neuro ophthalmology NEET PG 2024 2025 previous year questions high yield topics

ls /home/daytona/workspace/ 2>/dev/null || mkdir -p /home/daytona/workspace/neur…

mkdir -p /home/daytona/workspace/neuro-ophtho-flashcards

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// ── CONTENT ───────────────────────────────────────────────────────────────────

addCoverSlide();

// ═══════════════════════════════════════════════════════════════════════
// SECTION 1 – VISUAL FIELD DEFECTS
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 1", "Visual Field Defects & Pathway Lesions", "1A237E", "0D1B2A");

addQ(1,"Visual Fields",
  "A patient has complete blindness in the LEFT eye with normal vision in the right eye. Where is the lesion?",
  "Pre-chiasmal = monocular loss");
addA(1,"Visual Fields",
  "Lesion: LEFT optic nerve (or retina)\n\nPre-chiasmal lesions cause monocular visual loss.\n• Optic nerve lesions are anterior to the chiasm\n• Examples: optic neuritis, AION, optic nerve compression\n• RAPD will be present in the affected eye",
  "Monocular blindness = ipsilateral optic nerve or retina");

addQ(2,"Visual Fields",
  "What visual field defect is produced by a lesion at the centre of the optic chiasm?",
  "Chiasm = ONLY cause of bitemporal defect");
addA(2,"Visual Fields",
  "Bitemporal Hemianopia\n\n• The chiasm carries NASAL fibres from BOTH eyes (they cross)\n• Central chiasm lesion knocks out both sets of nasal fibres\n• = loss of BOTH temporal fields\n• MC cause: Pituitary adenoma compressing chiasm from below",
  "Bitemporal hemianopia = chiasmal lesion = pituitary adenoma (MC)");

addQ(3,"Visual Fields",
  "Temporal lobe lesion. What visual field defect results, and what is the classic description?",
  "'Pie in the sky' vs 'Pie on the floor' – know both");
addA(3,"Visual Fields",
  "Contralateral SUPERIOR Homonymous Quadrantanopia\n('Pie in the sky')\n\n• Temporal lobe carries Meyer's loop = inferior optic radiation fibres\n• These fibres subserve the SUPERIOR visual field\n• Temporal lobe lesion → SUPERIOR field loss\n\nContrast: Parietal lobe lesion → inferior fibres → INFERIOR quadrantanopia ('Pie on the floor')",
  "Temporal → Superior ('sky'). Parietal → Inferior ('floor')");

addQ(4,"Visual Fields",
  "Occipital cortex infarction (PCA territory). What is the characteristic visual field defect?",
  "Macular sparing is the key differentiator from optic tract lesions");
addA(4,"Visual Fields",
  "Congruent Homonymous Hemianopia WITH MACULAR SPARING\n\n• Most congruent = most posterior (cortex)\n• Macular cortex has dual blood supply (MCA + PCA) → spared\n• Optic tract/radiation lesions = NO macular sparing\n• Occipital lesion = macula spared\n\nCongruence: anterior lesions = incongruent; posterior = congruent",
  "Macular sparing = occipital (PCA) cortex infarct");

addQ(5,"Visual Fields",
  "What field defect is seen in a parietal lobe lesion involving the optic radiation?",
  "");
addA(5,"Visual Fields",
  "Contralateral INFERIOR Homonymous Quadrantanopia\n('Pie on the floor')\n\n• Superior optic radiation fibres run through parietal lobe\n• They subserve INFERIOR visual field\n• Parietal lobe lesion → loss of inferior contralateral field\n• Also: optokinetic nystagmus (OKN) abnormality toward lesion side",
  "Parietal → Inferior homonymous quadrantanopia");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 2 – PAPILLOEDEMA & IIH
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 2", "Papilloedema, IIH & Optic Disc Disorders", "004D40", "0D1B2A");

addQ(6,"Papilloedema",
  "Define papilloedema. What is the earliest sign on fundoscopy?",
  "Do not use 'papilloedema' for unilateral disc swelling");
addA(6,"Papilloedema",
  "Papilloedema = Optic disc swelling SPECIFICALLY due to RAISED INTRACRANIAL PRESSURE\n\nEarliest signs:\n1. Loss of spontaneous venous pulsations\n2. Disc hyperaemia\n3. Blurring of disc margins (nasal margin first)\n4. Peripapillary flame haemorrhages\n5. Paton lines (concentric folds)\n\nVision: Usually PRESERVED early; enlarged blind spot on fields",
  "First sign = absent venous pulsations. VA preserved early.");

addQ(7,"Papilloedema",
  "How do you differentiate papilloedema from pseudopapilloedema (disc drusen)?",
  "Disc drusen in children commonly mimics papilloedema");
addA(7,"Papilloedema",
  "Feature              | Papilloedema  | Disc Drusen\n──────────────────── | ─────────────| ──────────────\nVenous pulsations    | Absent        | Present\nDisc haemorrhages    | Present       | Absent\nFA leakage           | Present       | Absent\nAutofluorescence     | Normal        | Drusen bright\nUltrasound           | Normal        | Calcification\nVisual acuity        | Preserved     | Preserved",
  "Autofluorescence + ultrasound calcification = disc drusen (pseudopapilloedema)");

