Neuro Final Exam

Neuroanatomy & Diseases of the Neurological System

CUMULATIVE FINAL EXAM PRACTICE — 75 Questions

South College Atlanta · Summer 2026 · Weeks 1–9

Anatomy (5) · Movement Disorders (5) · CNS Tumors (5) · Seizures (5) · MS/MG (4) · Spinal Cord (5) · Dementia (4) · ALS/PLS (2) · Syncope (3) · POTS/CRPS/Phantom Pain (2) · Headaches (4) · Meningitis/Encephalitis (3) · Hydrocephalus (2) · Intracranial Hemorrhage/Stroke/CN Palsy (5) · Parkinson's (3) · Neurologic Exam (4) · Peripheral Neuropathy (2) · Basal Ganglia/Eye (2) · Vascular (3) · Red Flags (2) · Integration (5)

Weighted to match professor's final exam outline — heavier on Weeks 6–9

PART I — QUESTIONS (75 Items)

Q1. [Anatomy]

A 67-year-old man presents after a sudden onset of left-sided weakness and left homonymous hemianopia. Angiography shows occlusion at the junction of the internal carotid artery and the posterior communicating artery. Which Circle of Willis vessel, when patent, provides collateral flow between the anterior and posterior circulations?

A. Anterior communicating artery

B. Posterior communicating artery

C. Basilar artery

D. Middle cerebral artery

Q2. [Anatomy]

A patient presents with sudden loss of vision in the left eye only. Fundoscopy reveals a pale, swollen optic disc with a 'cherry-red spot' at the macula. Which vessel is occluded?

A. Ophthalmic artery

B. Middle cerebral artery

C. Central retinal artery

D. Posterior cerebral artery

Q3. [Anatomy]

A patient suffers a unilateral lesion at the LEFT optic tract (post-chiasmal). Which visual field defect results?

A. Bitemporal hemianopia (loss of peripheral vision in both eyes)

B. Left monocular blindness

C. Left homonymous hemianopia (loss of RIGHT visual field in both eyes)

D. Right homonymous hemianopia (loss of LEFT visual field in both eyes)

Q4. [Anatomy]

A patient with a T10 spinal cord hemisection (Brown-Séquard syndrome) on the right side. Which correctly describes the sensory deficits BELOW the lesion?

A. Right side: loss of pain and temperature; Left side: loss of proprioception

B. Right side: loss of proprioception and vibration; Left side: loss of pain and temperature

C. Bilateral loss of all sensation

D. Right side: loss of pain only; Left side: loss of vibration only

Q5. [Anatomy]

A 55-year-old man has a lesion of the anterior spinal artery at T4, sparing the posterior spinal arteries. Which pattern of deficits is expected?

A. Loss of proprioception and vibration below T4 with intact motor function

B. Loss of motor function and pain/temperature below T4 with intact proprioception and vibration

C. Complete bilateral loss of all sensation and motor function below T4

D. Ipsilateral motor loss only with contralateral sensory loss

Q6. [Movement Disorders]

A 70-year-old woman has had a bilateral symmetric tremor for 20 years that is present when she holds a cup of coffee (action tremor) but disappears at rest. It improves with a small amount of wine. Multiple family members are affected. Neurologic exam is otherwise normal. What is the diagnosis and first-line treatment?

A. Parkinson's disease; levodopa/carbidopa

B. Essential tremor; propranolol or primidone

C. Physiologic tremor; avoid caffeine

D. Intention tremor; deep brain stimulation

Q7. [Movement Disorders]

A 9-year-old boy has had multiple motor tics (eye blinking, shoulder shrugging) AND vocal tics (throat clearing, barking sounds) for 14 months. Symptoms began before age 18. He has no other medical conditions. What is the diagnosis and first-line treatment?

A. Provisional tic disorder; observation

B. Tourette syndrome; patient/family education and behavior modification, then antipsychotics (haloperidol) if needed

C. Persistent motor tic disorder; clonazepam

D. OCD with tics; SSRI

Q8. [Movement Disorders]

A 48-year-old man with schizophrenia on haloperidol for 12 years develops repetitive involuntary lip smacking, tongue protrusion, facial grimacing, and irregular hand movements. What is the diagnosis, mechanism, and correct first step in management?

A. Parkinson's disease; dopamine deficiency; start levodopa

B. Tardive dyskinesia; dopamine receptor upregulation from chronic blockade; remove/reduce the causative agent for at least 6 months

C. Huntington's disease; HTT gene mutation; genetic testing

D. Acute dystonic reaction; dopamine receptor blockade; give benztropine IM now

Q9. [Movement Disorders]

A 44-year-old man with heavy alcohol use is admitted to the hospital. On post-admission day 3, he develops severe agitation, confusion, whole-body tremors, fever of 39.1°C, tachycardia HR 130, diaphoresis, and visual hallucinations. What is the diagnosis, what electrolyte must be checked urgently, and what is the first-line treatment?

A. Wernicke's encephalopathy; check thiamine; give thiamine IV

B. Delirium tremens; check magnesium and potassium; benzodiazepines (IV/PO lorazepam or diazepam)

C. Septic encephalopathy; blood cultures; broad-spectrum antibiotics

D. Alcohol intoxication; blood alcohol level; supportive care

Q10. [Movement Disorders]

A 40-year-old man presents with choreiform movements, personality change, depression, and executive dysfunction. His father died of the same condition at 55. Genetic testing shows >50 CAG repeats on the HTT gene. What is the treatment for his chorea?

A. Levodopa/carbidopa

B. VMAT-2 inhibitors: tetrabenazine or deutetrabenazine (Austedo)

C. Pyridostigmine

D. IVIg

Q11. [CNS Tumors]

A 60-year-old man presents with progressive headaches, personality changes (disinhibition), and seizures. MRI shows an irregular ring-enhancing bifrontal mass crossing the corpus callosum ('butterfly glioma'). Biopsy confirms the diagnosis. What is the diagnosis, grade, and average survival?

A. Meningioma; Grade I; excellent prognosis

B. Glioblastoma multiforme (GBM); Grade IV; average 12 months

C. Pilocytic astrocytoma; Grade I; curable with surgery

D. Primary CNS lymphoma; variable; treated with methotrexate

Q12. [CNS Tumors]

Using the 'Flat Pig' mnemonic for pituitary adenomas: a 30-year-old woman presents with amenorrhea, galactorrhea, and decreased libido. Serum prolactin is 450 ng/mL. MRI pituitary shows a 7mm lesion. What is the first-line treatment, and what makes this unique among pituitary tumors?

A. Surgical transsphenoidal resection

B. Radiation therapy

C. Dopamine agonist (bromocriptine or cabergoline) — the ONLY pituitary tumor treated primarily medically

D. Hormone replacement only

Q13. [CNS Tumors]

A 45-year-old woman has an incidentally found well-circumscribed, homogeneously enhancing dural-based mass on MRI (obtained for headaches). She has no neurologic symptoms. What is the most likely diagnosis and appropriate management?

