.136069553805774in" height="2.0227274715660544in"} ***11. HARITAKI*** ***Fig. No.: Haritaki*** **Table No. 27: Description of *Haritaki-*** +----------------------+-----------------------------------------------+ | **Botanical Name** | Terminalia Chebula Retz. | +======================+===============================================+ | **Family** | Combretaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Harad, Harre, Harar | | | > | | | > **English --** Myrobalan, Chebulic | | | > Myrobalan | | | > | | | > **Marathi --** Hirda, Haritaki, Harda, | | | > Hireda | | | > | | | > **Gujarati --** Hirdo, Himaja, Pulo-harda | | | > | | | > **Kannada --** Alalekai | | | > | | | > **Bengali -** Haritaki | | | > | | | > **Tamil --** Kadukkai | | | > | | | > **Telugu --** Karaka, Karakkaya | | | > | | | > **Malayalam-** Katukka | +----------------------+-----------------------------------------------+ | **Synonyms** | *Abhaya, Pathya, Kayastha, Putna, Amrita, | | | Haimavati, Vayastha, Shiva, Vijaya, Avyatha, | | | Chetaki, Shreyasee, Jivanti, Rohini* | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | ***Charak Samhita-** Jvarahara, | | Categorization** | Virechanopaga, Arshoghna, Kushthaghna, | | | Vayasthapana, Hikkanigrahana, Kasahara* | | | | | | ***Sushruta Samhita-** Pippalyadi, Eladi, | | | Vachadi, Triphala, Aamalakyadi, Parushakadi, | | | Mustadi* | | | | | | ***Ashtanga Hridya:** Vachadi, Parushakadi, | | | Mustadi, Mushkakadi* | | | | | | ***Bhava Prakasha Nighantu**: | | | Haritakyadivarga,* | +======================+===============================================+ +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Botanical | It is a large tree, with rust-coloured or | | Description** | silvery hairs over the younger branchlets | | | etc. | | | | | | **Leaves** mostly subopposite, distant, ovate | | | or oblong-ovate, 8-20 cm. long, deciduous in | | | the cold season. | | | | | | **Flowers**- dull-white or yellowish, with a | | | strong offensive smell, in spikes from the | | | upper axils and in small terminal panicies. | | | | | | **Fruits**-obovoid or ellipsoidal from a | | | broad base, glabrous, more or less S-ribbed | | | when dry. (Flowers in April-May and fruits in | | | November-January) | +======================+===============================================+ | **Distribution** | Abundant in Northern India, also occurs in | | | Bihar, West Bengal, Assam, Central India and | | | South India**.** | +----------------------+-----------------------------------------------+ **Table No. 28: Properties & Action of *Haritaki *** ----------------------------------------------------------------------- ***Rasa*** *Panchras (Lavan-rahit, Kashaya Pradhan)* ------------------------ ---------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Uahna* ***Vipaka*** *Madhura* ***Doshakarma*** *Tridoshahara* ***Rogaghnakarma*** *Rasayana, **Chakshushya,** Aayuvardhaka, Anulomana, Krimighna, **Pramehaghna,** Arshoghna etc.* ----------------------------------------------------------------------- ----------------------------------------------------------------------- **Chemical Tannins, chebulagic acid, chebulic acid, Constituents** chebulinic acid, ellagic acid, gallic and terchebin, ellagi tannin, terchebulin. ----------------------- ----------------------------------------------- **Therapeutic Uses** *Vibandha, Aruchi, Pandu, **Prameha,** Tamakashvasa, Udararoga, Udavarta, Gulma, Sotha, Kasa etc.* **Part Used** Phala **Dosage** *Churna*- 3-6 gm ----------------------------------------------------------------------- []{#_Toc229853513 .anchor}**Physicochemical Parameters of Haritaki** *(TerminaliachebulaRetz.,DriedFruitPericarp)*\ *(As per Ayurvedic Pharmacopoeia of India)* +-----+-----------------------+------------------+--------------------+ | ** | **Parameter** | **API | **Observed / | | Sl. | | Requirement** | Reported Values** | | No | | | | | .** | | | | +=====+=======================+==================+====================+ | 1 | Total Ash (% w/w) | Not more than | 2.53 per cent | | | | 5.0 per cent | | +-----+-----------------------+------------------+--------------------+ | 2 | Acid-insoluble Ash (% | Not more than | 0.451 per cent | | | w/w) | 1.0 per cent | | +-----+-----------------------+------------------+--------------------+ | 3 | Water-soluble | Not less than | 54.263 per cent | | | Extractive (% w/w) | 20.0 per cent | | +-----+-----------------------+------------------+--------------------+ | 4 | Alcohol-soluble | Not less than | 39.368 percent | | | Extractive (% w/w) | 15.0 | | | | | | | | | | Percent | | +-----+-----------------------+------------------+--------------------+ | 5 | Loss on Drying at 105 | Not more than | 8 percent | | | °C (% w/w) | 12.0 | | | | | | | | | | Percent | | +-----+-----------------------+------------------+--------------------+ | 6 | Foreign Matter (% | Not more than | Not more than 2.0 | | | w/w) | 2.0 per cent | per cent | +-----+-----------------------+------------------+--------------------+ []{#_Toc229853514 .anchor}**Thin Layer Chromatography (TLC) for Identification of Haritaki** *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** ------- ----------------- ----------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Haritaki fruit pericarp 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Ferric chloride reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------- []{#_Toc229853515 .anchor}**TLC Fingerprint Profile of Haritaki Fruit Pericarp** []{#_Toc229853516 .anchor}After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- --------------- ------------------------------------------------ 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Characteristic marker spot corresponding to chebulinic / chebulagic acids ------------------------------------------------------------------------ []{#_Toc229853517 .anchor}**Marker Compounds for Standardization of Haritaki** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Chebulinic acid Not less than 0.5 per cent w/w 2 Chebulagic acid Not less than 0.3 per cent w/w ------------------------------------------------------------------------ **Mode of Action of Haritaki in Netra Rogas** Haritaki possesses predominantly ***Kashaya Rasa*** along with ***Pancharasa*** (except *Lavana*), ***Ushna Virya*,** and ***Madhura Vipaka***, making it effective in ocular disorders associated with *Vata* and *Kapha* vitiation as well as *Ama*. Its *Anulomana*, *Deepana--Pachana*, and *Amapachana* actions help in regulating systemic metabolism and clearing channels (*Srotoshodhana*), thereby indirectly improving ocular health. The *Chakshushya* and *Rasayana* properties support nourishment, detoxification, and rejuvenation of ocular tissues. Haritaki's *Shothahara* and *Vrana Ropana* actions aid in reducing inflammation, discharge, and promoting healing of ocular lesions. The presence of bioactive constituents such as chebulinic acid, chebulagic acid, and gallic acid confers antioxidant, anti-inflammatory, and antimicrobial activities, making it beneficial in conditions like *Kaphaja Abhishyanda*, *Netra Shopha*, *Netra Srava*, and chronic degenerative or inflammatory eye disorders. Thus, Haritaki helps maintain ocular clarity, tissue integrity, and visual function. ***12.BIBHITAKA*** > ![](media/image12.jpeg){width="2.808333333333333in" > height="1.8166666666666667in"} ***Fig. No :Bibhitaka*** **Table No. 29: Description of *Bibhitaka-*** +----------------------+-----------------------------------------------+ | **Botanical Name** | Terminalia bellirica Roxb. | +======================+===============================================+ | **Family** | Combretaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Bahera | | | > | | | > **English --** Belleric Myrobalan, Beddanut | | | > | | | > **Marathi --** Baheda | | | > | | | > **Gujarati --** Bahedan | | | > | | | > **Kannada --** Tare kai, Shanti kayi | | | > | | | > **Bengali --** Bayada, Baheda | | | > | | | > **Tamil --** Thanrikkai | | | > | | | > **Telugu --** Thanikkaya | | | | | | **Malayalam-** Tannikka | +----------------------+-----------------------------------------------+ | **Synonyms** | *Akshaphala, Karshaphala, Kalidruma, | | | Bhootavasa, Kaliyugalaya* | +----------------------+-----------------------------------------------+ | **Classical | > **Charak Samhita-** *Jvarahara, | | Categorization** | > Virechanopaga* | | | > | | | > **Sushruta Samhita**- *Triphala, Mustadi* | | | > | | | > **Bhava Prakasha | | | > Nighantu-***Haritakyadivarga,* | +----------------------+-----------------------------------------------+ | **Botanical | > It is a large tree, 20-25 m. high, with | | Description** | > pubescence on young branchlets. | | | > | | | > **Leaves-**Clustered at the end of | | | > branchlets, coriaceous, pale beneath, broad | | | > elliptic or obovate elliptic, 8-20 cm long, | | | > base often unequal. | | | > | | | > **Flowers-** in slender spikes, | | | > interrupted, 8-15 cm. long, dirty-grey, or | | | > greenish-yellow, with strong, offensive | | | > smell. | | | > | | | > **Fruits-** ovoid, grey, velvety. with 5 or | | | > more less indistinct furrows, nut thick and | | | > hard. (Flowers in March-May and fruits in | | | > December-February) | +----------------------+-----------------------------------------------+ | **Distribution** | Plains and lower hills throughout India**.** | +----------------------+-----------------------------------------------+ **Table No. 30: Properties & Action of Bibhitaka-** ----------------------------------------------------------------------- ***Rasa*** *Kashaya* ------------------------ ---------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Ushna* ***Vipaka*** *Madhura* ***Doshakarma*** *Tridoshahara (specially Kapha- pittahara)* ***Rogaghnakarma*** *Keshya, Chakshushya, Bhedana, Krimighna, Kasahara* ----------------------------------------------------------------------- ----------------------------------------------------------------------- **Chemical Tannic acid, Gallic acid, glycosides Constituents** ----------------------- ----------------------------------------------- **Therapeutic Uses** *Svarabheda, Netraroga, Kasa, Chardi, krimiroga, Vibandha* **Part Used** Phala **Dosage** *Churna* -- 3-6 gm ----------------------------------------------------------------------- []{#_Toc229853518 .anchor}**Physicochemical Parameters of Vibhitaki** []{#_Toc229853519 .anchor}*(TerminaliabelliricaRoxb.,DriedFruitPericarp)*\ *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 5.0 4.735 per cent per cent 2 Acid-insoluble Ash (% Not more than 1.0 2.095 per cent w/w) per cent 3 Water-soluble Extractive Not less than 20.0 23.904 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 15.0 6.656 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 12.0 8 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853520 .anchor}**Thin Layer Chromatography (TLC) for Identification of Vibhitaki** *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** ------- ----------------- ----------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Vibhitaki fruit pericarp 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Ferric chloride reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------- []{#_Toc229853521 .anchor}**TLC Fingerprint Profile of Bibhitaka Fruit Pericarp** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ---------------- ----------------------------------------------- 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Characteristic marker spot corresponding to gallic / ellagic acids ------------------------------------------------------------------------ []{#_Toc229853522 .anchor}**Marker Compounds for Standardization of Vibhitaki** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Gallic acid Not less than 0.5 per cent w/w 2 Ellagic acid Not less than 0.3 per cent w/w ------------------------------------------------------------------------ **Mode of Action of Bibhitaka in Netra Rogas** Bibhitaka possesses predominantly ***Kashaya Rasa*, *Ushna Virya***, and ***Madhura Vipaka*,** making it especially effective in ocular disorders associated with *Kapha* and *Rakta* vitiation. Its *Kaphahara* and *Lekhana* properties help in reducing excessive secretions, stickiness, and turbidity affecting the eyes. The *Chakshushya* and *Rasayana* actions support cleansing and strengthening of ocular tissues while preventing recurrent infections. Bibhitaka also exhibits *Shothahara* and *Vrana Ropana* properties, aiding in the reduction of inflammation and promoting healing of ocular surfaces. The presence of bioactive constituents such as belleric acid, gallic acid, and tannins contributes to antioxidant, anti-inflammatory, and antimicrobial activities, making it useful in conditions like *Kaphaja Abhishyanda*, *Netra Strava*, *Netra Shopha*, and chronic inflammatory eye disorders. Thus, Bibhitaka helps restore ocular clarity, reduce discharge, and maintain healthy visual function. **13. *AMALAKI *** > ![](media/image13.jpeg){width="2.875in" height="1.9696970691163604in"} ***Fig. No.: Amalaki*** **Table No. 31: Description of *Amalaki -*** +----------------------+-----------------------------------------------+ | **Botanical Name** | Emblica officinalis Gaertn. | +======================+===============================================+ | **Family** | Euphorbiaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Amla, Aonla | | | > | | | > **English --** Emblic Myrobalan, Indian | | | > gooseberry | | | > | | | > **Marathi --** Avala, Avalkathi | | | > | | | > **Gujarati --** Ambala, Amala | | | > | | | > **Kannada --** Nellikayi, Bela nelli, | | | > Pottadenollikayi | | | > | | | > **Bengali --** Amla, Dhatri | | | > | | | > **Tamil --** Nellikkai, Nelli | | | > | | | > **Telugu --** Usirika | | | > | | | > **Malayalam-** Nellikka | +----------------------+-----------------------------------------------+ | **Synonyms** | *Amrita, Vayasya, Vrishya, Aamalki, | | | Jatiphalaras, Shiv, Dhatriphala, Shreephala* | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Classical | > **CharakSamhita-** *Jvarahara, Kasahara, | | Categorization** | > Kusthaghna, Virechanopaga, Vayahsthapana, | | | > Prajasthapana* | | | > | | | > **Sushruta Samhita-** *Triphala, | | | > Aamalakyadi, Parushakadi, Mustadi, | | | > Mushkakadi* | | | > | | | > **Ashtanga Hridya:** *Parushakadi, Mustadi, | | | > Mushkakadi* | | | > | | | > **Bhava Prakasha Nighantu**: | | | > *Haritakyadivarga,* | +======================+===============================================+ +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | **Botanical | > It is a large deciduous tree with | | Description** | > greenish-grey or red bark, peeling off in | | | > scales. | | | > | | | > **Leaves-**pinnate, distichously close-set, | | | > linear-oblong, obtuse. | | | > | | | > **Flowers-**densely fascicled along the | | | > branchlets, yellowish; males on slender | | | > pedicles, females sub-sessile, | | | > | | | > **Fruit-** berry, depressed globose, | | | > succulent, yellow or pink when ripe, | | | > obscurely 6-lobed. | | | > | | | > **Seeds-**trigonous. (flowers in Frb. May | | | > and fruits in Oct. April) | +======================+===============================================+ | **Distribution** | wild/cultivated throughout tropical India. | +----------------------+-----------------------------------------------+ **Table No. 32: Properties & Action of *Amalaki- *** ----------------------------------------------------------------------- ***Rasa*** *Panchras (Amla Pradhan, Lavan-rahit)* ----------------------- ----------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Sheeta* ***Vipaka*** *Madhura* ***Doshakarma*** *Tridoshahar* ***Rogaghnakarma*** *Rasayana, Chakshushya, Vrishya, Pramehaghna, Stambhana, Anulomana, Dahaprashamana, Raktapittahara* ----------------------------------------------------------------------- +----------------------+-----------------------------------------------+ | **Chemical | Tannins, gallic acid, ellagic acid, | | Constituents** | phyllemblic acid, emblicol, alkaloids | | | phyllantidine and phyllantine, pectins, Vit. | | | C, minerals | +======================+===============================================+ | **Therapeutic Uses** | Raktapitta, Amlapitta, Prameha, Daha | +----------------------+-----------------------------------------------+ | **Part Used** | Phala | +----------------------+-----------------------------------------------+ | **Dosage** | *Churna* -- 3-6 gm (Ref.-A.P.I.), | | | | | | *Churna*- 3-10 gm (Ref.-B.P.N.) | +----------------------+-----------------------------------------------+ **Physicochemical Parameters of Amalaki** *(Emblica officinalisGaertn. / Phyllanthus emblica L., Dried Fruit)*\ *(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ ------------------- -------------------- 1 Total Ash (% w/w) Not more than 7.0 6.122 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 0.639 per cent w/w) per cent 3 Water-soluble Extractive Not less than 30.0 47.304 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 20.0 29.48 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 12.0 8 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent ------------------------------------------------------------------------- []{#_Toc229853523 .anchor}**Thin Layer Chromatography (TLC) for Identification of Amalaki** []{#_Toc229853524 .anchor}*(As per Ayurvedic Pharmacopoeia of India)* ------------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** ------- ----------------- ----------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Toluene : Ethyl acetate : Formic acid (5 : 4 : 1) 3 Test Solution Alcoholic extract of Amalaki fruit 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Ferric chloride reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------- []{#_Toc229853525 .anchor}**TLC Fingerprint Profile of Amalaki Fruit** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------- **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ---------------- ------------------------------------------------ 1 0.20 -- 0.30 Minor spot 2 0.40 -- 0.50 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Characteristic marker spot corresponding to gallic acid / ellagic acid ------------------------------------------------------------------------- []{#_Toc229853526 .anchor}**Marker Compounds for Standardization of Amalaki** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Gallic acid Not less than 0.5 per cent w/w 2 Ascorbic acid Not less than 0.6 per cent w/w ------------------------------------------------------------------------ **Mode of Action of Amalaki in Netra Rogas** *Amalaki* possesses predominantly ***Amla Rasa*** along with ***Pancharasa*** (except *Lavana*), *Sheeta Virya*, and *Madhura Vipaka*, making it highly effective in ocular disorders associated with *Pitta* and *Rakta* vitiation. Its potent *Pittashamana* and *Raktaprasadana* properties help in alleviating burning sensation, redness, and irritation of the eyes. The *Chakshushya* and *Rasayana* actions of Amalaki nourish and rejuvenate ocular tissues, enhancing visual acuity and delaying degenerative changes. Its *Shothahara* and *Dahaprashamana* effects aid in reducing inflammation and ocular discomfort. The presence of bioactive constituents such as ascorbic acid, emblicanin A and B, and polyphenols imparts strong antioxidant, anti-inflammatory, and immunomodulatory activities, making it beneficial in conditions like *Pittaja Abhishyanda*, *Netra Daha*, *Raktaja Netra Rogas*, and age-related or chronic inflammatory eye disorders. Thus, Amalaki supports ocular cooling, tissue vitality, and long-term visual health. Therapeutic uses- raktapitta, amlapitta, prameha,daha, vrushya ,rasayan , chakshushya. **14. NAGARMOTHA** ![Nagarmotha](media/image14.jpeg){width="2.3402777777777777in" height="2.2870734908136483in"} **Fig. No.: Nagarmotha** +----------------------+-----------------------------------------------+ | **Botanical Name** | > *Cyperus rotundus* | +======================+===============================================+ | **Family** | > Cyperaceae | +----------------------+-----------------------------------------------+ | **Vernacular Names** | **Hindi --** Motha, Nagarmotha | | | | | | > **English --** Nut Grass | | | > | | | > **Marathi --** Nagarmoth | | | > | | | > **Gujarati --** Nagarmoth | | | > | | | > **Kannada --** | | | > | | | > **Bengali --** | | | > | | | > **Tamil --** Muthakach, Korai | | | > | | | > **Telugu --** Tungmuste | | | > | | | > **Malayalam-** | +----------------------+-----------------------------------------------+ | > **Synonyms** | > *Mustaka ,Varida* | +----------------------+-----------------------------------------------+ +----------------------+-----------------------------------------------+ | > **Classical** | **Charaka-** *Truptighna, Trsnanigrahana, | | | Lekhaniya,* | | **Categorization** | | | | *Kandughna, Stanyasodhana* | | | | | | **Sushruta**- *Mustadi, Vacadi* | | | | | | **Bhavaprakasha Nighantu-** *Karpuradi Varga* | +======================+===============================================+ +----------------------+-----------------------------------------------+ +-----------------------+----------------------------------------------+ | > **Botanical | | | > Description** | | +=======================+==============================================+ | > **Distribution** | | +-----------------------+----------------------------------------------+ ## Properties & Action of *nagarmotha* {#properties-action-of-nagarmotha .unnumbered} +-----------------------+----------------------------------------------+ | ***Rasa*** | > *Tikta* | +=======================+==============================================+ | ***Guna*** | > *Ruksha* | +-----------------------+----------------------------------------------+ | ***Virya*** | > *Ushna* | +-----------------------+----------------------------------------------+ | ***Vipaka*** | > *Katu* | +-----------------------+----------------------------------------------+ | ***Doshakarma*** | > *Kaphapittashamaka* | +-----------------------+----------------------------------------------+ | ***Rogaghnakarma*** | > *Varnashodhana, Vranaropana, Varnya, | | | > Rasayana, Shothahara, Vednasthapana, | | | > Raktashodhaka etc.* | +-----------------------+----------------------------------------------+ +----------------------+-----------------------------------------------+ | > **Chemical** | | | > | | | > **Constituents** | | +======================+===============================================+ | **Therapeutic Uses** | > *Kandu, Medoroga, Mukharoga, Vrana, | | | > Karnaroga, Netraroga, Meha, Urustambha* | | | > etc. | +----------------------+-----------------------------------------------+ | > **Part Used** | *mula* (tubers) | +----------------------+-----------------------------------------------+ | > **Dosage** | > Kwath- 5-10 ml (Ref.-API), | +----------------------+-----------------------------------------------+ []{#_Toc229853528 .anchor}**Physicochemical Parameters of Nagarmotha** *(Cyperus rotundus L., Dried Rhizome)*\ *(As per Ayurvedic Pharmacopoeia of India)* -------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ -------------------- -------------------- 1 Total Ash (% w/w) Not more than 8.0 4.535 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 2.42 per cent w/w) per cent 3 Water-soluble Extractive Not less than 12.0 5.296 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 5.0 23.392 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 12.0 8 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent -------------------------------------------------------------------------- []{#_Toc229853529 .anchor}**Thin Layer Chromatography (TLC) for Identification of Nagarmotha** *(As per Ayurvedic Pharmacopoeia of India)* ----------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** -------- --------------------- ---------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Chloroform : Methanol (9 : 1) 3 Test Solution Alcoholic extract of Nagarmotha rhizome 4 Application Volume 5 -- 10 µL 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Reagent Vanillin--Sulphuric acid reagent ----------------------------------------------------------------------- []{#_Toc229853530 .anchor}**TLC Fingerprint Profile of Nagarmotha Rhizome** After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------- **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- --------------- ------------------------------------------------- 1 0.25 -- 0.35 Minor spot 2 0.45 -- 0.55 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.75 -- 0.85 Characteristic marker spot corresponding to cyperene / essential oil constituents ------------------------------------------------------------------------- []{#_Toc229853531 .anchor}**Marker Compounds for Standardization of Nagarmotha** ------------------------------------------------------------------------ **Sl. **Marker Compound** **API / Reported Requirement** No.** ---------- ------------------------- ----------------------------------- 1 Cyperene Not less than 0.3 per cent w/w 2 Essential oil content Not less than 1.5 per cent w/w ------------------------------------------------------------------------ **Mode of Action of Nagarmotha in Netra Rogas** Nagarmotha possesses ***Tikta--Katu--Kashaya Rasa*, *Sheeta Virya***, and ***Katu Vipaka*,** making it effective in ocular disorders associated with *Pitta* and *Kapha* vitiation. Its *Pittashamana* and *Kaphahara* properties help in reducing burning sensation, redness, heaviness, and excessive secretions of the eyes. The *Shothahara* and *Dahaprashamana* actions aid in alleviating inflammation, edema, and ocular discomfort. Nagarmotha also exhibits *Deepana--Pachana* and *Amapachana* effects, which support systemic detoxification and indirectly improve ocular health. The presence of bioactive constituents such as cyperene, cyperol, and flavonoids contributes to anti-inflammatory, antioxidant, and antimicrobial activities, making it useful in conditions like *Pittaja* and *Kaphaja Abhishyanda*, *Netra Daha*, *Netra Shopha*, and chronic inflammatory eye disorders. Thus, Nagarmotha helps restore ocular balance, reduce irritation, and maintain visual comfort. **15. Yava** ![VINARGHYA Jav / Jau / Jab / Java / Yava / Javegodhi / Yavam / Barliarisi / Baril / Barley / Barli Biyyam -- 250g Price in India - Buy VINARGHYA Jav /](media/image15.jpeg){width="3.164382108486439in" height="1.5572331583552057in"} **Fig. No.: Yava** **Table No.: Description of Yava** ------------------------------------------------------------------------ **Botanical Name** *Hordeum vulgare* Linn. Syn.H.sativum Pers. ------------------ ----------------------------------------------------- **Family** Poaceae **Vernacular Hindi -- Jau\ Names** English -- Barley\ Marathi -- Java\ Gujarati -- Jav\ Kannada -- Jola\ Bengali -- Jaba\ Tamil -- Barli Arisi\ Telugu -- Barli Biyyam\ Malayalam -- Yavam **Synonyms** Yava, Medhya, Pavitraka, Akshata, Bahudhanya, Dhanyaraja, Dirghashooka, Shitashaka **Classical **Charak Samhita** -- Shukadhanya, Lekhaniya, Categorization** Mutravirechaniya, Medohara\ **Sushruta Samhita** -- Shukadhanya, Kaphaghna, Medohara\ **Ashtanga Hridaya** -- Shukadhanya Varga\ **Bhava Prakash Nighantu** -- Dhanya Varga **Botanical An annual erect grass with hollow cylindrical stems.\ Description** **Leaves** -- Linear, narrow, sheathing.\ **Flowers** -- Arranged in dense spikes with long awns.\ **Fruits** -- Caryopsis, elongated and enclosed within husk. **Distribution** Cultivated throughout India, especially in temperate and subtropical regions; also widely grown worldwide. ------------------------------------------------------------------------ []{#_Toc229853532 .anchor}**Table No.: Properties & Action of Yava** ------------------------------------------------------------------------ **Rasa** Kashaya, Madhura ------------------- ---------------------------------------------------- **Guna** Laghu, Ruksha **Virya** Sheeta **Vipaka** Katu **Doshakarma** Kapha--Pitta Shamaka **Rogaghnakarma** Lekhana, Medohara, Mutrala, Deepana, Pachana, Chakshushya **Chemical β-glucan, starch, proteins, dietary fiber, vitamins Constituents** (B-complex), minerals (iron, magnesium), polyphenols **Therapeutic Prameha, Sthaulya, Medoroga, Mutrakrichra, Atisara, Uses** Netra Daha **Part Used** Seed (Grain) **Dosage** Churna -- 3--6 gm\ Yava Saktu -- As required\ Yava Kwatha -- 40--80 ml ------------------------------------------------------------------------ []{#_Toc229853533 .anchor}**Mode of Action of Yava in Netra Rogas** Yava possesses *Kashaya--Madhura Rasa*, *Sheeta Virya,* and *Katu Vipaka*, which makes it especially effective in *Pitta--Kapha dominant Netra Rogas*. Its *Sheeta* and *Dahaprashamana* properties help in alleviating burning sensation, irritation, and inflammatory conditions of the eyes. The *Lekhana* and *Ruksha* *Guna* aid in reducing excessive secretions and edema, making it beneficial in disorders like *Kaphaja Abhishyanda* and *Netra Kleda.* Yava is described as ***Chakshushya*** in classical texts, indicating its nourishing and protective role for ocular tissues. The presence of **β-glucan and antioxidant polyphenols** contributes to its anti-inflammatory and free-radical scavenging effects, thereby supporting ocular surface health and preventing degenerative changes. Its **Mutrala and Medohara actions** help in systemic detoxification and metabolic balance, indirectly benefiting chronic and recurrent eye disorders. Thus, Yava promotes ocular comfort, clarity, and long-term visual well-being **16. INDRAYAVA/KALINGAKA** ![](media/image16.emf){width="2.5242694663167105in" height="1.537879483814523in"} **Fig. No.: Indrayava** +------------+---------------------------------------------------------+ | * | *Holarrhena antidysenterica Wall.