addQ(8,"IIH",
  "Typical patient with IIH: What are the 5 Modified Dandy Criteria for diagnosis?",
  "Normal MRI is mandatory – must exclude SOL first");
addA(8,"IIH",
  "IIH (Idiopathic Intracranial Hypertension) – Modified Dandy Criteria:\n\n1. Signs/symptoms of raised ICP (headache, papilloedema)\n2. Raised CSF opening pressure (>25 cmH₂O adults; >28 obese)\n3. Normal CSF composition (no cells, normal glucose/protein)\n4. Normal neuroimaging (no mass, no hydrocephalus)\n5. No other identifiable cause",
  "Obese young woman + bilateral papilloedema + normal MRI + raised CSF = IIH");

addQ(9,"IIH",
  "What drugs cause IIH? Name the first-line treatment.",
  "Steroid WITHDRAWAL can cause IIH – not just steroid use");
addA(9,"IIH",
  "Drugs causing IIH – Mnemonic 'TOVA':\n• Tetracyclines (minocycline, doxycycline)\n• OCP / Obesity\n• Vitamin A / Retinoids (isotretinoin)\n• Adrenal insufficiency / Steroid withdrawal\n\nAlso: lithium, nalidixic acid, growth hormone\n\nFirst-line treatment:\n1. WEIGHT LOSS (most important)\n2. Acetazolamide (carbonic anhydrase inhibitor)\n3. Topiramate (also causes weight loss)\n4. Serial LP, optic nerve sheath fenestration if vision threatened",
  "1st line = Weight loss + Acetazolamide. 'TOVA' for drug causes.");

addQ(10,"Papilloedema",
  "What is Foster Kennedy Syndrome vs Pseudo-Foster Kennedy Syndrome?",
  "One has raised ICP; the other does NOT");
addA(10,"Papilloedema",
  "Foster Kennedy Syndrome (TRUE):\n• Frontal lobe SOL (olfactory groove meningioma MC)\n• Ipsilateral: optic ATROPHY (direct nerve compression)\n• Contralateral: PAPILLOEDEMA (raised ICP)\n• + Ipsilateral anosmia (frontal lobe)\n\nPseudo-Foster Kennedy:\n• Sequential bilateral AION\n• Active AION in one eye (disc swollen)\n• Old AION = atrophy in other eye\n• NO raised ICP involved",
  "True Foster Kennedy = frontal SOL + raised ICP. Pseudo = bilateral sequential AION");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 3 – PUPIL DISORDERS
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 3", "Pupillary Disorders & Reflexes", "BF360C", "0D1B2A");

addQ(11,"Pupil",
  "What is the Swinging Flashlight Test? What does a positive RAPD mean?",
  "RAPD = afferent defect. Pupils are EQUAL in pure afferent lesions.");
addA(11,"Pupil",
  "RAPD (Relative Afferent Pupillary Defect) = Marcus Gunn Pupil\n\nTest: Swing light between eyes every 2-3 seconds\n• Light in normal eye → BOTH pupils constrict\n• Light swung to diseased eye → BOTH pupils DILATE (paradoxical)\n\nPositive RAPD = afferent pathway lesion (optic nerve or severe retinal disease)\n\nKey rules:\n• RAPD = optic nerve disease (hallmark)\n• Pupils are EQUAL SIZE in afferent lesions\n• ANISOCORIA = efferent pathway abnormality",
  "RAPD positive = optic nerve lesion. Equal pupils = afferent defect.");

addQ(12,"Pupil",
  "Adie (Tonic) Pupil: Features + pharmacological test?",
  "Supersensitive to 0.1% pilocarpine = cholinergic denervation hypersensitivity");
addA(12,"Pupil",
  "Adie's (Tonic) Pupil:\n• Unilateral large pupil (mydriasis)\n• ABSENT or very poor light reaction\n• SLOW TONIC near response (pupil constricts slowly, re-dilates slowly)\n• Light-near dissociation present\n\nPharmacological test:\n• 0.1% pilocarpine → Adie pupil CONSTRICTS (hypersensitive)\n• Normal pupil: NO response to 0.1% pilocarpine\n\nHolmes-Adie Syndrome: Adie pupil + absent knee/ankle jerks\nCause: Ciliary ganglion damage (viral/idiopathic)",
  "0.1% pilocarpine constricts Adie pupil = denervation hypersensitivity");

addQ(13,"Pupil",
  "Argyll Robertson Pupil: What are the features and what is the cause?",
  "Accommodation Retained, Light Refused = syphilis");
addA(13,"Pupil",
  "Argyll Robertson Pupil:\n• Bilateral SMALL, irregular pupils (miosis)\n• ABSENT light reflex\n• PRESERVED near reflex (accommodation-convergence)\n= Light-near DISSOCIATION\n\nMnemonic: 'AR = Accommodation Retained, Light Refused'\n\nCause: Neurosyphilis (also DM – incomplete form)\nSite of lesion: Pretectal nucleus (dorsal midbrain)\n\nDifference from Adie:\nAdie = large pupil, near reaction tonic/slow\nAR = small pupil, near reaction brisk",
  "AR pupil = Syphilis. Small + absent light + intact near = pretectal lesion");

addQ(14,"Pupil",
  "Compare Adie pupil vs Argyll Robertson pupil in a table.",
  "Common PYQ – both have light-near dissociation but are OPPOSITE in size");
addA(14,"Pupil",
  "Feature            | Adie Pupil           | Argyll Robertson\n────────────────── | ─────────────────── | ───────────────────\nSize               | LARGE (mydriasis)    | SMALL (miosis)\nLight reaction     | Absent/reduced       | Absent\nNear reaction      | Slow/tonic           | Brisk/intact\nLaterality         | Usually unilateral   | Bilateral\nCause              | Ciliary ganglion     | Neurosyphilis / DM\nTest               | 0.1% pilocarpine+    | –\nAssociation        | Holmes-Adie (arefl.) | Tabes dorsalis",
  "Both have light-near dissociation. Adie = large. AR = small.");