A. GBM; immediate surgical resection

B. Meningioma; observation if asymptomatic, surgery only if symptomatic

C. Brain metastasis; chemotherapy

D. Primary CNS lymphoma; methotrexate

Q14. [CNS Tumors]

A 55-year-old man with known lung cancer develops headaches, right arm weakness, and seizures. MRI shows multiple enhancing lesions at the gray-white junction in different lobes. Which primary tumor most commonly metastasizes to the brain, and what percentage of cancer patients develop brain metastases?

A. Colon cancer; 10%

B. Lung cancer (40%); 30% of cancer patients

C. Breast cancer; 50% of cancer patients

D. Melanoma (40%); 5% of cancer patients

Q15. [CNS Tumors]

A 9-year-old boy is diagnosed with Neurofibromatosis Type 1 (NF1). His uncle has NF2. Which features correctly distinguish NF1 from NF2?

A. NF1: bilateral vestibular schwannomas; NF2: café au lait spots

B. NF1: café au lait spots, freckling, fibromas, optic gliomas (96% of NF); NF2: bilateral vestibular schwannomas, meningiomas, tinnitus, hearing loss

C. Both have identical clinical features

D. NF1: only affects adults; NF2: only affects children

Q16. [Seizures]

An 8-year-old girl repeatedly 'zones out' in class for 10-20 seconds at a time, with sudden onset and sudden return to activity. No loss of tone. EEG shows 3-Hz generalized spike-and-wave. What is the diagnosis, when do these typically resolve, and what is the treatment?

A. Focal impaired awareness seizure; persists into adulthood; levetiracetam

B. Absence seizure; typically resolves by age 18; ethosuximide

C. Myoclonic seizure; lifelong; valproate

D. PNES; no age resolution; CBT

Q17. [Seizures]

A 23-year-old man has a witnessed generalized tonic-clonic seizure that lasts 9 minutes continuously. EMS gives lorazepam 4mg IV — the seizure continues. What is the diagnosis and second-line treatment?

A. Simple febrile seizure; observation only

B. Status epilepticus (>5 min continuous); second-line: levetiracetam, valproate, or fosphenytoin IV

C. PNES; video EEG monitoring

D. Alcohol withdrawal seizure; additional benzodiazepines only

Q18. [Seizures]

A 32-year-old woman with epilepsy has episodes of lip smacking, repetitive hand movements, and impaired awareness lasting 3 minutes. She has no memory of the events. Where do 75% of these seizures originate, and what is the first-line treatment?

A. Frontal lobe; carbamazepine

B. Temporal lobe; levetiracetam (Keppra)

C. Occipital lobe; valproate

D. Parietal lobe; lamotrigine

Q19. [Seizures]

A 29-year-old woman with epilepsy presents for prenatal counseling. She is currently on valproic acid. Which statement is most accurate?

A. Valproic acid is safe in pregnancy and should be continued

B. Valproic acid has the highest teratogenic risk (neural tube defects, lower IQ, autism); preferred ASMs in pregnancy are levetiracetam and lamotrigine

C. All ASMs are equally teratogenic

D. No ASMs are safe in pregnancy

Q20. [Seizures]

A patient presents with events they describe as 'seizures' but: they remember every event, events last 15-30 minutes, they involve pelvic thrusting and forced eye closure, and no tongue biting or incontinence occurs. EEG during the event is COMPLETELY NORMAL. What is the diagnosis and gold standard diagnostic test?

A. Focal aware seizure; MRI brain

B. Status epilepticus; lorazepam IV now

C. PNES (psychogenic non-epileptic seizures); video EEG monitoring during an event

D. Absence seizure; EEG showing 3-Hz spike-wave

Q21. [MS / MG]

A 30-year-old woman has had two episodes of neurologic deficits over 18 months, separated by time and space. MRI shows ovoid periventricular and juxtacortical T2 hyperintensities. CSF shows oligoclonal bands. What are the MS diagnostic criteria, most common disease course, and treatment for an acute relapse?

A. Barkhof criteria; primary progressive; plasma exchange

B. McDonald criteria; relapsing-remitting (85%); high-dose IV methylprednisolone 1,000mg x 3 days

C. McDonald criteria; secondary progressive; oral prednisone

D. IIH criteria; relapsing-remitting; acetazolamide

Q22. [MS / MG]

A patient with RRMS on natalizumab (Tysabri) for 2 years develops progressive cognitive decline, confusion, and MRI shows multifocal white matter lesions. What is this complication, what virus causes it, and which other MS medications share this risk?

A. MS relapse; no viral cause; treat with steroids

B. PML (progressive multifocal leukoencephalopathy); JC virus; also associated with fingolimod, dimethyl fumarate, ocrelizumab

C. NMOSD; AQP4-IgG antibodies; switch to azathioprine

D. Drug toxicity; no viral cause; stop natalizumab and observe

Q23. [MS / MG]

A 27-year-old woman presents with bilateral ptosis worse at end of day, diplopia, and proximal limb weakness that IMPROVES with rest. Pupils are NORMAL. Sensory exam and reflexes are INTACT. Upward gaze for 60 seconds worsens her ptosis. What is the diagnosis, pathophysiology, and first-line outpatient treatment?

A. Multiple sclerosis; CNS demyelination; high-dose steroids

B. Myasthenia gravis; autoimmune destruction of AChR at NMJ; pyridostigmine (acetylcholinesterase inhibitor)

C. Lambert-Eaton syndrome; presynaptic VGCCab; 3,4-diaminopyridine

D. ALS; motor neuron degeneration; riluzole

Q24. [MS / MG]

A 35-year-old woman has optic neuritis AND severe longitudinally extensive transverse myelitis affecting 3+ spinal cord segments. MRI shows no periventricular lesions typical of MS. Serum test is positive for aquaporin-4 IgG antibodies. What is the diagnosis?

A. Multiple sclerosis; treat with interferon beta

B. NMOSD (neuromyelitis optica spectrum disorder); antibodies against aquaporin-4 water channels

C. Acute disseminated encephalomyelitis (ADEM); post-viral demyelination

D. Clinically isolated syndrome; monitor with serial MRI

Q25. [Spinal Cord]

A 35-year-old man is stabbed on the RIGHT side of his thoracic spine. He has right-sided loss of motor function and proprioception below T6, and left-sided loss of pain and temperature below T6. What syndrome is this, and what is the correct treatment approach for spinal cord reperfusion?

A. Anterior cord syndrome; anterior spinal artery thrombectomy

B. Brown-Séquard syndrome; MAP >85 mmHg and high-dose steroids to reperfuse the spinal cord

C. Central cord syndrome; cervical collar only

D. Posterior cord syndrome; physical therapy immediately

Q26. [Spinal Cord]

A 72-year-old woman with severe cervical spondylosis falls backward. She develops bilateral upper extremity weakness GREATER THAN lower extremity weakness, with some loss of pain/temperature. Reflexes are brisk. She can walk slowly. What syndrome is this, which direction causes it, and what treatment restores spinal cord perfusion?

