Vitiligo

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vitiligo

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Vitiligo

Definition

Vitiligo is an acquired autoimmune disease of the skin characterized by well-defined, milky-white macules and patches resulting from T-cell-mediated destruction of epidermal melanocytes. Leukotrichia (white hairs) within lesions reflects concurrent loss of follicular melanocytes.

Fitzpatrick's Dermatology, Ch. 76
Dermatology 2-Volume Set 5e, Ch. 66

Epidemiology

Prevalence: ~0.5-1% worldwide; up to >8% in parts of India
Peak onset: ages 10-30 years; ~50% of cases begin before age 20
No definitive sex predilection, though females seek care more often
Can occur in bone marrow transplant recipients from donors with vitiligo (supports immune transfer)
Monozygotic twin concordance only ~23%, supporting an important environmental/non-genetic component

Pathogenesis

The convergence theory unifies multiple pathogenic mechanisms:

1. Intrinsic melanocyte defects Melanocytes in vitiligo patients have intrinsic abnormalities - they are more susceptible to oxidative stress, have dilated rough endoplasmic reticulum (unfolded protein response), and produce excess reactive oxygen species (ROS).

2. Cellular stress and danger signals Stressed melanocytes release DAMPs - HSP-70 (heat shock protein 70) and HMGB1. These activate plasmacytoid dendritic cells and innate lymphoid cells to secrete IFN-α and IFN-γ.

3. Immune activation cascade

Activated keratinocytes produce CXCL9 and CXCL10
These recruit CD4+ helper and CD8+ cytotoxic T cells (which express CXCR3) to the skin
CD8+ T cells produce IFN-γ and TNF, directly destroying melanocytes
CD8+ T cells are both necessary and sufficient for melanocyte destruction

4. Resident memory T cells Express CD69, CD103, CD49a and persist in previously affected skin, explaining why vitiligo recurs in the same areas after treatment.

5. Genetic factors Multiple susceptibility loci identified. Key candidate genes are involved in melanogenesis, immune regulation, and apoptosis. ~7% of first-degree relatives of vitiligo patients are also affected. Many susceptibility genes are shared with other autoimmune diseases.

6. Chemical/environmental triggers Phenolic compounds (e.g., industrial chemicals) act as tyrosine analogs and initiate the cellular stress response in melanocytes, exacerbating or inducing vitiligo.

Clinical Features

Lesion Characteristics

Well-defined, milk-white macules/patches with smooth, convex margins
Surrounding skin may appear normal or hyperpigmented (normal or hyperpigmented border)
Trichrome vitiligo: intermediate tan zones between normal skin and fully depigmented areas (especially in early disease)
Leukotrichia: white hairs within depigmented patches
Rarely: inflammatory erythematous border (can mimic tinea corporis)

Clinical Types / Distribution

Type	Description
Generalized (most common)	Symmetric involvement; face, chest, hands, axillae, groin
Acrofacial	Distal fingers and facial orifices (lips, tips)
Segmental	Unilateral, Blaschkoid pattern; spreads for 1-2 years then stabilizes
Focal	Single or few macules in one area, often trigeminal (especially in children)
Mucosal	Oral/genital mucosa only
Universal	Nearly entire body surface depigmented

Predilection Sites

Face (especially around orifices - eyes, nose, mouth, ears), dorsal hands, upper chest, axillae, groin, elbows, knees, nipples, umbilicus, genitals, anus. Koebner phenomenon is common - lesions appear at sites of trauma.

Fig. - Segmental vitiligo (face/neck):

Segmental vitiligo showing depigmented patch around mouth and neck

Fig. - Generalized vitiligo (back):

Generalized vitiligo with widespread depigmented patches on the back and limbs

Signs of Active Disease

Confetti-like lesions
Hypomelanotic lesions with poorly defined borders
Trichrome pattern
Inflammatory (erythematous) border
Koebnerization

Associated Conditions

Vitiligo correlates with increased risk of other autoimmune diseases, especially:

Autoimmune thyroid disease (~15% of adults, ~5-15% of children with vitiligo)
Alopecia areata
Pernicious anemia
Type 1 diabetes mellitus
Addison's disease
Rheumatoid arthritis, lupus
Up to 20% of patients have at least one comorbid autoimmune disorder

Notable associated syndromes:

Vogt-Koyanagi-Harada (VKH) syndrome: uveitis + aseptic meningitis + otic involvement + vitiligo/poliosis
Alezzandrini syndrome: unilateral facial depigmentation + ipsilateral ocular changes
Halo nevi: depigmented halo around melanocytic nevi - associated with vitiligo

Paradoxically, vitiligo is associated with a decreased risk of melanoma and other skin cancers.