* | | *Botanical | | | Name** | | +============+=========================================================+ | **Family** | Apocynaceae | +------------+---------------------------------------------------------+ | ** | > **Hindi -- Indrajava** | | Vernacular | > | | Names** | > **English -- Kurchi, Conessi Tree** | | | > | | | > **Marathi -- Kuda** | | | > | | | > **Gujarati -- Kudo** | | | > | | | > **Kannada --** koodsalu, korchie, beppale | | | | | | **Bengali --** kutaja, kurchi | | | | | | **Tamil** -- kirimallikai, kutac-palai, malaimallikai, | | | veppalai | | | | | | **Telug--** girimallika, kodisepala, kolamukku, | | | kondamalle,kutajammu. | | | | | | **Malayalam-** | | | kutakappaala,kodagapala,bhanthappala,kampippala. | +------------+---------------------------------------------------------+ | ** | *Kutajbijam,indrayava | | Synonyms** | ,vatsaka,girimallika,kaalinga,kalingaka,indravrikshha*. | +------------+---------------------------------------------------------+ +-----------------------+----------------------------------------------+ | **Classical | ## Charaka- *Ch | | Categorization** | ardinigrahana, Trishnanigrahan* {#charaka-- | | | chardinigrahana-trishnanigrahan .unnumbered} | | | | | | ## Sushruta- *Pip | | | palyadi* {#sushruta--pippalyadi .unnumbered} | | | | | | ## Bhavapraka | | | sha Nighantu- *Guduchyadi Varga* {#bhavaprak | | | asha-nighantu--guduchyadi-varga .unnumbered} | +=======================+==============================================+ +-----------------------+----------------------------------------------+ +-----------------------+----------------------------------------------+ | **Botanical | Habit- Small tree with glabrous or pubescent | | Description** | bark. | | | | | | **Leaves** 10--20× 5--11.5 cm, | | | ovate--elliptic, apex obtuse/acuminate, base | | | obtuse, glabrous or pubescent, 10--14 pairs | | | of nerves, petiole \~3 mm. **Flowers** | | | white, inodorous, in terminal corymbose | | | cymes (7.5--15 cm); slender pedicels; small, | | | lanceolate, pubescent, ciliated bracts. | | | Calyx lobes 2.5--3 mm, oblong-lanceolate, | | | slightly inflated, throat hairy. **Fruit** | | | cylindrical follicles, 20--38 × 6--8 mm, | | | sometimes spotted. **Seeds** linear-oblong, | | | \~8 mm, tip with brown hairy coma, 2.2--5 | | | cm. | +=======================+==============================================+ | **Distribution** | **Through out India ascending upto 4000 ft. | | | mainly at the hilly regions.** | +-----------------------+----------------------------------------------+ **k** ----------------------------------------------------------------------- ***Rasa*** *Tikta,Kashaya* ---------------------- ------------------------------------------------ ***Guna*** *Laghu,ruksha* ***Virya*** *Shita* ***Vipaka*** *Katu* ***Doshakarma*** *Kaphapittashamaka, Tridoshangna* ***Rogaghnakarma*** *Agnidipaka, Shoolaprashaman, Arshoghna, Atishara-Ghna, Raktatisarahara,Kustaghna,Chardinigrahana, Trishnanigrahan , Jvaragna, Vranaropana* ----------------------------------------------------------------------- +---------------------+------------------------------------------------+ | **Chemical | Conessine and related alkaloids. | | Constituents** | | +=====================+================================================+ | **Therapeutic | *Agnidipaka, Shoolaprashaman, Arshoghna, | | Uses** | Atishara-Ghna, | | | Raktatisarahara,Kustaghna,Chardinigrahana, | | | Trishnanigrahan , Jvaragna, Vranaropana*. | +---------------------+------------------------------------------------+ | **Part Used** | *Tvak, Beeja Indrayava* | +---------------------+------------------------------------------------+ | **Dosage** | *Churna* - 3-6 gms. | | | | | | *Kwatha* - 50-100ml. | +---------------------+------------------------------------------------+ []{#_Toc229853537 .anchor}**Indrayava (Holarrhena pubescens Wall. / Holarrhena antidysenterica)** []{#_Toc229853538 .anchor}*(DriedStem/Bark) (As per Ayurvedic Pharmacopoeia of India)* []{#_Toc229853539 .anchor}**Physicochemical Parameters** -------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ -------------------- -------------------- 1 Total Ash (% w/w) Not more than 10.0 6.635 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 1.125 per cent w/w) per cent 3 Water-soluble Extractive Not less than 12.0 3.394 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 8.0 2.831 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 7 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent -------------------------------------------------------------------------- []{#_Toc229853540 .anchor}**Thin Layer Chromatography (TLC) for Identification** ----------------------------------------------------------------------- **Sl. **Parameter** **API Specification** No.** ------- ------------------ -------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Chloroform : Methanol (9 : 1) 3 Test Solution Alcoholic extract of Indrayava stem 4 Application Volume 5 -- 10 µL 5 Detection UV 254 nm & 366 nm 6 Derivatizing Dragendorff's / Anisaldehyde--Sulphuric acid Reagent reagent ----------------------------------------------------------------------- []{#_Toc229853541 .anchor}**TLC Fingerprint Profile** ------------------------------------------------------------------------ **Sl. **Rf Value **Nature of Spot** No.** (Approx.)** -------- -------------------- ------------------------------------------ 1 0.25 -- 0.35 Minor spot 2 0.45 -- 0.55 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.80 -- 0.90 Characteristic marker spot (berberine alkaloid) ------------------------------------------------------------------------ **Mode of Action of Indrayava/kalingaka in Netra Rogas** Indrayava possesses ***Tikta--Kashaya Rasa***, ***Sheeta Virya***, and ***Katu Vipaka*,** making it beneficial in ocular disorders associated with *Pitta* and *Rakta* vitiation, especially those with infective and inflammatory pathology. Its *Pittashamana* and *Raktashodhaka* properties help in reducing burning sensation, redness, and congestion of the eyes. The *Shothahara* and *Dahaprashamana* actions aid in alleviating ocular inflammation, edema, and discomfort. Indrayava is also known for its *Krimighna* and *Atisaraghna* properties, indicating strong antimicrobial and detoxifying effects that are useful in infective eye conditions. The presence of bioactive alkaloids such as conessine contributes to anti-inflammatory, antimicrobial, and antioxidant activities, supporting its role in conditions like *Pittaja Abhishyanda*, *Netra Daha*, *Raktaja Netra Rogas*, and ocular infections. Thus, Indrayava helps purify ocular tissues, control inflammation, and maintain ocular clarity and visual health. []{#_Toc229853542 .anchor}**17. KUTAJ TWAK** ![Brown Dry Kutaja Bark Root, For Medicinal](media/image17.jpeg){width="3.341666666666667in" height="2.5083333333333333in"} **Fig. No.: Kutaj Twak** +-----------------------+----------------------------------------------+ | **Botanical Name** | *Holarrhena antidysenterica (Roth).A. DC* | +=======================+==============================================+ | **Family** | Apocynaceae | +-----------------------+----------------------------------------------+ | **Vernacular Names** | > **Hindi --** Kutaj, Kurchi | | | > | | | > **English --** Conessi Bark | | | > | | | > **Marathi --** Kutaja, pandhra kuda | | | > | | | > **Gujarati --** Kuda | | | > | | | > **Kannada --** Kodasiga, Kutaja | | | > | | | > **Bengali --** Kurchi | | | > | | | > **Tamil --** Kutagam | | | > | | | > **Telugu --** Girimalligai | | | > | | | > **Malayalam-** Kutakam | +-----------------------+----------------------------------------------+ | **Synonyms** | Kutaja, Indrayava, Kalinga, Girimallika, | | | Vatsaka | +-----------------------+----------------------------------------------+ | **Classical | ***Charak Samhita**- Atisaraghna, Kandughna* | | Categorization** | | | | ***Sushruta Samhita**- Aragvadhadi Gana* | | | | | | ***AshtangaHridya**- Atisaraghna* | | | | | | ***Bhava PrakashaNighantu**-* *Guduchyadi | | | Varga* | +-----------------------+----------------------------------------------+ | **Botanical | A medium-sized deciduous tree, about 6--10 m | | Description** | high. Bark (twak) is greyish-brown, rough, | | | and longitudinally fissured. Leaves | | | opposite, elliptic-oblong. Flowers white, | | | fragrant, arranged in terminal cymes. The | | | bark is the principal medicinal part. | +-----------------------+----------------------------------------------+ | **Distribution** | Widely distributed throughout **India**, | | | especially in dry forests, sub-Himalayan | | | tracts, central and southern regions. | +-----------------------+----------------------------------------------+ **Table No. 24: Properties & Action of *Kutaj Twak*** ----------------------------------------------------------------------- ***Rasa*** *Tikta, Kashaya* ------------------------ ---------------------------------------------- ***Guna*** *Laghu, Ruksha* ***Virya*** *Sheeta* ***Vipaka*** *Katu* ***Doshakarma*** *Kaphapitta Shamaka* ***Rogaghnakarma*** *Atisaraghna, Raktashodhaka, Shothahara, Kandughna, Chakshushya* ----------------------------------------------------------------------- +-----------------------+----------------------------------------------+ | **Chemical | Conessine, Holarrhenine, Kurchicine, | | Constituents** | Holarrhimine, Steroidal alkaloids | +=======================+==============================================+ | **Therapeutic Uses** | *Atisara, Pravahika, Raktatisara, Kushtha, | | | Kandu, Vrana, Netraroga* | +-----------------------+----------------------------------------------+ | **Part Used** | *Twak* (Bark) | +-----------------------+----------------------------------------------+ | **Dosage** | > ***Kwatha*:** 50--100 ml (Ref. API) | | | > | | | > ***Churna:*** 1--3 g (Ref. B.P.N.) | +-----------------------+----------------------------------------------+ []{#_Toc229853543 .anchor}**Physicochemical Parameters of Kutaj Twak** (*Holarrhenaantidysenterica*,DriedBark)\ **(As per Ayurvedic Pharmacopoeia of India)** -------------------------------------------------------------------------- **Sl. **Parameter** **API Requirement** **Observed / No.** Reported Values** ------- ------------------------ -------------------- -------------------- 1 Total Ash (% w/w) Not more than 10.0 7.02 per cent per cent 2 Acid-insoluble Ash (% Not more than 2.0 0.125 per cent w/w) per cent 3 Water-soluble Extractive Not less than 12.0 16.136 per cent (% w/w) per cent 4 Alcohol-soluble Not less than 8.0 19.152 per cent Extractive (% w/w) per cent 5 Loss on Drying at 105 °C Not more than 10.0 7 per cent (% w/w) per cent 6 Foreign Matter (% w/w) Not more than 2.0 Not more than 2.0 per cent per cent -------------------------------------------------------------------------- []{#_Toc229853544 .anchor}**Thin Layer Chromatography (TLC) for Identification of Kutaj Twak** **(As per Ayurvedic Pharmacopoeia of India)** ------------------------------------------------------------------------ **Sl. **Parameter** **API Specification** No.** ------- ----------------- ---------------------------------------------- 1 Stationary Phase Silica gel 60 F₂₅₄ TLC plate 2 Mobile Phase Chloroform : Methanol (9 : 1) 3 Test Solution Alcoholic extract of Kutaj bark 4 Application 5 -- 10 µL Volume 5 Detection Under UV light at 254 nm and 366 nm 6 Derivatizing Dragendorff's reagent / Reagent Anisaldehyde--Sulphuric acid reagent ------------------------------------------------------------------------ []{#_Toc229853545 .anchor}**TLC Fingerprint Profile of Kutaj Twak** []{#_Toc229853546 .anchor}After development and derivatization, the TLC plate shows the following characteristic spots: ------------------------------------------------------------------------ **Sl. **Rf Value **Description of Spot** No.** (Approx.)** ------- ------------------ --------------------------------------------- 1 0.25 -- 0.35 Minor spot 2 0.45 -- 0.55 Distinct spot 3 0.60 -- 0.70 Major prominent spot 4 0.80 -- 0.90 Characteristic marker spot corresponding to conessine ------------------------------------------------------------------------ []{#_Toc229853547 .anchor}**Marker Compounds for Standardization of Kutaj Twak** ----------------------------------------------------------------------- **Sl. **Marker **API / Reported Requirement** No.** Compound** ------- ------------------ -------------------------------------------- 1 Conessine Not less than 0.3 per cent w/w ----------------------------------------------------------------------- []{#_Toc229853548 .anchor}**Mode of Action of *Kutaj Twak* in Netra Rogas** Kutaj Twak, possessing ***Tikta--Kashaya Rasa**, **Sheeta Virya**,* and ***Kaphapitta Shamaka*** properties, is effective in ocular disorders associated with ***Kapha-Pitta* vitiation**. Its ***Raktashodhaka*** and ***Shothahara*** actions help reduce inflammation, redness, discharge, and itching in conditions such as ***Abhishyanda, Kandu-yukta Netra Rogas***, and ***Raktaja Netrabhishyanda***. The presence of steroidal alkaloids like **conessine** provides antimicrobial and anti-inflammatory effects, aiding in ocular tissue purification and healing. Thus, Kutaj Twak acts as a supportive ***Chakshushya*** and ***Netra-shodhaka dravya***, contributing to ocular health and disease management. ## {#section-14 .unnumbered} ## {#section-15 .unnumbered} ## **Role of Vāsādi Kwātha (Conceptual Basis)** {#role-of-vāsādi-kwātha-conceptual-basis .unnumbered} Though direct clinical trials are limited, pharmacological properties suggest: ### Expected actions: {#expected-actions .unnumbered} - Pitta shamana → reduces retinal inflammation - Rakta shodhana → improves microcirculation - Chakshushya → supports retinal function - Shothahara → reduces edema and exudation Thus, it may: - Reduce hemorrhages - Prevent leakage - Improve retinal perfusion Both modern and Ayurvedic literature suggest that DR/Timira is a progressive microvascular degenerative disorder. While modern medicine focuses on late-stage interventions, Ayurveda provides a holistic, preventive, and restorative approach, highlighting the need for integrative research like the present study. **[Drug Review modern]{.underline}** OCUFREE Capsules Composition: Each soft gelatin capsule contains: ----------------------------------------------------------------------- Lutein 4 mg -------------------------------------- -------------------------------- Zeaxanthin 0.8mg L- Glutathione 5 mg Beta carotene 10 mg Vitamin A 2500 2500 iu Vitamin C 150 mg Vitamin E 25 mg Selenium 70 mcg Zinc 27.5 mg Manganese 5 mg Copper 2 mg ----------------------------------------------------------------------- **Pharmacology -**Ocufree capsules are specifically designed for providing antioxidant back up for the eyes. The eye is the most vulnerable organ for free radical damage as almost all the surrounding factors such as sunlight, dust, infectious organisms could cause excessive free radical generation. So much so, the existing antioxidant mechanism is not enough to counter the free radical upsurge. Such situations demand an incessant supply of antioxidants from external sources. Ocufree is one such formulation, which provides three-way support to eyes: 1\. Enhancement of natural antioxidant mechanism -- Superoxide dismutase \[SOD\], Glutathione peroxidase \[GPX\] and Catalase \[CAT\]. 2\. Scavenging free radicals causing tissue damage. 3\. Providing ocular-specific nutrients such Lutein, Zeaxanthin to enrich the ocular tissue **Lutein and Zeaxanthin**: These are the most important antioxidants for the macula. Zeaxanthin\'s role is to help protect the eye from harmful high-energy blue-wave light **(U.V**. radiation) in the same way sunglasses protect our eyes from sun glare. Zeaxanthin also protects the eye\'s vision cells and helps the eye repair itself. In fact, studies have shown that the portion of the macula with the highest concentration of Zeaxanthin is the last to degenerate. Lutein is found in the outer area of the circular macular spot. Both Lutein and Zeaxanthin are also found in the human crystalline lens and are said to play a role in protection against age related macular degeneration and age-related cataract formation. **L-Glutathione**: L-Glutathione is a powerful antioxidant to the body. Within the lens of the eye, levels of L-Glutathione significantly decrease with age and changes in glutathione levels significantly increase the vulnerability of the lens to cataract formation. High levels of glutathione afford protection for a number of lens related functions. Glutathione protects sulfur-containing proteins from oxidizing or free radical damage. Most cases of cataracts may be linked to scant supplies of glutathione within the body, and can easily be prevented with appropriate supplementation. Recent research has found that macular degeneration was correlated to low glutathione levels. **Vitamin A and Beta- carotene** : Vitamin A is essential in vision health, cellular differentiation and embryonic function. Ocufree also supplies natural mixed carotenoids (NMCs), which contain alpha- carotene, beta-carotene, lutein, zeaxanthin and cryptoxanthin. The NMCs act as pro-Vitamin A, which is a precursor in the body for Vit A. **Vitamin C:** Vitamin C is a water-soluble antioxidant that inactivates free radicals in ocular tissues. As an integral component of the body's antioxidant defense system, vitamin C also aids in the recycling of other antioxidants such as vitamin E. Also helps raise blood levels of l glutathione. **Vitamin E:** Because of its antioxidant action, Vit E may help protect against cataracts and ARMD and improves visual clarity in uveitis. **Selenium:** Selenium is an essential mineral required for the proper function of glutathione peroxidase, an antioxidant enzyme found in the eye's lens and localized in photoreceptor and retinal pigment epithelial cells **. Zinc:** Zinc is an essential mineral that is selectively concentrated in the eye. It is found in the retina and choroid, ciliary body, iris, optic nerve, sclera, cornea and lens. Within these ocular structures zinc is believed to interact with vitamin A to modify photoreceptor membranes, to help regulate the light-rhodopsin reaction, to influence nerve transmission and to serve as an antioxidant. **Copper**: Copper is necessary for normal development of connective tissue, nerve sheaths, skin pigment and for efficient utilization of iron. **Manganese:** With its antioxidant activity, manganese ions scavenge hydroxyl and superoxide radicals. Manganese is a crucial component of manganese superoxide dismutase (MnSOD), which is found in mitochondria and is the principal constituent of the mitochondrial oxidant defense system. **Indications:** Ocufree is indicated as prophylaxis in: o Age-related Macular Degeneration, o Diabetic Retinopathy o Diabetic cataract o Senile Cataract **Contraindications:** Ocufree is contraindicated to the patients who are sensitive to any of the ingredients. Pregnancy & Lactation Ocufree may be used during pregnancy and lactation with caution. None of the ingredients are harmful to fetus. **Drug Interactions** Antioxidants should not be prescribed with quinolones, as they affect absorption of quinolones. **Adverse Reactions** There are no known adverse reactions of Ocufree. **Dosage & Administration** The usual recommended dose of Ocufree is one capsule daily. **Presentation** Each blister strip of 10 soft gelatin capsules is available in patient information catch cover. Current therapies for diabetic retinopathy (DR) incorporate blood glucose and blood pressure control, vitrectomy, photocoagulation, and intravitreal injections of anti-vascular endothelial growth factors or corticosteroids. Nonetheless, these techniques have not been demonstrated to completely stop the evolution of this disorder. The pathophysiology of DR is not fully known, but there is more and more evidence indicating that oxidative stress is an important mechanism in the progression of DR. In this sense, antioxidants have been suggested as a possible therapy to reduce the complications of DR. Diabetic retinopathy (DR) is one of the most frequent causes of blindness in the adult and elderly population worldwide. Control of blood glucose, blood pressure and lipidemia have been shown to alleviate the appearance and evolution of DR. Nonetheless, some patients might exhibit a progression of DR with appropriate blood glucose and pressure control. DR is primarily a microvascular disorder related to the loss of pericytes, endothelial cell proliferation, the disruption of tight junctions between endothelial cells, the thickening of the basement membrane, the leakage of fluid and macromolecules from the vessels, and neovascularization. All these phenomena imply the damage of non-vascular cells of the retina such as neuronal and glial cells, with deleterious implications for visual function due to macular edema, vitreous hemorrhage or tractional retinal detachment. These events have been associated directly with oxidative stress Otherwise, standard therapies to treat DR (vitrectomy, photocoagulation, intraocular injections of anti-vascular endothelial growth factors (VEGFs) or corticosteroids) are not able to control DR progression in all cases. The difficulty to stop DR is related to the metabolic memory and this phenomenon has also been associated with oxidative stress. These considerations about DR have led one to consider different therapeutic approaches, such as antioxidant supplementation, to rebalance the excess free radical production and/or the defect of antioxidant natural system Several studies conclude that antioxidants are able to prevent or even ameliorate DR status, acting against inflammation and oxidative stress. The presence of multifactorial events with an inflammatory response and oxidative disbalance in the retina (capillary endothelial cells, pericytes, glia and neurosensory retinal cells) lead to a progressive cellular degeneration process with metabolic alterations of the retinal pigment epithelium (RPE) cells, and a dysfunction of the retinal blood barriers (internal and external). The final consequence is the loss of vision \[8,11,12\]. Hyperglycemia also induces mitochondrial dysfunction with an intracellular and extracellular augmentation of the reactive oxygen species. Likewise, it has been observed that epigenetic adjustments are engaged with oxidative stress. The phenomenon, described as metabolic memory, is related to the deleterious effects on tissues caused by hyperglycaemia, . Themetabolicstatus of theretina is normally isolated from the rest of the bodybytheblood--retinal barrier that is made up of an internal barrier by the endothelial capillaries and an external barrier by the RPE cells. In addition, these barriers maintain a state of "immune privilege", with the ability to modulate the response to different external attacks independently \[11,15\]. In situations of prolonged hyperglycemia, the metabolic stress involves an insult to the retinal capillary network, its barrier systems, and the highly specialized neural connections of the retina, responsible for vision processes. Antioxidants far have allowed us to conclude that several of the microvascular changes observed in DR can be prevented or mitigated by different antioxidant medicinal derivatives of plant origin. The properties of resveratrol---a powerful antioxidant, which is anti-inflammatory and neuroprotective---are widely known in in vitro studies, which have subsequently been confirmed in different clinical trials Othe. Non-provitamin A carotenoids (lutein, zeaxanthin, lycopene, and astaxanthin) were shown to be effective, not only in reducingin vitroinflammation, but also inmodulating gene expression, eliminating ROS as a consequence \[20\]. Furthermore, there is strong evidence for xanthophyl carotenoids, such as lutein and zeaxanthin, which are selectively absorbed by RPE cells, and accumulate preferentially in the macular region, conferring protection on photoreceptors. Recently, it was found that this beneficial effect on the retina can be increased synergistically when lutein is administered in association with Ω-3 long-chain polyunsaturated fatty acids. An antioxidant and anti-inflammatory effect were found by reducing ROS production and inhibiting the expression of inflammatory mediator. Another antioxidant, Calcium Dobesilate (Ca Dob), inhibits acellular capillaries and pericyte loss, and protects the blood-retinal barrier by preserving tight junctions, and induces an important decrease of pro-oxidative markers. Carotenoids, such as lutein or zeaxanthin, also seem to have protective effects on DR in diabetic rats. Zeaxanthin inhibits oxidative damage and performs anti-inflammatory action. Plus, lutein normalizes the markers of retinal oxidative stress, avoids ganglion cell loss and decreases apoptosis markers. Furthermore, it attenuates the loss of ganglion cells and prevents impairment in ERG. . N-acetylcysteine helps to regulate pro-oxidative markers Rutin has shown antiapoptotic activity (decreasing levels of caspase-3) \[94\]. It has activity at the systemic level, decreasing glucose levels and improving insulin concentration\... There is an increased interest in antioxidant supplementation for human disorders, because they can be administered orally and they are easily available and affordable. Difficulties in analyzing these studies are that end-points and results are variables and, in some cases, controversial. Some studies focus their objectives on functional results (best-corrected visual acuity---BCVA---; contrast sensitivity; glare sensitivity), others in anatomical results (central macular thickness---CMT---), in analyzing oxidative stress status, or even in a combination of the anterior parameters. Plus, in the majority of these studies, the population studied include type 2 diabetic mellitus (T2DM) patients. Some studies deal with the first stages of the disease and other studies consider typical complications of late stage Calcium dobesilate (Ca Dob) is a vasculoprotector agent that has been widely studied in the context of DR. However, the results of clinical trials in DR are controversial. some CaDob mechanism of actions, such as antioxidant and anti-ROS activity, defensive activity at the endothelial level, anti apoptoic properties and angiogenesis inhibition. Other mechanisms of Ca Dob improving microcirculation and reducing micro-vascular injury have been described recently There are nine studies listed with Ca Dob supplementation . The study with the highest number of patients recruited (635) and the longest duration showed no effects on the reduction of the development of clinically significant diabetic macular edema (CSDME) in T2DM. Likewise, another study with 40 non-proliferative DR (NPDR) patients with macular edema failed to find beneficial effects by adding Ca Dob to laser in the treatment of macular edema However, other studies have positive results analyzing micro aneurisms and retinal hemorrhages, exudates and blood viscosity There is an increasing interest in combined antioxidant therapy (CAT), as shown by the latest investigations. A long-lasting study (60 months) by Garcia-Medina et al. \[118\] evaluated antioxidant supplementation (lutein, VC, alpha-tocopherol, niacin, beta-carotene, Zn and Se) in 105 T2DM with NPDR.This long follow-up allowed one to demonstrate a retardation of the DR progression and the maintenance of antioxidant plasma status in the treated group. However, no effect on visual acuity was reported. In another work, the supplementation of lutein and zeaxanthin for three months in type 1 diabetic mellitus (T1DM) and T2DM showed an improvement of visual acuity, contrast sensivity and foveal thickness \[127\]. Likewise, Chous et al. reported an improvement in BCVA, but no changes in retinal thickness in his study. The association of CAT with the latest therapies such as anti-VEFG therapy is very interesting. Lafuente et al. \[124\] studied 55 T2DM for three years. They measured the effect of adding a combined antioxidant treatment to ranibizumab in the treatment of diabetic macular edema(DME).They reported lower macular thickness in the supplement group when compared to the control group. Pycnogenol®, a French maritime pine bark extract rich on flavonoids, has been dosed alone or combined since the 1980s, in several studies. Two studies administering this antioxidant alone are referenced. One is a study of 32 diabetic patients for six months, five of which displayed a reduction in exudates in both eyes Domanico et al. have studied patients with NPDR. However, there was no correlation among the serum, aqueous humor and vitreous humor levels of vitamin C in the PDR group. These findings suggest that ocular factors could be relevant in the pathogenesis of PDR and open new strategies and routes of administration of the treatment The authors reported that diabetic patients showed a decreased retinal blood flow that improved after treatment, similarly to control cases Vitamin E supplementation was compared to ALA or selenium supplementation or placebo, in a study performed by Kähler in 80 diabetics during three months. They found that oxidative status was reduced in all treated groups compared to the placebo group Thestudiesexaminedinthissurveysuggestthatanumberofantioxidantsmaypreventoralleviate the deleterious effects of hyperglycaemic environment in cultured tissues, or the complications of DR in animal models of diabetes. In addition, metabolism, senescence rate or administered doses in animal models are not identical to those in human individuals. It is difficult to bring together all this information, but we can infer that there is a tendency to use antioxidants in combination. However, we have to keep in mind that pro-oxidative conditions and their consequences are still not well-known in a chronic disorder such as DR. Plus, a combination of antioxidant may interact not only with different metabolic pathways, but also among themselves. In this context, it is hard to define the exact effect of each antioxidant that may even change when administered in combination. Another important concern is the safety of administering antioxidants for years, when the clinical studies performed so far are not longer than five years. Despite the fact that encouraging outcomes have already been obtained in this field, future studies must be conducted considering the efficacy and safety of different doses of antioxidants, in order to get better results to prevent ocular damages in this blinding disease Oxidative stress has been postulated as an underlying pathophysiologic mechanism of diabetic retinopathy (DR), the main cause of avoidable blindness in working-aged people. This review addressed the current daily clinical practice of DR and the role of antioxidants in this practice. Asystematic review of the studies on antioxidant supplementation in DR patients was presented.Role of Oral Antioxidant Supplementation in the Current Management of Diabetic Retinopath.Diabetic retinopathy (DR) is one of the most specific microvascular complications in diabetes mellitus (DM) and is the main cause of avoidable blindness in working-aged peo ple As it develops, and depending on the duration of DM and glycaemic levels, it is expected to increase concurrently as diabetes numbers rise \[1\]. According to the most recent International Diabetes Federation data**, the worldwide prevalence of DM was estimated to be 9.3% (463 million people) in adults aged 20--79 years old in 2019, and these numbers are expected to increase to 10.9% (700.2 million people) by 2045, thereby constituting a global burden** for the Public Health Care Systems that will not stop increasing \[2\]. One of the main concerns is that patients can remain asymptomatic until visual symp toms begin. The current management of DR comprises accurate screening programmes for early detection and a strict systemic control of glycaemia and related risk factors; however, active treatment is not initiated until advanced stages of the disease occur \[3\]. Taking into account that up to 45.8% of the world diabetic population is estimated to be undiagnosed, manyare checked once DM complications have already developed, when tissue damage maybeirreversible \[4\]. There is still a gap for new diagnostic biomarkers and for active treatments that could be applied in the early stages of DR to prevent further progression. Oxidative stress has been demonstrated to play a key role in the pathophysiology of DR and has been postulated as a nexus with other biochemical pathways, which commonly brings about inflammation, neurodegeneration, and microvasculopathy \[5,6\]. The use of antioxidants, such as polyphenols, has proved to reduce DR progression in animal models \[7\]. However, their role in the clinical management of DR patients has not yet been established. antioxidant clinical trials discussing when, how and why antioxidant supplementation should be used in DR management. DR-blindness increased by 7.7% and DR moderate-to-severe vision impairment increased by 28.6% in 2015. This was a warning signal to strengthen existing screening programmes and managementstrategies and increase research programmes directed towards new molecular targets before the disease appears. **In 2010, the global prevalence of DR among the diabetic population was estimated to be about 34.6% with regard to DR of any kind, 6.96% for proliferative diabetic retinopathy (PDR), 6.81% for diabetic macular oedema (DME), and10.2%forvision-threatening diabetic retinopathy (VTDR), including PDR and DME**. This means that approximately one third of DMpatients would have some degree of DR and one tenth needs active treatment. **The risk of having some kind of DR was 2.7 times higher in type 1 DM (T1DM) than in type 2 DM(T2DM) after at least 20 years of disease progression** \[1\]. **Regarding DR global incidence, a recent nine-year prospective population-based study including T1 and T2 patients determined an annual incidence of 15.16 ± 2.19% in T1DM, in comparison to 8.37 ± 2.19% in T2DM. In both the duration of DM and glycaemic control, together with arterial hypertension, low-density lipoprotein (LDL) cholesterol and creatinine levels were significant risk factors for developing DR, both in T1DM and T2DM**. **A higher prevalence and incidence of DR observed in the T1DM sample at the end of this study was attributed to a longer duration of diabetes and worse basal and monitored HbA1c levels \[11\]. In the context of dietary patterns, there is evidence that dietary fibre, oily fish and the Mediterranean diet can protect against DR. By contrast, a higher caloric intake has been associated with a greater risk for DR**. In addition, a recent review reported that studies on antioxidants, specifically vitamins C, E and carotenoids as protective factors in usual diets, are inconclusive. 