A. Anterior cord syndrome; hyperflexion; tPA

B. Central cord syndrome; hyperextension in a stenotic cervical canal; MAP >85 mmHg + surgical decompression if indicated

C. Brown-Séquard; penetrating trauma; MAP >65 mmHg

D. Posterior cord syndrome; flexion; NSAID therapy

Q27. [Spinal Cord]

A 50-year-old man presents with saddle anesthesia, urinary retention (800mL drained on Foley), bilateral leg weakness, absent rectal tone, and sexual dysfunction. MRI shows large central disc herniation at L4-L5. What is the diagnosis, imaging of choice, and time window for surgery?

A. Multiple sclerosis; MRI brain; no surgical window

B. Cauda equina syndrome; MRI lumbar spine (gold standard); surgical decompression within 48 hours

C. Spinal stenosis; CT myelogram; elective surgery

D. Conus medullaris syndrome; LP; steroids

Q28. [Spinal Cord]

A 48-year-old IV drug user presents with severe midline lumbar back pain, fever of 39.3°C, and new bilateral leg weakness developing over 24 hours. ESR is 85, CRP is 22. Blood cultures are positive for S. aureus. What is the diagnosis, imaging of choice, and treatment?

A. Disc herniation; CT without contrast; physical therapy

B. Spinal epidural abscess; MRI spine with contrast; surgical evacuation + IV antibiotics 4-8 weeks

C. Bacterial meningitis; LP; ceftriaxone + vancomycin

D. Vertebral compression fracture; X-ray; bracing

Q29. [Spinal Cord]

Which of the following correctly differentiates spinal stenosis from cauda equina syndrome?

A. Both cause saddle anesthesia and require emergent surgery

B. Spinal stenosis: neurogenic claudication (pain with walking, relieved by leaning forward/sitting); CES: acute saddle anesthesia + urinary retention = surgical emergency

C. Spinal stenosis requires emergency surgery; CES is managed conservatively

D. Both are managed with physical therapy and NSAIDs

Q30. [Dementia]

A 75-year-old man has a history of multiple strokes. He has cognitive decline with motor dysfunction, urinary incontinence, sensory changes, and memory impairment. His MRI shows multiple cortical and subcortical infarcts. His cognitive symptoms appeared ABRUPTLY after each stroke. What dementia subtype is this?

A. Alzheimer's disease; insidious onset, hippocampal atrophy

B. Vascular dementia; abrupt onset following cerebrovascular accident, neuroimaging confirms infarcts

C. Dementia with Lewy bodies; visual hallucinations + extrapyramidal symptoms

D. Frontotemporal dementia; behavioral/language variant, younger onset

Q31. [Dementia]

A 70-year-old woman has cognitive fluctuations with vivid visual hallucinations. She then develops extrapyramidal symptoms (rigidity, bradykinesia). The cognitive symptoms began ONE YEAR BEFORE the motor symptoms. What is the diagnosis and how does it differ from Parkinson's Disease Dementia?

A. Alzheimer's disease; no extrapyramidal symptoms

B. Dementia with Lewy Bodies (DLB); cognitive decline PRECEDES motor symptoms by ≥1 year (opposite of PDD)

C. Parkinson's Disease Dementia; Parkinson's motor symptoms precede dementia by ≥1 year

D. Frontotemporal dementia; behavioral variant

Q32. [Dementia]

A 58-year-old man presents with sexual disinhibition, socially inappropriate behavior, loss of empathy, and word-finding difficulties. His wife reports he 'has become a different person.' MRI shows pronounced frontal and temporal lobe atrophy. What type of dementia is this, what protein accumulates, and what is unique about its age of onset?

A. Alzheimer's disease; amyloid plaques and tau tangles; onset usually >65

B. Frontotemporal dementia (FTD); tau protein deposition; YOUNGER onset (45-65)

C. Vascular dementia; infarcts; onset follows stroke

D. Lewy body dementia; alpha-synuclein; onset varies

Q33. [Dementia]

A 75-year-old man presents with the triad of GAIT INSTABILITY, URINARY INCONTINENCE, and COGNITIVE DECLINE. MRI shows enlarged ventricles disproportionate to cortical atrophy. After large-volume lumbar puncture removing 30mL CSF, his gait noticeably improves. What is the diagnosis and definitive treatment?

A. Alzheimer's disease; donepezil

B. Normal pressure hydrocephalus (NPH); ventriculoperitoneal (VP) shunt placement

C. Vascular dementia; aspirin + statins

D. Parkinson's disease; levodopa/carbidopa

Q34. [Motor Neuron Disease]

A 58-year-old man has progressive weakness starting in his right hand with muscle fasciculations, atrophy, and hyperreflexia. He now has difficulty swallowing and speaking. Sensory exam is COMPLETELY INTACT. EMG shows fibrillations and positive sharp waves. What is the diagnosis and what distinguishes it from PLS?

A. PLS; only UMN signs, no fasciculations

B. ALS; affects BOTH UMN and LMN simultaneously with intact sensation; average survival 2-4 years

C. Multiple sclerosis; central demyelination

D. Myasthenia gravis; fatigable weakness, NMJ disease

Q35. [Motor Neuron Disease]

A 52-year-old woman has had slowly progressive lower extremity spasticity for 3 years with clumsiness, now involving both legs and dysarthria. Reflexes are BRISK. NO fasciculations. NO atrophy. Sensory exam is NORMAL. Which motor neuron disease is this?

A. ALS; both UMN and LMN signs

B. PLS (primary lateral sclerosis); slowly progressive UMN ONLY disease, normal lifespan but significant disability

C. GBS; ascending paralysis, areflexia

D. MS; relapsing-remitting demyelinating disease

Q36. [Syncope]

A 16-year-old girl has chronic fatigue, dizziness, and palpitations that worsen when she stands. Supine vitals: HR 90, BP 112/74. After 5 minutes of standing: HR 128, BP 108/72. She does NOT have orthostatic HYPOTENSION. Following a viral illness 3 months ago, symptoms began. What is the diagnosis and first-line non-pharmacologic treatment?

A. Vasovagal syncope; supine positioning and avoid triggers

B. POTS (postural orthostatic tachycardia syndrome); HR increase ≥30 bpm WITHOUT hypotension; 8-12g salt/day + 2-3L fluid/day + compression garments + slow exercise

C. Orthostatic hypotension; midodrine

D. Cardiac syncope; ECG and echocardiogram

Q37. [Syncope]

A 22-year-old medical student faints while watching a surgical procedure. Witnesses report pallor, slumping, and recovery within 60 seconds. She had nausea and tunnel vision just before the event. She is alert and oriented now with normal vitals and no neurologic deficits. What is the most likely diagnosis and treatment?