Diagnosis

Diagnosis is primarily clinical. Key tools:

Wood's lamp (UV-A light): Enhances contrast of depigmented lesions; particularly useful in fair-skinned patients - lesions fluoresce bright white
Skin biopsy: Absence of melanocytes on DOPA stain; sparse lymphocytic infiltrate at active edges
Lab workup for associated autoimmune diseases: TSH, anti-TPO antibodies, FBS, CBC, ANA

Disease Assessment Tools

Vitiligo Area Scoring Index (VASI)
Vitiligo European Task Force (VETF) score
Vitiligo Extent Score (VES)

Treatment

Repigmentation is possible only in areas with pigmented hair follicles (reservoir of melanocyte precursors). Lesions with leukotrichia respond poorly.

1. Topical Therapies

Agent	Notes
Topical corticosteroids	First-line for localized disease; moderate-to-potent class; risk of atrophy with prolonged use
Topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%)	Preferred for face and flexures; avoids atrophy; also used as maintenance (twice-weekly application)
Topical JAK inhibitors (ruxolitinib 1.5%)	Newer; FDA-approved for non-segmental vitiligo; targets JAK1/JAK2-IFN-γ pathway

2. Phototherapy

Narrowband UVB (NB-UVB): Most widely used phototherapy; 311-313 nm; effective for generalized disease; can combine with topical agents
PUVA (psoralen + UVA): Oral or topical psoralen + UVA exposure; effective but more side effects (nausea, phototoxicity, cataract risk with oral PUVA); used less now with NB-UVB available
Excimer laser (308 nm): Targeted NB-UVB; best for localized, resistant lesions

3. Systemic Therapies

Oral corticosteroids (mini-pulse): Weekly low-dose dexamethasone or betamethasone; used to halt rapid progression
Oral JAK inhibitors (ruxolitinib, baricitinib): Emerging; target CXCL9/10-CXCR3 and IFN-γ signaling; promising results in trials
Oral PUVA (less commonly used now)

4. Surgical Options (for stable, localized vitiligo)

Suction blister epidermal grafting - most widely used
Split-thickness skin grafting
Melanocyte-keratinocyte transplant procedure (MKTP)
Punch grafting

Surgical options require disease stability (no new lesions, no Koebner phenomenon) for at least 1-2 years.

5. Depigmentation

For extensive treatment-resistant vitiligo with minimal residual normal skin:

Monobenzyl ether of hydroquinone (MBEH) 20% applied 1-2x/day for 9-12 months
Requires lifelong strict photoprotection afterward
Can cause contact dermatitis; may depigment distant sites

6. Cosmetic

Camouflage cosmetics (cover-up makeup, self-tanning products)
Micropigmentation (tattooing): Especially useful for lips, nipples, distal fingers - areas with poor repigmentation response

Prognosis & Course

Course is unpredictable - may spread slowly, stabilize, or rarely progress rapidly
Segmental vitiligo: reaches full extent within 1-2 years then usually stabilizes
Generalized vitiligo: typically slow, chronic progression
Spontaneous partial repigmentation can occur (especially with sun exposure); complete spontaneous repigmentation is rare
After successful treatment, relapse rate ~40%

Mental Health Impact

Vitiligo carries significant psychosocial burden - social stigma, reduced self-esteem, anxiety, and depression are well-documented, particularly in darker-skinned individuals where contrast is more pronounced and in cultures with historical associations between depigmentation and leprosy. Psychological support is an integral part of management.

