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🧠 Complete Neurology MCQ Guide — All 20 Questions

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Q1. Which nerve is compressed in Carpal Tunnel Syndrome?

✅ Answer: a. Median nerve

• Numbness/tingling in the thumb, index, middle, and radial half of ring finger (median nerve distribution)
• Nocturnal pain/paresthesias (waking the patient at night)
• Weakness and atrophy of thenar muscles (abductor pollicis brevis)
• Positive Tinel's sign (tapping over carpal tunnel → tingling)
• Positive Phalen's test (wrist flexion for 60 sec → symptoms)

• Ulnar nerve → compressed at Guyon's canal (wrist) or cubital tunnel (elbow) → affects little finger + medial ring finger
• Radial nerve → wrist drop, compressed at radial groove of humerus ("Saturday night palsy")
• Peroneal nerve → compressed at fibular head → foot drop (this is a LEG nerve, not hand)

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Q2. Most appropriate definition of seizure?

✅ Answer: a. An abnormal discharge of cortical neurons causing a transient disturbance of cerebral function

• Cortical (not subcortical, not brainstem, not spinal cord)
• Transient disturbance
• Of cerebral (brain) function

• b. Subcortical neurons + spinal cord = Wrong — seizures don't arise from subcortical neurons
• c. Brainstem neurons causing tonic-clonic = Wrong — brainstem generates tonic posturing, not classic seizures
• d. Spinal cord neurons = Wrong — that would describe spinal myoclonus or reflex activity

• Seizure = single event of abnormal cortical discharge
• Epilepsy = ≥2 unprovoked seizures >24 hours apart

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Q3. Criterion for diagnosis of clinical Alzheimer's disease?

✅ Answer: b. Impairment of at least 2 areas of cognitive function

1. Dementia must first be established (cognitive decline from a prior level)
2. Insidious onset
3. Clear-cut history of worsening cognition
4. Impairment in ≥2 cognitive domains: memory, language, visuospatial, executive function, behavior/personality
5. No other explanation (not vascular, not toxic-metabolic)

• a. GCS <10 — GCS measures acute consciousness (trauma/coma), not used for Alzheimer's diagnosis
• c. MRI cortical atrophy — MRI can support diagnosis but is NOT a criterion; some patients have normal MRI early on
• d. Grasp/snout reflex — these are primitive reflexes seen in advanced disease but NOT a diagnostic criterion

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Q4. Pyridoxine dose causing mild sensory neuropathy?

✅ Answer: d. 500 mg daily (and technically c. 250 mg daily also fits the textbook range)

• ≥500 mg/day → causes severe sensory polyneuropathy (sensory neuronopathy/ganglionopathy)
• 250–3000 mg/day → sensory polyanglionopathy range cited
• 100 mg/day → used therapeutically (e.g., with INH for TB) — SAFE
• 50 mg/day → well within safe range

"High-dose pyridoxine (vitamin B6, 250–3000 mg/day) may cause a severe and remarkably uniform sensory polyanglionopathy."

• Painful paresthesias
• Sensory ataxia
• Perioral numbness
• Lhermitte sign (electric shock down spine with neck flexion)
• Low-amplitude/absent SNAPs on nerve conduction studies

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Q5. Which tract/column contains autonomic fibers in the spinal cord?

✅ Answer: b. Intermediolateral gray column

"There is an intermediolateral gray column extending from segments T1 through L2, which gives rise to preganglionic sympathetic autonomic fibers."

• Located in the lateral horn of spinal gray matter
• Present at T1–L2 (thoracolumbar = sympathetic outflow)
• Also at S2–S4 (parasympathetic outflow for pelvic organs)
• Contains preganglionic sympathetic neurons

• a. Anterior corticospinal tract → voluntary motor (corticospinal = pyramidal tract)
• c. Posterior column → fine touch, vibration, proprioception (dorsal column-medial lemniscal system)
• d. Ventral spinothalamic tract → crude touch and pressure

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Q6. Guillain-Barré variant with cranial nerve palsies, ophthalmoparesis, pupillary abnormalities, NO limb weakness?