A. Cardiac syncope; obtain ECG, Holter monitor, echocardiogram

B. Vasovagal syncope; place supine, avoid triggers (emotional stress, prolonged standing, pain, heat)

C. POTS; compression stockings and fluid loading

D. TIA; urgent MRI brain

Q38. [Syncope]

Which of the following features is most consistent with CARDIAC syncope and indicates the WORST prognosis among syncope types?

A. Clear prodrome of nausea and diaphoresis in a hot crowded room

B. Sudden onset without prodrome during exercise in a 55-year-old with a family history of sudden cardiac death

C. Orthostatic symptoms improving with sitting down

D. Brief syncopal episode associated with sight of blood

Q39. [POTS / CRPS / Phantom Pain]

A 35-year-old woman had a left wrist fracture 5 months ago. She now has burning pain in the left hand that is DISPROPORTIONATE to the original injury, with skin color changes (mottled redness), allodynia, temperature asymmetry, and edema. Budapest criteria are met. What is the diagnosis and what TWO therapies are the mainstay of treatment?

A. Phantom limb pain; mirror therapy

B. CRPS (complex regional pain syndrome); physiotherapy + psychotherapy (multidisciplinary)

C. Peripheral arterial disease; vascular surgery

D. Tarsal tunnel syndrome; orthotics and splinting

Q40. [POTS / CRPS / Phantom Pain]

A 50-year-old man had his right leg amputated below the knee 4 months ago. He experiences burning, stabbing, and throbbing sensations that feel as if they are coming from his amputated foot. What is the diagnosis, and what non-pharmacologic therapy uses visual feedback to retrain the brain?

A. CRPS; spinal cord stimulation

B. Phantom limb pain; mirror therapy (visual feedback reduces phantom pain)

C. Stump (residual limb) infection; wound care and antibiotics

D. Conversion disorder; CBT only

Q41. [Headaches]

A 35-year-old man has severe right-sided orbital pain with conjunctival injection, tearing, ptosis, and rhinorrhea occurring every night at the same time for 3 weeks. He paces around during the attacks (cannot lie still). Each episode lasts about 90 minutes. What is the diagnosis and rescue treatment?

A. Migraine; sumatriptan PO

B. Tension headache; NSAIDs and stress management

C. Cluster headache; 100% inhaled oxygen at 12-15 L/min via non-rebreather + subcutaneous sumatriptan

D. Trigeminal neuralgia; carbamazepine

Q42. [Headaches]

A 28-year-old woman has a 5-year history of severe unilateral, pulsating headaches lasting 4-72 hours, with nausea, photophobia, phonophobia, and aggravation by physical activity. She sometimes sees 'squiggly lines' across her vision before the headache starts. Which preventive therapy is indicated if she has ≥4-6 headache days per month?

A. NSAIDs daily; no preventive therapy needed

B. Beta-blockers (propranolol/metoprolol), topiramate, CGRP inhibitors, amitriptyline, or onabotulinumtoxin A (chronic migraine)

C. 100% oxygen inhalation

D. Carbamazepine

Q43. [Headaches]

A 55-year-old woman presents with sudden-onset 'worst headache of my life' that began during sexual intercourse. She has neck stiffness and photophobia. CT head is NEGATIVE. What is the next step and what does it rule out?

A. Discharge with NSAIDs; migraine most likely

B. Lumbar puncture to evaluate for xanthochromia; rule out subarachnoid hemorrhage (SAH) — thunderclap headache is SAH until proven otherwise

C. MRI brain with contrast; rule out tumor

D. Triptans; abort the migraine

Q44. [Headaches]

A 50-year-old woman has severe facial pain along the left cheek and jaw that is electrically shocking in quality, lasting seconds, triggered by chewing, brushing teeth, or talking. It is one of the worst pains she has experienced. What is the diagnosis and first-line treatment?

A. Cluster headache; inhaled oxygen

B. Trigeminal neuralgia; carbamazepine or oxcarbazepine (anticonvulsants)

C. TMJ dysfunction; botulinum toxin

D. Bell's palsy; corticosteroids within 72 hours

Q45. [Meningitis / Encephalitis]

A 16-year-old boy presents with acute headache, high fever, and neck stiffness. The next day a petechial rash develops. CSF shows: glucose 4 mg/dL, protein 82 mg/dL, WBC 119 (72% PMNs). Which organism is most likely, and what is the EMPIRIC treatment?

A. Streptococcus pneumoniae; penicillin only

B. Neisseria meningitidis; ceftriaxone + vancomycin + ±ampicillin (if >50 or immunocompromised)

C. HSV; acyclovir

D. Enterovirus; supportive care only

Q46. [Meningitis / Encephalitis]

Which CSF finding pattern correctly differentiates bacterial from viral meningitis?

A. Both show neutrophilic pleocytosis with low glucose

B. Bacterial: neutrophilic (PMN) pleocytosis + VERY high protein + LOW glucose + high opening pressure. Viral: lymphocytic pleocytosis + mildly elevated protein + NORMAL glucose

C. Bacterial: lymphocytic pleocytosis; Viral: neutrophilic pleocytosis

D. Both show normal glucose and normal protein

Q47. [Meningitis / Encephalitis]

A 30-year-old man presents with 5 days of fever, headache, ALTERED MENTAL STATUS, and new onset seizure. MRI shows inflammation primarily in the TEMPORAL and FRONTAL lobes. CSF shows elevated lymphocytes and elevated protein with NORMAL glucose. What is the most likely diagnosis, causative agent, and treatment?

A. Bacterial meningitis; S. pneumoniae; ceftriaxone + vancomycin

B. Viral encephalitis; HSV 1 (most common); acyclovir empirically while awaiting serology

C. Cryptococcal meningitis; Cryptococcus neoformans; fluconazole + amphotericin B

D. Prion disease; misfolded PrP; supportive care only

Q48. [Hydrocephalus]

A 72-year-old man has the triad of gait instability, urinary incontinence, and cognitive decline. MRI shows enlarged ventricles WITHOUT corresponding cortical atrophy. Gait improves significantly after LP removing 50mL CSF. What is the diagnosis, how does it differ from obstructive hydrocephalus, and what is the treatment?

A. Obstructive hydrocephalus; blocked CSF between ventricles; third ventriculostomy

B. Normal pressure hydrocephalus (NPH); communicating type — CSF flows between ventricles but absorption is impaired; VP shunt placement

C. Alzheimer's dementia; cortical atrophy; donepezil

D. Parkinson's disease; basal ganglia degeneration; levodopa

Q49. [Hydrocephalus]

A 45-year-old obese woman (BMI 35) with recent weight gain presents with daily pulsatile tinnitus, headaches, diplopia, and papilledema on fundoscopy. MRI brain is normal. LP reveals an opening pressure of 32 cm H2O with otherwise normal CSF. What is the diagnosis and first-line treatment?

