16 yr old female with (?) iih points to be asked in history and negative history

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IIH idiopathic intracranial hypertension history taking clinical points adolescent female

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History Taking in a 16-Year-Old Female with Suspected IIH

IIH (Idiopathic Intracranial Hypertension / Pseudotumor Cerebri) in a post-pubertal adolescent female closely mirrors the adult pattern - obese female of childbearing age with raised ICP and no structural cause. A thorough history is central to both diagnosis and ruling out secondary causes.

PRESENTING COMPLAINTS - Points to Elicit

1. Headache (Most Common Symptom - 84%)

  • Onset, duration, frequency - constant/daily/intermittent?
  • Character - typically diffuse, often retro-orbital; can be migraine-like (52%) or tension-type (22%)
  • Severity - progressive worsening?
  • Aggravating factors - Valsalva (coughing, sneezing, straining), positional change (bending forward), Valsalva-induced worsening suggests raised ICP
  • Relieving factors
  • Morning headache - worsening on waking (raised ICP)
  • Associated nausea/vomiting
  • Whether it wakes from sleep

2. Visual Symptoms (directly from papilledema/raised ICP)

  • Transient visual obscurations (TVOs) - 68%: brief dimming/"graying out" lasting up to 30 seconds, precipitated by standing up, bending over, bright light, or eye movement
  • Diplopia / double vision - horizontal diplopia (18%) from 6th nerve palsy (false localizing sign)
  • Blurred vision or decreased visual acuity - 32%
  • Progressive peripheral visual field loss - typically starts nasal inferior quadrant
  • Photophobia - 48%

3. Pulsatile Tinnitus (52%)

  • "Whooshing" or pulse-synchronous sound in ears
  • This is a highly specific symptom for raised ICP - ask specifically

4. Other Symptoms

  • Dizziness - 51%
  • Neck/back pain - 42-53%
  • Radicular pain - 19%
  • Cognitive difficulties / poor school performance - particularly noted in adolescent IIH
  • Irritability

HISTORY OF PRESENT ILLNESS - Systematic Questions

Weight History (Most Important Risk Factor in Adolescents)

  • Current weight and height (calculate BMI)
  • Recent weight gain - rapid weight gain is strongly associated; ask for timeline
  • Prior body weight, any recent change

Menstrual History (Critical in Female)

  • Menarche - age of onset (post-pubertal adolescent IIH resembles adult pattern)
  • Menstrual regularity - irregular cycles can suggest hormonal issues
  • Polycystic ovary syndrome (PCOS) - associated with obesity and IIH
  • Recent hormonal changes

Drug/Medication History (Extremely Important - Secondary Causes)

Ask specifically about ALL of the following:
DrugRelevance
Tetracyclines (doxycycline, minocycline)Common in acne treatment - strongly associated with IIH
Vitamin A / Retinoids (isotretinoin/Roaccutane)Very common in adolescents for acne - major cause
Oral contraceptive pills (OCPs)Hormonal association
CorticosteroidsEspecially withdrawal after prolonged use
Growth hormoneUsed in short stature/GH deficiency
Thyroid hormone replacementExcess LT4 can cause IIH in children
LithiumPsychiatric medications
Nalidixic acidAntibiotics
Iron supplements (excess)In high doses
Anabolic steroids
In a 16-year-old female, isotretinoin and doxycycline for acne are the single most common drug-related triggers to ask about.

Dietary History

  • Excessive Vitamin A intake - supplements, liver consumption
  • Diet and eating habits
  • Weight-gain history

PAST MEDICAL HISTORY

  • Prior episodes of similar headache or raised ICP
  • Thyroid disease - hypothyroidism is associated
  • Renal disease - hypertension
  • Obstructive sleep apnea - associated with IIH
  • Addison's disease (steroid withdrawal)
  • SLE or other autoimmune conditions - can cause raised ICP
  • Anemia - particularly iron deficiency
  • Hypercoagulable states - relevant to rule out cerebral venous sinus thrombosis (CVST)
  • Any known intracranial pathology, head trauma, infection

Surgical/Procedure History

  • Any prior lumbar punctures
  • Any prior eye surgeries or optic nerve issues

FAMILY HISTORY

  • Migraine (common differential)
  • Intracranial tumors
  • Hypercoagulable disorders (DVT, CVST in young relatives)

SOCIAL HISTORY

  • Diet (high vitamin A? High calorie?)
  • Physical activity
  • Smoking, alcohol
  • Any recreational drug use
  • Stress, sleep quality (OSA symptoms - snoring, daytime somnolence)