addQ(15,"Pupil",
  "What is Horner syndrome? Name the classic triad and the 3-neuron pathway.",
  "Anisocoria WORSE in dim light = Horner syndrome");
addA(15,"Pupil",
  "Horner Syndrome (Oculosympathetic Palsy):\n\nTriad: PTOSIS (partial 1-2mm) + MIOSIS + ANHIDROSIS\nAlso: enophthalmos (apparent), lower lid elevation\nAnisocoria worse in DIM LIGHT (Horner pupil won't dilate)\n\n3-Neuron Pathway:\n1st (Central): Hypothalamus → brainstem → Ciliospinal centre of Budge (C8-T2)\n2nd (Preganglionic): To superior cervical ganglion (near apex of lung)\n3rd (Postganglionic): Along internal carotid → cavernous sinus → dilator pupillae",
  "Horner = sympathetic palsy. Ptosis + Miosis + Anhidrosis. Worse in dark.");

addQ(16,"Pupil",
  "Which drug differentiates PREGANGLIONIC from POSTGANGLIONIC Horner syndrome?",
  "Cocaine confirms Horner; hydroxyamphetamine localises it");
addA(16,"Pupil",
  "Hydroxyamphetamine 1%:\n• Releases noradrenaline from postganglionic terminals\n• Preganglionic Horner: intact neuron → DILATES (positive)\n• Postganglionic Horner: damaged neuron → NO dilation\n\nCocaine 4-10%:\n• Blocks noradrenaline reuptake\n• Normal pupil: dilates; Horner (any level): NO dilation\n• Used to CONFIRM Horner syndrome\n\nApraclonidine 0.5%: Reverses anisocoria in both pre & postganglionic Horner",
  "Hydroxyamphetamine: positive (dilates) = preganglionic. No dilation = postganglionic.");

addQ(17,"Pupil",
  "Acute painful Horner syndrome – what must be urgently excluded?",
  "Don't miss this life-threatening cause");
addA(17,"Pupil",
  "Carotid Artery Dissection\n\n• Internal carotid artery (ICA) dissection\n• Postganglionic fibres run along ICA → damaged\n• Presents: acute painful Horner + ipsilateral face/neck pain\n• May cause stroke\n\nInvestigation: CT angiography / MR angiography\n\nOther causes by level:\n• Preganglionic: Pancoast tumour (apex lung), aortic aneurysm, cervical rib\n• Central: Lateral medullary syndrome (Wallenberg), MS, hypothalamic tumour",
  "Acute painful Horner = Carotid dissection until proven otherwise. Urgent CTA.");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 4 – OPTIC NEURITIS & OPTIC ATROPHY
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 4", "Optic Neuritis, Optic Atrophy & LHON", "1A237E", "0D1B2A");

addQ(18,"Optic Neuritis",
  "Classic presentation of demyelinating optic neuritis. What is the relationship to MS?",
  "Pain on eye movement is the clue");
addA(18,"Optic Neuritis",
  "Demyelinating Optic Neuritis:\n• Age: 20-40 yr, female predominance\n• Unilateral, PAINFUL (pain on eye movement – periorbital)\n• Subacute visual loss over hours-days\n• RAPD positive\n• Disc normal (RETROBULBAR – 'patient sees nothing, doctor sees nothing')\n• Colour vision lost early (especially red desaturation)\n• Uhthoff phenomenon (vision worsens with heat/exercise)\n\nMS link: 50% of ON patients develop MS within 15 years\nRecovery: >90% recover to 6/12 or better\n\nTreatment: IV methylprednisolone (speeds recovery, doesn't improve final VA)",
  "Optic neuritis = pain on eye movement + RAPD + normal disc + young female = MS");

addQ(19,"Optic Neuritis",
  "What is the difference between retrobulbar neuritis and papillitis on fundoscopy?",
  "The classic teaching: patient sees nothing / doctor sees nothing");
addA(19,"Optic Neuritis",
  "Retrobulbar Neuritis:\n• Inflammation BEHIND the globe (posterior optic nerve)\n• Fundoscopy: NORMAL disc\n• 'Patient sees nothing; doctor sees nothing'\n• Typical of demyelinating (MS-related) optic neuritis\n\nPapillitis:\n• Inflammation of the optic nerve HEAD (anterior)\n• Fundoscopy: SWOLLEN disc (disc oedema)\n• Seen in parainfectious optic neuritis (children, post-viral)\n• Also NMOSD (NMO spectrum disorder)\n\nNeuroretinitis:\n• Disc swelling + MACULAR STAR (fan-shaped exudates)\n• Cause: Bartonella henselae (cat scratch disease), syphilis",
  "Neuroretinitis = macular star = Bartonella (cat scratch disease)");

addQ(20,"Optic Neuritis",
  "What are the ONTT findings regarding oral vs IV steroids in optic neuritis?",
  "Oral steroids ALONE increased recurrence – avoid as monotherapy");
addA(20,"Optic Neuritis",
  "Optic Neuritis Treatment Trial (ONTT):\n\n1. IV methylprednisolone (1g/day × 3 days then oral taper):\n   → Speeds visual recovery by 4 weeks\n   → No improvement in FINAL visual outcome\n   → Delays MS onset\n\n2. Oral prednisolone alone (1 mg/kg/day):\n   → INCREASED rate of new attacks\n   → AVOID oral steroids alone for optic neuritis\n\n3. Placebo:\n   → Similar final outcome to IV steroids",
  "ONTT: IV steroids speed recovery but don't improve final VA. Oral alone = AVOID.");