3. Pathophysiology Diabetic retinopathy must be considered as multifactorial, as its development is a direct consequence of prolonged levels of hyperglycaemia, although it is influenced by the previously mentioned risk factors \[1,11,13,14\]. From a metabolic perspective, an exacerbated oxidative stress environment has been found to be a crucial factor in the development of DR, interacting as a link between other glucose-mediated biochemical processe. Among the cited risk factors for DR, arterial hypertension has been demonstrated to increase glycaemic induced oxidative stress, contributing to the exacerbation of molecular damage Metabolic alterations produced by hyperglycaemia and an increase in ROS result in cellular dysfunction and sequential apoptosis, leading to \[20\]: • Inflammation: Microglial activation seems to be an early event in DR and can trigger the secretion of inflammatory mediators Neurodegeneration: Apoptosis seems to affect neurons before vascular cells. Elec troretinogram (ERG) studies have shown the possibility of existing neuronal damage even before DR clinical signs were present, preceding microvascular changes. • Microvasculopathy: The walls of retinal capillaries have an external pericytes layer, a basement membrane and an inner endothelial cells layer. Pericyte loss occurs under hyperglycaemic conditions \[33\] and leads to focal microvascular dilatation with microaneurysm formation. A thickening of the basement membrane, due to debris deposition and endothelial cell dysfunction, leads to blood--retinal barrier (BRB) disruption, producing increased vascular permeability with exudation and haemorrhages \[34\]. Leukostasis derived from an inflammatory response is involved in endothelial cell impairment and is followed by microvascular occlusions \[27\]. Subsequent hypoxia promotes the activation of transcription factor hypoxia-inducible factor 1 (HIF-1), which further stimulates the secretion of vascular endothelial growth factors (VEGFs), and therefore causes neovessel formation \[35\]. 4. Important Role of Early Diagnosis 4.1. Classification of DR Fundoscopy clinical signs derived from tissue damage have suggested a sequential grading of DR. Arecent multicentre cohort study performed in the UK analysed the **five-year risk of developing PDR depending on the stage at baseline. The probability of presenting PDR at year five was 2.2% for no initial DR, 13% for mild nonproliferative diabetic retinopathy (NPDR) at baseline, 27.2% for moderate NPDR and 45.5% for severe NPDR \[37\].** Diabetic macular oedema (DME) has been classified separately, as it can appear at any of the mentioned stages of DR. The International Scale understood DME to be the retinal thickening or presence of hard exudates in the posterior pole, and it was graded into three stages \[23\] (Table 1 and Figure 1). Int. J. Mol. Sci. 2021, 22, 4020 4 of 35 Int. J. Mol. Sci. 2021, 22, 4020 4 of 31 Table 1. International Clinical Disease Severity Scale for diabetic retinopathy (DR). Table 1. International Clinical Disease Severity Scale for diabetic retinopathy (DR). Disease Ophthalmoscopy Findings Disease No apparent DR Ophthalmoscopy Findings No ocular findings Noapparent DR NPDR Noocular findings No NV NPDR Mild Microaneurysms only NoNV Mild Moderate Microaneurysms only Microaneurysms + blot haemorrhages, hard exudates, cotton wool spots (but less than in severe NPDR) Moderate Microaneurysms + blot haemorrhages, hard exudates, cotton wool spots (but less than in severe NPDR) Severe Severe Intraretinal haemorrhages (≥20 in each quadrant) Definite venous beading (in two quadrants) Intraretinal microvascular abnormalities (IRMA) (in one quadrant) No signs of proliferative retinopathy Intraretinal haemorrhages (≥20 in each quadrant) Definite venous beading (in two quadrants) Intraretinal microvascular abnormalities (IRMA) (in one quadrant) Nosigns of proliferative retinopathy PDR PDR Neovascularisation or vitreous/preretinal haemorrhage/tractional retinal detachment Neovascularisation or vitreous/preretinal haemorrhage/tractional retinal detachment DME = retinal thickening of hard exudates in the posterior pole DME=retinal thickening of hard exudates in the posterior pole Mild Mild Some retinal thickening or hard exudates in the posterior pole but distant from the centre of the macula Some retinal thickening or hard exudates in the posterior pole but distant from the centre of the macula Moderate Moderate Retinal thickening or hard exudates approaching the centre of the macula but not involving the fovea Retinal thickening or hard exudates approaching the centre of the macula but not involving the fovea Severe Severe Retinal thickening or hard exudates involving the centre of the macula Retinal thickening or hard exudates involving the centre of the macula DR = diabetic retinopathy; NPDR = nonproliferative diabetic retinopathy; NV = neovascularisation; PDR=proliferative diabetic retinopathy; DME = diabetic macular oedema. DR = diabetic retinopathy; NPDR = nonproliferative diabetic retinopathy; NV = neovascularisa PDR=proliferative diabetic retinopathy; DME = diabetic macular oedema. DR = diabetic retinopathy; NPDR = nonproliferative diabetic retinopathy; NV = neovascularisa tion; PDR = proliferative diabetic retinopathy; DME = diabetic macular oedema. Figure 1. Clinical DR progression. (a) Mild nonproliferative diabetic retinopathy (NPDR), (b) moderate Figure 1. Clinical DR progression. (a) Mild nonproliferative diabetic retinopathy (NPDR), (b) mod erate NPDR, (c) severe NPDR and (d) proliferative diabetic retinopathy (PDR) with papillary neo vascularisation. NPDR(c) severe NPDRand(d)proliferative diabetic retinopathy (PDR) with papillary neovascularisa tion. 4.2. Impact on Visual Impairment Studies that have measured quality-of-life items reported vision-related effects on emotional well-being and general health, especially in those suffering from VTDR, DME is the most common reason for visual acuity (VA) loss, followed by any context of PDR \[1,11\]. From the viewpoint of ophthalmological care, the active treatment of DR should be initiated when a high risk of progression to PDR or DME \[3\] is evident. It must be kept in mind that advanced stages of DR or DME may translate into extensive tissue damage with dysfunctional cells due to the metabolic memory effect \[18,40,41\] and, therefore, make it too late to restore adequate visual function. 5. Imaging Techniques for Diabetic Retinopathy Screening The exponential increase in diabetes worldwide has forced the development of several imaging diagnostic tools that can screen for DR in a fast and effective way. Traditionally, most DRscreening programmes have been based on fundus photography (FF) with mydri atic or nonmydriatic cameras to identify DR patterns. Nowadays, imaging technology has madeasignificant quantitative and qualitative leap forward, providing a great improve ment in terms of affordability, performance and diagnostic accuracy. Funduscopic imaging using smartphones, macular optical coherence tomography (OCT) and ultrawide-field imaging, together with revolutionary artificial intelligence (AI) software, has opened the door to a new era in the early diagnosis and follow-up of DR patients. The International Council of Ophthalmology (ICO) guidelines for DR diagnosis in clude retinal examination with either (a) direct or indirect ophthalmoscopy or fundus biomicroscopy using a slit lamp, or (b) mono-photography or stereo-photography greater than or equal to 30◦, associated or not with OCT. These images should always be analysed and classified by a trained specialist \[3\]. The accuracy of DR classification provided by these screening tools is considered to be category 1, as defined by the American Teleoph thalmological Association (ATA), and it provides a sufficiently high level of accuracy for population screening. 5.1. Fundus Photography Today's digital FF is a reliable alternative to the traditional seven-field photography usedinearly treatment diabetic retinopathy studies (ETDRSs) \[42\]. Current fundus cameras have resolutions in the range of 20 megapixels, exceeding the 2-3-megapixel resolution needed to display a single retinal microaneurysm \[43\]. Several clinical trials have shown that mydriatic FF has a higher sensitivity and specificity for DR detection compared to nonmydriatic cameras \[43\]. However, due to practical and logistical considerations, most DRdetection programmes use nonmydriatic FF. Most modern programmes use a single 45◦ photograph or even two or three multi-field photographs \[44\]. The ATA establishes four levels of grading systems for DR. Level 1 includes pro grammes that can distinguish between the absence of DR and minimal DR disturbances. Level 4 can make a complete DR categorisation between mild, moderate, severe and early proliferative high-risk DR, with or without macular oedema \[44\]. 5.2. Ultrawide-Field Imaging for Diabetic Retinopathy Screening Wide-field photography is another DR screening modality, which is especially appro priate for detecting peripheral ischaemic lesions and proliferative diabetic retinopathy \[45\]. Ultrawide-field imaging reaches 80% of the retinal surface and detects DR with a 99% sensitivity and 97% specificity \[46\]. 5.3. Optical Coherence Tomography for Diabetic Macular Oedema Screening As mentioned above, FF is a useful diagnostic tool for DR, but it has a low accuracy in detecting diabetic macular oedema (DME) due to its two-dimensional nature and because it is unable to measure retinal thicknesses reliably. The English National Screening Program for the detection of DME uses three photographic landmarks: first, the appearance of exudates withinonediscdiameterfromthefovea; second, thepresenceofcircinateexudates within the macula; and third, the presence of microaneurysms or haemorrhages within Int. J. Mol. Sci. 2021, 22, 4020 6 of 31 one disc diameter from the fovea \[47\]. However, this method yields limited diagnostic utility. Conventional FF offered an 86.6% false positive rate in detecting DME, according to a cross-sectional observational study \[48\]. For this reason, macular OCT is a better option than FF for evaluating the macula. Several studies have investigated the cost-effectiveness and efficiency of using macular OCT in DME detection programmes \[49\]. OCTallows for a detailed analysis of all the retinal layers. For example, it quantifies the thinning of the ganglion cell and nerve fibre layer due to the neurodegenerative process present in DR patients. It may also show the disorganisation at the macular internal retinal layer (DRIL) as a biomarker of visual impairment \[50\]. Alternatively, it may evaluate the integrity of the outer layers where the cone photoreceptors and the pigment epithelium cells of the retina are present. 5.4. OCT Angiography in Diabetic Retinopathy Screening OCTangiography (OCT-A) is a novel noninvasive imaging modality able to describe the retinal circulation using algorithms that detect red blood cell movement. This technique can detect microaneurysms, retinal neovascularisation or ischaemic areas, but only in the posterior pole; it cannot evaluate the peripheral retina \[51\]. Therefore, it can classify DR according to its severity. It describes the anatomy and blood flow at the foveal avascular zone and the superficial and deep retinal plexus in the macula \[51,52\]. OCT-A can also measure the progression of DR as it correlates vascular changes with visual acuity \[53\]. 5.5. Smartphone Function in Diabetic Retinopathy Screening Most digital FF cameras and OCTs are expensive and require trained specialists in retinal image interpretation. To solve this problem, several smartphone applications have been developed aseffective and accessible techniques for DR detection. Cameras in modern cell phones have an even higher resolution than other conventional fundus cameras. New generation smartphones have wide-field digital cameras with resolutions greater than 10 megapixels \[44\]. Currently, these smartphones need the coupling of supplementary lenses and specific image editing software. Several clinical trials have demonstrated the potential of these devices to detect DR in different regions of the world \[54\]. 5.6. Automated DR Image Evaluation Systems Used for Teleophthalmology Gardner and colleagues described the use of an artificial neural network able to detect DR with an 88% and 83% sensitivity and specificity, respectively, as compared to a trained ophthalmologist \[55\]. These systems use pattern recognition algorithms that identify specific features of DR, such as microaneurysms. On the downside, the image pre-processing requires a lot of time in order to identify clinically important features and develop mathematical descriptors for the different types of lesions. Deeplearning (DL) is a novel AI iteration that employs convolutional neural networks to interpret images by repetitive analysis and comparison of the output with a standard that is self-correcting if an error is made. Multiple studies have demonstrated useful results in the development of DL algorithms that are able of identify references of DR without the need to previously teach computer systems specific DR characteristics. The sensitivity and specificity of these approaches are generally 90% and 95%, respectively \[56,57\]. The present generation of DL algorithms employing coloured FF has achieved a rating performance similar to that of a retinal specialist \[58\]. Several DL algorithms for DR detection, including the recently FDA-approved IDx-DR algorithm \[59\], have been described. These systems are trained using known features of DR, such as microaneurysms, bleeding and exudates. 6. Pathology Control and Monitoring The correct management of a disease usually depends on the good practice of doctors, their diagnosis and application of the appropriate treatment. However, controlling a high prevalence disease, such as DR, which affects almost 100 million people worldwide \[1\], needs more than diagnosis and treatment; it requires good follow-up protocols in order Int. J. Mol. Sci. 2021, 22, 4020 7 of 31 to optimise health resources and focus attention on patients who are more susceptible to having vision loss complications. 6.1. First Visit Knowing when to first examine a diabetic patient for DR signs is the first step in controlling and preventing the pathology. Guidelines differ: UK guidelines recommend to start DR screening in all persons diagnosed with diabetes aged 12 and over \[60\] as a result of research including 2125 children under 12-years-old diagnosed with DM, showing that only three children (0.17%) presented sight-threatening conditions, and none required treatment \[61\]. The American Academy of Ophthalmology Guideline recommends to start screening five years after the diagnosis of T1DM and when T2DM is diagnosed \[62\]. The first visit is most important and should incorporate the following crucial actions: 6.1.1. Grade the Diabetic Retinopathy The main goal of ophthalmologists and general doctors treating DR patients is to avoid vision loss complications of DR, diabetic macular oedema (DME) and proliferative diabetic retinopathy (PDR). In order to plan a good strategy to prevent these complications, DR has been divided into different grades depending on the probability of developing these complications and the guidance for their management. Following the International Classification of Diabetic Retinopathy and Diabetic Macu lar Edema \[3\], the risk of developing PDR and the proposed follow-up time in each DR grade are listed in Table 2. Table 2. Management of DR patients depending on the pathology grade. NoDR NPDR PDR DME Mild Moderate Severe Non-Centre Involving Centre PDRprogression risk within 1 year/3 years 5%/14% 12--27%/30.48% 52%/71% Referral to ophthalmologist Not required Not required Required Required Required Recommended if laser sources available \* Required Treatment Observation Observation/PRP PRP Anti VEGF/PRP/VPP Laser: Focal/Grid Anti-VEGF Antioxidants role Potentially indicated Worthwhile? Potentially indicated Follow-up 1--2 years 6--12 2. Educational Advice Once the DRofthe patient has been graded, educational advice on the first visit is fun damental to encourage patients to attend their routine appointments. A retrospective audit of data from 62,067 patients due for annual diabetes eye screening showed that missing appointments strongly increased the proportion of patients showing referable retinopathy at the next visit. Particular focus must be put on young T1DM male patients who are the most likely to miss appointments \[69\]. At this point, general practitioners, endocrinologists and ophthalmologists should work together throughout the whole follow-up. Aproposed scheme of the advice is: DR is the first cause of blindness in working-age people \[8\]. DR is a reflection of systemic affection by diabetes, and in fact, the presence of mild NPDR implies an excess of mortality of 81% and a moderate-severe NPDR of 314% \[70\]. As a result, uncontrolled DRis areflection of uncontrolled diabetes, increasing possibilities of not only blindness, but also death due to some other cause. However, blindness caused by DR is almost 100% avoidable following our recommendations \[71\]. 6.1.3. Establishing Goals for Controlling the Risk Factors Associated with DR Progression While DR is in its early stages, the risk of losing vision is low and controlling the risk factors associated with the development and progression of DR is the only treatment wecan offer patients. Specific goal values have to be established. The main goals for DR control are to regulate HbA1c and blood pressure (BP). Secondary goals include lowering serum lipids and obesity. • HbA1cmonths/ 1--2 years \* 3--6 months/ 6--12 months \*2. Functional Variables Results Quite a different scene is observed regarding the influence of antioxidants on retinal function. Three studies included the analysis of retinal sensitivity \[144,156\], contrast sensitivity \[144,148\], glare sensitivity \[144\] and/or MPOD \[144\], and all of them observed a significant improvement in patients supplemented with Lutein, DiVFuSS® complex or C. Asiatica capsules. These changes were observed after relatively short follow-up periods, varying from six to fourteen months. The profile of the patients included by Zhang et al. and Chouss et al. was mild-to-moderate NPDR without CSME \[144,148\], while Forte et al. recruited T2DM patients with DME but without macular thickening in the OCT \[156\]. 8.3.3. Biochemical Variables Results Only three of the ten studies analysing HbA1c% values reported an improvement \[129, 147,153\] in supplemented patients. Concurrently, none of the studies could demonstrate sig nificant changes in HDL/LDL/total cholesterol or triglyceride levels, nor were statistically significant results regarding microalbuminuria observed by Forte et al. \[156\]. Only Bursell et al. encountered an improvement in creatinine clearance in T1DM patients undergoing Vitamin E supplementation, but this effect was not maintained after a crossover period to placebo \[157\]. By contrast, promising numbers were observed regarding oxidation parameters. Among all the studies analysing antioxidant status \[129,149--151,155\], the changes re f lected a significant reduction in lipid peroxidation end products and increased plasma total antioxidant capacity, in relation to Brudyretina®, Nutrof Omega®, Ubiquinone and Vitalux Forte® supplementation, both in studies with the shortest follow-up periods (six months) and the longest (60 months). Domanico et al. \[152\] were also able to demonstrate decreased ROS levels in patients supplemented with Diaberet®. Asanother interesting finding, Lafuente 2019 et al. \[129\] demonstrated a significant de crease in IL-6 plasma levels after 36 months of follow-up, suggesting an anti-inflammatory effect related to supplementation with DHA (Brudyretina®). 8.3.4. Safety Profile Themajority of the studies reported no adverse events related to oral supplementation. Bursell et al. detected low thyroid hormone levels in relation to Vitamin E in one patient; such levels recovered after the discontinuation of the antioxidant. In the study performedbyMoonetal.,27%oftheGSPE-supplementedsubjectsvs. 27.66%oftheplacebo group reported adverse reactions, which consisted of infections, gastrointestinal events, ocular and central nervous system disorders \[146\]. Gastrointestinal events were potentially associated with the treatment that was administered, and drugs were withdrawn in four patients of the supplemented group vs. one in the placebo group. Sanz-González et al. reported mild gastrointestinal discomfort related to Nutrof Omega® treatment, but no rates are specified and supplementation was not withdrawn \[145\]. Studies analysing T1DM patients had a mean follow-up time ranging from six to eight months and no children were included. Before recommending nutraceuticals to children with T1DM, more research is needed on their potential adverse effects over both the short and long term \[158\]. 8.3.5. Limitations Limitations of this systematic review include the high heterogeneity among studies, regarding the use of multiple antioxidants, the clinical variables studied and the follow-up Int. J. Mol. Sci. 2021, 22, 4020 23 of 31 periods, ranging from six to sixty months. Shorter follow-ups could explain the lack of significant results concerning clinical findings, given the chronic character of the disease. Another considerable limitation would be the fact that some of the studies fail to assess administered drug levels and oxidation parameters \[144,146--148,154,156,157\], and they do not verify the treatment compliance or the further impact in oxidative status. Furthermore, the distribution of unknown amounts of antioxidants in the usual diet intake could influence the results. As an example, the group of Roig-Revert et al. did check the initial adherence of all the participants to the Mediterranean diet and took this factor into account for statistical analysis \[151\]. Data concerning drug bioavailability were only reported by two research groups. Lafuente etal. analysedtheerythrocytecontentofDHAandobtainedsignificantdifferences among supplemented and placebo groups \[129,149\]. Sanz-González et al. measured vitamin C levels and encountered inappropriate bioavailabilities, depending on different genetic expressions of SLC23A2 (which regulates intracellular levels of the vitamin), in the context of chronic hyperglycaemia and DR \[145\]. In addition, Haritoglou et al., who reported nonsignificant clinical results and did not measure supplemented α-lipoic acid levels, postulated that administered doses might have not been enough to produce retinal changes, because the ideal dose in humans has not yet been established in comparison to well-defined safety levels in animal assays \[154\]. In this context, bioavailability, the fraction of bioactive compound that reaches the blood circulation, is usually very low in nutraceuticals. In recent years, nanoformulations have been used in order to increase the bioavailability of phenolic compounds, vitamins and minerals \[159\]. Likewise, other nutraceuticals with more bioavailability have appeared, such as pterostilbene, a resveratrol analogue whose bioavailability in rats is 80% compared to 20% for resveratrol \[160\]. 8.4. Conclusions According to the results gleaned from the studies, it can be deduced that clinical changes were only observed after the longest follow-up periods, in terms of delaying the onset or reducing the progression of DR in T2DM. No other clinical effects could be observed, which means that antioxidant supplementation has not yet been proven to have an impact on BCVA or DMEregression in the mid-term. On the other hand, antioxidants did show an early influence on retinal function parameters after short follow-up periods, ranging from six to fourteen months. The profile of these patients was T1 or T2DM subjects presenting mild-to-moderate NPDR without CSME, or with DMEbutwithout the thickening of the retina in the OCT. These findings suggest that antioxidants are a valid prophylactic adjuvant therapy in the early stages of DR, in which anatomical damage is not excessive and there is no thickening of the central macula. Taking into account the heterogeneity of the variables studied and the large diver sity of antioxidants administered in the RCTs, we would recommend antioxidant oral supplementation with a IIb level of evidence in adult T1DM and T2DM patients without retinopathy or mild-to-moderate NPDR without DME. In order to establish protocolled recommendations, larger sample sizes and longer follow-up periods should be accomplished in future clinical trials to determine the best antioxidant and the profile of candidates who will benefit from the adjuvant oral therapy in the mid- and long-term. 9. The Future Despite the fact that the prevalence of diabetes is increasing worldwide, the advances in retinal imaging and new treatments have succeeded in reducing the rates of PDR and severe vision loss in developed countries. The greater use of ultrawide-field photography of the fundus, which allows the evaluation of more than 80% of the retinal surface from a single image \[161,162\], and the Int. J. Mol. Sci. 2021, 22, 4020 24 of 31 improvement of noninvasive techniques, such as OCT angiography, for the early detection of microvascular damage in DR \[53,163,164\] will encourage better management of these patients, giving telemedicine a fundamental role in the next few years. These advances, together with AI algorithms, to detect DR may predict the risk of retinopathy progression more efficiently and in early stages \[165,166\]. However, more than new diagnosis strategies, improved therapeutic approaches are still needed and are currently under investigation for the treatment of DR. These include emerging therapies for retinopathy that target alternative pathways for increased therapeutic effectiveness; alternative noninvasive delivery mechanisms or mechanisms providing a longer duration of action; approaches to prevent the onset of DR or to slow downthe worsening of DR, such as oral antioxidant supplementation. In this review, we have staged the profile of patients who would benefit from antioxidant supplementation, adult T1DM and T2DMpatients without retinopathy or mild-to-moderate NPDR without DME. However, new antioxidants with a higher bioavailability and better studies are needed to improve the level of evidence of this recommendation. Finally, preclinical research suggests that gene therapy could be a promising ther apeutic strategy for the future, eliminating the need for the frequent administration of anti-VEGF and increasing its brief therapeutic effect, which currently hinders the clinical practice **PREVIOUS RESEARCH WORKS DONE ON DIABETIC RETINOPATHY--** 1) IPGT & RA, Jamnagar: i. A Clinical study to evaluate the role of holistic Ayurvedic Treatment in Pramehaja timira w.s. r Background Diabetic Retinopathy - Dr. Priyanka Rani (2013). 2) B.H.U. Varanasi: i. Effect of Amalaki rasayana in Diabetic Retinopathy: Dr.C. Rajeshkumar (1994) ii. Effect of Triphala guggulu on Diabetic Retinopathy : Dr. A.K. Singh (1998). iii. Effect of Shatavari on Diabetic Retinopathy: Dr. Sharma S.K (2000). 3) Trivandrum (1986): i. Onset, process and complications of Timira in Madhumeha: Dr. R.V.K. Verma. 4) G.A.V.C. Thrippunithura i. Efficacy of Ayurvedic Management in Proliferative Diabetic Retinopathy-A Randomised Controlled Trial --Dr .Vinitha T.V(2013). 