Sources: Fitzpatrick's Dermatology (9780071837781), Dermatology 2-Volume Set 5e (9780702082252), Andrews' Diseases of the Skin (9780323547536)

Recent evidence note (PMID 40192197): A 2025 systematic review on off-label topical ruxolitinib in dermatology confirms its growing use in vitiligo, supporting the JAK inhibitor class as an important emerging treatment option.

Auscultation in front and back amd which condn also the sounds

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Lung Auscultation: Front, Back & Clinical Correlations

Technique Basics

Use the diaphragm of the stethoscope for higher-pitched sounds (breath sounds, wheezes, crackles)
Use the bell for lower-pitched sounds (low-pitched rhonchi, cardiac sounds)
Apply directly to skin, not through clothing - full skin contact is required
Patient breathes through an open mouth with slow, deep breaths
Room must be quiet

Auscultation Areas: Anterior (Front)

Auscultate over the upper and mid-lung fields anteriorly:

Area	Lung Region Heard	Notes
Supraclavicular fossa (above clavicle)	Lung apex	Both sides
Infraclavicular area (below clavicle, 1st-2nd ICS)	Upper lobe	Both sides
2nd-4th ICS, mid-clavicular line	Upper + mid lobe (R), Upper lobe (L)
4th-5th ICS, anterior axillary line	Right middle lobe (R) / Lingula (L)	ONLY heard anteriorly

Key point: The right middle lobe and the lingula of the left lung can ONLY be auscultated anteriorly - they cannot be heard from the back.

Auscultation Areas: Posterior (Back)

The back provides access to the largest surface area of lung tissue (mostly lower lobes):

Area	Lung Region Heard	Notes
Suprascapular area (above spine of scapula)	Upper lobe apex
Interscapular area (T3-T7, between scapulae)	Upper and middle lobes	Best heard with arms crossed to move scapulae apart
Infrascapular area (below T7)	Lower lobes	Bilateral - most important zone posteriorly
Costovertebral angle / lung bases	Lower lobe bases	Often the earliest site for basal crackles (e.g., heart failure)

Compare left vs right at each level before moving down. Listen to at least 3 levels posteriorly (upper, mid, lower).

Systematic Sequence (Standard Approach)

Posterior (patient sitting or leaning forward):

Upper zones (between neck and spine of scapula)
Mid zones (interscapular)
Lower zones (below scapulae, down to bases)

Anterior (patient supine or sitting facing you):

Apices (supraclavicular)
Upper zones (infraclavicular)
Mid zones (right middle lobe / lingula)

Lateral (axillary lines - often forgotten):

Mid-axillary line at 4th-6th ICS
Important for detecting early pleural effusion and lower lobe pathology

Types of Breath Sounds

Normal Sounds

Sound	Characteristics	Normal Location
Vesicular (normal breath sounds)	Soft, low-pitched; inspiration louder and longer than expiration (3:1 ratio); no gap between I and E	Peripheral lung fields (all zones except trachea)
Bronchial (tracheal)	Loud, high-pitched, hollow; expiration = inspiration or louder; gap between I and E	Over trachea/manubrium only (normal there)
Bronchovesicular	Intermediate intensity and pitch; I:E roughly equal	1st and 2nd ICS anteriorly; between scapulae posteriorly

Adventitious (Abnormal) Sounds - ATS Classification

Sound	Characteristics	Mechanism	Clinical Condition
Fine crackles	Soft, high-pitched, short, discontinuous; mid-to-late inspiratory; like rubbing hair near the ear	Sudden opening of collapsed distal airways	Pulmonary fibrosis, early pulmonary edema, early pneumonia
Coarse crackles	Loud, low-pitched, longer, early inspiratory or expiratory; may clear with cough	Opening of secretion-laden distal airways	Bronchiectasis, COPD, pneumonia with secretions
Wheezes	Continuous (>250 ms), high-pitched (≥400 Hz), musical/hissing	Airway narrowing - oscillation of airway walls	Asthma, COPD (diffuse); endobronchial lesion (focal)
Rhonchi	Continuous (>250 ms), low-pitched (<200 Hz), snoring quality; may clear with cough	Secretions in large airways	COPD with secretions, chronic bronchitis
Stridor	Loud, high-pitched, mainly inspiratory; heard best over neck	Extrathoracic/upper airway obstruction	Croup, epiglottitis, anaphylaxis, foreign body - URGENT
Bronchial sounds in periphery	Abnormal when heard outside trachea/manubrium	Airless air spaces around a patent airway	Consolidation (pneumonia), atelectasis
Pleural friction rub	Creaking/grating, like leather rubbing; both inspiratory and expiratory; disappears when breath held	Inflamed pleural surfaces rubbing	Pleuritis, pulmonary infarction (PE), pleuropneumonia