addQ(21,"Optic Atrophy",
  "Classify optic atrophy into 4 types with appearances and causes.",
  "Primary vs secondary = margins (sharp vs blurred)");
addA(21,"Optic Atrophy",
  "Type         | Appearance                   | Causes\n──────────── | ──────────────────────────── | ──────────────────────────\nPrimary      | Flat WHITE disc, clear margins| MS post-neuritis, Leber's, compression, ethambutol, nutritional\nSecondary    | Dirty grey disc, blurred margins| Chronic papilloedema (raised ICP)\nConsecutive  | Atrophy + retinal changes     | CRVO, retinitis pigmentosa, chorioretinitis\nGlaucomatous | Cupped disc (C:D > 0.6)       | Glaucoma\n\nBand/Bow-tie atrophy: Nasal+temporal pallor → chiasm or optic tract lesion\nTemporal pallor only: Papillomacular bundle loss → post-demyelinating ON",
  "Band (bow-tie) atrophy = chiasm/tract lesion. Temporal pallor = post-demyelinating ON");

addQ(22,"Optic Atrophy",
  "Leber Hereditary Optic Neuropathy (LHON) – key features?",
  "Maternal inheritance = mitochondrial DNA mutation");
addA(22,"Optic Atrophy",
  "LHON:\n• Inheritance: MATERNAL (mitochondrial DNA)\n• Affects: Young MALES predominantly (20-30 yr)\n• Bilateral PAINLESS severe visual loss (sequential, weeks apart)\n• Visual field: Central / CECOCENTRAL scotoma\n• Early fundus: Peripapillary TELANGIECTASIA + pseudoedema\n• Late: Primary optic atrophy\n\nGene mutations (most to least common):\n• ND4 (11778) – most common ~50%\n• ND1 (3460)\n• ND6 (14484)\n\nAssociation: Cardiac conduction defects (WPW pattern)\nTreatment: Idebenone (mitochondrial antioxidant – some benefit)",
  "LHON: maternal inheritance, young males, cecocentral scotoma, ND4 mutation (MC)");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 5 – CRANIAL NERVE PALSIES
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 5", "III, IV & VI Nerve Palsies", "4A148C", "0D1B2A");

addQ(23,"CN Palsy",
  "Complete 3rd nerve palsy – what are the clinical findings?",
  "Eye position: DOWN and OUT (lateral rectus + superior oblique unopposed)");
addA(23,"CN Palsy",
  "Complete CN III (Oculomotor) Palsy:\n\n• Complete PTOSIS (levator palpebrae superioris)\n• Eye: DOWN and OUT position\n  (lateral rectus CN VI unopposed; superior oblique CN IV unopposed)\n• Loss of elevation, depression, adduction\n• Dilated FIXED pupil (if compressive)\n\nMnemonic: '3 P's' – Ptosis, Palsy of muscles, Pupil dilated (if surgical)",
  "Complete CN III = ptosis + down&out eye + ± dilated pupil");

addQ(24,"CN Palsy",
  "Surgical vs Medical CN III palsy – KEY difference and clinical significance?",
  "This is a potential neurosurgical EMERGENCY");
addA(24,"CN Palsy",
  "Feature            | Surgical (Compressive) | Medical (Microvascular)\n────────────────── | ───────────────────── | ──────────────────────\nPupil              | FIXED, DILATED         | SPARED (normal)\nCause              | PCom aneurysm          | DM, HTN, atherosclerosis\nEmergency?         | YES                    | No\nAction             | Urgent CT/CTA          | Observe, treat DM/HTN\nPain               | Often severe           | Mild/absent\n\nWHY pupil spared in medical:\nPupillomotor fibres = on outer surface (supplied by vasa nervorum → spared in ischaemia)\nMotor fibres = central (affected in ischaemia, spared in compression)",
  "Dilated pupil in CN III = ANEURYSM (PCom) – neurosurgical emergency!");

addQ(25,"CN Palsy",
  "CN IV (Trochlear) palsy – what muscle is weak, and what compensatory posture does the patient adopt?",
  "Longest intracranial course → most traumatized CN");
addA(25,"CN Palsy",
  "CN IV (Trochlear) Palsy:\n\n• Weakens: SUPERIOR OBLIQUE (depressor + intortor when eye adducted)\n• Effect: Hypertropia (affected eye HIGHER than normal eye)\n• Diplopia: Vertical, worse on LOOKING DOWN (stairs problem)\n\nCompensatory head posture:\n• Head tilts AWAY from affected side (contralateral tilt)\n• Chin depressed, face turned away from palsy\n\nDiagnosis: Parks-Bielschowsky 3-step test\n\nMC cause: TRAUMA (CN IV has longest intracranial course – very vulnerable)\nAlso: Congenital (most common cause of vertical diplopia overall)",
  "CN IV: head tilt AWAY from palsy, vertical diplopia worse on downgaze. MC cause = trauma.");