✅ Answer: c. Miller-Fisher Syndrome

1. Ophthalmoplegia (external eye muscle paralysis)
2. Ataxia (cerebellar-type gait)
3. Areflexia (absent reflexes)

• a. CIDP (Chronic Inflammatory Demyelinating Polyneuropathy) — chronic (>8 weeks), limb weakness and sensory loss
• b. Lambert-Eaton Myasthenic Syndrome (LEMS) — presynaptic NMJ disorder, proximal limb weakness, hyporeflexia, autonomic dysfunction; caused by anti-VGCC antibodies (often paraneoplastic with small cell lung cancer)
• d. Ramsay-Hunt Syndrome — VZV reactivation in geniculate ganglion → facial palsy + ear vesicles + sensorineural hearing loss

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Q7. Mechanism of action of donepezil in Alzheimer's disease?

✅ Answer: c. Prevents breakdown of acetylcholine

• Blocks the enzyme acetylcholinesterase which normally breaks down acetylcholine (ACh) in the synapse
• This increases synaptic ACh → improves cholinergic neurotransmission
• Basis: Cholinergic hypothesis of Alzheimer's — basal forebrain cholinergic neurons (nucleus basalis of Meynert) degenerate in AD, reducing ACh

• a. Clears amyloid plaques → that's aducanumab/lecanemab (anti-amyloid monoclonal antibodies)
• b. Increases synaptic density → not a mechanism of any current AD drug
• d. Prevents neuronal death → not donepezil's mechanism (neuroprotection is theoretical with some agents)

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Q8. Which tumor is highly epileptogenic?

✅ Answer: b. Oligodendroglioma

• Presents with seizures (most common presenting symptom, ~80%)
• Frontal lobe predilection
• Calcifications on CT ("popcorn calcifications")
• IDH mutation + 1p/19q co-deletion (hallmark molecular marker)
• Better prognosis than astrocytomas

• a. Ependymoma → arises from ventricular lining, causes hydrocephalus; less epileptogenic (more posterior fossa in children)
• c. Pilocytic astrocytoma → WHO grade I, most common in cerebellum in children; rarely causes seizures
• d. Pineoblastoma → pineal region, causes Parinaud syndrome (vertical gaze palsy), not seizures

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Q9. Most common pathogen causing bacterial meningitis in adults?

✅ Answer: d. Streptococcus pneumoniae

"Streptococcus pneumoniae remains the predominant pathogen in adult patients, accounting for over half of cases."

• a. H. influenzae → was #1 before Hib vaccine; now rare
• b. Listeria → important in elderly/immunocompromised, NOT most common overall
• c. N. meningitidis → most common in adolescents/young adults, causes epidemics in college dorms

• Empirical: Ceftriaxone + Vancomycin (+ dexamethasone to reduce inflammation)
• Add Ampicillin if Listeria suspected (elderly, immunocompromised)

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Q10. Which is part of the tetrad of narcolepsy?

✅ Answer: b. Cataplexy

"Narcolepsy was characterized by a tetrad of symptoms: (1) excessive sleepiness, (2) cataplexy, (3) sleep paralysis, (4) hypnagogic hallucinations."

1. Excessive daytime sleepiness (EDS) — sudden irresistible sleep attacks
2. Cataplexy — sudden loss of muscle tone triggered by strong emotion (laughing, surprise); patient is conscious but collapses
3. Sleep paralysis — transient inability to move at sleep onset/offset
4. Hypnagogic hallucinations — vivid hallucinations at sleep onset (or hypnopompic = at awakening)

• a. Catamenial epilepsy — seizures related to menstrual cycle; nothing to do with narcolepsy
• c. Catatonia — psychiatric, seen in schizophrenia/mood disorders; waxy flexibility, mutism
• d. Catecholamine surge — not a narcolepsy feature

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Q11. CSF: lymphocytosis, AFB smear positive, low glucose, high protein, elevated pressure — which infection?

✅ Answer: c. Tuberculous meningitis

• Subacute onset (days-weeks)
• Basal meningitis → cranial nerve palsies (especially CN III, VI)
• Hydrocephalus risk
• CSF: low glucose (<45), very high protein (>100), lymphocytes
• Tuberculomas on MRI

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Q12. Argyll-Robertson pupil, absent lower extremity reflexes, impaired vibration/position sense, sensory ataxic gait, history of syphilis 30 years ago?