A. Communicating hydrocephalus; VP shunt immediately

B. Idiopathic intracranial hypertension (IIH/pseudotumor cerebri); weight reduction + acetazolamide

C. Bacterial meningitis; ceftriaxone + vancomycin

D. Obstructive hydrocephalus from tumor; third ventriculostomy

Q50. [Intracranial Hemorrhage]

A 25-year-old man is hit in the right temporal region with a bat. He briefly loses consciousness, then appears completely normal for 3 hours ('lucid interval'), then rapidly deteriorates with vomiting, decreasing LOC, and a fixed dilated RIGHT pupil. CT shows a biconvex (lens-shaped) hyperdense lesion that does NOT cross suture lines. What is the diagnosis and treatment?

A. Subdural hematoma; conservative management

B. Epidural hematoma (EDH); emergent surgical evacuation — neurosurgical emergency

C. Subarachnoid hemorrhage; nimodipine + BP control

D. Intracerebral hemorrhage; antihypertensives

Q51. [Intracranial Hemorrhage]

A 75-year-old anticoagulated woman on warfarin (INR 3.8) falls and presents 3 weeks later with progressive lethargy, confusion, and headache. CT shows a crescent-shaped HYPODENSE lesion crossing the coronal suture. What is the diagnosis, and how does ACUTE SDH differ from CHRONIC SDH on CT?

A. EDH; both appear hyperdense

B. Chronic subdural hematoma; ACUTE SDH = hyperdense (white); CHRONIC SDH = hypodense (dark/similar to CSF)

C. Subarachnoid hemorrhage; bright blood in sulci

D. Intracranial contusion; scattered petechial hemorrhages

Q52. [Intracranial Hemorrhage]

A 38-year-old woman presents with sudden-onset 'thunderclap' headache, neck stiffness, and photophobia. CT head is negative. LP shows xanthochromic (yellow) CSF. What is the diagnosis, most common cause, and acute treatment?

A. Bacterial meningitis; S. pneumoniae; ceftriaxone + vancomycin

B. Subarachnoid hemorrhage (SAH); ruptured cerebral aneurysm (most common); emergent neurosurgical consultation for coiling or clipping

C. Viral encephalitis; HSV; acyclovir

D. Migraine with aura; no aneurysm; triptans

Q53. [Stroke / Hemorrhage]

A 62-year-old man with hypertension presents with sudden-onset left facial drooping, left arm/leg weakness, and aphasia for 45 minutes that FULLY RESOLVED. CT head is negative for hemorrhage. What is the diagnosis, what test is always done first, and what is the stroke risk within 90 days?

A. TIA; MRI brain first; 5% stroke risk in 90 days

B. TIA; CT head first (to rule out hemorrhage), then MRI brain; 15% risk of stroke within 90 days

C. Ischemic stroke with spontaneous recanalization; immediate tPA

D. Todd's paralysis post-seizure; EEG

Q54. [Cranial Nerve Palsy]

A 45-year-old man develops sudden unilateral right-sided facial weakness affecting BOTH the upper and lower face (cannot wrinkle forehead, cannot close eye), with loss of taste on the anterior 2/3 of tongue and hyperacusis. He had an upper respiratory infection 2 weeks ago. What is the diagnosis and treatment?

A. Central (UMN) facial palsy from stroke; CT head emergently

B. Bell's palsy (peripheral CN VII palsy); corticosteroids within 72 hours + supportive eye care

C. Trigeminal neuralgia; carbamazepine

D. Hemifacial spasm; botulinum toxin

Q55. [Parkinson's Disease]

A 65-year-old man has asymmetric resting pill-rolling tremor in his right hand, cogwheel rigidity, BRADYKINESIA (required criterion), masked facial expression (hypomimia), micrographia, stooped posture, and shuffling gait. He reports losing his sense of smell 2 years ago. What is the first-line pharmacotherapy and how should PD-related hallucinations be managed?

A. Propranolol; haloperidol for hallucinations

B. Levodopa/carbidopa (first-line); hallucinations treated with quetiapine (Seroquel) or pimavanserin (Nuplazid) — AVOID typical antipsychotics

C. Amantadine alone; risperidone for hallucinations

D. Deep brain stimulation; clozapine for hallucinations

Q56. [Parkinson's Disease]

A patient's neurologist notes that his parkinsonism symptoms do NOT respond to levodopa. He has autonomic failure, cerebellar ataxia, and parkinsonian features. What type of parkinsonism is this, and why does exogenous dopamine not help?

A. Idiopathic Parkinson's; levodopa should work — increase the dose

B. Atypical parkinsonism (e.g., Multiple System Atrophy); exogenous dopamine does NOT help because pathology is downstream of the dopamine pathway (protein buildup, not just dopamine depletion)

C. Essential tremor; treat with propranolol

D. Drug-induced parkinsonism; remove the offending drug

Q57. [Parkinson's Disease]

A 36-year-old man has dystonia, tremor, ataxia, and dysarthria. He has Kayser-Fleischer rings visible in his corneas. Serum ceruloplasmin is low and 24-hour urine copper is markedly elevated. What is the diagnosis and treatment?

A. Huntington's disease; VMAT-2 inhibitors

B. Wilson's disease (copper accumulation); penicillamine or trientine (copper chelation) + zinc

C. Essential tremor; propranolol

D. Multiple system atrophy; supportive care only

Q58. [Neurologic Exam]

On neurologic exam, a patient cannot wrinkle his forehead or close his right eye, has drooping of the right corner of his mouth, and loses taste on the right anterior 2/3 of the tongue. Which nerve is affected, and is this an UMN or LMN lesion?

A. CN V; UMN lesion

B. CN VII (facial nerve); LMN lesion — both upper AND lower face affected

C. CN VII; UMN lesion — only lower face affected (forehead spared)

D. CN XII; LMN lesion

Q59. [Neurologic Exam]

Using the reflex mnemonic '1-2 Buckle My Shoe (S1-2), 3-4 Shut the Door (L3-4), 5-6 Pick Up Sticks (C5-6), 7-8 Shut the Gate (C7-8),' which reflex corresponds to the C5-6 spinal levels?

A. Patellar reflex

B. Achilles reflex

C. Biceps and brachioradialis reflexes

D. Triceps reflex

Q60. [Neurologic Exam]

A patient can walk without arms for support when rising from a chair, maintains normal arm swing, but on tandem gait has difficulty. Romberg test: stands well with eyes OPEN but sways significantly with eyes CLOSED. What does this pattern indicate?