addQ(26,"CN Palsy",
  "CN VI (Abducens) palsy – clinical features. Why is it a 'false localizing sign'?",
  "Always consider raised ICP when VI palsy found with no obvious cause");
addA(26,"CN Palsy",
  "CN VI (Abducens) Palsy:\n\n• Weakens: LATERAL RECTUS\n• Effect: ESOTROPIA (convergent squint)\n• Diplopia: Horizontal, UNCROSSED, worse on gaze toward affected side\n• Limitation of abduction\n\nFalse localizing sign in raised ICP:\n• CN VI has the LONGEST intracranial course\n• Stretched over petrous ridge when ICP raised\n• Palsy does NOT indicate where the SOL is → false localizing\n\nGradenigo Syndrome:\n• Petrous apex lesion (otitis media / mastoiditis complication)\n• CN VI palsy + facial pain (CN V) + ipsilateral middle ear disease",
  "CN VI = false localizing sign in raised ICP. Gradenigo = petrous apex (VI + V + ear).");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 6 – AION / GCA
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 6", "AION, GCA & Ischaemic Optic Neuropathy", "B71C1C", "0D1B2A");

addQ(27,"AION",
  "What is the typical visual field defect in AION? What is the 'disc at risk'?",
  "AION = altitudinal field defect (not hemianopia, not central scotoma)");
addA(27,"AION",
  "AION (Anterior Ischaemic Optic Neuropathy):\n\nVisual field defect: ALTITUDINAL (usually inferior)\n• Sudden visual loss, often noticed on waking\n• Painless\n\n'Disc at Risk' (NAION):\n• Small optic disc with SMALL or absent cup\n• Crowded nerve fibre arrangement\n• Congestion → ischaemia when systemic hypotension occurs\n• Often with DM, HTN, hyperlipidaemia, OSA\n\nContrast: Optic neuritis = central scotoma, RAPD, painful, young\nAION = altitudinal, RAPD, painless, older",
  "AION = altitudinal field defect + disc at risk + older patient. Painless.");

addQ(28,"AION / GCA",
  "GCA (Giant Cell Arteritis) – clinical features, investigation, and immediate treatment?",
  "DO NOT wait for biopsy results before starting steroids");
addA(28,"AION / GCA",
  "GCA (Arteritic AION) – age > 70 yr:\n\nSymptoms:\n• Headache (temporal), scalp tenderness\n• Jaw claudication (pathognomonic)\n• Temporal artery tender + non-pulsatile\n• Sudden severe visual loss (pale chalky disc)\n• Systemic: fever, weight loss, PMR symptoms\n\nInvestigations:\n• ESR > 50 mm/hr (often > 80), CRP raised\n• Temporal artery biopsy (skip lesions → take long segment)\n\nTreatment – IMMEDIATE:\n• IV methylprednisolone 1g/day × 3 days (if vision threatened)\n• Oral prednisolone 1 mg/kg if no visual loss\n• Aspirin 100 mg/day (reduces stroke/visual loss risk)\n• DO NOT wait for biopsy – start steroids at once",
  "GCA: jaw claudication + ESR >50 + sudden visual loss → IMMEDIATE IV steroids");

addQ(29,"AION",
  "Non-arteritic AION (NAION) vs Arteritic AION (GCA) – comparison.",
  "ESR and jaw claudication are the key differentiators");
addA(29,"AION",
  "Feature         | NAION               | AAION (GCA)\n─────────────── | ─────────────────── | ───────────────────────\nAge              | 50-70 yr            | > 70 yr\nESR/CRP          | Normal              | ELEVATED\nPain             | Painless            | Headache/scalp tender\nJaw claudication | No                  | YES (pathognomonic)\nDisc at risk     | YES (small cup)     | Not required\nFellow eye risk  | ~15% in 5 years     | VERY HIGH if untreated\nTreatment        | RF modification     | Immediate steroids\nBiopsy           | Not needed          | Temporal artery biopsy",
  "GCA: jaw claudication + ESR raised. NAION: disc at risk + normal ESR.");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 7 – MIXED HIGH-YIELD PYQs
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 7", "Rapid-Fire High-Yield PYQ Scenarios", "004D40", "0D1B2A");

addQ(30,"PYQ Scenario",
  "30-year-old woman. Painful unilateral visual loss, pain on eye movement, RAPD present, disc appears NORMAL. Diagnosis?",
  "Normal disc + pain on eye movement = retrobulbar not papillitis");
addA(30,"PYQ Scenario",
  "RETROBULBAR OPTIC NEURITIS\n(Demyelinating – possible first presentation of MS)\n\nKey clues:\n• Young woman → demyelinating optic neuritis\n• Pain on eye movement → optic nerve sheath inflammation\n• RAPD → afferent optic nerve lesion\n• Normal disc → inflammation is POSTERIOR (retrobulbar)\n\nManagement:\n• MRI brain (look for demyelinating plaques)\n• IV methylprednisolone (speeds recovery)\n• Neurology referral for MS monitoring",
  "Pain on eye movement + RAPD + normal disc + young = retrobulbar optic neuritis / MS");

addQ(31,"PYQ Scenario",
  "65-year-old diabetic man. CN III palsy with NORMAL pupil. Cause? Is this an emergency?",
  "Pupil-sparing = microvascular. Dilated pupil = aneurysm = EMERGENCY");
addA(31,"PYQ Scenario",
  "MICROVASCULAR CN III PALSY\n(Diabetic/hypertensive – NOT an emergency)\n\nReasoning:\n• Normal (spared) pupil → central pupillomotor fibres NOT affected\n• In ischaemia: outer motor fibres affected (supplied by vasa nervorum)\n• Inner pupillomotor fibres (superficial) are spared\n\nManagement:\n• Control DM, HTN\n• Usually resolves in 3-4 months\n• If pupil becomes dilated later → urgent CTA to exclude aneurysm\n\nContrast: Any CN III palsy with dilated fixed pupil = aneurysm until proven otherwise",
  "Pupil-sparing CN III = microvascular (DM/HTN). NOT an emergency. Resolves in months.");