Vocal Resonance Tests

Done during auscultation to differentiate consolidation vs. effusion:

Test	Method	Normal	Consolidation	Pleural Effusion
Bronchophony	Patient says "99"	Muffled	Loud and clear	Absent/muffled
Egophony	Patient says "E"	Sounds like "E"	Sounds like "A" (E-to-A change)	Absent (except at effusion upper border)
Whispered pectoriloquy	Patient whispers "1-2-3"	Faint/inaudible	Clearly heard	Absent

Clinical Correlations: Auscultation Findings by Disease

Disorder	Breath Sounds	Added Sounds	Other
Pneumonia (consolidation)	Bronchial breath sounds (periphery)	Crackles (fine/coarse)	Bronchophony, egophony, whispered pectoriloquy all increased; dullness on percussion
Pleural effusion (large)	Absent/decreased	None (or rub above effusion line)	Dullness; stony dullness; trachea shifted AWAY; decreased fremitus; egophony at upper border only
Pneumothorax	Absent on affected side	None	Hyperresonance; trachea shifted AWAY (tension PTX); absent fremitus
Bronchial asthma (acute)	Vesicular with prolonged expiration	Expiratory wheezes (may be pan-inspiratory/expiratory)	Hyperresonant; decreased expansion; decreased fremitus
COPD	Decreased/quiet breath sounds	Wheezes, rhonchi	Hyperinflation; pursed-lip breathing; barrel chest
Atelectasis	Absent/decreased	None	Dullness; trachea shifted TOWARD affected side; decreased fremitus
Pulmonary fibrosis (ILD)	Normal or reduced	Fine "Velcro" crackles (bilateral, basal, end-inspiratory)	Clubbing; restrictive spirometry
Pulmonary edema (CHF)	Decreased at bases	Bilateral basal fine crackles (initially), progressing upward	S3 gallop; JVD; orthopnea
Bronchiectasis	Coarse or bronchial	Coarse crackles, wheezes	Persistent; sputum production
Pulmonary embolism	Usually normal	Pleural rub (if infarction)	Tachycardia; may have minimal auscultatory findings
Foreign body (large airway)	Decreased unilaterally	Focal wheeze (unilateral, monophonic)	Stridor if upper airway
Lung collapse (lobar)	Absent over that lobe	None	Trachea shifted toward collapse

Quick Memory Summary

Bronchial sounds in periphery = consolidation or atelectasis (airless lung around open bronchus)
Fine crackles at bases = pulmonary edema or fibrosis
Coarse crackles clearing with cough = secretions (bronchiectasis, COPD)
Diffuse expiratory wheeze = asthma or COPD
Monophonic/unilateral wheeze = endobronchial obstruction
Absent breath sounds + hyperresonance = pneumothorax
Absent breath sounds + dull percussion = effusion or total atelectasis
Pleural rub = pleuritis/infarct
Stridor = upper airway emergency

Sources: Murray & Nadel's Textbook of Respiratory Medicine (9780323655873); Textbook of Family Medicine 9e (9780323239905); Goldman-Cecil Medicine (9780323930345)

Clot in brain

A "clot in the brain" can refer to two main conditions: an ischemic stroke (clot blocking a blood vessel, cutting off blood supply) or a cerebral venous sinus thrombosis (clot in the brain's draining veins). Let me pull comprehensive textbook content on both.