A. Cerebellar ataxia; Romberg is positive in cerebellar disease

B. Sensory ataxia (proprioceptive deficit); positive Romberg = SENSORY ataxia (posterior column or peripheral nerve)

C. Vestibular dysfunction only; no other significance

D. Normal finding; no pathology

Q61. [Neurologic Exam]

During a motor strength exam, a patient holds both arms extended with palms up and eyes closed for 20 seconds. The RIGHT arm slowly drifts DOWN and PRONATES. What does this indicate?

A. Normal finding; both arms drift slightly

B. Pronator drift = subtle corticospinal tract (UMN) weakness on the RIGHT side

C. Cerebellar disease causing bilateral drift

D. Sensory deficit preventing proprioceptive awareness of arm position

Q62. [Peripheral Neuropathy]

A 62-year-old woman with a 20-year history of type 2 diabetes has bilateral burning pain, numbness in both feet in a stocking distribution, absent ankle reflexes, and decreased vibration sense distally. She also has orthostatic hypotension and gastroparesis. What is the diagnosis and only two FDA-approved medications for painful diabetic neuropathy?

A. CIDP; IVIg + corticosteroids

B. Diabetic peripheral neuropathy (DPN); DULOXETINE (Cymbalta) and PREGABALIN (Lyrica)

C. GBS; plasma exchange

D. CRPS; physiotherapy and psychotherapy

Q63. [Peripheral Neuropathy]

A 45-year-old woman has progressive symmetric weakness starting from her feet over 6 days following a GI illness. She now has ascending weakness to her waist with AREFLEXIA and hypotonia. Sensory changes are minimal. Babinski is ABSENT. She has tachycardia and labile blood pressure. What is the diagnosis and most feared complication?

A. CIDP; symptoms >8 weeks; IVIg + steroids

B. GBS (AIDP); most feared complication = RESPIRATORY FAILURE (25% of cases); IVIg 2g/kg OR plasma exchange

C. MS relapse; IV methylprednisolone

D. Spinal cord compression; emergent MRI

Q64. [Basal Ganglia]

A patient with Parkinson's disease has decreased dopamine from SNc degeneration. How does this affect the direct and indirect basal ganglia pathways, and what is the clinical result?

A. Dopamine activates indirect pathway (decreases movement) and inhibits direct pathway — net result: increased movement

B. Dopamine activates direct pathway (increases movement) and inhibits indirect pathway — in PD, both are impaired → NET RESULT: decreased movement (bradykinesia, rigidity)

C. Dopamine has no effect on basal ganglia pathways

D. Dopamine only affects the indirect pathway

Q65. [Eye Anatomy]

A patient has a fixed, dilated (mydriatic) pupil on the left with ptosis and the eye deviated 'down and out.' Pupillary light reflex is absent in the LEFT eye with no consensual response when light is shone in the right eye. What nerve is affected, what is the most important cause to exclude, and how do you assess its function?

A. CN IV palsy; trauma; head tilt test

B. CN III (oculomotor) palsy; POSTERIOR COMMUNICATING ARTERY ANEURYSM — pupil-involving CN III palsy = PComm aneurysm until proven otherwise; assess with accommodation, EOMs, swinging light test

C. Horner's syndrome; first-order neuron; check for anhidrosis

D. CN VI palsy; ischemic; eye turns medially

Q66. [Vascular Disorders]

A 68-year-old man with hypertension presents with sudden onset of left-sided weakness, left facial droop, and aphasia. NIHSS score is 12. CT head is NEGATIVE for hemorrhage. He was last seen well 2 hours ago. What is the most appropriate treatment?

A. Aspirin 325mg and observation

B. IV tPA (alteplase) within 4.5 hours of symptom onset; goal tPA within 45 minutes of ED arrival; correct lab = glucose

C. Heparin drip immediately

D. Warfarin and discharge

Q67. [Vascular Disorders]

A 65-year-old man has a CT head showing intracerebral hemorrhage in the left basal ganglia. BP is 218/124. What is the most common cause of spontaneous intracerebral hemorrhage, and what is the immediate BP management goal?

A. Ruptured AVM; surgical excision immediately

B. Hypertension (#1 cause); gradually lower BP to 150/90 mmHg with labetalol or nicardipine

C. Amyloid angiopathy; warfarin reversal first

D. Bleeding disorder; FFP and platelets

Q68. [Vascular Disorders]

A 45-year-old woman is found to have an unruptured cerebral aneurysm on MRA obtained for headache evaluation. She is asymptomatic. The aneurysm is 4mm. What determines management, and what IS the gold standard imaging for a RUPTURED aneurysm presenting as SAH?

A. All aneurysms should be immediately clipped surgically

B. Unruptured: management based on size/location (watch vs. intervene); SAH: CT head first → if negative → LP for xanthochromia → then CTA/MRA

C. Angiography for both ruptured and unruptured — always first test

D. MRI with gadolinium is gold standard for both

Q69. [Red Flags]

Which of the following headache features represents the MOST serious red flag requiring EMERGENT neuroimaging?

A. Bilateral headache that is worse in the morning and improves after eating

B. Thunderclap onset ('worst headache of life') with neck stiffness = SAH until proven otherwise

C. Headache triggered by red wine in a known migraineur

D. Daily headaches for 6 months in a 35-year-old with no other symptoms

Q70. [Red Flags]

A 55-year-old woman with breast cancer has new-onset seizures and progressive headache. MRI shows multiple lesions at the gray-white junction. Which tumor-related red flag feature is present, and what does the gray-white junction location suggest?

A. Single lesion in the cerebellum; suggests primary GBM

B. Multiple lesions at the gray-white junction in a cancer patient = METASTATIC DISEASE until proven otherwise; red flag features include history of systemic cancer, progressive headache, new focal deficits, and seizures

C. Bitemporal hemianopia from pituitary compression

D. Enhancement along the meninges; suggests meningioma

Q71. [Integration]

A 70-year-old man has ataxic gait, absent ankle jerks, impaired vibration and proprioception in the feet, and autonomic dysfunction. CBC shows macrocytosis (MCV 108). Which test should be ordered first, and what classic B12 deficiency syndrome can produce these findings?

A. CT head without contrast; rule out stroke

B. Serum vitamin B12 (and methylmalonic acid/homocysteine); Subacute combined degeneration (SCD) of the spinal cord — posterior AND lateral column demyelination from B12 deficiency

C. EMG/NCS alone; diabetic neuropathy

D. MRI brain with contrast; MS plaques

Q72. [Integration]

A 55-year-old man with a 40 pack-year smoking history develops proximal muscle weakness that IMPROVES with repeated exercise. He also has dry mouth, orthostatic hypotension, constipation, and sluggish pupils. What is the diagnosis, its association with malignancy, and how does it differ from MG?