NEGATIVE HISTORY (Important to Specifically Ask and Document as Absent)

These help fulfill the diagnostic criteria and rule out secondary causes:

Symptoms to Rule Out Other Diagnoses

SymptomRules Out
No fever, meningism (neck stiffness, photophobia, phonophobia in context of fever)Meningitis / encephalitis
No focal neurological deficits (limb weakness, sensory loss, ataxia)Intracranial mass, stroke
No seizuresStructural lesion, CNS infection
No altered consciousness, confusionMass lesion, metabolic cause
No thunderclap headacheSAH (subarachnoid hemorrhage)
No progressive ascending weaknessGBS (raised CSF protein can occasionally raise ICP)
No history of head traumaPost-traumatic CSF issues
No orthostatic component (worse lying, better standing)Low pressure headache / CSF leak

Risk Factor Negatives

Negative HistorySignificance
No use of tetracyclines / isotretinoin / vitamin A supplementsExcludes drug-induced
No corticosteroid use or recent withdrawalExcludes steroid-related
No OCP useReduces hormonal cause
No family history of thrombosisReduces CVST risk
No recent viral illness, vaccinationsCan precede IIH in children
Not pregnantCVST, eclampsia, IIH of pregnancy
No symptoms of hypothyroidism (cold intolerance, weight gain, constipation)Hypothyroidism-associated IIH
No symptoms of adrenal insufficiencySteroid withdrawal
No history of anemia symptomsIron deficiency anemia-related IIH

DIAGNOSTIC CRITERIA REMINDER (Modified Dandy / Friedman 2013)

For context when structuring history:
  • A. Papilledema present
  • B. Normal neurological exam (except 6th nerve palsy allowed)
  • C. Neuroimaging: normal parenchyma, venous thrombosis excluded
  • D. Normal CSF constituents
  • E. LP opening pressure > 25 cm H2O
History should systematically address each of these criteria and provide evidence against all secondary causes.

Summary Table for Quick Reference

DomainKey Points to Ask
HeadacheCharacter, timing, Valsalva aggravation, morning worsening
VisionTVOs, diplopia, blurred vision, visual field loss
Pulsatile tinnitusPulse-synchronous whooshing
Drug historyIsotretinoin, doxycycline, Vit A supplements, OCP, steroids, GH
WeightBMI, recent rapid weight gain
MenstrualMenarche, regularity, PCOS
Negative historyNo fever, no focal deficits, no seizures, no trauma, no thrombosis risk
Exclude CVSTNo prior DVT, hypercoagulable history, combined OCP

Sources: Bradley and Daroff's Neurology in Clinical Practice; Cummings Otolaryngology; Medscape IIH Clinical Presentation; MDPI Pediatric IIH Obesity Review 2025; Springer Pediatric IIH study

Decrease vision with blurring of vision history for neurology

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decreased vision blurred vision history taking neurology approach localization visual pathway

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https://pmc.ncbi.nlm.nih.gov/articles/PMC10564074

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History Taking: Decreased Vision / Blurring of Vision (Neurology)

The single most important first step in any neurological history for visual loss is localization along the visual pathway - this determines the entire differential diagnosis. History is the primary tool for localization.

STEP 1 - THE MASTER QUESTION: Monocular or Binocular?

Ask the patient: "Have you checked by covering each eye separately?" This is non-trivial - patients often misidentify binocular hemianopia as monocular loss.
MonocularBinocular
Localizes toIpsilateral eye or optic nerve (pre-chiasmal)Chiasm or retrochiasmal
ExamplesOptic neuritis, NAION, retinal artery occlusionBitemporal hemianopia (chiasm), homonymous hemianopia (optic tract/radiation/cortex)

STEP 2 - ONSET AND TIME COURSE (Most Critical Localizing Feature)

A. Sudden onset (seconds to minutes) - Vascular

  • Transient + monocular (amaurosis fugax): embolic, carotid artery disease - "curtain descending over the eye," lasts minutes, altitudinal
  • Retinal migraine: transient monocular loss with headache, vasospastic
  • TVO (Transient Visual Obscurations): seconds-long, postural (standing up), from raised ICP / papilledema
  • Sudden persistent monocular: CRAO (central retinal artery occlusion), AION - maximal at onset, minimal recovery