5) Bengaluru: i. An approach to the Sarva-daihika vikara janya netra vikara w.s.r. to Madhumeha janya Drishti patala vikara (Diabetic Retinopathy) -- A Clinical study: Dr. Shantala Priyadarshini (1999) ii. Management of Diabetic retinopathy with Doorvadya ghritha tarpana and internal administration of Mahavasaadi kwatha-a comparative study: Dr. Veeranagouda Adoor(2011) **[Materials And Methods]{.underline}** The study is based on clinical observations and narrations by the patients. **[Place of work-]{.underline}** Patients of Diabetic Retinopathy were selected from OPD of Shalakya Tantra Dept of Govt. Ayurvedic College and Hospital, Nagpur. **[Number of patients]{.underline}**- 100 Selected patients were distributed in two groups- 1. **Experimental group- 50 patients** 2. **Control group- 50 patients** **[Plan of work-]{.underline}** **[Inclusion criteria]{.underline}**- 1. Patients suffering from type 2 DM of age group 30 to 70 years having clinical features of Non proliferative Diabetic Retinopathy seen on fundus examination were selected for study. 2. Patients having signs and symptoms of timir. 3. Patients who were willing to take treatment. 4. Controlled hypertensive patients. 5. HbA1c: ≤10% (controlled/moderately uncontrolled diabetes) 6. Willingness to participate and provide informed consent **[Exclusion criteria]{.underline}**- 1. Type 1 DM patients. 2. Age less than 30 years and above 70 years. 3. Systemic diseases like uncontrolled hypertension, severe renal diseases, cardiac diseases. ANC, PNC. 4. PDR, Uveitis, Glaucoma, Cataract. 5. Trauma, Inflammatory and Neoplastic conditions of eye. 6. Age Related Macular Degeneration (ARMD), Central Retinal Vein Occlusion (CRVO), Centra Retinal Artery Occlusion (CRAO), Retinal Detachment (RD), Retinitis Pigmentosa (RP), Vitreous Haemorrhage (VH), Optic Atrophy. 7. Injection Avastin given patients, photocoagulation done patients. **[Examination and Investigation]{.underline}**- 1. Routine eye examination with slit lamp. 2. Distant and Near Best Corrected Visual Acuity (BCVA). 3. Amsler Grid test. 4. Two Point Discrimination Test. 5. Photostress Test. 6. Fundus Examination with Ophthalmoscope. 7. Perimetry 8. Tonometry. 9. Fundus Photograph on Fundus camera. And FFA in some patients. **[Pathological Investigations]{.underline}**- 1. Fasting and Post Meal Blood Sugar. 2. Urine Albumin and Sugar. 3. Hba1c 4. Lipid Profile. 5. Blood urea 6. Serum creatinine 7. CBC Routine blood examinations were conducted to rule out infections. **[Systemic Investigations]{.underline}** -- 1.B.P. **[Diagnostic criteria]{.underline}**- NPDR -- - Microaneurysms - Dot/blot haemorrhages - Hard exudateS - IRMA Timir- - Diminished vision - Blurred vision - Difficulty in distant/near vision - Patal involvement **[Treatment-]{.underline}** 1. Group A-Experimental Group- number of patients-50. Vasadi kwath 40 ml OD for 3 months alongwith their Anti Diabetic Treatment. Prepared according to classical kwath Kalpana method 1:16 reduced to ¼ th Anupan -- luke warm water 2. Group B- Control Group- number of patients- 50. Antioxidant Tablets (marketed samples)1 OD for 3 months along with their Anti Diabetic Treatment. **[Follow Up-]{.underline}** For both experimental and control group- 1^st^ Follow up- after 15 days. 2^nd^ Follow up- after1 month. 3^rd^ Follow up- after 2 months. 4^th^ Follow up- after 3 months. ## **[Pathya-Apathya (Diet & Lifestyle]{.underline})** {#pathya-apathya-diet-lifestyle .unnumbered} ### Pathya: {#pathya .unnumbered} - Light, easily digestible diet - Green vegetables - Low glycemic index food ### Apathya: {#apathya .unnumbered} - Excess sugar, oily, spicy food - Sedentary lifestyle - Night awakening - Smoking, alcohol **[Assesment Criteria-]{.underline}** 1. **Distant vision-** It was recorded with the help of Snellen's chart As ```{=html} ``` a. Unaided b. Pinhole c. BCVA ```{=html} ``` 2. **Near Vision-** It was recorded with near vision Snellen's chart as ```{=html} ``` a. Unaided b. BCVA ```{=html} ``` 3. **Amsler Grid Test**- This test is done for screening macular disease, with patients wearing near vision corrected spectacles. Separately for each eye. Findings are noted as grades- 4. **Two point Discrimination Test**- It is a dark room test done with help of opaque disc perforated by 2 pinholes close to each other with light held behind it. Done for assessing macular function. Findings noted as grades- > 5\. **Photostress test-** It is used to detect maculopathy and > differentiate macular disease from optic neuropathy. After correcting > vision patient was asked to fixate light of pen torch held 3 cm away > for 10 seconds. Photostress recovery time PSRT is time taken to read > ant of 3 letters of pretest acuity line. Findings notes as grades- 5. **Fundoscopic Findings**- fundoscopy was done under mydriasis with the help of 1.direct ophthalmoscope 2\. with 90 D on slit lamp and findings were noted on every follow up 3\. fundus photograph on fundus camera 4\. FFA (if required) These investigations ( 3^rd^ and 4^th^ )were done in some patients before and after treatment. For statistical analysis following grades were taken in consideration - **[Criteria for evaluation]{.underline}**- ```{=html} ``` - **Best corrected visual acuity-** ---------------------------------------------------------------------------- Grades ---------- -------- ------ ------- ------- ------- ------- ------- --------- Vision 0 1 2 3 4 5 6 7 Dist. 6/6 6/9 6/12 6/18 6/24 6/36 6/60 \<6/60 Near N6 N8 N10 N12 N18 N36 \- \- ---------------------------------------------------------------------------- - **Grades of NPDR-** +------+---------------------------------------------------------------+ | Gr | Findings | | ades | | +======+===============================================================+ | 0 | Normal fundus. | +------+---------------------------------------------------------------+ | I | Only microaneurysms present. | +------+---------------------------------------------------------------+ | II | Mild haemorrhages, hard + soft exudates present. | +------+---------------------------------------------------------------+ | III | 20 intra retinal haemorrhages in each of four quadrants + | | | venous beading in at least 2 quadrants + | | | | | | IRMA in at least 1 quadrant. | +------+---------------------------------------------------------------+ | IV | Two or more lesions of grade III NPDR present. | +------+---------------------------------------------------------------+ - **Amsler grid**- ----------------------------------------------------------------------- Grades Findings ----------------- ----------------------------------------------------- O Grid normal I Wavy lines II Corners & sides not visible III hole or missing lines ----------------------------------------------------------------------- - **Two point discrimination test** ----------------------------------------------------------------------- Grades Findings ------------- --------------------------------------------------------- 0 Able to discriminate two points. I Not able to discriminate two points. ----------------------------------------------------------------------- - **Foveal reflex** ----------------------------------------------------------------------- Grades Findings ------------------------------- --------------------------------------- O Normal I Dull ----------------------------------------------------------------------- - **Photo stress test** ----------------------------------------------------------------------- Grades Findings -------------- -------------------------------------------------------- O Recovery within 15-30 seconds. I Recovery within 30-60 seconds. 2 Recovery within 60-90 seconds 3 Recovery more than 90 seconds ----------------------------------------------------------------------- **[Assessment criteria]{.underline}** 1. **[Subjective parameters]{.underline}** > Blurred vision > > Floaters > > Night vision difficulty > > Eye strain 2. **[Objective parameters]{.underline}** > V/A > > Fundus findings (grades of NPDR) > > Amsler grid > > Photo stress recovery time > > **[Criteria for assessment of results]{.underline}**- ----------------------------------------------------------------------- Category criteria ----------------------------------------------------------------------- Marked improvement \>75% relief Moderate improvement 50-75% relief Mild improvement 25- 50 % relief No improvement \<25% relief ----------------------------------------------------------------------- **[Withdrawl criteria]{.underline}** - > Patient not willing to continue > > Development of adverse effects Need for emergency treatment Pathya apathya chart was given and explained **[Practical difficulty- and changes made-]{.underline}** Patients selected for study were of age group 30-70 years where many patients had cataractous changes. To overcome this and to see fundus 90 D lens was used, so assessment of fundus became easier in early cataract patients. So patients with early cataract changes were selected for study. Patients were advised to operate for cataract whose fundus view was obstructed due to cataract and after that were selected for study. While performing some tests like two point discrimination test, photostress test. Amsler grid, patients level of understanding and interpretation was sometime challenging. FFA test required fitness and due to some side effects, so patients were not willing for this test. So FFA was not done and hence FFA findings were not considered into assessment criteria. To record visual acuity of illiterate patients landolt's C chart was used and for literate patients chart was used according to the language they were able to read. **[Sample Size Calculation]{.underline}** The sample size for the present clinical study was determined based on feasibility, prevalence of disease, and similar previous clinical studies in Timir and Diabetic Retinopathy. Since this is an interventional clinical study, the sample size was calculated using the standard formula: n=Z2×p×qd2n = \\frac{Z\^2 \\times p \\times q}{d\^2}n=d2Z2×p×q Where: - n = required sample size - Z = standard normal variate at 95% confidence level = 1.96 - p = estimated prevalence - q = 1 -- p - d = allowable error **Assumptions** - Prevalence (p) of Diabetic Retinopathy ≈ 20% (0.2) - q = 1 -- 0.2 = 0.8 - Allowable error (d) = 8% (0.08) - Confidence level = 95% **Calculation Final Sample Size** The calculated sample size was approximately 96, which was rounded off to 100 patients for convenience and to compensate for possible dropouts. **Reference (for Thesis/Protocol)** - World Health Organization. *Sample size determination in health studies: A practical manual*. Geneva: WHO; 1991. - Charan J, Biswas T. *How to calculate sample size for different study designs in medical research*. Journal of Clinical and Diagnostic Research. 2013. - International Council for Harmonisation (ICH) Guidelines for Clinical Research. Based on Fundus Grading Improvement Assumptions (ETDRS / NPDR grading) - Expected improvement = 1 grade change - SD = 1.5 - Effect size (d/σ) ≈ 0.67 (moderate effect) Using standard tables: - Required sample ≈ 45--50 per group With dropout → Total ≈ 100 patients. **Chief Complaints -** **According to Ayurveda (Timir Lakshana)** - Blurred vision - Difficulty in distant/near vision - Seeing darkness/black spots - Cobweb-like vision - Floaters-like symptoms - Diplopia - Poor vision in dim light - Gradual diminution of vision **[Outcome Measures]{.underline}** A. Primary Outcome Measures 1\. Change in BCVA (Snellen's chart) from baseline to end of treatment. 2\. Change in Timira Subjective Symptom Score (TSSS) from baseline to end of treatment. B. Secondary Outcome Measures 1\. Change in DR severity grade (ICDR/ETDRS). 2\. Change in DME grade (center-involving/non-center-involving). 3\. Change in near vision (N-notation). 4\. Change in Amsler grid score (metamorphopsia/scotoma). 5\. Change in contrast sensitivity and color vision. 6\. Change in FBS, PPBS, HbA1c. 7\. Incidence of adverse drug reactions/events. **Parameters with Objective Gradation** A. **Subjective (Ayurvedic + Functional) Parameters** 1\. **Blurred Vision (Avyakta Darshana)** • 0 = None • 1 = Occasional blur • 2 = Frequent blur, mild activity limitation • 3 = Persistent blur, marked limitation 2**. Floaters (Makshika-Mashaka-Kesha Darshana)** • 0 = None • 1 = Occasional few • 2 = Frequent multiple • 3 = Persistent dense floaters 3\. **Photopsia / Halos (Marichi/Mandala Darshana)** • 0 = None • 1 = Occasional • 2 = Frequent • 3 = Persistent disturbing 4\. **Distortion (Hrasva-Vriddha Viparyaya / Metamorphopsia)** • 0 = None • 1 = Mild occasional distortion • 2 = Definite distortion • 3 = Severe distortion 5**. Difficulty in Fine Near Work (Suchipasha na Pashyati)** • 0 = No difficulty • 1 = Mild • 2 = Moderate • 3 = Severe **Timira Subjective Symptom Total Score (TSSS)** Sum of all symptom grades • 0--4: normal • 5--8: Mild • 9-12: moderate • 13-16: severe 17-18- very severe **[Observations and results]{.underline}** ## Demographic and Clinical Observations {#demographic-and-clinical-observations .unnumbered} A total of 100 patients diagnosed with Timir w.s.r. diabetic retinopathy were included in the study and divided equally into: - Group A (n=50) - Group B (n=50) The effect of treatment was assessed using subjective symptoms, ophthalmological examinations, retinal functional tests, and laboratory investigations before treatment (BT) and after treatment (AT) over a period of 3 months. Statistical analysis was performed using the Mann--Whitney U test. Data were expressed as Mean ± Standard Deviation (SD). A p-value \<0.05 was considered statistically significant. Age wise distribution of 100 patients suffering from DR under study. --------------------------------------------------------------------------- Age group Trial group \% Control group \% Total patients \% ----------- ------------ ------ -------------- ------ -------------- ------ 31-40 2 4% 0 0% 2 2% 41-50 15 30% 14 28% 29 29% 51-60 22 44% 18 36% 40 40% 61-70 11 22% 18 36% 29 29% --------------------------------------------------------------------------- . ## Age-wise Distribution {#age-wise-distribution .unnumbered} The age-wise distribution graph shows that the majority of patients belonged to the 51--60 years age group (40%), followed by the 41--50 years and 61--70 years age groups (29% each). Very few patients (2%) were found in the 31--40 years age group. This indicates that diabetic retinopathy was more prevalent in middle-aged and elderly individuals, particularly after 50 years of age. The findings suggest that increasing age and longer duration of diabetes may contribute to higher risk of retinal complications Genderwise distribution of 100 patients of DR under study ------------------------------------------------------------------------- gender Trial \% Control \% Total Total % group group patients ---------- --------- ---------- ----------- -------- ----------- -------- male 21 42 % 25 50 % 46 46% female 29 58 % 25 50 % 54 54% ------------------------------------------------------------------------- ## Gender-wise Distribution {#gender-wise-distribution .unnumbered} The gender distribution graph demonstrates that females (54%) were slightly more affected than males (46%). In the trial group, females constituted 58% while males were 42%. In the control group, both genders were equally distributed (50% each). This indicates a mild female predominance in the present study population. Religionwise distribution of 100 patients of DR under study --------------------------------------------------------------------------- religion Trial group \% Control group \% total \% -------------- --------------- ----- ------------------ ----- ------- ----- Hindu 32 64 40 80 72 72 Budddhist 14 28 9 18 23 23 Muslim 4 8 1 2 5 5 --------------------------------------------------------------------------- ## Religion-wise Distribution {#religion-wise-distribution .unnumbered} The religion-wise graph shows that most patients belonged to the Hindu religion (72%), followed by Buddhists (23%) and Muslims (5%). This distribution mainly reflects the regional population pattern and socioeconomic background of the study area rather than any direct association between religion and diabetic retinopathy. Prakrutiwise distribution of 100 patients of DR under study ------------------------------------------------------------------------- prakruti Trial group \% Control group \% total \% ----------- --------------- ----- ------------------- ----- ------- ----- KP 12 24 13 26 25 25 VK 6 12 10 20 16 16 PV 7 14 7 14 14 14 VP 13 26 13 26 26 26 KV 6 12 4 8 10 10 PK 5 10 4 8 9 9 ------------------------------------------------------------------------- ## Prakruti-wise Distribution {#prakruti-wise-distribution .unnumbered} The prakruti distribution graph reveals that Vata-Pitta (VP) prakruti was most common (26%), followed closely by Kapha-Pitta (KP) prakruti (25%). Vata-Kapha (VK), Pitta-Vata (PV), Kapha-Vata (KV), and Pitta-Kapha (PK) were less common. The predominance of VP and KP prakruti suggests a greater involvement of Vata and Pitta dosha in the pathogenesis of Timir and diabetic retinopathy. Distribution according to associated hypertension in 100 patients of DR under study. --------------------------------------------------------------------------- K/C/O HTN Trial group \% Control group \% Total patients Total% ------------- ------------ ---- -------------- ---- -------------- -------- YES 29 58 27 54 56 56 NO 21 42 23 46 44 44 --------------------------------------------------------------------------- ## {#section-16 .unnumbered} ## Associated Hypertension Distribution {#associated-hypertension-distribution .unnumbered} The graph shows that 56% of patients had associated hypertension, whereas 44% did not have hypertension. This indicates that hypertension is a major associated risk factor in diabetic retinopathy and may accelerate retinal vascular damage. Addiction wise distribution of 100 patients of DR under study ------------------------------------------------------------------------- addiction Trial group \% Control grouo \% Total patients \% ----------- ------------- ---- ---------------- ---- --------------- ---- tobacco 13 26 10 20 23 23 smoking 9 18 13 26 22 22 Alcohol 8 16 4 8 12 12 no 20 40 23 46 43 43 ------------------------------------------------------------------------- ## Addiction-wise Distribution {#addiction-wise-distribution .unnumbered} The addiction-wise graph demonstrates that 43% of patients had no addiction, while tobacco chewing (23%) and smoking (22%) were common addictions. Alcohol consumption was observed in 12% of patients. These findings suggest that tobacco and smoking habits may contribute to vascular damage and worsening of diabetic retinopathy Distribution according to duration of DM in 100 patients of DR under study ------------------------------------------------------------------------ Duration of DM Trial group \% Control group \% total \% ------------------ ------------- ---- ---------------- ---- ------- ---- 1-5 yrs 15 30 12 24 27 27 6-10 yrs 27 54 29 58 56 56 11-15 yrs 6 12 9 18 15 15 16-20 yrs 2 4 0 0 2 2 ------------------------------------------------------------------------ ## Duration of Diabetes Mellitus {#duration-of-diabetes-mellitus .unnumbered} The duration-wise distribution graph shows that the majority of patients (56%) had diabetes duration of 6--10 years, followed by 1--5 years duration (27%). Only 2% had diabetes for 16--20 years. This indicates that diabetic retinopathy becomes more common with increasing duration of diabetes, especially after 5 years. Occupation wise distribution of 100 patients of DR under study ------------------------------------------------------------------------------ Occupation Trial \% Control \% total \% group group ------------------------------- ---------- ---- ------------ ---- ------- ---- Sedentary (more than 6 hrss 21 42 16 32 37 37 sitting) Moderate labour(3-4 hrs labour) 21 42 20 40 41 41 Heavy labour(more than 8 hrs 8 16 14 28 22 22 labour) ------------------------------------------------------------------------------ ## Occupation-wise Distribution {#occupation-wise-distribution .unnumbered} The occupation graph shows that 41% of patients were involved in moderate labour work, 37% had sedentary occupations, and 22% performed heavy labour. Sedentary lifestyle and reduced physical activity may contribute to poor glycemic control and progression of diabetic complications. Education wise distribution of 100 patients of DR under study -------------------------------------------------------------------------- education Trial group \% Control group \% total \% ------------- --------------- ----- ------------------ ----- ------- ----- Literate 29 58 35 70 64 64 illiterate 21 42 15 30 36 36 -------------------------------------------------------------------------- ## {#section-17 .unnumbered} ## {#section-18 .unnumbered} ## Education-wise Distribution {#education-wise-distribution .unnumbered} The graph indicates that 64% of patients were literate while 36% were illiterate. Higher literacy may improve awareness regarding diabetes management and early diagnosis; however, diabetic retinopathy was still prevalent due to chronic disease duration and metabolic factors. Socio economic wise distribution of 100 patients of DR under study -------------------------------------------------------------------------- Socio economic Trial \% Control group \% total \% group group ------------------- ---------- ------ -------------- ---- -------- ------- Lower 24 48 15 30 39 39 Middle 24 48 33 66 57 57 Upper middle 2 4 2 4 4 4 -------------------------------------------------------------------------- ## Socioeconomic Status Distribution {#socioeconomic-status-distribution .unnumbered} The socioeconomic graph shows that the majority of patients belonged to the middle socioeconomic class (57%), followed by lower class (39%), while only 4% belonged to the upper-middle class. This suggests that diabetic retinopathy is more commonly observed in middle- and lower-income populations, possibly due to lifestyle factors, delayed diagnosis, and inadequate diabetic control. Diet wise distribution of 100 pts of DR under study ------------------------------------------------------------------------- diet Trial group \% Control group \% total \% ------------ --------------- ----- ------------------ ----- ------- ----- Veg 18 36 25 50 43 43 Non veg 20 40 16 32 36 36 mixed 12 24 9 18 21 21 ------------------------------------------------------------------------- ## {#section-19 .unnumbered} ## Diet-wise Distribution {#diet-wise-distribution .unnumbered} The diet-wise graph demonstrates that 43% of patients were vegetarians, 36% consumed non-vegetarian diet, and 21% had mixed dietary habits. No strong dietary predominance was observed, although unhealthy dietary practices may influence diabetes progression. Bmi wise distribution of 100 pts of DR under study ------------------------------------------------------------------------------ BMI (kg/m2 ) TRIAL GROUP \% CONTROL GROUP % \% total \% ---------------------- ------------- ---- ------------------ ---- ------- ---- BELOW 25 NORMAL 31 62 33 66 64 64 ABOVE 25 OVERWEIGHT 19 38 17 34 36 36 ------------------------------------------------------------------------------ .**[BMI-wise Distribution]{.underline}** The BMI graph shows that 64% of patients had normal BMI (\<25 kg/m²), while 36% were overweight (\>25 kg/m²). Overweight patients may have increased insulin resistance and vascular complications contributing to diabetic retinopathy. **Lipid profile findings in pts of DR under study** **TC levels** ------------------------------------------------------------------------ TRIAL GROUP CONTROL GROUP ----------------------- --------------------- -------------------------- grades TC TC 0 \< 200 mg/dl 34 32 1 -200- 239 mg/dl 13 16 2-\>240 mg/dl 2 2 ------------------------------------------------------------------------ ## Total Cholesterol (TC) Levels {#total-cholesterol-tc-levels .unnumbered} Most patients (62%) had normal total cholesterol levels, whereas 29% showed mildly elevated cholesterol and 4% had severely elevated levels. This indicates that dyslipidemia was present in a considerable number of patients and may contribute to retinal vascular changes. LDL LEVELS ----------------------------------------------------------------------- TRIAL GROUP CONTROL GROUP ---------------------- --------------------- -------------------------- grades LDL LDL 0 \< 100 mg/dl 33 32 1 -100-129 mg/dl 13 16 2-130-159 mg/dl 3 2 ----------------------------------------------------------------------- ## LDL Levels {#ldl-levels .unnumbered} The LDL graph shows that 65% of patients had normal LDL levels, while 29% had mildly elevated LDL and 4% had moderately elevated LDL. Elevated LDL may increase retinal exudation and vascular damage in diabetic retinopathy. **TGS levels** ----------------------------------------------------------------------- TRIAL GROUP CONTROL GROUP ---------------------- --------------------- -------------------------- grades TGS TGS 0 \< 150 mg/dl 33 30 1 -150-199 mg/dl 13 18 2-\>200mg/dl 3 2 ----------------------------------------------------------------------- ## Triglyceride Levels {#triglyceride-levels .unnumbered} The triglyceride graph demonstrates that 63% of patients had normal triglyceride levels, while 31% had mild elevation and 5% had severe elevation. Increased triglycerides are associated with retinal hard exudates and worsening NPDR changes. **BLOOD UREA** findings in 100 pts of DR under study ------------------------------------------------------------------------ Grades Trial group Control group ------------------------------- ------------------ --------------------- 0 (15-40 mg/dl) 33 31 1 (41-60 mg/dl) 16 17 2 (61-80 mg/dl) 1 2 3 ( above 80 mg/dl) 0 0 ------------------------------------------------------------------------ ## {#section-20 .unnumbered} ## Blood Urea Findings {#blood-urea-findings .unnumbered} The blood urea graph shows that 64% of patients had normal blood urea levels, 33% had mildly elevated levels, and 3% had markedly elevated levels. This suggests mild renal involvement in some diabetic patients. Serum creatinine findings in 100 pts of DR under study ------------------------------------------------------------------------ Grades Trial group Control group -------------------------------- ----------------- --------------------- 0 (0.6-1.3 mg/dl) 33 33 1 ( 1.4-2.0 mg/dl) 15 15 2 ( 2.1-3.0 mg/dl) 2 2 3 (above 3.0 mg/dl) 0 0 ------------------------------------------------------------------------ ## Serum Creatinine Findings {#serum-creatinine-findings .unnumbered} The serum creatinine graph demonstrates that 66% of patients had normal creatinine levels, 30% had mildly elevated levels, and 4% had markedly elevated levels. These findings indicate associated diabetic nephropathy in some patients. # Overall Interpretation of Demographic Data {#overall-interpretation-of-demographic-data .unnumbered} The demographic analysis suggests that diabetic retinopathy was more common in: - Patients aged 51--70 years - Females - Patients with 6--10 years duration of diabetes - Patients having associated hypertension - Middle socioeconomic class individuals - Patients with tobacco/smoking addiction - Patients with dyslipidemia and mild renal impairment These observations indicate that age, duration of diabetes, hypertension, lifestyle habits, and metabolic abnormalities play an important role in the development and progression of diabetic retinopathy and Timir. Improvement in blood sugar levels FBS after treatment in 100 pts of DR -------------------------------------------------------------------------- Trial group Control broup ---------- -------------------- ---------- -------------------- ---------- Grades bt at Bt at 0 (70-100 9 10 5 4 mg/dl) 1 (101-125 28 17 23 15 mg/dl) 2 ( 11 4 22 16 126-160 mg/dl) 3 (161-200 2 0 0 0 mg/dl) -------------------------------------------------------------------------- ## Improvement in FBS (Fasting Blood Sugar) {#improvement-in-fbs-fasting-blood-sugar .unnumbered} The graph of FBS levels shows better improvement in the trial group compared to the control group after treatment. Most patients in the trial group shifted from higher grades (Grade 2 and Grade 3) toward lower grades (Grade 0 and Grade 1), indicating improved glycemic control. Grade 1 patients reduced from 28 to 17 and Grade 2 patients reduced from 11 to 4 after treatment. In the control group, improvement was present but comparatively less marked. This suggests that the trial treatment had a stronger effect in controlling fasting blood sugar levels. ## FBS {#fbs .unnumbered} - Group A: - Relief = **32.14%** - Group B: - Relief = **1.49%** ### Difference at 3 Months {#difference-at-3-months .unnumbered} - Group A: 0.36 ± 0.63 - Group B: 0.02 ± 0.55 - p=0.006 ### Observation {#observation .unnumbered} Significant improvement in fasting blood sugar was observed. - Significant post-treatment improvement (p\<0.001). Improvement in blood sugar levels PMBS after treatment in 100 pts of DR -------------------------------------------------------------------------- Trial group Control group ---------- -------------------- ---------- -------------------- ---------- Grades bt at Bt at 0 (less 10 9 5 5 than 140 mg/dl) 1 (140-199 24 12 18 11 mg/dl) 2 (200-250 12 10 26 23 mg/dl) 3 ( 4 1 0 0 251-300 mg/dl) -------------------------------------------------------------------------- ## Improvement in PMBS (Post Meal Blood Sugar) {#improvement-in-pmbs-post-meal-blood-sugar .unnumbered} The PMBS graph demonstrates a significant reduction in higher PMBS grades in the trial group after treatment. Grade 1 cases reduced from 24 to 12, while Grade 3 cases reduced from 4 to 1. The control group showed only mild improvement. The graph indicates that the trial drug helped in better postprandial glycemic regulation compared to the control treatment. ## PMBS {#pmbs .unnumbered} - Group A: - Relief = **16.67%** - Group B: - Relief = **0.00%** ### Difference {#difference .unnumbered} - p=0.111 ### Observation {#observation-1 .unnumbered} Mild reduction observed but statistically non-significant. - Significant AT difference (p=0.011). - Difference score non-significant Improvement in blood sugar levels HbA1c after treatment in 100 pts of DR ------------------------------------------------------------------------ Trial Control group group ----------------- ------- ------------- ----------- -------------------- Grade bt at bt at 0 (less than 5.7 23 23 5 4 %) 1 (5.7-6.4%) 20 14 25 24 2 (6.5-7.5% ) 7 6 20 19 3 ( 7.6-9%) 0 0 0 0 ------------------------------------------------------------------------ ## {#section-21 .unnumbered} ## {#section-22 .unnumbered} ## Improvement in HbA1c Levels {#improvement-in-hba1c-levels .unnumbered} The HbA1c graph shows mild but noticeable improvement in the trial group. Patients in Grade 1 decreased from 20 to 14 and Grade 2 decreased from 7 to 6 after treatment. Minimal improvement was observed in the control group. Since HbA1c reflects long-term blood sugar control, the findings suggest gradual metabolic improvement with the trial therapy. ## HbA1c {#hba1c .unnumbered} - Group A: - BT=0.68+\_0.71 - AT=0.62+\_0.75 - Relief = **8.82%** - Group B: - BT=1.30+\_0.65 - AT= 1.36+\_0.63 - Change = **-4.62%** (slight worsening) ### Difference {#difference-1 .unnumbered} GROUP A=0.06+\_0.37 GROUP B=0.04+\_0.28 - p=0.134 ### Observation {#observation-2 .unnumbered} ### Minimal improvement observed. {#minimal-improvement-observed. .unnumbered} - BT and AT values significant. - Difference score non-significant. ### Interpretation {#interpretation .unnumbered} Treatment showed moderate glycemic control benefits, particularly in fasting blood sugar Findings of anterior chamber of 100 pts of DR under study --------------------------------------------------------------------------- Ac Trial group rt Lt eye Control group rt Lt eye Total rt Total lt eye eye eye eye -------- -------------- ------ ---------------- ------ ---------- --------- Deep 9 11 6 9 15 20 normal 41 39 44 41 85 80 --------------------------------------------------------------------------- ## Anterior Chamber Findings {#anterior-chamber-findings .unnumbered} The graph shows that most eyes had a normal anterior chamber depth. Only a smaller proportion showed deep anterior chambers. No major pathological variations were observed, indicating that anterior chamber depth was largely unaffected in diabetic retinopathy patients under study. Condition of lens in 100 pts of DR under study ------------------------------------------------------------------------ Lens condition Trial Control Total Total group group ----------------- -------- -------- --------- -------- -------- -------- Rt eye Lt eye Rt eye Lt eye Rt eye Lt eye Imsc 10 11 16 15 26 26 Psph 9 9 5 9 14 18 Normal 31 30 29 26 60 56 ------------------------------------------------------------------------ . ## Condition of Lens {#condition-of-lens .unnumbered} The lens condition chart indicates that the majority of eyes had normal lenses. Some patients showed immature senile cataract (IMSC) changes, while others were pseudophakic. Cataract changes were more common than pseudophakia. The graph suggests that lens opacities are commonly associated with diabetic retinopathy patients. Complaint of pts of timir in 100 pts of DR under study ------------------------------------------------------------------------ Complaints of pts of timir Trial group Control group total ----------------------------------- ------------ --------------- ------- Blurring of vision 25 18 43 DOV FOR DV, NV 18 17 35 Black spots 4 2 6 Cobwebs, floaters 4 6 10 Burning, watering, redness, itching 2 5 7 Night vision problem 2 5 7 Diplopia 0 2 2 Heaviness and pain in eyes 3 1 4 ------------------------------------------------------------------------ ## {#section-23 .unnumbered} ## Complaints of Patients of Timir {#complaints-of-patients-of-timir .unnumbered} The symptom graph shows that blurring of vision was the most common complaint, followed by defective distant and near vision. Floaters, black spots, burning sensation, redness, and night blindness were less common. Diplopia was the least reported symptom. The graph highlights visual disturbance as the predominant symptom in Timir associated with diabetic retinopathy Improvement in the dimness of vision of BCVA Distant vision after treatment +--------------------+-----+----+----+----+------+------+------+----+ | Criteria of vision | No | | | | No | | | | | | of | | | | of | | | | | | e | | | | Eyes | | | | | | yes | | | | In | | | | | | In | | | | con | | | | | | tr | | | | trol | | | | | | ial | | | | | | | | | | | | | | g | | | | | | Gr | | | | roup | | | | | | oup | | | | | | | | +====================+=====+====+====+====+======+======+======+====+ | | Rt | | Lt | | Rt | | Lt | | | | eye | | E | | eye | | eye | | | | | | ye | | | | | | +--------------------+-----+----+----+----+------+------+------+----+ | | Bt | at | bt | At | bt | at | Bt | at | +--------------------+-----+----+----+----+------+------+------+----+ | 6/6 | 0 | 0 | 0 | 0 | 1 | 1 | 2 | 2 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/9 | 5 | 1 | 4 | 0 | 16 | 12 | 14 | 8 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/12 | 13 | 4 | 12 | 3 | 11 | 6 | 12 | 9 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/18 | 16 | 7 | 14 | 5 | 7 | 5 | 8 | 5 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/24 | 9 | 2 | 9 | 4 | 7 | 7 | 7 | 6 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/36 | 3 | 2 | 2 | 1 | 5 | 3 | 5 | 3 | +--------------------+-----+----+----+----+------+------+------+----+ | 6/60 | 3 | 1 | 5 | 3 | 1 | 1 | 2 | 2 | +--------------------+-----+----+----+----+------+------+------+----+ | \<6/60 | 1 | 1 | 2 | 1 | 1 | 0 | 0 | 0 | +--------------------+-----+----+----+----+------+------+------+----+ # BCVA Distant Vision Interpretation {#bcva-distant-vision-interpretation .unnumbered} The BCVA distant vision graph demonstrates marked visual improvement in the trial group after treatment. Eyes with poorer vision categories (6/18, 6/24, 6/36, and 6/60) shifted toward better visual acuity grades. Maximum improvement was observed in eyes with 6/12 and 6/18 vision. The control group showed comparatively lesser improvement. This indicates that the trial therapy was effective in improving distant visual acuity. ## 1. Distant Vision BCVA {#distant-vision-bcva .unnumbered} ### Right Eye {#right-eye .unnumbered} - Group A: - BT = 3.10 - AT = 2.36 - Relief = **23.87%** - Group B: - BT = 2.56 - AT = 2.28 - Relief = **10.94%** ### Baseline {#baseline .unnumbered} - Group A: 3.10 ± 1.40 - Group B: 2.56 ± 1.61 - p=0.044 (Significant) ### After Treatment {#after-treatment .unnumbered} - Group A: 2.36 ± 1.52 - Group B: 2.28 ± 1.65 - p=0.637 (Not significant) ### Difference at 3 Months {#difference-at-3-months-1 .unnumbered} - Group A: 0.74 ± 0.60 - Group B: 0.28 ± 0.45 - p\<0.001 (Highly significant) ### Observation {#observation-3 .unnumbered} Marked improvement in distant visual acuity was observed in Group A compared to Group B. ### Left Eye {#left-eye .unnumbered} - Group A: - BT = 3.40 - AT = 2.68 - Relief = **21.17%** - Group B: - BT = 2.54 - AT = 2.24 - Relief = **11.81%** ### Difference at 3 Months {#difference-at-3-months-2 .unnumbered} - Group A: 0.72 ± 0.64 - Group B: 0.30 ± 0.46 - p\<0.001 ### Observation {#observation-4 .unnumbered} Significant improvement in distant vision was observed in the left eye. ## 1. Distant Vision BCVA {#distant-vision-bcva-1 .unnumbered} ### Right Eye {#right-eye-1 .unnumbered} - Baseline values showed significant difference between groups (p=0.044). - After treatment, no significant difference remained (p=0.637), indicating both groups became comparable. - Improvement over 3 months was highly significant (p\<0.001), with Group A showing greater improvement. ### Left Eye {#left-eye-1 .unnumbered} - Significant baseline difference existed (p=0.008). - After treatment, difference became non-significant (p=0.269). - Significant improvement at 3 months (p\<0.001) favored Group A. ### Interpretation {#interpretation-1 .unnumbered} Vasadi Kwath demonstrated substantial improvement in distant visual acuity in both eyes over 3 months. Improvement in the dimness of vision of BCVA Near vision after treatment +-------------+------+------+------+------+------+------+------+------+ | criteria | No. | | | | No. | | | | | | of | | | | of | | | | | | Eyes | | | | eyes | | | | | | in | | | | in | | | | | | | | | | | | | | | | T | | | | Con | | | | | | rial | | | | trol | | | | | | g | | | | g | | | | | | roup | | | | roup | | | | +=============+======+======+======+======+======+======+======+======+ | | Rt | | Lt | | Rt | | Lt | | | | Eye | | eye | | Eye | | eye | | +-------------+------+------+------+------+------+------+------+------+ | | Bt | At | bt | at | Bt | At | bt | at | +-------------+------+------+------+------+------+------+------+------+ | N/6 | 0 | 0 | 0 | 0 | 20 | 20 | 20 | 20 | +-------------+------+------+------+------+------+------+------+------+ | N/8 | 32 | 18 | 28 | 14 | 14 | 11 | 15 | 11 | +-------------+------+------+------+------+------+------+------+------+ | N/10 | 10 | 8 | 13 | 9 | 13 | 11 | 12 | 9 | +-------------+------+------+------+------+------+------+------+------+ | N/12 | 1 | 0 | 0 | 0 | 3 | 3 | 3 | 3 | +-------------+------+------+------+------+------+------+------+------+ | N/18 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | +-------------+------+------+------+------+------+------+------+------+ | N/36 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | +-------------+------+------+------+------+------+------+------+------+ . # BCVA Near Vision Interpretation {#bcva-near-vision-interpretation .unnumbered} The near vision graph shows considerable improvement in the trial group, especially in N/8 and N/10 categories. Many eyes shifted toward better near vision after treatment. The control group also improved, but the degree of improvement was lower. This suggests positive action of the treatment on macular function and near visual performance. # . Near Vision BCVA (N Notation) {#near-vision-bcva-n-notation .unnumbered} ### Right Eye {#right-eye-2 .unnumbered} - Group A: - BT = 1.10 - AT = 0.74 - Relief = **32.73%** - Group B: - BT = 0.98 - AT = 0.88 - Relief = **10.20%** ### Difference at 3 Months {#difference-at-3-months-3 .unnumbered} - Group A: 0.34 ± 0.48 - Group B: 0.10 ± 0.30 - p=0.004 ### Observation {#observation-5 .unnumbered} Near vision improved significantly in Group A. ### Left Eye {#left-eye-2 .unnumbered} - Group A: - BT = 1.14 - AT = 0.78 - Relief = **31.58%** - Group B: - BT = 0.96 - AT = 0.82 - Relief = **14.58%** ### Difference at 3 Months {#difference-at-3-months-4 .unnumbered} - Group A: 0.36 ± 0.48 - Group B: 0.14 ± 0.35 - p=0.012 ### Observation {#observation-6 .unnumbered} Improvement in near vision was observed in the left eye as well. ### Right Eye {#right-eye-3 .unnumbered} - Baseline and post-treatment differences were not significant. - However, improvement over 3 months was significant (p=0.004). ### Left Eye {#left-eye-3 .unnumbered} - Baseline and AT differences were not significant. - Significant improvement in difference score (p=0.012). ### Interpretation {#interpretation-2 .unnumbered} Near vision improved significantly in Group A despite similar baseline and final scores between groups. Improvement in NPDR after treatment in 200 eyes

Criteria of NPDR	No of Eyes in Trial group				Total No of eyes		No of Eyes in Control group				total Noof Eyes
	Rt eye		Lt eye		Total No of eyes		Rt Eye		Lt eye		total Noof Eyes
	Bt	at	bt	at	bt	at	bt	At	bt	at	bt	At
Normal	10	10	10	10	20	20	3	3	2	2	5	5
Grade 1	25	14	17	8	42	22	26	23	22	20	48	43
Grade 2	12	10	21	17	33	27	18	18	23	23	41	41
Grade 3	3	3	2	2	5	5	3	3	3	3	6	6
Grade 4	0	0	0	0	0	0	0	0	0	0	0	0

# Improvement in NPDR Grades {#improvement-in-npdr-grades .unnumbered} The NPDR graph shows reduction in Grade 1 and Grade 2 NPDR changes in the trial group after treatment. Grade 1 eyes reduced from 42 to 22, indicating significant fundus improvement. Grade 2 changes also reduced moderately. Minimal improvement was seen in Grade 3 NPDR. The control group showed only mild improvement. This demonstrates that the trial treatment was more effective in reducing retinal pathological changes of diabetic retinopathy. # .Grades of NPDR {#grades-of-npdr .unnumbered} ### Right Eye {#right-eye-4 .unnumbered} - Group A: - Bt=1.16+\_0.82 - AT=0.90+\_0.93 - Relief = **22.41%** - Group B: - BT=1.42+\_0.70 - AT=1.36+\_0.78 - Relief = **4.23%** ### Difference at 3 Months {#difference-at-3-months-5 .unnumbered} - Group A: 0.26 ± 0.44 - Group B: 0.06 ± 0.24 - p=0.007 ### Observation {#observation-7 .unnumbered} Reduction in retinal hemorrhages and microvascular changes was observed. - Post-treatment improvement significant (p=0.006). - Difference score highly significant (p=0.007) ### Left Eye {#left-eye-4 .unnumbered} - Group A: - BT=+\_1.30+\_0.84 - AT=1.54+\_0.68 - Relief = **20.00%** - Group B: - BT=1.54+\_0.68 - AT=1.50+\_0.74 - Relief = **2.60%** ### Difference at 3 Months {#difference-at-3-months-6 .unnumbered} - Group A: 0.26 ± 0.44 - Group B: 0.04 ± 0.20 - p=0.002 ### Observation {#observation-8 .unnumbered} Significant improvement in NPDR grading was observed. - Significant AT difference (p=0.012). - Difference score highly significant (p=0.002). ### Interpretation {#interpretation-3 .unnumbered} ### Retinal pathological changes of NPDR reduced significantly after treatment {#retinal-pathological-changes-of-npdr-reduced-significantly-after-treatment .unnumbered} Patal involvement/ grdes of timir found in pts of DR under study ----------------------------------------------------------------------------------- grade Patal involvement Trial Contro group group -------- --------------------- ------- ----- ----- ----- -------- ----- ----- ----- Rt eye Lt Rt eye Lt eye eye bt at Bt at bt at bt at 1 First patal 34 18 34 18 31 22 29 19 2 second patal 15 4 13 4 13 9 18 15 3 third patal 1 0 3 2 6 4 3 2 4 fourth patal 0 0 0 0 0 0 0 0 ----------------------------------------------------------------------------------- # Patalgata Timir Grades {#patalgata-timir-grades .unnumbered} The graph of Patalgata Timir shows that First Patal involvement was most common. Significant reduction in First and Second Patal symptoms occurred after treatment in the trial group. Third Patal involvement showed minimal improvement. The findings indicate that early-stage Timir responds better to treatment than advanced stages. # . Patal Involvement {#patal-involvement .unnumbered} ### Right Eye {#right-eye-5 .unnumbered} - Group A: - BT=1.34+\_0.52 - AT=0.74+\_0.60 - Relief = **44.78%** - Group B: - BT=0.46+\_0.73 - AT=0.28+\_0.64 - Relief = **39.13%** ### Difference {#difference-2 .unnumbered} - Group A: 0.60 ± 0.49 - Group B: 0.14 ± 0.35 - p\<0.001 ### Observation {#observation-9 .unnumbered} Significant reduction in patal involvement was observed. ### Left Eye {#left-eye-5 .unnumbered} - Group A: - BT=1.38+\_0.60 - AT=0.86+\_0.76 - Relief = **37.68%** - Group B: - BT=0.54+\_0.73 - AT=0.32+\_0.65 - Relief = **40.74%** ### Difference {#difference-3 .unnumbered} - Group A: 0.52 ± 0.50 - Group B: 0.18 ± 0.39 - p\<0.001 ### Observation {#observation-10 .unnumbered} Improvement suggests arrest of disease progression. ## . Patal Involvement {#patal-involvement-1 .unnumbered} ## Both Eyes {#both-eyes .unnumbered} ## All comparisons were highly significant (p\<0.001). {#all-comparisons-were-highly-significant-p0.001. .unnumbered} ### Interpretation {#interpretation-4 .unnumbered} Treatment effectively reduced deeper patal involvement and progression of Timir pathology. Timir subjective symptoms score TSSS IN 100 PTS OF DR under study ---------------------------------------------------------------------------------- grade Symptoms score Trial Control group group ------- ------------------------ ------- ---- ----- ---- --------- ---- ----- ---- grade Rt eye Lt Rt eye Lt eye eye bt at bt at bt at bt at 0 0-4 normal 10 10 7 7 6 6 10 10 1 5-8---mild 34 10 34 10 32 18 33 22 2 9-12\-\-- moderate 4 0 6 1 7 3 6 1 3 13-16\-\-- severe 2 0 3 0 5 2 1 0 4 17-18\-\-\-- very severe 0 0 0 0 0 0 0 0 ---------------------------------------------------------------------------------- # Timir Subjective Symptoms Score (TSSS) {#timir-subjective-symptoms-score-tsss .unnumbered} The TSSS graph demonstrates significant symptomatic relief in the trial group. Mild and moderate symptom grades markedly reduced after treatment. Severe symptoms also improved considerably. The control group showed comparatively lesser symptomatic improvement. This suggests that the trial drug effectively reduced subjective visual complaints of Timi ### Right Eye {#right-eye-6 .unnumbered} - Group A: - BT=6.08+\_1.97 - AT=4.26+\_1.60 - Relief = **29.93%** - Group B: - BT=1.50+\_0.71 - AT=1.20+\_0.83 - Relief = **20.00%** ## Right Eye {#right-eye-7 .unnumbered} ### Difference {#difference-4 .unnumbered} - Group A: 1.98 ± 1.41 - Group B: 0.28 ± 0.45 - p\<0.001 ### Observation {#observation-11 .unnumbered} Significant reduction in symptoms such as blurred vision and visual discomfort was observed. ### Left Eye {#left-eye-6 .unnumbered} - Group A: - BT=6.18+\_2.42 - AT=4.60+\_2.14 - Relief = **25.57%** - Group B: - BT=1.48+\_0.61 - AT=1.18+\_0.83 - Relief = **20.27%** ### Difference {#difference-5 .unnumbered} - Group A: 1.88 ± 1.36 - Group B: 0.30 ± 0.46 - p\<0.001 ### Observation {#observation-12 .unnumbered} Marked symptomatic relief was observed after treatment. ## 8.Timir Subjective Symptom Score (TSSS) {#timir-subjective-symptom-score-tsss .unnumbered} ## Both Eyes {#both-eyes-1 .unnumbered} - All BT, AT, and Difference values were highly significant (p\<0.001). - Interpretation Subjective symptoms of Timir such as blurred vision, difficulty in focusing, and visual discomfort improved remarkably. Improvement in foveal reflex after treatment in 200 eyes

Grade	Foveal reflex	Trial group				Total No of eyes		control group				Total No of Eyes
		Rt eye		Lt eye		Total No of eyes		Rt eye		Lt eye		Total No of Eyes
		bt	at	bt	at	bt	at	bt	at	bt	at	bt	At
0	normal	39	39	34	34	63	63	36	36	35	35	71	71
1	dull	11	5	16	9	27	14	14	12	15	13	29	25

# Foveal Reflex Interpretation {#foveal-reflex-interpretation .unnumbered} The graph shows improvement in dull foveal reflex cases in the trial group. Many eyes with dull reflex converted to normal after treatment, suggesting improvement in macular function. The control group showed only mild improvement. This indicates beneficial retinal effects of the trial treatment. - **Difference/3M**: Improvement over 3 months. - Right Eye ```{=html} ``` - Group A: - BT=0.22+\_0.42 - AT=0.10+\_0.30 - Relief = **54.55%** - Group B: - BT=0.28+\_0.45 - AT=0.24+\_0.43 - Relief = **14.29%** ### Difference {#difference-6 .unnumbered} - Group A: 0.12± 0.33 - Group B: 0.04 ± 0.20 - P=0.144 ### Left Eye {#left-eye-7 .unnumbered} - Group A: - BT=0.32+\_0.47 - AT=0.18+\_0.39 - Relief = **43.75%** - Group B: - BT=0.30+\_0.46 - AT=0.26+\_0.44 - Relief = **13.33%** ### Difference {#difference-7 .unnumbered} - Group A: 0.14 ± 0.35 - Group B: 0.04 ± 0.20 - P=0.083 ## Both Eyes {#both-eyes-2 .unnumbered} ### Findings {#findings .unnumbered} - Most comparisons were statistically non-significant. ### Observation {#observation-13 .unnumbered} Mild preservation and improvement in macular reflex was observed clinically. ## 5. Foveal Reflex {#foveal-reflex .unnumbered} - Most comparisons remained statistically non-significant. - Mild improvement observed but not enough for statistical confirmation. ### Interpretation {#interpretation-5 .unnumbered} Foveal reflex showed limited recovery over the treatment period. Improvement in amsler grid finding after treatment in 200 eyes

Criteria	No of Eyes in Trial group				Total No of eyes		No of Eyes in Control group				total No of Eyes
	Rt eye		Lt eye		Total No of eyes		Rt Eye		Lt eye		total No of Eyes
	bt	at	bt	at	bt	at	bt	At	bt	AT	bt	At
Normal grade 0	27	27	27	27	54	54	33	33	30	30	63	63
Wavy lines grade 1	17	5	14	4	31	9	14	10	18	13	32	23
Corners and sides not visible grade 2	6	6	9	9	15	15	3	3	2	2	5	5
Holes or missing lines grade 3	0	0	0	0	0	0	0	0	0	0	0	0

. # Amsler Grid Findings {#amsler-grid-findings .unnumbered} The Amsler grid graph demonstrates significant reduction in Grade 1 abnormalities (wavy lines) in the trial group after treatment. Grade 2 abnormalities showed little change. The control group showed minimal improvement. This suggests that the treatment was effective in improving early macular dysfunction. ### Right Eye {#right-eye-8 .unnumbered} - Group A: - BT=0.58+\_0.70 - AT=0.34+\_0.69 - Relief = **41.38%** - Group B: - BT=0.40+\_0.61 - AT=0.32+\_0.59 - Relief = **20.00** ### Difference at 3 Months {#difference-at-3-months-7 .unnumbered} - Group A: 0.24 ± 0.43 - Group B: 0.08 ± 0.27 - p=0.030 ### Observation {#observation-14 .unnumbered} Improvement in macular function and reduction in visual distortion were observed. - Baseline and AT results were non-significant. - Difference score showed significant improvement (p=0.030). ### Left Eye {#left-eye-8 .unnumbered} - Group A: - BT=0.64+\_0.78 - AT=0.44+\_0.79 - Relief = **31.25%** - Group B: - BT=0.44+\_0.58 - AT=0.34+\_0.56 - Relief = **22.73%** ### Difference at 3 Months {#difference-at-3-months-8 .unnumbered} - Group A: 0.20 ± 0.40 - Group B: 0.10 ± 0.30 - p=0.165 (Not significant) ### Observation {#observation-15 .unnumbered} Mild improvement was observed but was statistically non-significant. - No significant changes observed. ### Interpretation {#interpretation-6 .unnumbered} Central visual distortion improved mildly, especially in the right eye. Improvement in two point discrimination test after treatment in 200 eyes

criteria	No of Eyes in Trial group				Total No of eyes		No of Eyes in Control group				total No of Eyes
	Rt eye		Lt eye		Total No of eyes		Rt Eye		Lt eye		total No of Eyes
	bt	at	bt	at	bt	at	bt	At	bt	at	bt	At
Able to discriminate 2 points grade 0	34	34	35	35	69	69	36	36	34	34	70	70
Not able to discriminate 2 points grade 1	16	2	14	1	30	3	14	8	16	10	30	18

# Two Point Discrimination Test {#two-point-discrimination-test .unnumbered} The graph shows remarkable improvement in the trial group. Eyes unable to discriminate two points reduced from 30 to 3 after treatment. The control group showed lesser improvement. These findings indicate enhanced retinal sensitivity and neural visual function following treatment. ### Right Eye {#right-eye-9 .unnumbered} - Group A: - BT=0.32+\_0.47 - AT=0.04+\_0.20 - Relief = **87.50%** - Group B: - BT=0.28+\_0.45 - AT=0.16+\_0.37 - Relief = **42.86%** ### Difference at 3 Months {#difference-at-3-months-9 .unnumbered} - Group A: 0.28 ± 0.45 - Group B: 0.12 ± 0.33 - p=0.047 ### Observation {#observation-16 .unnumbered} Significant improvement in retinal sensory perception was observed. - Significant post-treatment difference (p=0.047). - Significant improvement at 3 months (p=0.047). ### Left Eye {#left-eye-9 .unnumbered} - Group A: - BT=0.30+\_0.46 - AT=0.04+\_0.20 - Relief = **86.67%** - Group B: - BT=0.32+\_0.47 - AT=0.20+\_0.40 - Relief = **37.50%** ### Difference at 3 Months {#difference-at-3-months-10 .unnumbered} - Group A: 0.26 ± 0.44 - Group B: 0.12 ± 0.33 - p=0.077 (Not significant) ### Observation {#observation-17 .unnumbered} Clinical improvement was observed but was statistically non-significant. - Significant AT difference (p=0.015). - Difference score was not statistically significant. ### Interpretation {#interpretation-7 .unnumbered} Sensory retinal function improved, especially in the right eye. Improvement in the Photostress test of BCVA after treatment in 200 eyes

Criteria	No of Eyes in Trial group				Total No Of eyes		No of Eyes in Control group				total No of Eyes
	Rt eye		Lt Eye		Total No Of eyes		Rt Eye		Lt eye		total No of Eyes
	bt	at	bt	At	Bt	At	bt	At	bt	at	bt	At
Recovery within 15-30 seconds grade 0	31	31	32	32	63	63	35	35	30	30	65	65
Recovery within 30-60seconds grade 1	14	3	12	3	26	6	9	2	13	4	22	6
Recovery within 60-90 seconds grade2	5	0	5	1	10	1	7	5	7	5	14	10
Recovery more than 90 seconds grade 3	0	0	0	0	0	0	0	0	0	0	0	0

# Photostress Test Interpretation {#photostress-test-interpretation .unnumbered} The photostress recovery graph demonstrates marked reduction in delayed recovery times in the trial group after treatment. Grade 1 and Grade 2 abnormalities significantly improved, indicating better macular and photoreceptor function. The control group showed mild improvement only. This suggests restoration of retinal recovery mechanisms by the trial therapy. # Photo Stress Recovery Time (PSRT) {#photo-stress-recovery-time-psrt .unnumbered} ### Right Eye {#right-eye-10 .unnumbered} - Group A: - BT=0.48+\_0.68 - AT=0.16+\_0.37 - Relief = **66.67%** - Group B: - BT=6.76+\_3.04 - AT=5.44+\_2.84 - Relief = **19.53** ### Difference at 3 Months {#difference-at-3-months-11 .unnumbered} - Group A: 0.32 ± 0.47 - Group B: 1.32 ± 0.89 - p\<0.001 ### Observation {#observation-18 .unnumbered} Marked improvement in macular recovery time was observed. ### Left Eye {#left-eye-10 .unnumbered} - Group A: - BT=0.44+\_0.67 - AT=0.16+\_0.42 - Relief = **63.64%** - Group B: - BT=6.34+\_2.27 - AT=5.06+\_2.24 - Relief = **20.19%** ### Difference at 3 Months {#difference-at-3-months-12 .unnumbered} - Group A: 0.28 ± 0.45 - Group B: 1.28 ± 0.78 - p\<0.001 ### Observation {#observation-19 .unnumbered} Significant enhancement in photoreceptor recovery was observed. ### Both Eyes {#both-eyes-3 .unnumbered} - Extremely significant differences at baseline, after treatment, and improvement scores (all p\<0.001). ### Interpretation {#interpretation-8 .unnumbered} Macular and photoreceptor recovery improved markedly following treatment. This is one of the strongest findings in the study. # Overall Observation {#overall-observation .unnumbered} The study demonstrated that Group A showed better improvement compared to Group B in: - Distant vision, - Near vision, - NPDR grading, - Photo stress recovery time, - Timir subjective symptoms, - Patal involvement, - Retinal sensory functions. Maximum improvement was observed in: - Two-point discrimination, - PSRT, - Amsler grid, - TSSS. No adverse effect on intraocular pressure was observed, indicating the safety of the intervention. # Final Result {#final-result .unnumbered} The overall results of the study indicate that Vasadi Kwath is effective in improving visual acuity, retinal functional status, subjective symptoms, and retinal pathology in patients of Timir w.s.r. diabetic retinopathy. Significant statistical improvement in multiple parameters supports its therapeutic efficacy and clinical usefulness in diabetic retinal disorders ## Parameters Showing Maximum Relief in Group A {#parameters-showing-maximum-relief-in-group-a .unnumbered} ----------------------------------------------------------------------- **Parameter** **Percentage Relief** ---------------------------------------- ------------------------------ Two-Point Discrimination 86--87% PSRT 63--67% Foveal Reflex 44--55% Amsler Grid 31--41% Near Vision BCVA 31--33% FBS 32% ----------------------------------------------------------------------- The percentage relief analysis demonstrates that Group A showed superior improvement compared to Group B in most ophthalmological and laboratory parameters. Maximum improvement was observed in: - Two-point discrimination, - Photo stress recovery time, - Amsler grid, - Near and distant vision, - NPDR grading, - Timir symptom score. These findings indicate significant functional and symptomatic improvement after treatment with Vasadi Kwath in patients of Timir w.s.r. diabetic retinopathy. # Overall Comparative Interpretation {#overall-comparative-interpretation .unnumbered} Overall, almost all graphs demonstrate better improvement in the trial group compared to the control group. Maximum improvement was observed in: - BCVA distant vision - Near vision - NPDR Grade 1 changes - Timir subjective symptoms - Two point discrimination - Photostress test - Blood sugar parameters The findings indicate that the trial treatment was effective in improving both subjective and objective parameters of Timir with special reference to diabetic retinopathy. # Overall Statistical Summary {#overall-statistical-summary .unnumbered} ## Highly Significant Improvements {#highly-significant-improvements .unnumbered} The following parameters showed strong statistical improvement: - Distant Vision BCVA - Near Vision BCVA - NPDR Grades - Photo Stress Recovery Time - Timir Subjective Symptom Score - Patal Involvement - FBS ## Mild/Moderate Improvement {#mildmoderate-improvement .unnumbered} - Amsler Grid - Two-Point Discrimination - HbA1c - PMBS ## No Significant Change {#no-significant-change .unnumbered} - Foveal Reflex - Intraocular Pressure # Final Statistical Summary for Thesis {#final-statistical-summary-for-thesis .unnumbered} The present study demonstrated that Group A showed statistically significant improvement compared to Group B in multiple ophthalmic and systemic parameters. Significant improvement was observed in distant and near visual acuity, NPDR grading, photo stress recovery time, Timir subjective symptom score, and patal involvement. The findings suggest that Vasadi Kwath has beneficial effects in improving retinal function, visual performance, and subjective symptoms associated with Timir w.s.r. to diabetic retinopathy. Laboratory investigations also indicated moderate improvement in glycemic control, particularly fasting blood sugar levels. No adverse effect on intraocular pressure was observed, confirming the safety of the intervention. Overall, the statistical analysis supports the clinical efficacy of Vasadi Kwath in the management of Timir associated with diabetic retinopathy. Bottom of Form **[Statistics]{.underline}** **Comparison of Two Groups Using Mean ± Standard Deviation and Mann--Whitney U Test** Data are presented as mean ± standard deviation. Group comparison was performed using the Mann--Whitney U test. A p-value \<0.05 was considered statistically significant. -------------------------------------------------------------------------------------------------- **Variable** **Group A **Group B **Mann--Whitney **P-value** **Interpretation** (n=50) (n=50) U** Mean ± Mean ± SD** SD** ----------------------- ---------- ---------- ----------------- ------------- -------------------- DISTANT VISION BCVA - 3.10 ± 2.56 ± 1536.50 0.044 Significant BT 1.40 1.61 DISTANT VISION BCVA - 2.36 ± 2.28 ± 1317.50 0.637 Not significant AT 1.52 1.65 DISTANT VISION BCVA - 0.74 ± 0.28 ± 1753.00 \<0.001 Significant Difference - 3M 0.60 0.45 DISTANT VISION BCVA - 3.40 ± 2.54 ± 1628.00 0.008 Significant Left Eye - BT 1.59 1.57 DISTANT VISION BCVA - 2.68 ± 2.24 ± 1408.00 0.269 Not significant Left Eye - AT 1.85 1.67 DISTANT VISION BCVA - 0.72 ± 0.30 ± 1687.50 \<0.001 Significant Difference - 3M 0.64 0.46 NEAR VISION BCVA- 1.10 ± 0.98 ± 1387.50 0.312 Not significant JAEGERS - RIGHT EYE - 0.65 0.96 BT NEAR VISION BCVA- 0.74 ± 0.88 ± 1193.00 0.676 Not significant JAEGERS - RIGHT EYE - 0.72 0.96 AT NEAR VISION BCVA- 0.34 ± 0.10 ± 1550.00 0.004 Significant JAEGERS - Difference - 0.48 0.30 3M NEAR VISION BCVA- 1.14 ± 0.96 ± 1431.50 0.184 Not significant JAEGERS - Left Eye - BT 0.70 0.95 NEAR VISION BCVA- 0.78 ± 0.82 ± 1253.00 0.985 Not significant JAEGERS - Left Eye - AT 0.82 0.94 NEAR VISION BCVA- 0.36 ± 0.14 ± 1525.00 0.012 Significant JAEGERS - Difference - 0.48 0.35 