A. Myasthenia gravis; thymoma; worsens with use

B. Lambert-Eaton myasthenic syndrome (LEMS); SMALL CELL LUNG CANCER (50-70%); IMPROVES with repeated use (opposite of MG)

C. ALS; no malignancy association; LMN + UMN signs

D. CIDP; no malignancy; IVIg + steroids

Q73. [Integration]

A 30-year-old woman with bipolar disorder on long-term lithium and haloperidol presents with cognitive decline, RAPID progression (weeks), myoclonus, and focal neurologic deficits. EEG shows periodic sharp waves. CSF shows elevated 14-3-3 protein. MRI shows cortical ribboning on DWI. What is the diagnosis and prognosis?

A. Medication toxicity; discontinue lithium and haloperidol; full recovery expected

B. Prion disease (CJD); RAPID progressive dementia + myoclonus + periodic EEG sharp waves + 14-3-3 protein in CSF = CJD; NO CURE; death typically within months

C. Viral encephalitis; acyclovir

D. Autoimmune encephalitis; NMDA-R antibodies; steroids + IVIg

Q74. [Integration]

A 20-year-old college student in a dorm presents with fever of 40°C, severe headache, photophobia, neck stiffness, and a rapidly spreading maculopapular rash that becomes petechial. He is confused and tachycardic. What is the most likely organism, treatment, and important public health action?

A. HSV encephalitis; acyclovir; no public health action needed

B. Neisseria meningitidis; ceftriaxone 2g IV/IM immediately (do not wait for LP) + vancomycin; CHEMOPROPHYLAXIS for close contacts (rifampin, ceftriaxone, or ciprofloxacin) + DROPLET precautions

C. Streptococcus pneumoniae; penicillin; no contact precautions

D. Listeria monocytogenes; ampicillin; contact precautions

Q75. [Integration]

A 60-year-old man presents with weakness, double vision, and difficulty swallowing that have worsened throughout the day. He had a home-canned vegetable meal 18 hours ago. He has a DESCENDING paralysis with autonomic features (constipation, urinary retention, dry mouth, dilated FIXED pupils). What is the diagnosis, mechanism, and treatment?

A. GBS; post-infectious; IVIg

B. Botulism (Clostridium botulinum toxin); DESCENDING flaccid paralysis + autonomic symptoms from PRESYNAPTIC acetylcholine blockade; antitoxin (heptavalent HBAT) + supportive care

C. MG; AChR antibodies; pyridostigmine

D. LEMS; VGCC antibodies; 3,4-diaminopyridine

PART II — ANSWER KEY WITH CLINICAL RATIONALES

Q1. [Anatomy]  Answer: B

The Circle of Willis connects the anterior (ICA → ACA, MCA) and posterior (vertebral → basilar → PCA) circulations. The POSTERIOR COMMUNICATING ARTERY (PComm) bridges between the ICA and the posterior cerebral artery. An aneurysm at the PComm can compress CN III (causing a 'blown pupil' — dilated, non-reactive). The anterior communicating artery bridges the two ACAs. Together they allow collateral flow if one vessel is occluded.

Q2. [Anatomy]  Answer: C

Central retinal artery occlusion (CRAO) causes sudden, painless, MONOCULAR vision loss. The classic fundoscopic finding is a pale retina with a cherry-red spot at the fovea (the foveal blood supply from the choroidal circulation is preserved). The central retinal artery is the FIRST branch of the ophthalmic artery (itself the first branch of the ICA). CRAO is associated with thrombotic vascular events from the internal carotid artery.

Q3. [Anatomy]  Answer: C

The left optic tract carries fibers representing the RIGHT visual field (left temporal retina + right nasal retina). Damage to the LEFT optic tract causes LEFT HOMONYMOUS HEMIANOPIA — loss of the RIGHT visual field in BOTH eyes. Key rule: retro-chiasmal lesions cause contralateral homonymous deficits. Bitemporal hemianopia = chiasmal lesion (classic pituitary adenoma). Monocular blindness = optic nerve lesion (pre-chiasmal).

Q4. [Anatomy]  Answer: B

Brown-Séquard = hemisection of the spinal cord. IPSILATERAL side (right): loss of motor function (CST) + loss of proprioception and vibration (dorsal column — these fibers do NOT decussate until the medulla). CONTRALATERAL side (left): loss of pain and temperature (spinothalamic tract — these fibers decussate within 1-2 segments of entry). Key mnemonic: Same side loses motor + position; Opposite side loses pain + temperature.

Q5. [Anatomy]  Answer: B

Anterior spinal artery (ASA) syndrome = anterior cord syndrome. The ASA supplies the ANTERIOR 2/3 of the cord (corticospinal tract + spinothalamic tract). Deficit: bilateral loss of MOTOR (CST) + bilateral loss of PAIN and TEMPERATURE (STT). INTACT: proprioception and vibration (dorsal columns, supplied by posterior spinal arteries). The artery of Adamkiewicz is a critical supply to the thoracolumbar ASA and can be damaged during aortic surgery.

Q6. [Movement Disorders]  Answer: B

Essential tremor (ET) is the most common movement disorder. Bilateral, symmetric ACTION tremor (not resting), improves with alcohol, familial pattern (50-70%), normal neurologic exam. Key differentiators from PD: NO resting tremor, NO bradykinesia, NO micrographia, symmetric. Treatment: propranolol (first-line beta-blocker) or primidone (anti-epileptic). For refractory cases: deep brain stimulation, focused ultrasound, botulinum toxin.

Q7. [Movement Disorders]  Answer: B

Tourette syndrome DSM-5 criteria: (1) ≥2 motor tics AND ≥1 vocal tic, (2) >1 year duration, (3) onset before age 18, (4) not secondary to medication or medical condition. This patient meets all criteria. First-line: patient and family EDUCATION + behavior modification (CBIT — comprehensive behavioral intervention). Pharmacologic second-line: haloperidol or pimozide (FDA-approved). Frequently co-occurs with ADHD and OCD — treat comorbidities separately.

Q8. [Movement Disorders]  Answer: B

Tardive dyskinesia (TD): drug-induced involuntary repetitive movements, typically face/torso/limbs from long-term dopamine-blocking medications. Mechanism: chronic D2 receptor blockade → receptor UPREGULATION → hypersensitivity. First step: REMOVE or reduce the causative medication and allow ≥6 months. FDA-approved treatment if symptoms persist: VMAT-2 inhibitors — valbenazine (Ingrezza) or deutetrabenazine (Austedo). Acute dystonic reaction occurs within hours of a dose (not years), treated with benztropine.

Q9. [Movement Disorders]  Answer: B

Delirium tremens (DTs): occurs 2-4 DAYS after last drink. Features: confusion, agitation, autonomic hyperactivity (fever, tachycardia, severe HTN, diaphoresis), whole-body tremors, ±seizures. Critical labs: POC glucose → CMP with MAGNESIUM and potassium (dehydration + severe electrolyte imbalances). Treatment: ICU admission, IV fluids + electrolytes, THIAMINE before glucose, magnesium, BENZODIAZEPINES (first-line). Progression: minor withdrawal → major withdrawal → DTs → Wernicke → Korsakoff → coma/death.