B. Subacute onset (hours to days) - Inflammatory / Demyelinating

  • Optic neuritis - worsens over hours to a few days, then improves
  • Hours-to-days onset with painful eye movements = optic neuritis until proven otherwise

C. Slowly progressive (weeks to months) - Compressive / Infiltrative

  • Pituitary tumor (bitemporal), meningioma, glioma
  • Toxic/nutritional optic neuropathy
  • Hereditary optic neuropathies (Leber's - subacute but typically young male)

D. Stepwise / Stuttering - Vascular

  • MS relapses, vascular TIA

STEP 3 - DETAILED CHARACTERIZATION OF VISION LOSS

Nature of loss - ask specifically:

  • Decreased acuity - can't read / see far? (central field affected)
  • Field loss - "missing piece of vision" - which quadrant/side?
  • Color vision affected? - red desaturation (optic nerve sign; "does red look washed out or faded compared to other eye?")
  • Contrast sensitivity - things look "washed out" or dim despite normal acuity (optic neuritis)
  • Positive symptoms - flashing lights (photopsia - migraine, retinal detachment), floaters, zigzag (scintillating scotoma of migraine aura)
  • Negative symptoms - simply missing area of vision (ischemia, optic nerve)

Pattern of field loss - key localizing clues:

Field DefectLocalization
Central scotomaOptic nerve (optic neuritis, NAION, toxic)
Altitudinal (superior or inferior half)Optic nerve (NAION - inferior altitudinal loss)
Bitemporal hemianopiaOptic chiasm (pituitary lesion)
Homonymous hemianopiaOptic tract / LGN / optic radiation / cortex (ipsilateral side to defect)
Congruous homonymousMore posterior (occipital cortex)
Incongruous homonymousMore anterior (optic tract)
Quadrantanopia (pie in sky)Temporal lobe (Meyer's loop)
Quadrantanopia (pie on floor)Parietal lobe

STEP 4 - ASSOCIATED SYMPTOMS (Localizing + Etiological)

Pain with vision loss - key discriminator:

PainNo Pain
Optic neuritisYes - eye pain on movement (90%), precedes loss by hours
NAIONNoYes
Retinal artery occlusionNoYes
Arteritic AION (GCA)Jaw claudication, scalp tenderness, temporal headache
Uveitis / scleritisDeep aching pain
Angle closure glaucomaSevere periocular pain + halos, nausea

Headache - ask character, onset, location:

  • ICP-related: morning headache, positional, with nausea/vomiting + TVOs = papilledema/IIH
  • Thunderclap = SAH (acute visual loss from SAH)
  • GCA: temporal headache + jaw claudication + > 50 years

Diplopia (double vision):

  • Horizontal diplopia = 6th nerve palsy (false localizing sign of raised ICP, or brainstem)
  • Vertical diplopia = 4th nerve palsy
  • Variable diplopia - worse at end of day / after sustained gaze = Myasthenia Gravis

Other neurological symptoms:

  • Limb weakness/sensory loss, ataxia, dysarthria, dysphagia - MS, stroke, brainstem lesion
  • Facial numbness, hemibody sensory loss - optic tract to cortex lesion
  • Uhthoff's phenomenon - vision worsens with heat or exercise → highly specific for demyelinating disease (optic neuritis / MS)
  • Seizures - cortical lesion (posterior cortex - visual cortex involvement)
  • Cognitive decline, personality change - diffuse cortical disease

STEP 5 - PAST HISTORY (Etiological Clues)

HistorySuggests
Prior episode in same or other eye with recoveryMS / optic neuritis recurrence
Known MSOptic neuritis relapse
Hypertension, diabetes, hyperlipidemia, smoking, AF, carotid diseaseVascular (NAION, CRAO, stroke)
Autoimmune disease (SLE, Sjögren, sarcoidosis)Optic neuropathy from systemic disease
Raised ICP features (prior headache, papilledema)IIH, mass lesion
Pituitary/brain tumor historyCompressive visual loss
Thyroid disease (Graves')Dysthyroid orbitopathy
Amblyopia ("lazy eye"), ocular traumaNon-neurological cause
Family history of visual loss, premature deathsLeber's hereditary optic neuropathy (LHON), glaucoma
Diabetes insipidus, polyuriaNeurosarcoidosis, craniopharyngioma