addQ(32,"PYQ Scenario",
  "75-year-old with sudden visual loss, jaw pain while chewing, temporal headache. ESR = 90. Urgent next step?",
  "Don't wait for biopsy – start steroids NOW");
addA(32,"PYQ Scenario",
  "GIANT CELL ARTERITIS (GCA)\n\nUrgent next step: IMMEDIATE IV methylprednisolone\n(Do NOT wait for biopsy results)\n\nWhy urgent?\n• Fellow eye at very high risk of ischaemia within hours-days\n• Once other eye loses vision, it is permanent\n• Biopsy can be done within 1-2 weeks of starting steroids\n  (histology remains positive for weeks)\n\nJaw claudication = pain when chewing = PATHOGNOMONIC of GCA\nESR > 50 (often > 80) = characteristic\n\nStart: IV methylprednisolone 1g/day + aspirin 100mg/day",
  "GCA: start IV steroids IMMEDIATELY. Don't wait for biopsy. Both eyes at risk.");

addQ(33,"PYQ Scenario",
  "Obese 25-year-old woman. Bilateral papilloedema, daily headache, diplopia. Normal CT and MRI. CSF opening pressure = 30 cmH₂O. Diagnosis and treatment?",
  "Diplopia = CN VI false localizing sign in raised ICP");
addA(33,"PYQ Scenario",
  "IDIOPATHIC INTRACRANIAL HYPERTENSION (IIH)\n\nDiagnosis confirmed by:\n• Young obese woman (classic demographic)\n• Bilateral papilloedema\n• Normal neuroimaging\n• Raised CSF pressure (>25 cmH₂O)\n• Normal CSF composition\n\nDiplopia → CN VI palsy = false localizing sign (raised ICP stretches CN VI)\n\nTreatment:\n1. WEIGHT LOSS (primary intervention – most effective)\n2. Acetazolamide (first-line medication)\n3. Topiramate (also causes weight loss)\n4. Optic nerve sheath fenestration (if vision threatened)\n5. LP/VP shunt (refractory cases)",
  "IIH: obese young woman + papilloedema + normal MRI + raised CSF pressure");

addQ(34,"PYQ Scenario",
  "A patient has right eye OPTIC ATROPHY and left eye PAPILLOEDEMA. Most likely diagnosis?",
  "Classic Foster Kennedy presentation");
addA(34,"PYQ Scenario",
  "FOSTER KENNEDY SYNDROME\n\nCause: Frontal lobe space-occupying lesion\n(MC = Olfactory groove meningioma)\n\nMechanism:\n• Ipsilateral optic atrophy: direct compression of ipsilateral optic nerve\n• Contralateral papilloedema: raised ICP from the expanding mass\n• + Ipsilateral anosmia (olfactory nerve compression)\n\nImportant contrast:\nPseudo-Foster Kennedy = sequential bilateral AION\n• Active AION one eye (swollen disc) + old AION other eye (atrophy)\n• NO raised ICP\n• No frontal SOL",
  "Ipsilateral atrophy + contralateral papilloedema = Foster Kennedy = frontal SOL");

addQ(35,"PYQ Scenario",
  "Young male with bilateral visual loss (sequential, painless), cecocentral scotoma, family history on MOTHER'S side only. Diagnosis?",
  "Maternal inheritance = mitochondrial = LHON");
addA(35,"PYQ Scenario",
  "LEBER HEREDITARY OPTIC NEUROPATHY (LHON)\n\nKey features here:\n• Young male (20-30 yr)\n• Bilateral painless visual loss, often sequential\n• Cecocentral scotoma (involving central vision + blind spot)\n• MATERNAL inheritance (mitochondrial DNA)\n\nMost common mutation: ND4 (position 11778)\n\nFundus:\n• Early: Peripapillary telangiectasia\n• Late: Primary optic atrophy\n\nAssociation: Cardiac conduction defects (WPW pattern)\nTreatment: Idebenone (modest benefit)\nGenetic counselling for maternal relatives",
  "LHON = maternal (mitochondrial) inheritance + young male + cecocentral scotoma");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 8 – ONE-LINER RAPID REVIEW
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 8", "One-Liner Rapid Review", "37474F", "0D1B2A");

addQ(36,"One-Liner",
  "What causes bitemporal hemianopia?",
  "Only ONE structure causes true bitemporal hemianopia");
addA(36,"One-Liner","Optic chiasm lesion ONLY\n\nMC cause: Pituitary adenoma (compresses chiasm from below)\nOther causes: Craniopharyngioma (children), meningioma, aneurysm\nNote: Superior bitemporal defect first = pituitary adenoma (grows up into chiasm)","Bitemporal hemianopia = chiasm only = pituitary adenoma (MC)");

addQ(37,"One-Liner",
  "What is the visual field defect in a complete optic tract lesion?",
  "Tract = first place where fibres from same side of both eyes combine");
addA(37,"One-Liner","Contralateral Homonymous Hemianopia (INCONGRUENT)\n\n• Incongruent because fibres are not fully sorted yet\n• Wernicke hemianopic pupil reaction may be present\n• Can cause bow-tie atrophy in both discs\n• Ipsilateral disc: superior + inferior pallor (temporal retinal fibres)\n• Contralateral disc: bow-tie (nasal + temporal nasal fibres)","Optic tract = incongruent homonymous hemianopia + possible RAPD");