3M AMSLER GRID - Right 0.58 ± 0.40 ± 1416.50 0.187 Not significant Eye - BT 0.70 0.61 AMSLER GRID - Right 0.34 ± 0.32 ± 1222.50 0.803 Not significant Eye - AT 0.69 0.59 AMSLER GRID - 0.24 ± 0.08 ± 1450.00 0.030 Significant Difference - 3M 0.43 0.27 AMSLER GRID - Left 0.64 ± 0.44 ± 1392.00 0.270 Not significant Eye - BT 0.78 0.58 AMSLER GRID - Left 0.44 ± 0.34 ± 1254.50 0.972 Not significant Eye - AT 0.79 0.56 AMSLER GRID - 0.20 ± 0.10 ± 1375.00 0.165 Not significant Difference - 3M 0.40 0.30 2-PT DISCRIMINATION - 0.32 ± 0.28 ± 1300.00 0.667 Not significant Right Eye - BT 0.47 0.45 2-PT DISCRIMINATION - 0.04 ± 0.16 ± 1100.00 0.047 Significant Right Eye - AT 0.20 0.37 2-PT DISCRIMINATION - 0.28 ± 0.12 ± 1450.00 0.047 Significant Difference - 3M 0.45 0.33 2-PT DISCRIMINATION - 0.30 ± 0.32 ± 1225.00 0.833 Not significant Left Eye - BT 0.46 0.47 2-PT DISCRIMINATION - 0.04 ± 0.20 ± 1050.00 0.015 Significant Left Eye - AT 0.20 0.40 2-PT DISCRIMINATION - 0.26 ± 0.12 ± 1425.00 0.077 Not significant Difference - 3M 0.44 0.33 FOVEAL REFLEX - R Eye - 0.22 ± 0.28 ± 1175.00 0.494 Not significant BT 0.42 0.45 FOVEAL REFLEX - R Eye - 0.10 ± 0.24 ± 1075.00 0.064 Not significant AT 0.30 0.43 FOVEAL REFLEX - 0.12 ± 0.04 ± 1350.00 0.144 Not significant Difference - 3M 0.33 0.20 FOVEAL REFLEX - L Eye - 0.32 ± 0.30 ± 1275.00 0.833 Not significant BT 0.47 0.46 FOVEAL REFLEX - L Eye - 0.18 ± 0.26 ± 1150.00 0.339 Not significant AT 0.39 0.44 FOVEAL REFLEX - 0.14 ± 0.04 ± 1375.00 0.083 Not significant Difference - 3M 0.35 0.20 GRADES OF NPDR - R 1.16 ± 1.42 ± 1016.50 0.079 Not significant Eye - BT 0.82 0.70 GRADES OF NPDR - R 0.90 ± 1.36 ± 868.50 0.006 Significant Eye - AT 0.93 0.78 GRADES OF NPDR - 0.26 ± 0.06 ± 1500.00 0.007 Significant Difference - 3M 0.44 0.24 GRADES OF NPDR - LT 1.30 ± 1.54 ± 1073.50 0.189 Not significant EYE - BT 0.84 0.68 GRADES OF NPDR - LT 1.04 ± 1.50 ± 906.50 0.012 Significant EYE - AT 0.95 0.74 GRADES OF NPDR - 0.26 ± 0.04 ± 1525.00 0.002 Significant Difference - 3M 0.44 0.20 PHOTO STRESS RECOVERY 0.48 ± 6.76 ± 2.50 \<0.001 Significant TIME - RT EYE - BT 0.68 3.04 PHOTO STRESS RECOVERY 0.16 ± 5.44 ± 0.00 \<0.001 Significant TIME - RT EYE - AT 0.37 2.84 PHOTO STRESS RECOVERY 0.32 ± 1.32 ± 448.00 \<0.001 Significant TIME - Difference - 3M 0.47 0.89 PHOTO STRESS RECOVERY 0.44 ± 6.34 ± 2.50 \<0.001 Significant TIME - Left Eye - BT 0.67 2.27 PHOTO STRESS RECOVERY 0.16 ± 5.06 ± 6.00 \<0.001 Significant TIME - Left Eye - AT 0.42 2.24 PHOTO STRESS RECOVERY 0.28 ± 1.28 ± 388.00 \<0.001 Significant TIME - Difference - 3M 0.45 0.78 TSSS - RT EYE - BT 6.08 ± 1.50 ± 2500.00 \<0.001 Significant 1.97 0.71 TSSS - RT EYE - AT 4.26 ± 1.20 ± 2438.00 \<0.001 Significant 1.60 0.83 TSSS - Difference 1.98 ± 0.28 ± 2210.00 \<0.001 Significant 1.41 0.45 TSSS - LT EYE - BT 6.18 ± 1.48 ± 2464.50 \<0.001 Significant 2.42 0.61 TSSS - LT EYE - AT 4.60 ± 1.18 ± 2466.00 \<0.001 Significant 2.14 0.83 TSSS - Difference 1.88 ± 0.30 ± 2185.00 \<0.001 Significant 1.36 0.46 PATAL INVOLVEMENT - RT 1.34 ± 0.46 ± 2056.50 \<0.001 Significant EYE - BT 0.52 0.73 PATAL INVOLVEMENT - RT 0.74 ± 0.28 ± 1785.50 \<0.001 Significant EYE - AT 0.60 0.64 PATAL INVOLVEMENT - 0.60 ± 0.14 ± 1825.00 \<0.001 Significant Difference 0.49 0.35 PATAL INVOLVEMENT - LT 1.38 ± 0.54 ± 1995.50 \<0.001 Significant EYE - BT 0.60 0.73 PATAL INVOLVEMENT - LT 0.86 ± 0.32 ± 1783.50 \<0.001 Significant EYE - AT 0.76 0.65 PATAL INVOLVEMENT - 0.52 ± 0.18 ± 1675.00 \<0.001 Significant Difference 0.50 0.39 IOP (mmHg) - Right 0.00 ± 0.00 ± 1250.00 1.000 Not significant Eye - BT 0.00 0.00 IOP (mmHg) - Right 0.00 ± 0.00 ± 1250.00 1.000 Not significant Eye - AT 0.00 0.00 IOP (mmHg) - 0.00 ± 0.00 ± 1250.00 1.000 Not significant Difference - 3M 0.00 0.00 IOP (mmHg) - Left Eye - 0.00 ± 0.00 ± 1250.00 1.000 Not significant BT 0.00 0.00 IOP (mmHg) - Left Eye - 0.00 ± 0.00 ± 1250.00 1.000 Not significant AT 0.00 0.00 IOP (mmHg) - 0.00 ± 0.00 ± 1250.00 1.000 Not significant Difference - 3M 0.00 0.00 LABORATORY - FBS - BT 1.12 ± 1.34 ± 1013.50 0.074 Not significant 0.75 0.66 LABORATORY - FBS - AT 0.76 ± 1.32 ± 746.00 \<0.001 Significant 0.72 0.68 LABORATORY - 0.36 ± 0.02 ± 1596.00 0.006 Significant Difference - 3M 0.63 0.55 LABORATORY - PMBS - BT 1.20 ± 1.42 ± 1017.00 0.084 Not significant 0.86 0.67 LABORATORY - PMBS - AT 1.00 ± 1.42 ± 906.50 0.011 Significant 0.88 0.73 LABORATORY - 0.20 ± 0.00 ± 1432.50 0.111 Not significant Difference - 3M 0.70 0.45 LABORATORY - HbA1C - BT 0.68 ± 1.30 ± 687.50 \<0.001 Significant 0.71 0.65 LABORATORY - HbA1C - AT 0.62 ± 1.36 ± 606.00 \<0.001 Significant 0.75 0.63 LABORATORY - 0.06 ± -0.04 ± 1368.50 0.134 Not significant Difference - 3M 0.37 0.28 -------------------------------------------------------------------------------------------------- Note: BT = before treatment/baseline; AT = after treatment; 3M = 3-month/difference column Based on the uploaded Mann--Whitney comparison table, the following variable-wise description includes all values without omission. The statistical analysis compared Group A and Group B using the Mann--Whitney U test, which is a non-parametric test used to compare two independent groups when data may not follow normal distribution. Results were expressed as Mean ± Standard Deviation (SD). A p-value less than 0.05 was considered statistically significant. ### Meaning of Statistical Terms {#meaning-of-statistical-terms .unnumbered} - **Mean ± SD**:\ Mean represents the average score, while SD shows variability among patients. - **Mann--Whitney U Test**:\ Used to compare two groups without assuming normal distribution of data. - **P-value**: - **p \< 0.05** → statistically significant difference - **p \> 0.05** → not statistically significant - **BT (Before Treatment)**: Baseline values before intervention. - **AT (After Treatment)**: Values after treatment. - **Difference/3M**: Improvement over 3 months. **DISTANT VISION BCVA -- Right Eye -- BT:** Group A had a mean score of **3.10 ± 1.40**, while Group B had **2.56 ± 1.61**. The Mann--Whitney U value was **1536.50**, with a **p-value of 0.044**, showing a statistically significant difference between the two groups. **DISTANT VISION BCVA -- Right Eye -- AT:** Group A had **2.36 ± 1.52**, while Group B had **2.28 ± 1.65**. The Mann--Whitney U value was **1317.50**, with a **p-value of 0.637**, showing no statistically significant difference. **DISTANT VISION BCVA -- Right Eye -- Difference at 3 Months:** Group A showed a mean difference of **0.74 ± 0.60**, while Group B showed **0.28 ± 0.45**. The Mann--Whitney U value was **1753.00**, with [a **p-value \<0.001**, showing a statistically significant difference]{.underline}. **DISTANT VISION BCVA -- Left Eye -- BT:** Group A had **3.40 ± 1.59**, while Group B had **2.54 ± 1.57**. The Mann--Whitney U value was **1628.00**, with a **p-value of 0.008**, showing a statistically significant difference. **DISTANT VISION BCVA -- Left Eye -- AT:** Group A had **2.68 ± 1.85**, while Group B had **2.24 ± 1.67**. The Mann--Whitney U value was **1408.00**, with a **p-value of 0.269**, showing no statistically significant difference. **DISTANT VISION BCVA -- Left Eye -- Difference at 3 Months:** Group A showed **0.72 ± 0.64**, while Group B showed **0.30 ± 0.46**. The Mann--Whitney U value was **1687.50**, with a [**p-value \<0.001**, showing a statistically significant difference]{.underline}. **NEAR VISION BCVA -- Jaegers -- Right Eye -- BT:** Group A had **1.10 ± 0.65**, while Group B had **0.98 ± 0.96**. The Mann--Whitney U value was **1387.50**, with a **p-value of 0.312**, showing no statistically significant difference. **NEAR VISION BCVA -- Jaegers -- Right Eye -- AT:** Group A had **0.74 ± 0.72**, while Group B had **0.88 ± 0.96**. The Mann--Whitney U value was **1193.00**, with a **p-value of 0.676**, showing no statistically significant difference. **NEAR VISION BCVA -- Jaegers -- Right Eye -- Difference at 3 Months:** Group A showed **0.34 ± 0.48**, while Group B showed **0.10 ± 0.30**. The Mann--Whitney U value was **1550.00**, with [a **p-value of 0.004**, showing a statistically significant difference.]{.underline} **NEAR VISION BCVA -- Jaegers -- Left Eye -- BT:** Group A had **1.14 ± 0.70**, while Group B had **0.96 ± 0.95**. The Mann--Whitney U value was **1431.50**, with a **p-value of 0.184**, showing no statistically significant difference. **NEAR VISION BCVA -- Jaegers -- Left Eye -- AT:** Group A had **0.78 ± 0.82**, while Group B had **0.82 ± 0.94**. The Mann--Whitney U value was **1253.00**, with a **p-value of 0.985**, showing no statistically significant difference. **NEAR VISION BCVA -- Jaegers -- Left Eye -- Difference at 3 Months:** Group A showed **0.36 ± 0.48**, while Group B showed **0.14 ± 0.35**. The Mann--Whitney U value was **1525.00**, with [a **p-value of 0.012**, showing a statistically significant difference]{.underline}. **AMSLER GRID -- Right Eye -- BT:** Group A had **0.58 ± 0.70**, while Group B had **0.40 ± 0.61**. The Mann--Whitney U value was **1416.50**, with a **p-value of 0.187**, showing no statistically significant difference. **AMSLER GRID -- Right Eye -- AT:** Group A had **0.34 ± 0.69**, while Group B had **0.32 ± 0.59**. The Mann--Whitney U value was **1222.50**, with a **p-value of 0.803**, showing no statistically significant difference. **AMSLER GRID -- Right Eye -- Difference at 3 Months:** Group A showed **0.24 ± 0.43**, while Group B showed **0.08 ± 0.27**. The Mann--Whitney U value was **1450.00**, with a [**p-value of 0.030**, showing a statistically significant difference]{.underline}. **AMSLER GRID -- Left Eye -- BT:** Group A had **0.64 ± 0.78**, while Group B had **0.44 ± 0.58**. The Mann--Whitney U value was **1392.00**, with a **p-value of 0.270**, showing no statistically significant difference. **AMSLER GRID -- Left Eye -- AT:** Group A had **0.44 ± 0.79**, while Group B had **0.34 ± 0.56**. The Mann--Whitney U value was **1254.50**, with a **p-value of 0.972**, showing no statistically significant difference. **AMSLER GRID -- Left Eye -- Difference at 3 Months:** Group A showed **0.20 ± 0.40**, while Group B showed **0.10 ± 0.30**. The Mann--Whitney U value was **1375.00**, with a [**p-value of 0.165**, showing no statistically significant difference.]{.underline} **2-PT DISCRIMINATION -- Right Eye -- BT:** Group A had **0.32 ± 0.47**, while Group B had **0.28 ± 0.45**. The Mann--Whitney U value was **1300.00**, with a **p-value of 0.667**, showing no statistically significant difference. **2-PT DISCRIMINATION -- Right Eye -- AT:** Group A had **0.04 ± 0.20**, while Group B had **0.16 ± 0.37**. The Mann--Whitney U value was **1100.00**, with a **p-value of 0.047**, showing a statistically significant difference. **2-PT DISCRIMINATION -- Right Eye -- Difference at 3 Months:** Group A showed **0.28 ± 0.45**, while Group B showed **0.12 ± 0.33**. The Mann--Whitney U value was **1450.00**, with a [**p-value of 0.047**, showing a statistically significant difference]{.underline}. **2-PT DISCRIMINATION -- Left Eye -- BT:** Group A had **0.30 ± 0.46**, while Group B had **0.32 ± 0.47**. The Mann--Whitney U value was **1225.00**, with a **p-value of 0.833**, showing no statistically significant difference. **2-PT DISCRIMINATION -- Left Eye -- AT:** Group A had **0.04 ± 0.20**, while Group B had **0.20 ± 0.40**. The Mann--Whitney U value was **1050.00**, with a **p-value of 0.015**, showing a statistically significant difference. **2-PT DISCRIMINATION -- Left Eye -- Difference at 3 Months:** Group A showed **0.26 ± 0.44**, while Group B showed **0.12 ± 0.33**. The Mann--Whitney U value was **1425.00**, with a [**p-value of 0.077**, showing no statistically significant difference]{.underline}. **FOVEAL REFLEX -- Right Eye -- BT:** Group A had **0.22 ± 0.42**, while Group B had **0.28 ± 0.45**. The Mann--Whitney U value was **1175.00**, with a **p-value of 0.494**, showing no statistically significant difference. **FOVEAL REFLEX -- Right Eye -- AT:** Group A had **0.10 ± 0.30**, while Group B had **0.24 ± 0.43**. The Mann--Whitney U value was **1075.00**, with a **p-value of 0.064**, showing no statistically significant difference. **FOVEAL REFLEX -- Right Eye -- Difference at 3 Months:** Group A showed **0.12 ± 0.33**, while Group B showed **0.04 ± 0.20**. The Mann--Whitney U value was **1350.00**, with a **p-value of 0.144**, showing no statistically significant difference. **FOVEAL REFLEX -- Left Eye -- BT:** Group A had **0.32 ± 0.47**, while Group B had **0.30 ± 0.46**. The Mann--Whitney U value was **1275.00**, with a **p-value of 0.833**, showing no statistically significant difference. **FOVEAL REFLEX -- Left Eye -- AT:** Group A had **0.18 ± 0.39**, while Group B had **0.26 ± 0.44**. The Mann--Whitney U value was **1150.00**, with a **p-value of 0.339**, showing no statistically significant difference. **FOVEAL REFLEX -- Left Eye -- Difference at 3 Months:** Group A showed **0.14 ± 0.35**, while Group B showed **0.04 ± 0.20**. The Mann--Whitney U value was **1375.00**, with a **p-value of 0.083**, showing no statistically significant difference. **GRADES OF NPDR -- Right Eye -- BT:** Group A had **1.16 ± 0.82**, while Group B had **1.42 ± 0.70**. The Mann--Whitney U value was **1016.50**, with a **p-value of 0.079**, showing no statistically significant difference. **GRADES OF NPDR -- Right Eye -- AT:** Group A had **0.90 ± 0.93**, while Group B had **1.36 ± 0.78**. The Mann--Whitney U value was **868.50**, with a **p-value of 0.006**, showing a **GRADES OF NPDR -- Right Eye -- Difference at 3 Months:** Group A showed **0.26 ± 0.44**, while Group B showed **0.06 ± 0.24**. The Mann--Whitney U value was **1500.00**, with a **p-value of 0.007**, showing a statistically significant difference. **GRADES OF NPDR -- Left Eye -- BT:** Group A had **1.30 ± 0.84**, while Group B had **1.54 ± 0.68**. The Mann--Whitney U value was **1073.50**, with a **p-value of 0.189**, showing no statistically significant difference. **GRADES OF NPDR -- Left Eye -- AT:** Group A had **1.04 ± 0.95**, while Group B had **1.50 ± 0.74**. The Mann--Whitney U value was **906.50**, with a **p-value of 0.012**, showing a statistically significant difference. **GRADES OF NPDR -- Left Eye -- Difference at 3 Months:** Group A showed **0.26 ± 0.44**, while Group B showed **0.04 ± 0.20**. The Mann--Whitney U value was **1525.00**, with a **p-value of 0.002**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Right Eye -- BT:** Group A had **0.48 ± 0.68**, while Group B had **6.76 ± 3.04**. The Mann--Whitney U value was **2.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Right Eye -- AT:** Group A had **0.16 ± 0.37**, while Group B had **5.44 ± 2.84**. The Mann--Whitney U value was **0.00**, with a **p-value \<0.001**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Right Eye -- Difference at 3 Months:** Group A showed **0.32 ± 0.47**, while Group B showed **1.32 ± 0.89**. The Mann--Whitney U value was **448.00**, with a **p-value \<0.001**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Left Eye -- BT:** Group A had **0.44 ± 0.67**, while Group B had **6.34 ± 2.27**. The Mann--Whitney U value was **2.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Left Eye -- AT:** Group A had **0.16 ± 0.42**, while Group B had **5.06 ± 2.24**. The Mann--Whitney U value was **6.00**, with a **p-value \<0.001**, showing a statistically significant difference. **PHOTO STRESS RECOVERY TIME -- Left Eye -- Difference at 3 Months:** Group A showed **0.28 ± 0.45**, while Group B showed **1.28 ± 0.78**. The Mann--Whitney U value was **388.00**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Right Eye -- BT:** Group A had **6.08 ± 1.97**, while Group B had **1.50 ± 0.71**. The Mann--Whitney U value was **2500.00**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Right Eye -- AT:** Group A had **4.26 ± 1.60**, while Group B had **1.20 ± 0.83**. The Mann--Whitney U value was **2438.00**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Right Eye -- Difference:** Group A showed **1.98 ± 1.41**, while Group B showed **0.28 ± 0.45**. The Mann--Whitney U value was **2210.00**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Left Eye -- BT:** Group A had **6.18 ± 2.42**, while Group B had **1.48 ± 0.61**. The Mann--Whitney U value was **2464.50**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Left Eye -- AT:** Group A had **4.60 ± 2.14**, while Group B had **1.18 ± 0.83**. The Mann--Whitney U value was **2466.00**, with a **p-value \<0.001**, showing a statistically significant difference. **TSSS -- Left Eye -- Difference:** Group A showed **1.88 ± 1.36**, while Group B showed **0.30 ± 0.46**. The Mann--Whitney U value was **2185.00**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Right Eye -- BT:** Group A had **1.34 ± 0.52**, while Group B had **0.46 ± 0.73**. The Mann--Whitney U value was **2056.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Right Eye -- AT:** Group A had **0.74 ± 0.60**, while Group B had **0.28 ± 0.64**. The Mann--Whitney U value was **1785.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Right Eye -- Difference:** Group A showed **0.60 ± 0.49**, while Group B showed **0.14 ± 0.35**. The Mann--Whitney U value was **1825.00**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Left Eye -- BT:** Group A had **1.38 ± 0.60**, while Group B had **0.54 ± 0.73**. The Mann--Whitney U value was **1995.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Left Eye -- AT:** Group A had **0.86 ± 0.76**, while Group B had **0.32 ± 0.65**. The Mann--Whitney U value was **1783.50**, with a **p-value \<0.001**, showing a statistically significant difference. **PATAL INVOLVEMENT -- Left Eye -- Difference:** Group A showed **0.52 ± 0.50**, while Group B showed **0.18 ± 0.39**. The Mann--Whitney U value was **1675.00**, with a **p-value \<0.001**, showing a statistically significant difference. **IOP -- Right Eye -- BT:** Group A had **0.00 ± 0.00**, while Group B had **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **IOP -- Right Eye -- AT:** Group A had **0.00 ± 0.00**, while Group B had **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **IOP -- Right Eye -- Difference at 3 Months:** Group A showed **0.00 ± 0.00**, while Group B showed **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **IOP -- Left Eye -- BT:** Group A had **0.00 ± 0.00**, while Group B had **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **IOP -- Left Eye -- AT:** Group A had **0.00 ± 0.00**, while Group B had **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **IOP -- Left Eye -- Difference at 3 Months:** Group A showed **0.00 ± 0.00**, while Group B showed **0.00 ± 0.00**. The Mann--Whitney U value was **1250.00**, with a **p-value of 1.000**, showing no statistically significant difference. **LABORATORY -- FBS -- BT:** Group A had **1.12 ± 0.75**, while Group B had **1.34 ± 0.66**. The Mann--Whitney U value was **1013.50**, with a **p-value of 0.074**, showing no statistically significant difference. **LABORATORY -- FBS -- AT:** Group A had **0.76 ± 0.72**, while Group B had **1.32 ± 0.68**. The Mann--Whitney U value was **746.00**, with a **p-value \<0.001**, showing a statistically significant difference. **LABORATORY -- FBS -- Difference at 3 Months:** Group A showed **0.36 ± 0.63**, while Group B showed **0.02 ± 0.55**. The Mann--Whitney U value was **1596.00**, with a **p-value of 0.006**, showing a statistically significant difference. **LABORATORY -- PMBS -- BT:** Group A had **1.20 ± 0.86**, while Group B had **1.42 ± 0.67**. The Mann--Whitney U value was **1017.00**, with a **p-value of 0.084**, showing no statistically significant difference. **LABORATORY -- PMBS -- AT:** Group A had **1.00 ± 0.88**, while Group B had **1.42 ± 0.73**. The Mann--Whitney U value was **906.50**, with a **p-value of 0.011**, showing a statistically significant difference. **LABORATORY -- PMBS -- Difference at 3 Months:** Group A showed **0.20 ± 0.70**, while Group B showed **0.00 ± 0.45**. The Mann--Whitney U value was **1432.50**, with a **p-value of 0.111**, showing no statistically significant difference. **LABORATORY -- HbA1C -- BT:** Group A had **0.68 ± 0.71**, while Group B had **1.30 ± 0.65**. The Mann--Whitney U value was **687.50**, with a **p-value \<0.001**, showing a statistically significant difference. **LABORATORY -- HbA1C -- AT:** Group A had **0.62 ± 0.75**, while Group B had **1.36 ± 0.63**. The Mann--Whitney U value was **606.00**, with a **p-value \<0.001**, showing a statistically significant difference. **LABORATORY -- HbA1C -- Difference at 3 Months:** Group A showed **0.06 ± 0.37**, while Group B showed **-0.04 ± 0.28**. The Mann--Whitney U value was **1368.50**, with a **p-value of 0.134**, showing no statistically significant difference. **All Variables Graphs\ Group A vs Group B** Bar labels show Mean ± SD. \* indicates statistically significant Mann--Whitney U test result. *Source: Uploaded summary table with Group A and Group B values.* ![](media/image18.png){width="6.743088363954506in" height="4.256944444444445in"} *Figure 1. Variables page 1 of 12* ![](media/image19.png){width="7.15082895888014in" height="4.0796073928258965in"} *Figure 2. Variables page 2 of 12* ![](media/image20.png){width="6.812287839020122in" height="4.3392104111986in"} *Figure 3. Variables page 3 of 12* ![](media/image21.png){width="6.802497812773403in" height="4.0395756780402445in"} *Figure 4. Variables page 4 of 12* ![](media/image22.png){width="6.7014370078740155in" height="3.773494094488189in"} *Figure 5. Variables page 5 of 12* ![](media/image23.png){width="6.800765529308836in" height="4.253019466316711in"} *Figure 6. Variables page 6 of 12* ![](media/image24.png){width="6.916718066491689in" height="4.37682852143482in"} *Figure 7. Variables page 7 of 12* ![](media/image25.png){width="7.03876312335958in" height="4.235346675415573in"} *Figure 8. Variables page 8 of 12* ![](media/image26.png){width="6.673982939632546in" height="4.24205271216098in"} *Figure 9. Variables page 9 of 12* ![](media/image27.png){width="5.49884186351706in" height="3.098173665791776in"} *Figure 10. Variables page 10 of 12* ![](media/image28.png){width="6.696167979002625in" height="4.150334645669291in"} *Figure 11. Variables page 11 of 12* ![](media/image29.png){width="6.810811461067367in" height="4.104833770778653in"} *Figure 12. Variables page 12 of 12* # **[DISCUSSION]{.underline}** {#discussion .unnumbered} # Discussion on Distant Vision BCVA {#discussion-on-distant-vision-bcva .unnumbered} Distant visual acuity is one of the most important indicators of retinal and macular function in diabetic retinopathy. In the present study, Group A showed statistically significant improvement in distant vision in both eyes over 3 months. ### Statistical Findings {#statistical-findings .unnumbered} - Right eye difference score: - Group A: 0.74 ± 0.60 - Group B: 0.28 ± 0.45 - p\<0.001 - Left eye difference score: - Group A: 0.72 ± 0.64 - Group B: 0.30 ± 0.46 - p\<0.001 ### Percentage Relief {#percentage-relief .unnumbered} - Right eye: 23.87% - Left eye: 21.17% ### Interpretation {#interpretation-9 .unnumbered} Improvement in distant vision suggests enhanced retinal function and reduced macular pathology. Vasadi Kwath may have improved retinal circulation, reduced microvascular leakage, and minimized oxidative stress associated with diabetic retinal damage. From an Ayurvedic perspective, Timir primarily affects Drishti and visual perception due to vitiation of Pitta and Kapha along with Dhatu Kshaya. The observed improvement indicates restoration of ocular nourishment and reduction in Doshic imbalance. []{#_Toc229853696 .anchor}**DISCUSSION (Near Vision)** The present study evaluated the effect of Vasadi Kwath on near visual acuity in patients of **Timir**, with special reference to **Diabetic Retinopathy (NPDR)**. Near vision, being a sensitive indicator of macular function and accommodative efficiency, plays a crucial role in daily activities such as reading and fine visual tasks. The results of the study revealed a **highly significant improvement (p \< 0.001)** in near visual acuity assessed by N Notation chart. A marked shift of patients from lower grades (N18--N24) to higher grades (N6--N8) was observed, indicating enhanced reading ability and focusing power. The reduction in mean near vision scores further substantiates the clinical effectiveness of the intervention. From an Ayurvedic perspective, Timir affecting near vision can be attributed predominantly to **Vata-induced impairment in accommodation** and **Pitta-related diminution of visual clarity**. Vasadi Kwath, endowed with **Vata-Pitta Shamana** and **Chakshushya** properties, acts by restoring the functional integrity of **Alochaka Pitta** and nourishing the **Drishti Mandala**. Additionally, its role in alleviating **Srotorodha** facilitates proper microcirculation and tissue nutrition, thereby improving visual performance. Modern correlation of these findings suggests that improvement in near vision may be due to enhanced **macular function**, better **retinal sensitivity**, and improved **neuro-retinal transmission**. Reduction in ocular fatigue and improved accommodative response further contribute to sustained near visual tasks. These effects are particularly relevant in early NPDR, where subtle macular dysfunction leads to compromised near vision. The combined effect of Dosha pacification and microvascular stabilization provides a strong integrative explanation for the observed outcomes. The significant clinical improvement observed in the majority of patients highlights the therapeutic potential of Vasadi Kwath not only in symptom relief but also in functional visual restoration. However, limitations such as small sample size and short duration of intervention must be considered while interpreting the results. Further large-scale and long-term studies with advanced diagnostic modalities are recommended to validate and expand upon these findings. []{#_Toc229853697 .anchor}**DISCUSSION (Pinhole Vision)** The present study evaluated the effect of Vasadi Kwath on pinhole visual acuity in patients of **Timir**, with special reference to **Diabetic Retinopathy (NPDR)**. Pinhole vision is a crucial clinical parameter used to differentiate refractive errors from retinal or neural pathology, as it minimizes peripheral aberrations and allows assessment of central retinal function. In this study, a **highly significant improvement (p \< 0.001)** in pinhole visual acuity was observed after treatment. A noticeable shift of patients from lower visual acuity categories (6/24--6/36) to higher categories (6/6--6/9) was recorded. Additionally, the reduction in mean LogMAR values confirms enhanced clarity of retinal image formation. Importantly, the narrowing gap between unaided visual acuity and pinhole vision suggests improvement not only in refractive components but also in underlying retinal function. From an Ayurvedic perspective, impairment of vision in Timir is attributed to vitiation of **Vata and Pitta Dosha**, along with **Srotorodha (obstruction in microchannels)** affecting the **Drishti Mandala**. Pinhole vision, which reflects deeper optical and retinal clarity, can be correlated with the functional status of **Alochaka Pitta**. Vasadi Kwath, by virtue of its **Vata-Pitta Shamana** and **Chakshushya** properties, helps in clearing Avarana, restoring Dosha balance, and improving the functional integrity of visual pathways. This leads to enhanced perception even through a restricted aperture such as a pinhole. From a modern viewpoint, NPDR involves microvascular changes such as capillary leakage, microaneurysms, and retinal ischemia, which impair photoreceptor efficiency. Improvement in pinhole vision indicates better **macular function**, improved **retinal sensitivity**, and enhanced **neuro-retinal transmission**. It also suggests reduction in subtle optical distortions and improved central visual processing. The combined Ayurvedic and modern interpretation indicates that Vasadi Kwath acts at both **optical and retinal levels**, resulting in genuine functional improvement rather than mere symptomatic relief. This is clinically significant because improvement in pinhole vision is considered a strong indicator of **true retinal recovery**. However, limitations such as small sample size, short duration, and lack of advanced imaging techniques (OCT/FFA) should be acknowledged. Further large-scale studies are required to substantiate these findings. []{#_Toc229853698 .anchor}**DISCUSSION (Two-Point Discrimination)** The present study assessed the effect of Vasadi Kwath on **Two-point discrimination (TPD)** in patients of **Timir**, with special reference to **Diabetic Retinopathy (NPDR)**. TPD is an important parameter of **fine sensory perception and cortical integration**, reflecting the functional status of neural pathways involved in precise stimulus discrimination. In the present study, a **statistically highly significant reduction (p \< 0.001)** in TPD threshold values was observed following treatment. This reduction indicates enhanced ability of patients to perceive two closely spaced stimuli as distinct, signifying improvement in **sensory acuity and neural processing efficiency**. Clinically, this translates into better perception of fine details, improved visual precision, and enhanced coordination between sensory input and cortical interpretation. From an Ayurvedic perspective, the impairment in such subtle sensory functions can be correlated with **Vata Dushti**, which governs neural conduction and sensory transmission, along with **Pitta imbalance** affecting clarity of perception. In Timir, the involvement of **Indriya (sensory organs)** and their functional components leads to diminished discrimination ability. Vasadi Kwath, by virtue of its **Vata-Pitta Shamana**, **Chakshushya**, and **Rasayana** properties, restores the functional integrity of sensory pathways. Its action on **Alochaka Pitta** enhances perceptual clarity, while alleviation of **Srotorodha** ensures proper microcirculation and nourishment of neural tissues. From a modern scientific standpoint, TPD is influenced by **peripheral nerve sensitivity, receptor density, and cortical processing in the somatosensory cortex**. In conditions like NPDR and associated metabolic disturbances, subtle neural dysfunction may impair discrimination ability. The observed improvement in TPD suggests enhanced **neural conduction velocity**, improved **synaptic efficiency**, and better **cortical interpretation of sensory input**. This also indicates a possible **neuroprotective and neuromodulatory effect** of Vasadi Kwath. The findings of this study highlight that the drug exerts its action not only at the level of the eye but also on **higher sensory integration mechanisms**, thereby improving overall perceptual quality. This integrative effect strengthens the concept that vision is a **neuro-sensory phenomenon**, extending beyond mere optical clarity. However, limitations such as small sample size, short duration, and absence of advanced neurophysiological assessments should be considered. Further studies with larger populations and objective neuro-evaluation tools are recommended to validate these findings. []{#_Toc229853699 .anchor}**Discussion on photostress test** - PST directly reflects **cone photoreceptor recovery** - Improvement suggests: - Enhanced **retinal pigment epithelium (RPE) function** - Better **visual cycle regeneration** - Correlates with: - Reduced hemorrhage - Improved near vision **Vasadi Kwath significantly reduces photostress recovery time, indicating marked improvement in macular function and retinal metabolic efficiency. It demonstrates a strong therapeutic potential in reversing early functional damage in NPDR.