STEP 6 - DRUG AND TOXIC HISTORY

Toxic optic neuropathy = bilateral, painless, slowly progressive, central/cecocentral scotoma, red desaturation
  • Ethambutol - TB treatment, dose-dependent bilateral optic neuropathy
  • Methanol - ingestion, rapid severe bilateral visual loss
  • Hydroxychloroquine - macular toxicity (bull's eye maculopathy)
  • Tobacco / alcohol - nutritional/tobacco amblyopia
  • Amiodarone - bilateral optic neuropathy
  • Vigabatrin - bilateral visual field constriction
  • Sildenafil - NAION risk
  • Vitamin B12 deficiency - nutritional optic neuropathy
  • Isotretinoin, tetracyclines - IIH/raised ICP

STEP 7 - SYSTEMIC/CONSTITUTIONAL HISTORY

SymptomSuggests
Weight loss, fatigue, night sweatsMalignancy (infiltrative optic neuropathy), lymphoma
Jaw claudication, scalp tenderness, temporal artery tenderness, fatigue, polymyalgiaGCA (arteritic ISCHEMIC optic neuropathy) - emergency
Fever, rash, lymphadenopathySarcoidosis, Lyme, viral
Oral/genital ulcersBehcet's disease
Skin rash (butterfly rash, photosensitivity)SLE
Dry eyes/mouthSjögren's
Symptoms of raised ICP: headache, vomiting, diplopia, TVOsPapilledema from any cause
Obesity, recent weight gainIIH
PregnancyIIH, CVST, eclampsia

STEP 8 - NEGATIVE HISTORY (Important to Elicit and Document)

NegativeSignificance
No pain on eye movementAgainst optic neuritis
No improvement after first episodeAgainst typical optic neuritis
No Uhthoff's phenomenonAgainst demyelination
No jaw claudication, scalp tenderness, fever, raised ESRAgainst GCA
No prior episodesAgainst MS relapse
No drug exposure (ethambutol etc.)Against toxic optic neuropathy
No fever/meningismAgainst infective/inflammatory meningitis
No limb weakness/sensory symptomsAgainst posterior stroke if isolated visual loss
No traumaAgainst traumatic optic neuropathy
No family history of visual loss in young menAgainst LHON

Quick Reference - Key Differential Clues by Pattern

ConditionEyeOnsetPainRecoveryKey Feature
Optic neuritisMonocularDaysYes (on movement)Yes (weeks)Uhthoff, young woman, MS risk
NAIONMonocularSuddenNoMinimalVascular risk, altitudinal loss, crowded disc
Arteritic AION (GCA)MonocularSuddenYes (headache, jaw)Minimal>50 yr, raised ESR, emergency
CRAOMonocularSuddenNoMinimalEmbolic, AF, carotid disease
Amaurosis fugaxMonocularTransient (mins)NoFullCurtain, carotid stenosis
Retinal migraineMonocularTransientHeadacheFullVasospasm, migraine history
TVOs (papilledema)BilateralSeconds, posturalHeadacheFullIIH, seconds-brief, Valsalva
Pituitary tumorBitemporal fieldWeeks-monthsHeadacheVariableBitemporal hemianopia, endocrine sx
Occipital strokeHomonymousSuddenHeadacheVariableVascular risk, macular sparing
Toxic optic neuropathyBilateralWeeksNoVariableDrug/nutritional history
Uhthoff MSMonocularWith heat/exerciseNoYesDemyelination

Sources: Bradley and Daroff's Neurology in Clinical Practice; Continuum: Diagnostic Approach to Vision Loss (PMC10564074); Stroke Manual; Wills Eye Manual

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Decrease vision with blurring of vision history for neurology

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Here is a complete, ready-to-use History-Taking Proforma for Decreased Vision / Blurring of Vision from a neurology perspective:

HISTORY-TAKING PROFORMA

Chief Complaint: Decreased Vision / Blurring of Vision


1. PATIENT IDENTIFICATION

  • Name | Age | Sex | Occupation | Handedness
  • Referred by: self / ophthalmologist / GP / neurologist

2. PRESENTING COMPLAINT

"Decreased vision / blurring of vision since ___"

3. HISTORY OF PRESENTING COMPLAINT

A. LATERALITY - (First and Most Important Question)

  • Right eye only
  • Left eye only
  • Both eyes
  • "Did you check by covering each eye separately?"
Monocular = pre-chiasmal (eye or optic nerve) Binocular = chiasmal or retrochiasmal

B. ONSET

  • Sudden (seconds) - vascular: embolism, ischemia
  • Subacute (hours to days) - inflammatory: optic neuritis
  • Gradual (weeks to months) - compressive, toxic, hereditary
  • Episodic / Recurrent - MS, migraine, IIH (TVOs)
  • Exact date and time of onset: ___