addQ(38,"One-Liner",
  "Name the bright autofluorescent structure on fundus autofluorescence (FAF) that mimics papilloedema.",
  "");
addA(38,"One-Liner","Optic Disc DRUSEN\n\nDrusen = calcium deposits within the optic nerve head\n• Appear highly autofluorescent on FAF (bright)\n• Calcified on ultrasound (highly reflective)\n• Can mimic papilloedema clinically\n• BURIED drusen in CHILDREN = most dangerous mimic\n• FA: no leakage (vs papilloedema which leaks)","Disc drusen = bright on FAF + calcified on ultrasound = pseudopapilloedema");

addQ(39,"One-Liner",
  "Neuroretinitis: What does it look like on fundoscopy, and what is the MC infectious cause?",
  "Macular star is the key feature");
addA(39,"One-Liner","Neuroretinitis:\n• Optic disc SWELLING + MACULAR STAR\n• Macular star = hard exudates arranged in star pattern around macula (around fovea)\n• Arises from disc oedema tracking into outer plexiform layer\n\nMC cause: Bartonella henselae (Cat Scratch Disease)\nOther: Syphilis, Lyme disease, Toxoplasma\n\nDoes NOT progress to MS (unlike typical optic neuritis)","Neuroretinitis = disc swelling + macular star = Bartonella (cat scratch)");

addQ(40,"One-Liner",
  "What is Uhthoff's phenomenon and which condition is it associated with?",
  "");
addA(40,"One-Liner","Uhthoff's Phenomenon:\n• Transient worsening of vision with HEAT or EXERCISE\n• Associated with: DEMYELINATING OPTIC NEURITIS (MS)\n• Mechanism: Heat slows conduction in already-demyelinated fibres\n• Fully reversible when temperature normalises\n• Not a sign of disease progression","Uhthoff = vision worsens with heat/exercise = demyelinating optic neuritis / MS");

addQ(41,"One-Liner",
  "A patient after temporal lobe surgery has difficulty seeing objects in the upper part of the visual field on the opposite side. Name the structure damaged.",
  "");
addA(41,"One-Liner","Meyer's Loop (Inferior Optic Radiation – Temporal lobe)\n\n• Meyer's loop: inferior fibres of optic radiation that sweep forward into temporal lobe\n• These fibres carry information from the SUPERIOR visual field\n• Damage → Contralateral SUPERIOR homonymous quadrantanopia\n• 'Pie in the sky'\n• A complication of temporal lobe surgery or ATL for epilepsy","Meyer's loop damage = 'pie in the sky' = superior contralateral quadrantanopia");

addQ(42,"One-Liner",
  "Normal CSF opening pressure in adults (lying position)?",
  "IIH diagnosed when pressure > 25 cmH₂O in adults");
addA(42,"One-Liner","Normal CSF pressure (lumbar puncture, lateral decubitus/lying position):\n\n10 – 18 cmH₂O in adults\n\nIIH diagnostic threshold:\n• Adults: > 25 cmH₂O\n• Obese adults: > 28 cmH₂O\n\nNote: Measure in lateral decubitus (lying on side)\n• Upright position gives falsely high values","Normal CSF = 10-18 cmH₂O. IIH >25 cmH₂O (adults).");

addQ(43,"One-Liner",
  "What is Gradenigo syndrome? Which cranial nerves are involved?",
  "Petrous apex lesion – often complication of otitis media");
addA(43,"One-Liner","Gradenigo Syndrome (Petrous Apex Syndrome):\n\nTriad:\n1. CN VI palsy (lateral rectus weakness → horizontal diplopia)\n2. CN V involvement (facial/retro-orbital pain, trigeminal neuralgia)\n3. Ipsilateral middle ear disease (otitis media / mastoiditis)\n\nCause: Petrous apex osteomyelitis (complication of otitis media)\nAlso: Petrous apex tumours, cholesteatoma\n\nHistorical importance: Frequent NEET PG question","Gradenigo = CN VI + facial pain (V) + ear disease = petrous apex lesion");

addQ(44,"One-Liner",
  "What is the 'swinging flashlight test' finding in a left EFFERENT defect (CN III palsy on left)?",
  "Efferent defect ≠ RAPD – pupils are unequal but both respond sluggishly");
addA(44,"One-Liner","Left CN III Palsy (Efferent defect):\n• Left pupil is FIXED and DILATED at baseline\n• Swinging flashlight test:\n  – Light in right eye: RIGHT pupil constricts, left pupil does NOT constrict\n  – Light in left eye: RIGHT pupil constricts consensually, left pupil STILL does NOT constrict\n\nKey: The left pupil is ALWAYS dilated regardless of which eye is illuminated\n→ This is efferent, NOT RAPD\n\nRAPD: Both pupils react (constrict/dilate together), but dilate when diseased eye lit","Efferent defect: dilated pupil doesn't respond to ANY light. RAPD: both pupils react together.");

addQ(45,"One-Liner",
  "What is the significance of 'temporal pallor' of the optic disc?",
  "Most often linked to one very common clinical condition");
addA(45,"One-Liner","Temporal Pallor of Optic Disc:\n\n• Indicates atrophy of the PAPILLOMACULAR BUNDLE\n• These fibres enter the temporal aspect of the optic disc\n• Classic cause: Post-DEMYELINATING OPTIC NEURITIS\n  (temporal pallor is the residual sign after optic neuritis resolves)\n\nOther causes: toxic/nutritional optic neuropathy (alcohol-tobacco amblyopia, B12 deficiency)\n\nBand (bow-tie) atrophy = nasal AND temporal pallor → chiasm/tract lesion","Temporal pallor = papillomacular bundle loss = hallmark of post-demyelinating optic neuritis");