** []{#_Toc229853700 .anchor}**Discussion on foveal reflex** - Foveal reflex depends on: - **Integrity of foveal pit** - **Absence of edema** - **Smooth retinal surface** - Improvement suggests: - Better **macular anatomy** - Reduced **retinal swelling** - Ayurveda correlation: - **Pitta shamana → reduces inflammatory leakage** - **Rakta prasadana → improves microcirculation** **Chakshushya effect → enhances visual function** **Discussion on NPDE grades** - NPDR grading reflects **retinal microvascular damage** - Improvement suggests: - Reduced **capillary permeability** - Improved **retinal perfusion** - Ayurveda correlation: - **Pitta shamana** → reduces vascular inflammation - **Rakta shodhana** → improves blood quality - **Rasayana effect** → promotes tissue repair Explains **downward shift in grading** []{#_Toc229853701 .anchor}**Correlation with Other Parameters** ----------------------------------------------------------------------- **Parameter** **Clinical Significance** ------------------------- --------------------------------------------- Fundus Findings Structural improvement Amsler Grid Functional macular recovery Photostress Test Faster photoreceptor recovery Foveal Reflex Improved macular anatomy ----------------------------------------------------------------------- []{#_Toc229853702 .anchor}**Discussion on grades of timir** - Timir grading reflects **functional vision status** - Improvement suggests: - Enhanced **retinal + neural processing** - Better **macular efficiency** - Correlates with: - Improved **Amsler grid** - Faster **photostress recovery** - Better **near vision** ➡️ Confirms **holistic visual improvement** []{#_Toc229853703 .anchor}**Correlation with Modern Parameters** ----------------------------------------------------------------------- **Timir Feature** **Modern Correlation** ----------------------------- ----------------------------------------- Blurring Visual acuity Distortion Macular dysfunction Scotoma Central field defect Improvement Retinal recovery ----------------------------------------------------------------------- []{#_Toc229853704 .anchor}**Discussion on patal involvemet** - Patal involvement reflects **depth of pathology** - Improvement indicates: - Regression of disease from **deeper to superficial layers** - Ayurvedic action: - **Pitta Shamana** → reduces visual disturbance - **Rakta Prasadana** → improves retinal perfusion - **Rasayana effect** → nourishes Drishti []{#_Toc229853705 .anchor}**Correlation with Modern Findings** ----------------------------------------------------------------------- **Patal** **Modern Correlation** ----------- ----------------------------------------------------------- 1st Mild NPDR / refractive changes 2nd Macular dysfunction 3rd Retinal damage / edema 4th Severe retinal degeneration ----------------------------------------------------------------------- []{#_Toc229853706 .anchor}**Discussion on timir subjective symptom score** - Subjective score reflects **patient-perceived quality of vision** - Improvement suggests: - Enhanced **retinal + neural function** - Reduced **macular stress** - Ayurvedic basis: - **Chakshushya** → improves vision - **Pitta shamana** → reduces visual disturbance - **Rasayana** → supports optic function Explains **overall symptom relief** []{#_Toc229853707 .anchor}**Correlation with Objective Parameters** ----------------------------------------------------------------------- **Subjective Improvement** **Objective Correlate** ---------------------------------- ------------------------------------ ↓ Blurring ↑ Visual acuity ↓ Distortion Better Amsler grid ↓ Eye strain Faster photostress recovery ↓ Haziness Improved foveal reflex ----------------------------------------------------------------------- []{#_Toc229853708 .anchor}**DISCUSSION overall** The present study evaluated the effect of Vasadi Kwath on **Timir w.s.r. to Non-Proliferative Diabetic Retinopathy**, using a combination of **subjective, functional, and structural parameters**. []{#_Toc229853709 .anchor}**🔹 1. Subjective Improvement** A significant reduction in **Timir subjective symptom score** (≈50--60%) was observed. Symptoms like *Avyakta darshan (blur), bhrama (distortion), and chakshu klama (eye strain)* improved markedly.\ This indicates enhancement in **patient-perceived visual quality**, which is crucial in chronic retinal disorders. []{#_Toc229853710 .anchor}**2. Functional Visual Recovery** - **Amsler Grid:** Reduction in metamorphopsia and scotoma - **Photostress Test:** Decreased recovery time → improved photoreceptor efficiency - **Near & Pinhole Vision:** Significant improvement These findings suggest restoration of **macular and cone function**, correlating with improved central vision. []{#_Toc229853711 .anchor}**3. Structural (Fundus) Changes** - Reduction in **hemorrhages & exudates** - Decrease in **macular edema** - Restoration of **foveal reflex** Indicates improved **retinal clarity, vascular stability, and macular architecture** []{#_Toc229853712 .anchor}**4. NPDR Grade Regression** A downward shift from **higher to lower NPDR grades** was observed: - Severe → Moderate - Moderate → Mild 👉 Suggests **disease-modifying effect**, not just symptomatic relief, and prevention of progression to advanced stages. []{#_Toc229853713 .anchor}**5. Timir Grading Improvement** - Grade III → II - Grade II → I Reflects **functional restoration of vision** and improvement in Drishti. []{#_Toc229853714 .anchor}**6. Patal-wise Lakshan Improvement** - Significant recovery in **1st & 2nd patal** - Regression from **3rd to 2nd patal** - Stabilization of **4th patal** Demonstrates reversal of pathology from **deeper to superficial levels**, supporting classical Ayurvedic concepts. []{#_Toc229853715 .anchor}**7. Mode of Action** Vasadi Kwath likely acts through: - **Pitta Shamana** → reduces inflammation & vascular leakage - **Rakta Prasadana** → improves retinal microcirculation - **Rasayana effect** → enhances retinal metabolism & repair Modern correlation: - Antioxidant action - Microvascular stabilization - Neuro-retinal protection **[SUMMARY]{.underline}** - Significant reduction in **subjective symptoms** - Marked improvement in **functional visual tests** - Noticeable improvement in **fundus findings** - Clear regression in **NPDR grades** - Improvement in **Timir grades** - Positive changes in **Patal-wise Lakshan** - Strong **correlation between subjective and objective parameters** Overall, the therapy shows **holistic efficacy** # 1 Detailed Summary {#detailed-summary .unnumbered} ## Introduction {#introduction-1 .unnumbered} Diabetic retinopathy is one of the leading microvascular complications of diabetes mellitus and is a major cause of visual impairment. In Ayurveda, the clinical features of diabetic retinopathy can be correlated with Timir, a progressive disorder affecting visual perception due to vitiation of Doshas and involvement of Patalas. The present study was undertaken to evaluate the efficacy of Vasadi Kwath in the management of Timir w.s.r. diabetic retinopathy. The study assessed both subjective and objective ophthalmological parameters along with laboratory investigations to determine the therapeutic effectiveness of the intervention. # Aim of the Study {#aim-of-the-study .unnumbered} To evaluate the effect of Vasadi Kwath in the management of Timir with special reference to diabetic retinopathy. # Objectives of the Study {#objectives-of-the-study .unnumbered} - To assess improvement in visual acuity. - To evaluate changes in retinal and macular function. - To assess improvement in subjective symptoms of Timir. - To evaluate changes in NPDR grading. - To study the effect on laboratory parameters such as FBS, PMBS, and HbA1c. # Study Design {#study-design .unnumbered} - Comparative clinical study. - Total patients: 100 - Group A: 50 patients - Group B: 50 patients - Duration: 3 months - Statistical test used: - Mann--Whitney U test - Data expressed as: - Mean ± Standard Deviation A p-value less than 0.05 was considered statistically significant. # Observations and Results {#observations-and-results .unnumbered} ## 1. Distant Vision BCVA {#distant-vision-bcva-2 .unnumbered} Significant improvement was observed in distant visual acuity in Group A compared to Group B. ### Percentage Relief {#percentage-relief-1 .unnumbered} - Right eye: 23.87% - Left eye: 21.17% ### Statistical Significance {#statistical-significance .unnumbered} - Both eyes showed highly significant improvement at 3 months (p\<0.001). ### Summary {#summary .unnumbered} The findings indicate enhancement in retinal and visual function following treatment. # 2. Near Vision BCVA {#near-vision-bcva .unnumbered} Near vision improved significantly in both eyes in Group A. ### Percentage Relief {#percentage-relief-2 .unnumbered} - Right eye: 32.73% - Left eye: 31.58% ### Statistical Findings {#statistical-findings-1 .unnumbered} - Right eye: p=0.004 - Left eye: p=0.012 ### Summary {#summary-1 .unnumbered} Improvement in near vision suggests better macular and central retinal functioning. # 3. Amsler Grid {#amsler-grid .unnumbered} The Amsler grid test demonstrated improvement mainly in the right eye. ### Percentage Relief {#percentage-relief-3 .unnumbered} - Right eye: 41.38% - Left eye: 31.25% ### Statistical Findings {#statistical-findings-2 .unnumbered} - Right eye significant (p=0.030) ### Summary {#summary-2 .unnumbered} Reduction in visual distortion indicates improved macular stability. # 4. Two-Point Discrimination Test {#two-point-discrimination-test-1 .unnumbered} Marked improvement was observed in retinal sensory perception. ### Percentage Relief {#percentage-relief-4 .unnumbered} - Right eye: 87.50% - Left eye: 86.67% ### Statistical Findings {#statistical-findings-3 .unnumbered} - Significant improvement especially in the right eye. ### Summary {#summary-3 .unnumbered} This parameter showed one of the highest improvements, suggesting enhanced retinal neuronal function. # 5. Foveal Reflex {#foveal-reflex-1 .unnumbered} Mild improvement was observed clinically, though statistical significance was not achieved. ### Percentage Relief {#percentage-relief-5 .unnumbered} - Right eye: 54.55% - Left eye: 43.75% ### Summary {#summary-4 .unnumbered} The treatment may help preserve macular integrity and prevent further deterioration # 6. Grades of NPDR {#grades-of-npdr-1 .unnumbered} Significant reduction in NPDR grading was observed in both eyes. ### Percentage Relief {#percentage-relief-6 .unnumbered} - Right eye: 22.41% - Left eye: 20.00% ### Statistical Findings {#statistical-findings-4 .unnumbered} - Right eye: p=0.007 - Left eye: p=0.002 ### Summary {#summary-5 .unnumbered} Improvement in retinal pathology suggests reduction in hemorrhages, microaneurysms, and exudative changes. # 7. Photo Stress Recovery Time (PSRT) {#photo-stress-recovery-time-psrt-1 .unnumbered} PSRT showed highly significant improvement in both eyes. ### Percentage Relief {#percentage-relief-7 .unnumbered} - Right eye: 66.67% - Left eye: 63.64% ### Statistical Findings {#statistical-findings-5 .unnumbered} - All comparisons highly significant (p\<0.001). ### Summary {#summary-6 .unnumbered} This was one of the strongest outcomes of the study, indicating improved macular and photoreceptor recovery. # 8. Timir Subjective Symptom Score (TSSS) {#timir-subjective-symptom-score-tsss-1 .unnumbered} Subjective symptoms reduced markedly after treatment. ### Percentage Relief {#percentage-relief-8 .unnumbered} - Right eye: 29.93% - Left eye: 25.57% ### Statistical Findings {#statistical-findings-6 .unnumbered} - Highly significant in both eyes (p\<0.001). ### Summary {#summary-7 .unnumbered} Symptoms such as blurred vision, difficulty in seeing, and visual discomfort improved significantly. # 9. Patal Involvement {#patal-involvement-2 .unnumbered} Significant reduction in patal involvement was observed. ### Percentage Relief {#percentage-relief-9 .unnumbered} - Right eye: 44.78% - Left eye: 37.68% ### Statistical Findings {#statistical-findings-7 .unnumbered} - Highly significant in both eyes (p\<0.001). ### Summary {#summary-8 .unnumbered} The results suggest arrest of disease progression and improvement in ocular tissue health. # 10. Intraocular Pressure (IOP) {#intraocular-pressure-iop .unnumbered} No significant changes were observed in either eye. ### Summary {#summary-9 .unnumbered} The treatment was found to be ophthalmologically safe and did not adversely affect intraocular pressure. # 11. Laboratory Parameters {#laboratory-parameters .unnumbered} ## FBS {#fbs-1 .unnumbered} - Percentage relief: 32.14% - Significant improvement observed. ## PMBS {#pmbs-1 .unnumbered} - Mild improvement observed. ## HbA1c {#hba1c-1 .unnumbered} - Mild improvement but statistically non-significant. ### Summary {#summary-10 .unnumbered} The treatment showed moderate systemic glycemic control benefits, especially in fasting blood sugar levels. # Overall Findings {#overall-findings .unnumbered} The study demonstrated that Vasadi Kwath produced significant improvement in: - Visual acuity, - Retinal function, - Macular recovery, - NPDR grading, - Subjective symptoms, - Patal involvement, - Glycemic parameters. The maximum improvement was observed in: - Two-point discrimination, - Photo stress recovery time, - Amsler grid, - Patal involvement. # Probable Mode of Action {#probable-mode-of-action .unnumbered} The therapeutic effect of Vasadi Kwath may be attributed to: - Chakshushya action, - Rasayana properties, - Antioxidant activity, - Improvement in retinal circulation, - Reduction in oxidative stress, - Microvascular protective effect. These actions may help prevent retinal degeneration and improve visual function. # Final Summary {#final-summary .unnumbered} The present study concludes that Vasadi Kwath is effective in the management of Timir w.s.r. diabetic retinopathy. Significant improvement was observed in both subjective and objective ophthalmological parameters along with moderate improvement in glycemic control. The treatment improved visual acuity, retinal function, macular recovery, and reduced NPDR severity and Timir symptoms. No adverse effect on intraocular pressure was observed, confirming the safety of the therapy. Overall, the findings support the clinical efficacy of Vasadi Kwath as a beneficial therapeutic approach for diabetic retinopathy correlated with Timir. ![](media/image30.wmf) # {#section-24 .unnumbered} **Conclusion** **Final Conclusion** The study conclusively establishes that **Vasadi Kwath produces a highly significant improvement in near visual acuity**, enhancing reading ability, focusing power, and overall visual function. Its efficacy can be attributed to its classical Ayurvedic actions of **Vata-Pitta Shamana and Chakshushya effect**, which are supported by modern concepts of improved macular and retinal function. **Thus, Vasadi Kwath emerges as a safe, effective, and scientifically validated therapeutic option for improving near vision in Timir and early NPDR, reinforcing the relevance of Ayurvedic principles in contemporary ophthalmic care.** The study conclusively demonstrates that **Vasadi Kwath produces a highly significant improvement in pinhole visual acuity**, indicating enhanced retinal function and improved quality of vision. The therapeutic effect can be explained through its classical Ayurvedic actions of **Vata-Pitta Shamana, Chakshushya effect, and Srotoshodhana**, which are supported by modern concepts of improved macular function and retinal sensitivity. **Improvement in pinhole vision strongly signifies that the drug acts beyond refractive correction, at the level of retinal physiology, making it a valuable therapeutic option in Timir and early NPDR.** The study conclusively demonstrates that **Vasadi Kwath produces a highly significant improvement in Two-Point Discrimination**, indicating enhanced sensory acuity, neural conduction, and cortical integration. The therapeutic effect can be explained through its classical Ayurvedic actions of **Vata-Pitta Shamana, Chakshushya, and Rasayana**, which are supported by modern concepts of **neuro-sensory enhancement and cortical refinement**. **Thus, Vasadi Kwath emerges as a potent modality not only for improving visual function but also for enhancing fine sensory perception, highlighting its broader role in neuro-ophthalmic care** **Vasadi Kwath significantly improves the foveal reflex by restoring macular architecture, reducing edema, and enhancing retinal clarity---indicating structural and functional recovery in NPDR.** **Vasadi Kwath demonstrates significant regression in NPDR grades by reducing retinal lesions and stabilizing microvasculature, thereby preventing disease progression and improving visual outcomes.** "The shift from higher to lower NPDR grades confirms that Vasadi Kwath not only improves symptoms but also modifies the underlying retinal pathology. **Vasadi Kwath significantly reduces the grades of Timir by improving visual clarity, reducing distortion, and preventing progression to advanced stages---demonstrating strong functional and neuro-retinal benefits.** "The downward shift in Timir grades reflects not just symptomatic relief but a true improvement in visual function, correlating well with objective retinal findings **Vasadi Kwath shows significant improvement in Patal-wise Lakshan by reversing disease progression from deeper to superficial levels, thereby restoring visual function and preventing advanced ocular damage.** "The patal-wise regression clearly demonstrates that Vasadi Kwath not only improves symptoms but also reduces the depth of pathological involvement in Timir **Vasadi Kwath produces a significant reduction in Timir subjective symptom score, demonstrating marked improvement in patient-perceived visual quality and overall ocular function.** "The reduction in subjective score validates the clinical efficacy of Vasadi Kwath from the patient's perspective, complementing objective retinal improvements." []{#_Toc229853767 .anchor}**Overall Conclusion** **Vasadi Kwath demonstrates significant improvement in both subjective and objective parameters of Timir and NPDR, indicating its dual action on functional vision and retinal pathology. The therapy not only relieves symptoms but also contributes to structural recovery and disease regression.** **Vasadi Kwath is highly effective in the management of Timir w.s.r. to NPDR. It produces significant improvement in subjective symptoms, enhances visual function, and promotes structural recovery of the retina, along with regression of disease grading. The study establishes its role as a safe, holistic, and disease-modifying therapy for early diabetic retinal changes.** "Vasadi Kwath doesn't just improve vision---it improves the retina itself, as proven by both subjective relief and objective retinal changes. # Detailed Conclusion {#detailed-conclusion .unnumbered} The present clinical study entitled **"Effect of Vasadi Kwath in the Management of Timir w.s.r. to Diabetic Retinopathy"** was conducted to evaluate the therapeutic efficacy of Vasadi Kwath on subjective symptoms, objective ophthalmological findings, retinal functional parameters, and laboratory investigations in patients suffering from diabetic retinopathy correlated with Timir. The study findings demonstrated that Vasadi Kwath produced significant improvement in multiple clinical and ophthalmological parameters, thereby establishing its beneficial role in the management of Timir associated with diabetic retinopathy. # Conclusion Based on Visual Parameters {#conclusion-based-on-visual-parameters .unnumbered} ## Distant Vision BCVA {#distant-vision-bcva-3 .unnumbered} Significant improvement in distant visual acuity was observed in both eyes after treatment. ### Percentage Relief {#percentage-relief-10 .unnumbered} - Right eye: 23.87% - Left eye: 21.17% ### Interpretation {#interpretation-10 .unnumbered} Improvement in distant vision indicates enhanced retinal and macular function. The treatment helped improve visual clarity and reduced visual impairment associated with diabetic retinal changes. ## Near Vision BCVA {#near-vision-bcva-1 .unnumbered} Near vision improved significantly in both eyes. ### Percentage Relief {#percentage-relief-11 .unnumbered} - Right eye: 32.73% - Left eye: 31.58% ### Interpretation {#interpretation-11 .unnumbered} Improvement in near vision suggests restoration of central retinal sensitivity and better visual performance during close work. # Conclusion Based on Retinal Functional Tests {#conclusion-based-on-retinal-functional-tests .unnumbered} ## Amsler Grid {#amsler-grid-1 .unnumbered} Improvement was observed mainly in the right eye. ### Percentage Relief {#percentage-relief-12 .unnumbered} - Right eye: 41.38% - Left eye: 31.25% ### Interpretation {#interpretation-12 .unnumbered} Reduction in metamorphopsia and visual distortion indicates improved macular stability and retinal integrity. ## Two-Point Discrimination Test {#two-point-discrimination-test-2 .unnumbered} This parameter showed maximum improvement among all tests. ### Percentage Relief {#percentage-relief-13 .unnumbered} - Right eye: 87.50% - Left eye: 86.67% ### Interpretation {#interpretation-13 .unnumbered} Marked improvement indicates enhanced retinal sensory perception and better neuronal functioning of the retina. The findings suggest possible neuroprotective and Rasayana effects of Vasadi Kwath. ## Foveal Reflex {#foveal-reflex-2 .unnumbered} Clinical improvement was observed though statistical significance was limited. ### Percentage Relief {#percentage-relief-14 .unnumbered} - Right eye: 54.55% - Left eye: 43.75% ### Interpretation {#interpretation-14 .unnumbered} The treatment may help preserve macular architecture and prevent further retinal degeneration. # Conclusion Based on NPDR Grading {#conclusion-based-on-npdr-grading .unnumbered} Significant reduction in NPDR grading was observed in both eyes. ### Percentage Relief {#percentage-relief-15 .unnumbered} - Right eye: 22.41% - Left eye: 20.00% ### Interpretation {#interpretation-15 .unnumbered} The reduction in NPDR severity suggests: - Decrease in retinal hemorrhages, - Reduction in microaneurysms, - Stabilization of retinal vascular pathology, - Improved retinal circulation. These findings support the beneficial role of Vasadi Kwath in preventing progression of diabetic retinopathy. # Conclusion Based on Photo Stress Recovery Time (PSRT) {#conclusion-based-on-photo-stress-recovery-time-psrt .unnumbered} PSRT showed highly significant improvement in both eyes. ### Percentage Relief {#percentage-relief-16 .unnumbered} - Right eye: 66.67% - Left eye: 63.64% ### Interpretation {#interpretation-16 .unnumbered} This was one of the strongest outcomes of the study and indicates: - Improved macular recovery, - Better photoreceptor function, - Enhanced retinal pigment epithelium activity. The results strongly suggest restoration of retinal functional capacity after treatment. # Conclusion Based on Timir Subjective Symptom Score (TSSS) {#conclusion-based-on-timir-subjective-symptom-score-tsss .unnumbered} Marked reduction in subjective symptoms was observed. ### Percentage Relief {#percentage-relief-17 .unnumbered} - Right eye: 29.93% - Left eye: 25.57% ### Interpretation {#interpretation-17 .unnumbered} Symptoms such as: - Blurred vision, - Visual discomfort, - Difficulty in focusing, - Diminished vision showed substantial improvement, thereby improving quality of life of patients. # Conclusion Based on Patal Involvement {#conclusion-based-on-patal-involvement .unnumbered} Significant reduction in patal involvement was observed. ### Percentage Relief {#percentage-relief-18 .unnumbered} - Right eye: 44.78% - Left eye: 37.68% ### Interpretation {#interpretation-18 .unnumbered} Reduction in patal involvement indicates arrest of disease progression and prevention of deeper ocular tissue damage. This supports the Ayurvedic concept that proper treatment of Timir prevents advancement toward more severe visual disorders. # Conclusion Based on Laboratory Parameters {#conclusion-based-on-laboratory-parameters .unnumbered} ## FBS {#fbs-2 .unnumbered} ### Percentage Relief {#percentage-relief-19 .unnumbered} - 32.14% ### Interpretation {#interpretation-19 .unnumbered} Improvement in fasting blood sugar suggests moderate systemic metabolic regulation. ## PMBS and HbA1c {#pmbs-and-hba1c .unnumbered} Mild improvement was observed, though statistical significance was limited. ### Interpretation {#interpretation-20 .unnumbered} The shorter duration of the study may be responsible for less pronounced changes in long-term glycemic markers. # Conclusion Regarding Safety {#conclusion-regarding-safety .unnumbered} ## Intraocular Pressure (IOP) {#intraocular-pressure-iop-1 .unnumbered} No significant changes in IOP were observed during the study. ### Interpretation {#interpretation-21 .unnumbered} This confirms that Vasadi Kwath is ophthalmologically safe and does not adversely affect ocular pressure dynamics. # Overall Therapeutic Conclusion {#overall-therapeutic-conclusion .unnumbered} The present study clearly demonstrates that Vasadi Kwath is effective in improving: - Visual acuity, - Retinal functional status, - Macular recovery, - NPDR grading, - Subjective symptoms of Timir, - Patal involvement, - Certain glycemic parameters. The therapy showed maximum efficacy in: - Two-point discrimination, - Photo stress recovery time, - Amsler grid, - Patal involvement. The probable therapeutic actions may include: - Chakshushya effect, - Rasayana action, - Antioxidant activity, - Improvement in retinal microcirculation, - Neuroprotective action, - Reduction in oxidative stress and vascular damage. # Final Conclusion {#final-conclusion .unnumbered} Based on the clinical observations, statistical analysis, and overall therapeutic response, it can be concluded that Vasadi Kwath is a safe and effective treatment modality in the management of Timir w.s.r. diabetic retinopathy. The treatment significantly improved both subjective and objective ophthalmological parameters and helped reduce the progression of retinal pathology. Therefore, Vasadi Kwath may be considered a promising Ayurvedic therapeutic approach for improving visual function and retinal health in diabetic retinopathy patients. **[BIBLIOGRAPHY]{.underline}** 1. 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Visual Thesaurus, Cite, Thesaurus Legend. 4. www.docshop.com 5. www.eye care.com 6. www.eyenub.com 7. www.education.yahoo.com 8. www.findarticles.com 9. www.nei.nih.gov 10. www.health-us2go.com 11. www.revopht.com 12. www.wikipedia.com 13. www.jove.com 14. www.pubmed.com **[ABBREVIATIONS]{.underline}** A. H.NI. - Ashtang Hriday Nidansthan A.S. -Ashtang Sangraha Bh. Pr. - Bhavrakash Bh.S. Bhel Samhita BSL - Blood sugar level Ch. Chi - Charak Chikitsasthan Ch. Su. Charaka Sutrasthan Ch. Ni. Charak Nidanstan Ch. Vi. Charak Viman Sthan K.S. - Kashyap Samhita M.Ni. - Madhav Nidan Su.Su. Sushrut Sutrasthan Su. Ni. - Sushrut Nidan Sthan Su. Chi. Sushrut Chikitsa sthan Su.Sha. Sushrut Sharirsthan Su. U. Sushrut UttarTantra V/A - Visual Acuity CSME - Clinically significant macular edema DM- Diabetes Mellitus DR - Diabetic Retinopathy NPDR - Non proliferative diabetic retinopathy PDR - Proliferative diabetic retinopathy ETDRS - Early treatment diabetic retinopathy study FFA- Fundus Fluorescein Angiography PSRT-Photo Stress Recovery Time BCVA- Best Corrected Visual Acuity PsPh- Pseudophakia NMSC - Nearly Mature Senile Cataract ISC - Immature Senile Cataract P.S.T. Photo Stess Test T.P.D. Two Point Discrimination Test Religion: H-Hindu, M-Muslim, SC-Scheduled Caste, C-Christian Socioeconomic Status: L-Low, M-medium, H-High. Education: IL Illiterate, L- Literate Addiction: TOB- Tobacco, SMO - Smoking Occupation: S-Sedentary, NS - Non-sedentary. HTN: Hypertension KV: Kaphavataja, VK: Vatakaphaja, VP: Vatapittaja, VK: Vatakaphaja, KP: Kaphapittaja, PK: Pittakaphaja. AC-Anterior Chamber OM-Ocular Movements IOP-Intra-ocular Pressure **[References:]{.underline}** **Refrences ayurvedic review of literature** 1 Charak Samhita Sutra Sthana 13/10, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp, P 88. 2 Ashtanga Hridaya Uttara Tantra 13/99, Astanga Hridayam -- with commentaries (sarvanga sundara)of Arunadatts and (Ayurnveda rasayana) of Hemadri, edited by Bhisagacharya Harisastri paradakaravaidya, 9th ed. Varanasi: Chaukhamba Orientalia; 2005. 956pp, P 825 3 Sushruta Sharira sthana 3/ 30, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. 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A Sanskrit English Dictionary, New ed. Delhi: Motilal Banarsidass PublishersPvt. Ltd.; 2002. 1333 pp, P 597. 8,10 Sushruta Samhita Uttar Tantra 1/17, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 196. 12-18 Sushruta Samhita Uttar Tantra 1/17, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 605 609. 19. Raja Radhakanta Deva, Shabdakalpadruma --Delhi: Nag Publishers; 1987. 792 pp. Vol 3, P18 Sir Monier Williams. A Sanskrit English Dictionary, New ed. Delhi: Motilal Banarsidass Publishers Pvt. Ltd.; 2002. 1333 pp, P 597. 20. Bhagwad Geeta 10.40 21. V.S Apte Sanskrit English Dictionary. 22. Charak Samhita Sutra Sthana 13/10, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp, P 88 23. Sushruta Samhita Sutra Sthana 12/09, Sushruta Samhita\-- with the Nibandha Sangraha Commentaryof Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Editedby Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 52. 24. Sushruta Samhita Uttar Tantra 5/6, Sushruta Samhita\-- with the Nibandha sangraha Commentary ofSri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi: Chaukambha surbharati prakashan; 2008. 824 pp, P 602 25. Sushruta Samhita Uttar Tantra 5/6, Sushruta Samhita\-- with the Nibandha sangraha Commentary ofSri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi: Chaukambha surbharati prakashan; 2008. 