C. DURATION & COURSE

  • Duration since onset: ___
  • Transient - lasted ___ minutes/hours, fully recovered
  • Persistent - still present
  • Progressive - worsening over time
  • Improving - spontaneous recovery (optic neuritis)
  • Stepwise / Fluctuating - vascular / MS relapse
  • Stable / Nonprogressive

D. NATURE OF VISION LOSS

(Ask each one specifically)
FeaturePresentAbsentDetails
Reduced visual acuity (near / far)
Blurring of vision
Visual field loss - missing areaWhich side/quadrant?
Central scotoma - central black spot
Altitudinal loss - upper/lower half
Peripheral field loss - tunnel vision
Color vision affected - red looks faded
Contrast sensitivity reduced - washed out
Diplopia - double visionHorizontal / vertical?
Positive symptoms - flashes, zigzags
Floaters
Halos around lights
Night blindness

E. ASSOCIATED PAIN

  • Pain on eye movement - cardinal sign of optic neuritis (present in ~90%)
    • Duration of pain: ___
    • Precedes vision loss? Y / N
    • Resolved within 7 days? Y / N (>7 days argues against ON)
  • Periocular / orbital aching pain - scleritis, uveitis
  • Temporal headache + jaw claudication + scalp tenderness - GCA / arteritic AION (EMERGENCY)
  • Severe periocular pain + nausea + halos - acute angle closure glaucoma
  • Headache - morning, postural, nausea/vomiting - raised ICP / papilledema
  • No pain whatsoever - NAION, CRAO, toxic optic neuropathy

F. TEMPORAL PROFILE - KEY DIFFERENTIATOR

TimingDiagnosis to Consider
Transient - seconds, postural (standing/bending)TVOs from papilledema / IIH
Transient - minutes, altitudinal, "curtain"Amaurosis fugax - embolic
Transient - with migraine headacheRetinal migraine / visual aura
Transient - with exercise or heat, recoversUhthoff's phenomenon - MS/demyelination
Subacute - days, pain on movement, recoversOptic neuritis
Sudden - maximal at onset, no pain, no recoveryNAION, CRAO
Gradual - weeks, bitemporal field lossChiasmal compression - pituitary tumor
Gradual - bilateral, cecocentral scotomaToxic / nutritional optic neuropathy

G. AGGRAVATING / RELIEVING FACTORS

  • Worse with heat / hot shower / exercise - Uhthoff's (MS)
  • Worse on standing / bending - TVOs (IIH)
  • Worse with eye movements - optic neuritis
  • Worse at end of day - myasthenia gravis (ptosis/diplopia)
  • Relieved by rest - MG
  • Postural component (worse lying flat) - raised ICP
  • Any specific triggers: bright light, exercise, meals, medications

H. SIMILAR EPISODES IN THE PAST

  • Previous episode in the same eye - recovered? MS / ON recurrence
  • Previous episode in the other eye - recovered? MS
  • Prior TIAs (transient weakness, speech disturbance) - vascular
  • Documented prior optic neuritis or MS diagnosis

4. ASSOCIATED NEUROLOGICAL SYMPTOMS

(Helps localize lesion beyond optic nerve)
SymptomPresentAbsentDetails
Limb weakness - focalWhich limb(s)?
Sensory loss / tingling / numbnessWhich distribution?
Facial numbness
Ataxia / balance problems / incoordination
Dysarthria / slurred speech
Dysphagia
Vertigo
Bladder/bowel dysfunctionUrgency, retention
Fatigue (disproportionate)MS hallmark
Cognitive disturbance / memory
Seizures
Hearing loss / tinnitusPulsatile?
Diplopia / squintNew or old?
PtosisUnilateral / bilateral

5. ASSOCIATED SYSTEMIC SYMPTOMS

SymptomPresentAbsentSuggests
Headache - character / timingICP, GCA, migraine
Nausea / vomitingRaised ICP
Jaw claudicationGCA - EMERGENCY
Scalp tenderness (combing hair)GCA
Fever / chillsInfective/inflammatory
Weight loss / night sweatsMalignancy, sarcoid
Dry eyes / dry mouthSjögren's
Oral/genital ulcersBehcet's disease
Skin rash (butterfly, photosensitivity)SLE
Joint pains / swellingAutoimmune
Polyuria / polydipsiaSarcoidosis, craniopharyngioma
Menstrual irregularity / galactorrhoeaPituitary lesion
Recent viral illness / vaccinationPost-viral optic neuritis
Obesity / recent weight gainIIH
Pulsatile tinnitusIIH / raised ICP