// ═══════════════════════════════════════════════════════════════════════
// SECTION 9 – MNEMONICS & RAPID SUMMARY
// ═══════════════════════════════════════════════════════════════════════
addSection("SECTION 9", "Mnemonics & Quick Summary Cards", "004D40", "0D1B2A");

addQ(46,"Mnemonic",
  "Give mnemonics for: (1) Horner syndrome features, (2) IIH drug causes, (3) Argyll Robertson pupil.",
  "These mnemonics appear directly in PYQ explanations");
addA(46,"Mnemonic",
  "1. Horner Syndrome – 'PAM':\n   Ptosis (partial) + Anhidrosis + Miosis\n\n2. IIH Drug Causes – 'TOVA':\n   Tetracyclines / OCP+Obesity / Vitamin A (retinoids) / Adrenal insufficiency (steroid withdrawal)\n\n3. Argyll Robertson – 'ARLA':\n   Accommodation Retained, Light Absent\n   OR: 'Prostitute's pupil – accommodates but doesn't react'\n\n4. CN III palsy positions:\n   '3 Ps': Ptosis + Paralysis (down & out) + Pupil dilated (if surgical)",
  "PAM (Horner) | TOVA (IIH drugs) | ARLA (AR pupil)");

addQ(47,"Summary",
  "Rank the 5 visual pathway lesions by CONGRUITY of the homonymous defect they produce.",
  "More posterior = more congruent");
addA(47,"Summary",
  "Congruity (LEAST → MOST):\n\n1. Optic tract: Most INCONGRUENT homonymous hemianopia\n2. Anterior optic radiation (temporal/parietal): Incongruent quadrantanopia\n3. Posterior optic radiation: More congruent quadrantanopia\n4. Occipital cortex: Most CONGRUENT homonymous hemianopia\n   + MACULAR SPARING (if PCA territory spared)\n\nRule: More POSTERIOR = more CONGRUENT\nRule: Macular sparing = ONLY with occipital cortex lesions",
  "Tract = incongruent. Cortex = most congruent + macular sparing");

addQ(48,"Summary",
  "What are the 3 causes of light-near dissociation (intact near, absent light reflex)?",
  "Syphilis is the classic but there are 3 main causes");
addA(48,"Summary",
  "LIGHT-NEAR DISSOCIATION\n(Near reflex intact; light reflex ABSENT/reduced)\n\n3 Main Causes:\n1. Argyll Robertson pupil (NEUROSYPHILIS)\n   – Bilateral small pupils\n2. Dorsal midbrain (Parinaud) syndrome\n   – Bilateral large pupils + upgaze palsy + convergence-retraction nystagmus\n3. Adie's (Tonic) pupil\n   – Unilateral large pupil, tonic slow near response\n\nAlso: Diabetes (incomplete AR pattern), MS, Lyme disease",
  "Light-near dissociation: Argyll Robertson (syphilis) | Parinaud (dorsal midbrain) | Adie");

addQ(49,"Summary",
  "Parinaud Dorsal Midbrain Syndrome – features?",
  "Upgaze palsy + convergence-retraction nystagmus = Parinaud");
addA(49,"Summary",
  "Parinaud Syndrome (Dorsal Midbrain):\n\nClassic Triad:\n1. UPGAZE PALSY (cannot look up – supranuclear)\n2. CONVERGENCE-RETRACTION nystagmus on attempted upgaze\n3. LIGHT-NEAR DISSOCIATION (bilateral dilated pupils)\n\nAdditional:\n• Eyelid retraction (Collier sign / 'setting sun' eyes in children)\n• Skew deviation\n\nCauses:\n• Pineal gland tumour (MC in young adults)\n• Hydrocephalus (aqueduct compression)\n• MS, infarction\n\nNote: These are large pupils (unlike AR = small pupils)","Parinaud = upgaze palsy + convergence-retraction nystagmus + dilated pupils = pineal tumour");

addQ(50,"Summary",
  "FINAL CARD: Recall the 10 most important one-liners for NEET PG neuro-ophthalmology.",
  "These are the highest-yield, exam-ready facts");
addA(50,"Summary",
  "Top 10 One-Liners:\n1. Bitemporal hemianopia = chiasm only = pituitary adenoma MC\n2. Macular sparing = occipital cortex infarct (PCA)\n3. Pie in sky = temporal (Meyer's loop); Pie on floor = parietal\n4. RAPD = optic nerve disease (afferent lesion)\n5. Dilated pupil CN III = aneurysm (PCom) – EMERGENCY\n6. Spared pupil CN III = microvascular (DM/HTN) – NOT emergency\n7. GCA: jaw claudication + ESR raised → immediate IV steroids\n8. IIH: obese young woman + bilateral papilloedema + normal MRI\n9. Argyll Robertson: small pupils, no light reflex, intact near = syphilis\n10. LHON: maternal inheritance, young male, cecocentral scotoma",
  "Revise these 10 daily for the week before NEET PG 2026!");

// ── Write file ────────────────────────────────────────────────────────────────
pres.writeFile({ fileName: "/home/daytona/workspace/neuro-ophtho-flashcards/NeuroOphtho_Flashcards_NEETPG2026.pptx" })
  .then(() => console.log("SUCCESS: PPTX created."))
  .catch(e => console.error("ERROR:", e));

cd /home/daytona/workspace/neuro-ophtho-flashcards && node flashcards.js

ls -lh /home/daytona/workspace/neuro-ophtho-flashcards/