✅ Answer: d. Tabes dorsalis

1. Argyll-Robertson pupil — "accommodates but doesn't react"; miotic pupil that constricts for near vision but NOT to light (syphilis hallmark)
2. Absent deep tendon reflexes (lower extremity)
3. Impaired vibration and proprioception → posterior column damage
4. Sensory ataxic gait (wide-based, stomping gait; worsens with eyes closed = Romberg +)
5. Lightning pains (lancinating pains in legs)

• a. ALS → motor neuron disease; upper + lower motor neuron signs; no sensory loss, no Argyll-Robertson
• b. GBS → acute/subacute ascending weakness with areflexia; no Argyll-Robertson
• c. Spinal epidural abscess → fever + back pain + progressive weakness; no Argyll-Robertson

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Q13. NMDA antagonist used in management of Alzheimer's disease?

✅ Answer: b. Memantine

• NMDA (N-methyl-D-aspartate) receptor antagonist
• Blocks excessive glutamate-mediated excitotoxicity
• Glutamate overactivation → calcium influx → neuronal death
• Memantine low-affinity, voltage-dependent block → protects neurons without blocking normal synaptic transmission

• a. Aducanumab → monoclonal antibody that clears amyloid plaques (anti-amyloid, controversial FDA approval 2021)
• c. Rivastigmine → AChE + BuChE inhibitor (not NMDA antagonist)
• d. Selegiline → MAO-B inhibitor used in Parkinson's disease

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Q14. Gene that increases vulnerability to Alzheimer's disease?

✅ Answer: c. Apolipoprotein E4 (APOE ε4)

• Most significant genetic risk factor for sporadic (late-onset) Alzheimer's
• APOE ε4 allele → increased amyloid deposition, reduced amyloid clearance
• Each copy of ε4 increases risk: 1 allele → 3× risk; 2 alleles → 8–12× risk
• Does NOT mean you WILL get Alzheimer's — it's a susceptibility gene, not a causative gene

• a. Alpha-synuclein → gene for Parkinson's disease / Lewy body dementia
• b. APOE ε2 → actually PROTECTIVE against AD
• d. Dystrophin → gene mutated in Duchenne Muscular Dystrophy (not AD)

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Q15. Mechanism of radiation therapy in brain tumors?

✅ Answer: b. Radiation can damage tumor DNA affecting its growth

• Ionizing radiation (X-rays, gamma rays, protons) causes double-strand DNA breaks
• Tumor cells have impaired DNA repair mechanisms → cannot fix these breaks → cell death
• Normal cells also damaged but have better repair capacity
• Effect is greatest on rapidly dividing cells

• a. "Simulates light damaging tumor cells" → completely fictional mechanism
• c. "Agitates cell membranes" → not the mechanism of radiation
• d. "Heats tumor tissue" → that would be hyperthermia therapy or focused ultrasound, not standard radiation

• Whole brain radiation (WBRT)
• Stereotactic radiosurgery (Gamma Knife, CyberKnife) — focused, single high dose
• Proton beam therapy

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Q16. Organism producing toxic spores causing paralysis if ingested in contaminated food?

✅ Answer: b. Clostridium botulinum

• Clostridium botulinum produces botulinum toxin (most potent biological toxin known)
• Toxin cleaves SNARE proteins (specifically synaptobrevin/VAMP, syntaxin, SNAP-25) → prevents ACh vesicle fusion at the neuromuscular junction
• Result: flaccid paralysis (descending, symmetric)
• Affects: presynaptic NMJ

• Descending paralysis (starts with cranial nerves: diplopia, dysphagia, dysarthria → then descends)
• NO fever (unlike meningitis)
• NO sensory loss
• Pupils may be dilated and unreactive (autonomic involvement)
• Respiratory failure (most dangerous)

1. Foodborne (ingested toxin — canned/preserved food)
2. Wound botulism (toxin from wound)
3. Infant botulism (ingested spores — honey in infants)

• a. Aspergillosis → fungal lung infection
• c. Cryptococcus neoformans → fungal meningitis (India ink +)
• d. Mycobacterium leprae → leprosy (peripheral neuropathy, skin lesions)

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Q17. Strongest single risk factor for Alzheimer's disease?