6. PAST MEDICAL HISTORY

  • Multiple sclerosis / demyelinating disease
  • Diabetes mellitus - type: ___, duration: ___, control: ___
  • Hypertension
  • Hyperlipidaemia
  • Atrial fibrillation / cardiac disease
  • Carotid artery disease / prior stroke / TIA
  • Autoimmune disease: SLE / Sjögren / sarcoidosis / Behcet's / vasculitis
  • Pituitary / brain tumor - prior surgery / radiation
  • Thyroid disease - hypo / hyper / Graves' orbitopathy
  • Raised ICP / IIH - prior episode
  • Glaucoma / other eye disease
  • Amblyopia ("lazy eye") in childhood
  • Migraine - with or without aura
  • Obstructive sleep apnea
  • HIV / immunocompromised state
  • TB (ethambutol use)
  • Renal / hepatic disease

7. DRUG HISTORY

(Toxic optic neuropathy - bilateral, painless, progressive, central scotoma)
DrugClassOcular Effect
EthambutolAnti-TBOptic neuropathy - dose/duration dependent
Isoniazid (INH)Anti-TBOptic neuropathy (B6 depletion)
HydroxychloroquineAntimalarial / rheumatologyMacular toxicity - bull's eye
AmiodaroneAntiarrhythmicBilateral optic neuropathy
VigabatrinAntiepilepticBilateral peripheral field constriction
Sildenafil / PDE5 inhibitorsNAION risk
Isotretinoin / tetracyclinesAcneIIH / raised ICP
Oral contraceptive pillIIH / thrombosis (CVST)
Steroids (prolonged / withdrawal)IIH, glaucoma
Methanol ingestionToxicSevere bilateral loss, emergency
Quinine / chloroquineMacular / retinal toxicity
Digoxin (toxicity)Yellow/green tinge, halos
  • Nutritional history - tobacco / alcohol ("tobacco-alcohol amblyopia")
  • Vitamin B12 / folate deficiency
  • Dietary history - malnutrition, vitamin A excess

8. FAMILY HISTORY

  • Visual loss in young male relatives - Leber's Hereditary Optic Neuropathy (LHON) - mitochondrial, males in their 20s-30s
  • Glaucoma - family history
  • MS in first-degree relatives
  • Migraine
  • Premature cardiovascular disease / stroke

9. PERSONAL AND SOCIAL HISTORY

  • Smoking - pack years
  • Alcohol - units/week (nutritional amblyopia, Wernicke's)
  • Occupation (chemical / solvent exposure, methanol risk)
  • Travel history (Lyme disease, tropical infections)
  • Sexual history (syphilis - tabes dorsalis, Argyll Robertson pupil)
  • IV drug use (HIV, infective endocarditis - embolic)
  • Pregnancy / recent postpartum (IIH, CVST, eclampsia)
  • BMI / obesity (IIH)

10. NEGATIVE HISTORY - MUST DOCUMENT

Negative PointRules Against
No pain on eye movementOptic neuritis
No Uhthoff's phenomenonMS / demyelination
No prior episode with recoveryMS relapse
No jaw claudication / scalp tendernessGCA (arteritic AION)
No fever / meningismInfective optic neuritis / meningitis
No drug exposure (ethambutol, etc.)Toxic optic neuropathy
No limb weakness / sensory symptomsStroke / posterior fossa lesion
No headache / raised ICP featuresIIH / papilledema
No traumaTraumatic optic neuropathy
No family history of visual loss (young males)LHON
No pituitary symptomsCompressive chiasmal lesion
No autoimmune symptomsNMO, SLE-optic neuropathy

11. SUMMARY - LOCALIZATION CHECKLIST

After taking history, complete this:
FeatureFindingLocalizes to
Monocular / Binocular
Transient / Persistent
Pain on eye movement?
Uhthoff?
Field pattern
Color vision affected?
Associated neuro symptoms?
Vascular risk factors?
Drug / toxic exposure?
Provisional Localization: ☐ Pre-chiasmal ☐ Chiasmal ☐ Retrochiasmal
Top Differential Diagnoses:




Based on: Bradley and Daroff's Neurology in Clinical Practice; Continuum: Diagnostic Approach to Vision Loss; Wills Eye Manual; Stroke Manual Visual Loss Guidelines
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