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ischemic stroke CT brain infarct

Diagnostic imaging series displaying nine axial Computed Tomography (CT) brain slices (labeled a-i) from patients with ischemic stroke. Each slice demonstrates the localization of an infarct through a comparison of human and automated segmentation. The brain tissue is presented in standard grayscale, showing normal anatomical structures such as the ventricles and cerebral hemispheres. Superimposed on these scans are two primary markers: solid white regions and black perimeter outlines. The solid white areas represent the output of a 3D Convolutional Neural Network (CNN) trained on CT angiography (CTA) and non-contrast CT (NCCT) features to identify ischemic lesions. The black perimeters delineate the 'ground truth' infarcted regions manually segmented by radiologists. Across the series, the images illustrate varying degrees of spatial overlap and discrepancy between the AI model and the human experts, highlighting clinical challenges in automated lesion quantification, particularly near the cortical surface and periventricular white matter. This comparison is used to evaluate the diagnostic accuracy, sensitivity, and specificity of deep learning algorithms in neuroradiology.

This Comparison Chart illustrates the side-by-side diagnostic evaluation of an ischemic stroke using a customized computer-aided assessment interface. The left panel shows an axial Non-Contrast Computed Tomography (NCCT) scan of the brain, demonstrating the characteristic hyperdense skull and low-contrast parenchyma where early subtle hypodensity might represent an acute infarct. The right panel displays a corresponding Magnetic Resonance Image (MRI), likely a Diffusion-Weighted Imaging (DWI) sequence, of the same patient. This MRI shows a distinct, localized hyperintense (bright) lesion in the left hemisphere adjacent to the lateral ventricle, which clearly delineates the area of acute cerebral infarction. The comparison highlights the higher sensitivity of MRI over CT in the hyperacute and acute phases of stroke. The interface includes navigational controls and analysis buttons ('RUN', 'Select Other DIR', 'SAVE'), indicating its use as a clinical decision support tool designed to assist radiologists in identifying and localizing stroke-affected regions.

This diagnostic comparison contains six axial non-contrast head CT (NCCT) scans demonstrating the utility of 'Stroke Windows' in identifying acute ischemic stroke markers. The top row (a, c, e) shows head CTs in standard brain windows (level 35 HU, width 100 HU), while the bottom row (b, d, f) displays the corresponding levels in narrow stroke windows (level 35 HU, width 30 HU). The narrow windowing enhances tissue contrast to highlight early infarct signs. Key pathological findings visualized include: 1) Left sulcal effacement of the insular ribbon and hypodensity of the left basal ganglia (images a and b); 2) A right hyperdense middle cerebral artery (MCA) sign, indicative of acute thrombosis (images c and d); and 3) Hypodensity of the left basal ganglia (images e and f). These comparisons illustrate how adjusting window width and level can improve the visibility of subtle gray-white matter differentiation loss and vascular signs, facilitating earlier detection of ischemic territory in neuroradiology.

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Clot in the Brain

"Clot in the brain" refers to two distinct clinical conditions depending on which vessels are affected:

Type	Vessel Involved	Effect
Ischemic Stroke	Arteries (blocked)	Brain tissue dies from lack of blood supply
Cerebral Venous Thrombosis (CVT)	Veins/venous sinuses (blocked)	Blood backs up, causing venous infarction + raised ICP

PART 1: ISCHEMIC STROKE (Arterial Clot)

Definition

Ischemic stroke is death of brain tissue due to occlusion of a cerebral artery, cutting off oxygen and glucose supply. ~600,000 first-ever strokes occur annually in the US alone.

Types / Mechanisms

1. Thrombotic (~33%)

Clot forms directly at an atherosclerotic plaque, usually at vessel bifurcations (especially the internal carotid artery)
Turbulent flow at bifurcations causes plaque ulceration → platelet adhesion → thrombus formation
When stenosis exceeds 90% of vessel diameter, flow is critically reduced

2. Lacunar / Small-vessel (~20%)

Involve small terminal vessels; infarcts 2-20 mm in size
Affect: basal ganglia, thalamus, pons, internal capsule
Mechanism: lipohyalinosis (from hypertension) or microemboli
~80-90% of lacunar stroke patients have hypertension

3. Cardioembolic (~25%)

Clot travels from heart to brain
Atrial fibrillation is the most common cause (5x increased stroke risk)
Also: mural thrombus from MI, valvular disease, patent foramen ovale