✅ Answer: a. Increasing age

• Prevalence of AD doubles every 5 years after age 65
• Age 65: ~1–2%; Age 85+: ~30–50%
• Age is the single greatest non-modifiable risk factor

1. Age (strongest)
2. APOE ε4 genotype (strongest modifiable genetic risk)
3. Family history
4. Female sex
5. Cardiovascular risk factors (hypertension, diabetes, obesity)
6. Low educational level (reduced cognitive reserve)
7. Head trauma

• b. Alcoholism → causes Wernicke-Korsakoff syndrome (thiamine deficiency), not AD specifically
• c. Thiamine deficiency → Wernicke's encephalopathy (ophthalmoplegia, ataxia, confusion)
• d. Sedentary lifestyle → modifiable risk factor but NOT the strongest

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Q18. Main pathophysiology in Stiff Person Syndrome?

✅ Answer: a. Antibodies against glutamic acid decarboxylase (GAD)

• Autoimmune disorder with anti-GAD65 antibodies (in ~80%)
• GAD (glutamic acid decarboxylase) = enzyme that converts glutamate → GABA
• Anti-GAD antibodies → reduced GABA synthesis → loss of inhibitory tone → continuous motor neuron firing → muscle rigidity + spasms

• Progressive axial muscle rigidity (back and abdomen)
• Episodic painful muscle spasms (triggered by noise, touch, emotional stress)
• Lordosis (exaggerated lumbar)
• Hypersensitivity to sensory stimuli

• b. Anti-synaptobrevin → not a known autoimmune target for SPS (synaptobrevin is cleaved by botulinum toxin)
• c. Anti-AChR (acetylcholine receptor) → Myasthenia gravis
• d. Anti-VGCC (voltage-gated calcium channels) → Lambert-Eaton Myasthenic Syndrome

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Q19. Typical CSF abnormality in Guillain-Barré Syndrome?

✅ Answer: b. Elevated protein with normal WBC count

• Protein: elevated (>45 mg/dL, often >100)
• WBC: normal (<10 cells/µL)
• Glucose: normal
• Opening pressure: normal

• a. Elevated IgG index → Multiple sclerosis
• c. Oligoclonal bands → Multiple sclerosis
• d. Positive RPR → Neurosyphilis (tabes dorsalis, general paresis)

• Acute ascending flaccid paralysis
• Post-infectious (Campylobacter jejuni most common trigger, also CMV, EBV, flu)
• Demyelinating (AIDP most common in Western countries) or axonal (AMAN, AMSAN in Asia)
• Treatment: IVIG or plasmapheresis (equally effective); steroids NOT beneficial

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Q20. Periventricular demyelinating lesions at right angles to corpus callosum in MS?

✅ Answer: a. Dawson fingers

• Named after James Walker Dawson (1910)
• Periventricular plaques of demyelination in MS that orient perpendicular to the long axis of the corpus callosum (along medullary veins)
• On MRI (FLAIR/T2): appear as finger-like projections radiating outward from corpus callosum
• This pattern is pathognomonic for multiple sclerosis

• b. Leptomeningeal enhancement → meningitis or leptomeningeal carcinomatosis
• c. Rising sun phenomenon → describes enlarged fourth ventricle in obstructive hydrocephalus (Tectal plate glioma in children)
• d. Sundowning phenomenon → behavioral worsening in dementia patients in the evening (behavioral, NOT radiological)

• Dissemination in space (lesions in ≥2 of 4 CNS locations: periventricular, juxtacortical, infratentorial, spinal cord)
• Dissemination in time (new lesions on follow-up MRI, or simultaneous enhancing + non-enhancing lesions)

• Acute attack: IV methylprednisolone
• Disease modifying: interferons, glatiramer acetate, natalizumab, ocrelizumab, siponimod

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📋 Quick Answer Key

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