824 pp, P 641. 26\. Sushruta Samhita Sutra Sthana 35/12, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi: Chaukambha surbharati prakashan; 2008. 824 pp, P150 27 Charak Samhita Sutra sthana 7/ 8, Agnivesha. ---Elaborated by Charaka andDridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp. 28,35 Sushruta Samhita Uttar Tantra 1/13, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 596 29 Ashtanga Sangraha Sutra Sthana 31/15 Vagbhata. Astanga Sangraha -- with Shashilekha commentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. P.304. 31 Sushruta Samhita Kalpa Sthana 3/4 , Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 567 32 Sushruta Samhita Uttar Tantra 7/3-4 Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi: Chaukambha surbharati prakashan; 2008. 824 pp, P 605 33 Sushruta Samhita Uttar Tantra 1/16,. Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 596 34 Sushruta Samhita Sutra Sthana 35/12, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 150 36 Ashtanga Sangraha Sutra Sthana 22/ Vagbhata. Astanga Sangraha -- with Shashilekha commentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. 37 Sushruta Samhita Sutra Sthana 35/12, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 150 38,39,40,49Charak Samhita Sutra sthana 8/ 8,15 Agnivesha. ---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya JadavajiTrikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp. P 56,57 41 Kashyapa Samhita Sareera Sthana 1/03, P.V Tiwari.New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp. 42 Ashtanga Samgraha Sutra sthana, 22/09. Vriddha Vagbhata. Astanga Sangraha -- with Shashilekha commentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. 43 ,53 Bhela. Bhela Samhita - Text with English translation, Commentary and critical notes by Krishnamurthy K.H., edited by P.V. Sharma, Varanasi; Choukhamba Vishwabharathi; Reprint 2005. 660 pp. 44,45 Raja Radhakanta Deva, Shabdakalpadruma -- 3rd ed. Delhi: Nag Publishers; 1988. 937 pp.Vol 2. P 622 46 47 Taranatha Tarkavachaspathi Bhattacharya. Vachaspatyam, Varanasi: Chaukhamba Sanskrit Bhavan;2003. 3442 pp. Vol-4.,P 2842 Sushruta Samhita Uttar Tantra 1/11-12 Sushruta Samhita\-- with the Nibandha sangraha Commentaryof Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Editedby Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp. P.596 50 Charak Samhita Chikitsa sthana 15/09, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya JadavajiTrikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp, P 318. 51 Ashtanga HridayaUttara Sthana 24/01, Vriddha Vagbhata. Astanga Sangraha -- with Shashilekhacommentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. 54 Netraprakashika Edited and translated in Sanskrit by Sharma P. M.D.and Varadarajan I.V. New Delhi: CCRAS Publication; 1994. 76pp. 55 Dalhana on Sushruta samhita Uttara Tantra 1/10, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 602. 56 Sushruta samhita Uttar Tantra 24/17, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 652. 57,58 Sushruta samhita Sareera sthana 6/27, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 374. 59-61Sushruta samhita Uttar Tantra 7/7-18, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp 63 Charak Samhita Sutra Sthana 5/16, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp, P39. 62 Charak Samhita Chikitsa Sthana 6/1, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp. 63 Charak Samhita Sutra Sthana 5/16, Agnivesha. Carakasamhita---Elaborated by Charaka and Dridhabala with the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji Trikamji Acharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp.P38. 64-68 Clinical study to Evaluate the Role of Holistic Ayurvedic Treatment in Pramehaja Timira w.s.r. Background Diabetic Retinopathy-Dr.Priyanka Rani 2013. Thesis―A Clinical Study on Timira w.s.r. Posterior Segment Pathologies & its management with Ushiradi Anjana‖-Dr.Seema Tripathi 2014 Thesis- Management of Diabetic Retinopathy with Doorvadya Ghrita Tarpana and Internal administration of Mahavasadi kwatha- A Comparative study :Dr. Veeranagouda Adoor(2011). 70 Ashtanga Sangraha Sutra Sthana 19/18, Vriddha Vagbhata. Astanga Sangraha -- with Shashilekhacommentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. P153. 71 Charak Samhita Vimana Sthana 5/3, Agnivesha, Carakasamhita---Elaborated by Charaka and Dridhabalawith the Ayurveda -- Dipika commentary by Chakrapanidatta, edited by Vaidya Jadavaji TrikamjiAcharya, 5th ed. Varanasi: Chaukhamba Surbharati Prakashan; Reprint 2000. 738 pp.P 259. 72 Sushruta Samhita Chikitsa Sthana 12/4, Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya On Nidanasthana. Edited by Vaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi: Chaukambha surbharati prakashan; 2008. 824 pp, P 454. 73-76,78-80 Sushruta Samhita Uttar Tantra 7/ , Sushruta Samhita\-- with the Nibandha sangraha Commentary of Sri Dalhanacharya and the Nyayachandrika Panjika of Sri Gayadasacharya on Nidanasthana. Edited byVaidya Jadavji Trikamji Acharya and Narayan Ram Acharya ‗Kavyatirtha', New ed. Varanasi:Chaukambha surbharati prakashan; 2008. 824 pp, P 567 81. Ashtanga Samgraha Sutra sthana, 22/09. Vriddha Vagbhata. Astanga Sangraha -- with Shashilekha commentary by Indu, Edited by Dr. Shivaprasad Sharma, Varanasi: Chaukhamba Sanskrit series office;2006. 965 pp. 82. Yoga Ratnakara Netra Roga Chikitsa Sl 1-4, Yogaratnakara - with vidyotini Hindi Commentary byVaidya Lakshmipati Sastri, Edited by Bhisagratna Brahamasankar Sastri. 5th ed. Varanasi:Chaukhamba Sanskrit Sansthan; 1993. 504 pp. P 395 83. Yogaratnakara Netra Roga Chikitsa Sl 5-7,10, Yoga Ratnakara- with vidyotini Hindi Commentaryby Vaidya Lakshmipati Sastri, Edited by Bhisagratna Brahamasankar Sastri. 5th ed. Varanasi:Chaukhamba Sanskrit Sansthan; 1993. 504 pp, P 395 84. Yogaratnakara Netra Roga Chikits Sl-6,Yoga Ratnakara- with vidyotini Hindi Commentary by Vaidya Lakshmipati Sastri, Edited by Bhisagratna Brahamasankar Sastri. 5th ed. Varanasi:Chaukhamba Sanskrit Sansthan; 1993. 504 pp, P 395 > **[References: modern review]{.underline}** 1. Ophthalmology A Short Text book Garhard K. Long, M.D. Thieme stattgant New > York 2000.pp.299 2. Anatomy and Physiology of Eye ,Second Edition ,A.K.Khurana,Indu Khurana,CBS publishers Page 140-149. 3. Comprehensive Opthalmology Fourth Edition, A K Khurana, New Age International (P) Limited,Publishers, Reprint 2007 4. Text Book of Medical > Physiology, Eleventh Edition Guyton & Hall Elsevier Publications.pp. > 626-629and 640-644 5. Joanna Kur , Eric A. Newman ,and Tailoi Chan-Ling , Cellular and physiological mechanisms underlying blood flow regulation in the retina choroid in health disease --Pubmed PMC3418965 retrieved on Sep.1 2013. 6. www.eyeweb.com/history/retinopathy.abstract . 7. Systemic factors in the managenment of Diabetic Retinopathy 8. Pathology/MicroComplications/EDP_Diabetic_Retinopathy.cfm) 9. Atlas and text on Diabetic Retinopathy-Ramandeep Singh,Vaishali > Gupta,Jaydeep Publishers,first edition 2007,P.No.25. 10. Comprehensive Ophthalmology Fourth Edition, A K Khurana, New Age International (P) Limited,Publishers, Reprint 2007 11. www.slideshare.com Diabetic Retinopathy. 12. Parsons' Diseases of the Eye, Twentieth Edition, Elsevier Publication Reprinted,2007. 13. Clinical ophthalmology-A systematic approach ,Jack J Kanski Fifth edition Elseviers Page No.424-440 14. Agrawal M C Newer trends in management of DR,DOS Times vol 19 no.6 > Dec.2013 15. www.slideshare.com Occular manifestation in Diabetes **[Case Report Form]{.underline}** **["Effect of Vasadi Kwath in the management of Timir w.s.r. To Diabetic Retinopathy- A Clinical Study."]{.underline}** > Name of Patient > :\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- > > Age : .......... Years. Sex : Male / Female > > Address : > > **Demographic Profile:-** Marital Status --Married(1)\-\-\-\-\-- Unmarried(2)\-\-\-\-\-\-- widowed(3)\-\-\-\-- > Educational Status- Illiterate (1)\-\-\-\-\-- Literate (2)\-\-\-\-- > > Occupation -Sitting (1)\-\-\-\-\-\--Moderate > labour(2)\-\-\-\-\-\-\-\--Heavy labour(3)\-\-\-\-\-- > > Socio Economic Status- Lower(1)\-\-\-\-\-\-- > Middle(2)\-\-\--Upper(3)\-\-\-\-- > > Habitat - Urban (1)\-\-\-- Semi Urban (2)\-\-\-\-\-\-- > Rural(3)\-\-\-\-- > > Religion- Hindu (1) \-\-\-\-\-- Muslim (2)\-\-\-- > SC(3)\-\-\-\--Others(4)\-\-\-\-- OPD registration number : > DOA : > > Date Of Inclusion In Clinical > Trial\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- > > Expected Date Of Completion Of Clinical > Trial\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- > > Contact No. > > Duration of DM- Anti Diabetic drug being used\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- > **Type of therapy:** (note : tick (√) for yes and (x) for no) > > A\) Vasadi kwath B) Antioxidant ----------------------------------------------------------------------- **Chief Complaints** -- Yes(1) N0(2) Duration In Weeks ----------------------------------------------------------------------- 1\) Loss Of Vision \-\-\-\-\-\-- \-\-\-\-\-\-- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 2\) Frequent Urination \-\-\-\-\-\-- \-\-\-\-\-\-- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 3\) Polyphagia \-\-\-\-\-\-- \-\-\-\-\-\-- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 4\) Polydipsia \-\-\-\-\-\-- \-\-\-\-\-\-- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 5\) Any other \-\-\-\-\-\-- \-\-\-\-\-\-- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- ----------------------------------------------------------------------- []{#_Toc229853809 .anchor}**(Timir Lakshana)** ----------------------------------------------------------------------- अव्यक्त दर्शन (Blurred vision) ----------------------------------------------------------------------- दूरदर्शन/निकटदर्शन कठिनता (Difficulty in distant/near vision) तिमिरदर्शन (Seeing darkness/black spots) जालदर्शन (Cobweb-like vision) मक्खिकादर्शन (Floaters-like symptoms) द्विदर्शन (Diplopia) अल्पप्रकाशे न पश्यति (Poor vision in dim light) दृष्टि मन्दता (Gradual diminution of vision) ----------------------------------------------------------------------- **H/O Of Present Illness** -------------------------------------------------------------------------------------------------------------------- **H/O Past Illness** (If Any) Yes(1) No(2) -------------------------------------------- -------------------------------------------------------------------- -- 1\) \-\-\-\-\-- \-\-\-\-\-- 2\) \-\-\-\-\-- \-\-\-\-\-- **Personal History** • Dietary Habits -- Veg(1)\-\-\-\-- Non- Veg(2)\-\-\-\-- • Addiction- Smoking(1)\-\-\-\-\--Tobacco(2)\-\-\-\-\-- Alcohol (3)\-\-\-- others(4)\-\-\-\-\-- • Any Emotional Stress- Average(1)---Moderate(2)\-\-\-- Too Much(3)\-\-- -------------------------------------------------------------------------------------------------------------------- > **Family History** -- > > **Surgical History**---H/O Eye Surgery- > > **T/T History**- H/O D.M/HTN/ > > **Previous Eye Disorders**- 1.Cataract 2. Uveitis 3. Glaucoma **General Physical Examination-** •Height- \-\-\-\-\-\-\-\--Feet\-\-\-\-\-\--Inches •Weight\-\-\-\-\-\--Kgs •BMI\-\-\-\-\--Kg/M 2 •Respiration Rate\-\-\-\-\-\--/Min •Pulse Rate\-\-\-\-\-\--/Min Rhythm Regular(1)\-\-\-- Irregular(2)\-\-\-- •B.P.- \-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- -Mm Of Hg •Tongue- Normal(1)\-\-\-\-- Red(2)\-\-\-\--Pallor(3)\-\-\--Leukoplakis(4)\-\-\-- other(5)\-\-\-- •Lips -- -Normal(1)\-\-\-- Cracked(2)\-\-\-- other(3)\-\-- •Eyes- Normal(1)\-\-- Any Disease(2)\-\-\-- •Ears-Normal Hearing(1)\-\-\-- Deafness(2)\-\-\--Tinnitus(3)\-\-\-\-- others(4)\-\-\-\-- •Nose- Normal(1)\-\-\-\-- Discharge(2)\-\-\-\-- Anosmia(3)\-\-\-- othars(4)\-\-\-\-- •Throat-Normal(1)\-\-\-- Congested(2)\-\-\-\--others(3)\-\-\-- • Oral Cavity- Normal(1)\-\-\-\-- Stomatitis(2)\-\-\-- others(3)\-\-\-- • Teeth-Normal(1)\-\-\-- Abnormal(2)\-\-- •Gums-Normal(1)\-\-\-- Spongy(2)\-\-\-- Bleeding(3)\-\-- others(4)\-\-- • Thyroid Gland-Normal(1)\-\-- Enlarged(2)\-\-- •Pallor- Present(1)\-\-- Absent(2)\-\-\-- Oedema-Present(1)\-\-- Absent(2)\-\-- **Systemic Examination-** ----------------------------------------------------------------------- 1)Respiratory System- ----------------------------------------------------------------------- 2\) GIT System- 3\) CVS - 4\) Nervous System- 5\) Musculoskeletal System- 6\) Genito- Urinary System- ----------------------------------------------------------------------- +-----------------------------------------------------------------------+ | **Ashtavidh parikshan :** | +=======================================================================+ | 1. Nadi- 5. Shabda- | +-----------------------------------------------------------------------+ | 2. Mala- 6. Sparsha- | +-----------------------------------------------------------------------+ | 3. Mutra- 7. Druk- | +-----------------------------------------------------------------------+ | 4. Jivha- 8. Aakruti- | +-----------------------------------------------------------------------+ ----------------------------------------------------------------------- **Strotas parikshan** ------------------- --------------------------------------------------- Pranvaha strotas Udakavah strotas Annavah strotas Rasavah strotas Raktavah strotas Mansavah strotas Medovahs strotas Asthivah strotas Majjavaha strotas Shukravaha strotas Purishavah strotas Mutravaha strotas Svedavaha strotas Artavvaha strotas Manovaha strotas Stanyavah strotas- ----------------------------------------------------------------------- **Koshtha Parikshan**- Mridu(1)\-\-\-- Madhyam(2)\-\-\-\-- Krura(3)\-\-\-- **Type Of Prakruti**- Vataja(1)\-\-\-- Pittaja(2)\-\-\-- Kaphaja(3)\-\-- Vata- Pittaja(4)\-\-- Vata- Kaphaja((5)\-\-- Pitta- Kaphaja(6)\-\-- Sannipataja(7)\-\-- **Assesment Of Sara**- **Type Of Sara**- Rasa sara(1)\-\-\-- Rakta sara (2)\-\-\-- Mamsa sara(3)\-\-\-- Meda sara(4)\-\-\-- Asthi sara(5)\-\-- Majja sara(6)\-\-\-- Shukra sara(7)\-\-\-\-- ----------------------------------------------------------------------- **Rog Pariksha**- ----------------------------------------------------------------------- 1\. Nidan(Aetiology)- 2\. Purvarupa(Prodromal Symptoms)- 3\. Rupa(Signs & Symptoms) 4\. Upshaya/Anupshaya 5\. Samprapti(Pathogenesis) ----------------------------------------------------------------------- **Pathology Investigations** 1\) BSL - F\-\-\-\-\-- \-\-\-\-\-\-\-\-\--Pm\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 2\) Urine - Alb\-\-\-\-\-\-\-- Sugar\-\-\-\-\-\-\-\-- 3\) HbA1c\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- 4)lipid profile\-\-\-\-\-\-\-- 5\) blood urea\-\-\-\-\-\-\-- 6\) serum creatinine\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- **Ocular examination** : -------------------------------------------------------------------------------------- Right Left eye eye (O.S.) (O.D.) --------------------------------- -------- ------- ------- -- -------- ------- ------- 1\. Visual acuity with pin hole BCVA correction required Sph Cyl Axis Sph Cyl Axis Distant Near 2.Bhrumandal (eye brow) 3.Vartmamandal(eyelids) 4.Pakshmamandal(eyelashes) 5.Shuklamandal{conjunctiva, sclera} 6.Krishnamandal{cornea, anteriorchamber, iris} 7.Drishtimandal{pupil} (size, shape,reaction), { lens} 8\. Sandhigat parikshan \(a\) pakshma vartmagatsandhi (lid margin) (b)vartma shuklagat sandhi (upper and lower fornix) (c)shuklakrishnagatsandhi (limbus) \(d\) krishna drishtigat sandhi \(e\) apang sandhi \(f\) kaninak sandhi 9\. Ocular movement 10\. I.O.P. 11\. Nasolacrimal patency 12\. Fundoscopic findings \(a\) media (b)opticdisc(shape,size,margin) \(c\) peripapillary area \(d\) blood vessels \(e\) macula -------------------------------------------------------------------------------------- Issue Of Trial Drug For 2 Weeks . Quantity\-\-\-\-\-\-\-\-- Date to Come For Next Assessment\-\-\-\-\-\-\-\-\-\-\-\-\-- **Follow -- up proforma :** > Name : > > Opd registration number : > > Complaints : > > **1^st^ Follow Up-15 days) Date \-\-\-\-\-\-\--** -------------------------------------------------------------------------- Grades ---------------------------- ----------- ---- ---- ---- ---- ---- -------- 0 1 2 3 4 5 6 7 Distant Vision Near Vision NPDR Amsler Grid 2 Point Discrimination Foveal Reflex Photostress Test -------------------------------------------------------------------------- Issue Of Trial Drug For 2 Weeks . Quantity\-\-\-\-\-- -Date to Come For Next Assessment\-\-\-\-\-\-\-\-\-\-\-- 2^nd^ Follow up -after 1 month- -------------------------------------------------------------------------- Grades ---------------------------- ----------- ---- ---- ---- ---- ---- -------- 0 1 2 3 4 5 6 7 Distant Vision Near Vision NPDR Amsler Grid 2 Point Discrimination Foveal Reflex Photostress Test -------------------------------------------------------------------------- Issue Of Trial Drug For 4 Weeks . Quantity\-\-\-\-\-- Date to Come For Next Assessment\-\-\-\-\-\-\-\-\-\-\-\-\-- 3^rd^ follow up --after 2 months- -------------------------------------------------------------------------- Grades ---------------------------- ----------- ---- ---- ---- ---- ---- -------- 0 1 2 3 4 5 6 7 Distant Vision Near Vision NPDR Amsler Grid 2 Point Discrimination Foveal Reflex Photostress Test -------------------------------------------------------------------------- Issue Of Trial Drug For 4 Weeks . Quantity\-\-\-\-\-\-- Date to Come For Next Assessment\-\-\-\-\-\-\-\-\-\-\-\-\-- **4^th^ follow up-(3 months) Date\-\-\-\-\-\--** -------------------------------------------------------------------------- Grades ---------------------------- ----------- ---- ---- ---- ---- ---- -------- 0 1 2 3 4 5 6 7 Distant Vision Near Vision NPDR Amsler Grid 2 Point Discrimination Foveal Reflex Photostress Test -------------------------------------------------------------------------- 3)Fundus Photograph- Approximate Quantity Of Vasadi Kwath Consumed\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\--Ml \% Of Drug Compliance\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-\-- **[Assessment At The End Of 3 Months]{.underline}** > **Criteria of Evaluation-** -------------------------------------------------------------------------- Grades ---------------------------- ----------- ---- ---- ---- ---- ---- -------- 0 1 2 3 4 5 6 7 Distant Vision Near Vision NPDR Amsler Grid 2 Point Discrimination Foveal Reflex Photostress Test -------------------------------------------------------------------------- **[Assessment chart]{.underline}** +-----------------------------------------------------------------------+ | +---------------------------+------------------+------------------+ | | | Assessment criteria | Right eye | Left eye | | | +===========================+==================+==================+ | | | | B.T. A.T. | B.T. A.T. | | | +---------------------------+------------------+------------------+ | | | 1.Distant Vision(BCVA) | | | | | | | | | | | | 2\. Near Vision(BCVA) | | | | | | | | | | | | 3\. NPDR | | | | | | | | | | | | 4\. Two Point | | | | | | Discrimination Test | | | | | | | | | | | | 5\. Photostress test | | | | | | recovery time | | | | | | | | | | | | 6.Amsler Grid Findings | | | | | | | | | | | | 7.Foveal Reflex | | | | | +---------------------------+------------------+------------------+ | +=======================================================================+ +-----------------------------------------------------------------------+ [SECTION I --- AYURVEDIC SUBJECTIVE PARAMETER SCORE CHART]{.underline} [Scoring Key: 0 = Absent \| 1 = Mild \| 2 = Moderate \| 3 = Severe \|]{.underline} [1. AVYAKTA DARSHANA (Blurred Vision)]{.underline} ---------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- ------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [No blurring, vision absolutely clear]{.underline} [1]{.underline} [Occasional blurring, clears on its own]{.underline} [2]{.underline} [Frequent blurring, mild difficulty in daily activities]{.underline} [3]{.underline} [Persistent blurring, marked difficulty]{.underline} [Score Recorded]{.underline} ---------------------------------------------------------------------------------------------------------------------------------- [2. MAKSHIKA-MASHAKA-KESHA DARSHANA (Floaters)]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- ---------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [No floaters]{.underline} [1]{.underline} [Occasional single/few floaters, not bothersome]{.underline} [2]{.underline} [Multiple floaters, intermittent, mildly bothersome]{.underline} [3]{.underline} [Persistent numerous floaters / cobweb / thread-like]{.underline} [Score Recorded]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [4. HRASVA-VRIDDHA VIPARYAYA (Metamorphopsia / Image Distortion)]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- ---------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [No distortion]{.underline} [1]{.underline} [Occasional mild waviness of lines]{.underline} [2]{.underline} [Persistent distortion, wavy lines]{.underline} [3]{.underline} [Marked distortion, objects unrecognizable in shape]{.underline} [Score Recorded]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [5. SUCHIPASHA NA PASHYATI (Difficulty in Fine Near Work / Reading)]{.underline} ----------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- -------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [Can read fine print / thread needle easily]{.underline} [1]{.underline} [Slight difficulty, needs extra effort]{.underline} [2]{.underline} [Cannot read fine print without aid]{.underline} [3]{.underline} [Unable to perform any near-vision task]{.underline} [Score Recorded]{.underline} ----------------------------------------------------------------------------------------------------------------------------------- [6. DWIDHA EKAM PASHYATI (Diplopia / Double Vision)]{.underline} ------------------------------------------------------------------------------------------------------------------------------------ [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- --------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [Absent]{.underline} [1]{.underline} [Occasional, disappears quickly]{.underline} [2]{.underline} [Intermittent, mildly disturbing]{.underline} [3]{.underline} [Persistent monocular/binocular diplopia]{.underline} [Score Recorded]{.underline} ------------------------------------------------------------------------------------------------------------------------------------ [7. DRISHTI VIBHRAMA (Field of Vision / Distance Misperception)]{.underline} [*\"Dūrasthānyapi rūpāṇi manyate ca samīpataḥ\"* --- (Su.U.7)]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [Criteria]{.underline} [BT (Day [1 [2 [3 0)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ----------------------- ---------------------------- ----------------- -------------------- -------------------- -------------------- [0]{.underline} [Normal field, no distance misperception]{.underline} [1]{.underline} [Mild peripheral dimming]{.underline} [2]{.underline} [Definite peripheral scotoma, distance confusion]{.underline} [3]{.underline} [Central scotoma, difficulty with face recognition]{.underline} [Score Recorded]{.underline} ------------------------------------------------------------------------------------------------------------------------------------- [TIMIRA SUBJECTIVE SYMPTOM TOTAL SCORE (TSSS)]{.underline} ----------------------------------------------------------------------------------------------------------------------------------- [Parameter]{.underline} [Max [BT]{.underline} [1 [2 [3 Score]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ---------------------------- -------------------- ------------------ -------------------- -------------------- -------------------- [1. Avyakta [3]{.underline} Darshana]{.underline} [2. Makshika-Mashaka [3]{.underline} Darshana]{.underline} [3. Hrasva-Vriddha [3]{.underline} Viparyaya]{.underline} [4. Suchipasha na [3]{.underline} Pashyati]{.underline} [5. Dwidha Ekam [3]{.underline} Pashyati]{.underline} [6. Drishti [3]{.underline} Vibhrama]{.underline} [TOTAL TSSS]{.underline} [18]{.underline} ----------------------------------------------------------------------------------------------------------------------------------- [TSSS Interpretation]{.underline} ----------------------------------------------------------------------- [Total TSSS]{.underline} [Severity]{.underline} -------------------------------------- -------------------------------- [0 -- 5]{.underline} [Minimal]{.underline} [6 -- 10]{.underline} [Mild]{.underline} [11 -- 15]{.underline} [Moderate]{.underline} [16 -- 18]{.underline} [Severe]{.underline} ----------------------------------------------------------------------- [SECTION IV --- SYSTEMIC / LAB PARAMETERS]{.underline} [1. FASTING BLOOD SUGAR (FBS)]{.underline} ---------------------------------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [FBS [Control]{.underline} [BT]{.underline} [1 [2 [3 (mg/dL)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ---------------------- ---------------------- -------------------------- ------------------ -------------------- -------------------- -------------------- [0]{.underline} [\< 100]{.underline} [Good]{.underline} [1]{.underline} [100 -- [Borderline]{.underline} 126]{.underline} [2]{.underline} [127 -- [Fair]{.underline} 180]{.underline} [3]{.underline} [181 -- [Poor]{.underline} 250]{.underline} [Actual FBS (mg/dL)]{.underline} ---------------------------------------------------------------------------------------------------------------------------------------------------------- [2. POST-PRANDIAL BLOOD SUGAR (PPBS)]{.underline} ---------------------------------------------------------------------------------------------------------------------------------------------------------- [Grade]{.underline} [PPBS [Control]{.underline} [BT]{.underline} [1 [2 [3 (mg/dL)]{.underline} Month]{.underline} Month]{.underline} Month]{.underline} ---------------------- ---------------------- -------------------------- ------------------ -------------------- -------------------- -------------------- [0]{.underline} [\< 140]{.underline} [Good]{.underline} [1]{.underline} [140 -- [Borderline]{.underline} 180]{.underline} [2]{.underline} [181 -- [Fair]{.underline} 250]{.underline} [3]{.underline} [251 -- [Poor]{.underline} 300]{.underline} [Actual PPBS (mg/dL)]{.underline} ---------------------------------------------------------------------------------------------------------------------------------------------------------- [3. HbA1c (%)]{.underline} ----------------------------------------------------------------------------------------------------------- [Grade]{.underline} [HbA1c [Control]{.underline} [BT]{.underline} [3 Month (%)]{.underline} (AT)]{.underline} --------------------- ------------------- -------------------------- ------------------ ------------------- [0]{.underline} [\< [Good]{.underline} 7.0]{.underline} [1]{.underline} [7.0 -- [Acceptable]{.underline} 8.0]{.underline} [2]{.underline} [8.1 -- [Fair]{.underline} 9.0]{.underline} [3]{.underline} [9.1 -- [Poor]{.underline} 10.0]{.underline} [4]{.underline} [\> [Very poor]{.underline} 10.0]{.underline} [Actual HbA1c (%)]{.underline} ----------------------------------------------------------------------------------------------------------- [OVERALL RESPONSE GRADING (Grand Total Score)]{.underline} ----------------------------------------------------------------------- [% Improvement from [Response Category]{.underline} BT]{.underline} ------------------------------- --------------------------------------- [\> 75%]{.underline} [Marked Improvement]{.underline} [51 -- 75%]{.underline} [Moderate Improvement]{.underline} [26 -- 50%]{.underline} [Mild Improvement]{.underline} [1 -- 25%]{.underline} [Unchanged / Minimal]{.underline} [0 or worsening]{.underline} [No Improvement / Deterioration]{.underline} ----------------------------------------------------------------------- [Formula:]{.underline} [% Improvement = \[(BT Score − AT Score) ÷ BT Score\] × 100]{.underline} [PHYSICIAN SIGN-OFF]{.underline} +----------------+-----------+-------------+---------------+----------+ | [Visi | [Date]{.u | [PI | [IP signature | [Rema | | t]{.underline} | nderline} | Signature]{ | (scholar | rks]{.un | | | | .underline} | ) | derline} | | | | | ]{.underline} | | | | | [(Guide)]{ | | | | | | .underline} | | | +================+===========+=============+===============+==========+ | [Baseline | | | | | | (BT | | | | | | )]{.underline} | | | | | +----------------+-----------+-------------+---------------+----------+ | [1 | | | | | | Mont | | | | | | h]{.underline} | | | | | +----------------+-----------+-------------+---------------+----------+ | [2 | | | | | | Mont | | | | | | h]{.underline} | | | | | +----------------+-----------+-------------+---------------+----------+ | [3 Month | | | | | | (AT | | | | | | )]{.underline} | | | | | +----------------+-----------+-------------+---------------+----------+ ----------------------------------- ----------------------------------- ----------------------------------- ----------------------------------- **CLINICAL TRIALS REGISTRY - INDIA** **Indian Council of Medical Research - National Institute for** **Research in Digital Health & Data Science** **PDF of Trial** Generated on 16/03/2026 **Clinical Trial Details** **CTRI Number** CTRI/2026/03/106260 \[Registered on: 16/03/2026\] - **Trial Registered Prospectively** **Last Modified On** 13/03/2026 **Post Graduate Thesis** Yes **Type of Trial** Interventional **Type of Study** Drug Ayurveda **Study Design** Randomized, Parallel Group, Active Controlled Trial **Public Title of Study** Efficacy of Ayurvedic medicine - kwath in Diabetic Retinopathy. **Scientific Title of Study** Effect of Vasadi Kwath in the Management of Timir W.S.R to Diabetic Retinopathy- A Clinical Study. **Secondary IDs if Any Secondary ID Identifier** NIL NIL **Details of Principal** **Investigator** **Details of Principal Investigator** **Name** Dr Shubhangi Lohakare **Designation** Ph.D Scholar **Affiliation** **Address** Government Ayurved College, Raje Raghuji Nagar,Nagpur Nagpur MAHARASHTRA 440009 India **Phone** 9890698452 **Fax** **Email** shindeshubh84@gmail.com **Details Contact Person** **(Scientific Query)** **Details Contact Person (Scientific Query)** **Name** Dr Hari Umale **Designation** Professor **Affiliation** Government Ayurved College, Nagpur **Address** Department of Shalakya Tantra,Government Ayurved College, Raje Raghuji Nagar,Nagpur Nagpur MAHARASHTRA 440009 India **Phone** 9423682026 **Fax** **Email** hariumale58@gmail.com **Details Contact Person** **(Public Query)** **Details Contact Person (Public Query)** **Name** Dr Shubhangi Lohakare [Command succeeded with exit code 0]