4. Artery-to-Artery Embolism

Clot breaks off a proximal arterial plaque (e.g., carotid bifurcation) and travels distally
Classic example: amaurosis fugax (carotid plaque embolizes to ophthalmic artery → transient monocular blindness)

5. Other/Cryptogenic (~33%)

Arterial dissection (leading cause in young; carotid or vertebral; follows trauma, sneezing)
Hypercoagulable states: antiphospholipid antibodies, protein C/S deficiency, sickle cell, polycythemia
Oral contraceptives, pregnancy
Vasospasm: cocaine, amphetamines, migraine
Vasculitis, infections (varicella, fungal meningitis)

Risk Factors

Modifiable	Non-modifiable
Hypertension	Age
Atrial fibrillation	Male sex
Diabetes	Race (Black, Hispanic > White)
Smoking	Family history
Dyslipidemia	Prior stroke/TIA
Obesity, sedentary lifestyle
Carotid stenosis

Clinical Features - FAST + MORE

FAST mnemonic:

Face drooping (unilateral)
Arm weakness (unilateral)
Speech difficulty (dysarthria or aphasia)
Time to call emergency services

Additional features by territory:

Territory	Artery	Symptoms
Middle cerebral artery (MCA)	MCA	Contralateral hemiplegia (face + arm > leg), hemisensory loss, homonymous hemianopia, aphasia (dominant), neglect (non-dominant)
Anterior cerebral artery (ACA)	ACA	Contralateral leg weakness > arm, personality change, urinary incontinence
Posterior circulation	Vertebrobasilar	Diplopia, dysphagia, vertigo, ataxia, crossed deficits (face ipsilateral, body contralateral), coma
Lacunar	Lenticulostriate	Pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis, dysarthria-clumsy hand syndrome

Imaging

CT (non-contrast) - FIRST done:

Normal in first 6 hours (early ischemia may be invisible)
Early signs: loss of grey-white differentiation, hyperdense MCA sign (clot visible as white in vessel), sulcal effacement
Later: hypodense (dark) area in infarcted territory

CT with stroke windows enhances visibility of early infarct signs - narrowing the window width (30 HU instead of 100 HU) dramatically improves contrast, showing:

Hyperdense MCA sign = acute thrombosis in the MCA
Basal ganglia hypodensity = early infarct

MRI DWI (gold standard for acute stroke):

Bright (hyperintense) lesion visible within minutes of infarct
Far more sensitive than CT in hyperacute phase

CT brain showing hyperdense MCA sign (acute thrombosis) and early infarct signs with stroke windowing

CT brain with stroke windows: (c,d) hyperdense right MCA sign indicating acute thrombosis; (a,b) left insular ribbon loss and basal ganglia hypodensity; (e,f) early basal ganglia infarct

Management - Time is Brain!

NINDS Stroke Time Targets:

Step	Target
Door to doctor	10 min
Door to CT completion	25 min
Door to CT reading	45 min
Door to treatment (tPA)	60 min

Acute Treatment

1. IV Thrombolysis - tPA (Alteplase)

Indicated within 4.5 hours of symptom onset (or last known well)
Contraindications: hemorrhage on CT, recent surgery, anticoagulation, BP >185/110 (must treat first), blood glucose <50 or >400
Dose: 0.9 mg/kg (max 90 mg); 10% as bolus, rest over 60 min

2. Mechanical Thrombectomy

For large vessel occlusion (ICA, MCA M1 segment)
Window: up to 24 hours in selected patients (if salvageable penumbra on imaging)
Superior to tPA alone for proximal occlusions

3. Blood Pressure Management

Do NOT aggressively lower BP in acute ischemic stroke (collateral perfusion depends on it)
Only lower if BP >220/120 (or >185/110 before tPA)

4. Supportive

Oxygen only if SpO2 <95% (avoid hyperoxia)
Avoid dextrose solutions (hyperglycemia worsens infarct)
Withhold oral intake until swallowing assessed (aspiration risk)
Treat fever aggressively (even mild hyperthermia worsens outcome)

Secondary Prevention

Mechanism	Drug
Cardioembolic (AF)	Anticoagulation (DOAC or warfarin)
Non-cardioembolic	Antiplatelet (aspirin ± clopidogrel, or ticagrelor)
Atherosclerosis	Statin (high-intensity), antihypertensive
Carotid stenosis >70%	Carotid endarterectomy or stenting

PART 2: CEREBRAL VENOUS THROMBOSIS (CVT)

What It Is

CVT is clot formation in the draining veins and dural venous sinuses of the brain. It is rarer (0.5-1% of all strokes) but treacherous - easily missed and potentially fatal if untreated.

Sites Involved (Most to Least Common)

Superior sagittal sinus (most common)
Transverse sinus
Sigmoid sinus
Cavernous sinus (usually septic - from facial/orbital infection)
Deep cerebral veins (internal cerebral veins, vein of Galen)
Cortical veins

Causes / Risk Factors

Septic CVT:

Facial/orbital infection → cavernous sinus thrombosis
Otitis media/mastoiditis → lateral sinus thrombosis

Aseptic CVT:

Oral contraceptive pill (most common in young women)
Pregnancy and puerperium
Thrombophilia (factor V Leiden, protein C/S deficiency, antiphospholipid syndrome)
Dehydration
Malignancy
Behcet's disease, vasculitis
Head trauma
~15-20% idiopathic

Clinical Features

Headache (most common; gradual or thunderclap onset) - can be the only symptom early
Seizures (focal or generalized)
Focal neurological deficits (hemiparesis, aphasia) - often fluctuating and bilateral
Papilledema (raised ICP)
Altered consciousness / coma (severe cases)
Cavernous sinus thrombosis specifically: proptosis, chemosis, painful ophthalmoplegia, fever

Key distinction from arterial stroke: CVT symptoms are often subacute (days to weeks), bilateral, and may have seizures + headache + raised ICP together.

Imaging

CT (non-contrast):

Hyperdense (white) sinus/vein = acute thrombus
"Cord sign" = hyperdense cortical vein
Low-density parenchymal swelling

CT Venography / Post-contrast CT:

"Empty delta sign" = hypodense clot within an enhancing superior sagittal sinus (triangular shape)

MRI + MR Venography (gold standard):

Loss of normal flow void in sinus
T1 and T2 hyperintensity in thrombosed vessel
SWI: "blooming" hypointensity of thrombosed vein; prominent serpiginous draining veins (venous congestion)
MR Venography: loss of flow signal in affected sinus

Parenchymal changes (venous infarct):

Often hemorrhagic (venous infarcts bleed)
Bilateral, parasagittal distribution (SSS thrombosis)
Crosses arterial territories (unlike arterial strokes)

Treatment

Anticoagulation - first line:
- IV heparin or subcutaneous LMWH → followed by warfarin
- Indicated even in the presence of hemorrhagic infarction (unique - unlike arterial stroke)
- DOACs: emerging evidence, not yet definitively superior to warfarin
Reduce ICP: acetazolamide, repeated LP (for isolated intracranial hypertension), head elevation
Antiepileptics: if seizures occur
Antibiotics: if septic etiology
Thrombectomy / local thrombolysis: for patients deteriorating despite anticoagulation
Decompressive surgery: in severe cases with herniation risk
Thrombophilia screening in all patients

Key Comparison: Arterial vs Venous Stroke

Feature	Ischemic Stroke (Arterial)	CVT (Venous)
Onset	Sudden (seconds-minutes)	Subacute (days-weeks)
Headache	Less common	Very common, often prominent
Seizures	Less common	Common
Distribution	Arterial territory	Crosses arterial territories; bilateral
Hemorrhage	Less common	Frequently hemorrhagic
CT finding	Hypodense infarct; hyperdense artery	Hyperdense sinus; empty delta sign
Treatment	tPA, thrombectomy, antiplatelets	Anticoagulation (even with bleed!)
Common cause	AF, atherosclerosis	OCP, thrombophilia, pregnancy

Sources: Rosen's Emergency Medicine (9780323757898); Bradley and Daroff's Neurology in Clinical Practice (9780323642613); Grainger & Allison's Diagnostic Radiology (9780323760751)

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