Q10. [Movement Disorders]  Answer: B

Huntington's disease: autosomal DOMINANT, HTT gene CAG repeat >50, average onset age 40, average survival 15-20 years. Chorea = hyperkinetic (striatal neuron degeneration → impaired indirect pathway → uncontrolled thalamic output). FDA-approved treatment for CHOREA: VMAT-2 inhibitors — tetrabenazine or deutetrabenazine (Austedo). Note: deutetrabenazine is ALSO FDA-approved for tardive dyskinesia. Treat depression/anxiety/insomnia separately. Genetic counseling and prenatal testing for family members.

Q11. [CNS Tumors]  Answer: B

GBM is the most common and deadliest primary brain tumor in adults, ALWAYS Grade IV. Classic MRI: irregular RING-ENHANCING mass with central necrosis. Butterfly pattern (crossing corpus callosum) is pathognomonic. Average survival: 12 months. INCURABLE. Treatment: surgical debulking + radiation + temozolomide. Mass effect managed with dexamethasone. Personality changes suggest frontal lobe involvement. Red flag: progressive headache + personality change + seizure = CNS tumor until proven otherwise.

Q12. [CNS Tumors]  Answer: C

Prolactinoma is the most common secretory pituitary adenoma. 'Flat Pig' mnemonic = FSH, LH, ACTH, TSH, Prolactin, Inhibin, GH. Prolactin >200 is diagnostic; level correlates with tumor size. Women: amenorrhea + galactorrhea. Men: sexual dysfunction + gynecomastia. UNIQUE PEARL: prolactinoma is the ONLY pituitary tumor treated MEDICALLY (dopamine agonist: bromocriptine or cabergoline) rather than surgically. Dopamine normally OPPOSES prolactin release. To assess adrenal function from ACTH: check AM cortisol level (stimulation test).

Q13. [CNS Tumors]  Answer: B

Meningioma is the MOST COMMON benign CNS tumor (36%), arising from the meninges. Non-glial, slow-growing. MRI: dural-based, homogeneously enhancing, well-circumscribed mass. Management: OBSERVATION if asymptomatic — no surgery required for incidental asymptomatic meningioma. Surgery is indicated if causing symptoms (seizures, mass effect, neurologic deficits). Serial MRI to monitor growth. Key red flags warranting surgery: rapid growth, new symptoms, significant mass effect.

Q14. [CNS Tumors]  Answer: B

Brain metastases: 30% of cancer patients develop brain mets. Multiple lesions at the GRAY-WHITE JUNCTION = classic metastatic pattern (tumor cells lodge at the vascular transition zone). Primary tumor sources: LUNG = 40% (most common), Breast, Colon, Kidney, Melanoma = only 3% of brain mets but 40% of melanoma patients will develop them. Treatment is palliative (quality of life). Multiple enhancing lesions in a cancer patient = metastatic disease until proven otherwise.

Q15. [CNS Tumors]  Answer: B

NF1 (96% of cases): diagnosed in CHILDHOOD. Features: ≥6 café au lait spots (>5mm in children), axillary/inguinal freckling, cutaneous neurofibromas, Lisch nodules (iris hamartomas), optic gliomas. NF2 (rare): diagnosed in ADULTHOOD. Features: BILATERAL vestibular schwannomas (pathognomonic) + meningiomas. Symptoms: tinnitus, progressive hearing loss, balance difficulty. Both are autosomal dominant. Management: clinical monitoring + CNS tumor surveillance + appropriate specialist referrals.

Q16. [Seizures]  Answer: B

Absence seizures: generalized seizures with sudden, brief (< 20 seconds) lapses in awareness + sudden return, NO loss of body tone. Children accused of 'daydreaming.' EEG: 3-Hz generalized spike-and-wave. Typically RESOLVE by age 18. First-line: ETHOSUXIMIDE. No postictal phase. Distinguish from focal impaired awareness (temporal lobe origin, automatisms, postictal confusion). If untreated, can impair academic performance.

Q17. [Seizures]  Answer: B

Status epilepticus = seizure >5 minutes OR ≥2 seizures without return to baseline. Most seizures self-terminate in 1-3 minutes. Treatment ladder: (1) FIRST-LINE: benzodiazepines — lorazepam IV preferred, then diazepam IV or midazolam IM; (2) SECOND-LINE (concurrent): IV anticonvulsants — levetiracetam, valproate, or fosphenytoin; (3) THIRD-LINE (refractory): midazolam/pentobarbital/propofol infusion (medically induced coma). Check glucose immediately in all seizures.

Q18. [Seizures]  Answer: B

Focal IMPAIRED AWARENESS seizures with automatisms (lip smacking, hand movements) originate in the TEMPORAL LOBE in 75% of cases. Features: lapse in awareness + automatisms (unconscious repetitive behaviors). Patient has no memory of the event. Can last minutes to hours. If restrained: combative. First-line: LEVETIRACETAM (Keppra). Surgical option for refractory cases: lobectomy if foci is in the non-dominant temporal lobe.

Q19. [Seizures]  Answer: B

Valproic acid has the HIGHEST teratogenic risk: neural tube defects (10x increased risk), lower IQ, autism spectrum disorder. AVOID in all women of childbearing age if possible. Preferred ASMs in pregnancy: LEVETIRACETAM and LAMOTRIGINE (and oxcarbazepine). Folic acid supplementation is mandatory preconception. Note: OCPs reduce lamotrigine levels (potential breakthrough seizures); strong enzyme inducers (phenobarbital, phenytoin, carbamazepine) reduce OCP efficacy.

Q20. [Seizures]  Answer: C

PNES: sudden behavior changes that MIMIC seizures but do NOT correlate with abnormal EEG. Features suggesting PNES: patient RECALLS the event (true seizures cause amnesia), forced eye closure, pelvic thrusting, long episodes (>5 min), NO physical trauma (no tongue biting). Gold standard: VIDEO EEG MONITORING showing normal EEG during the clinical event. Associated with underlying psychiatric disorder, often history of sexual or physical abuse. Treatment: cognitive behavioral therapy (CBT). Never treat PNES with ASMs.

Q21. [MS / MG]  Answer: B

McDonald criteria: dissemination in SPACE (lesions in ≥2 of 4 areas: periventricular, juxtacortical, infratentorial, spinal cord) AND dissemination in TIME (new lesion on follow-up or simultaneous enhancing + non-enhancing lesions). RRMS = 85% of cases. CSF: oligoclonal bands + elevated IgG support diagnosis when MRI is equivocal. Acute relapse treatment: IV METHYLPREDNISOLONE 1,000mg daily x 3 days (shortens relapse but doesn't change long-term disability). MS is the leading cause of neurologic disability in young adults.

Q22. [MS / MG]  Answer: B

PML (Progressive Multifocal Leukoencephalopathy): FATAL demyelinating disease caused by JC virus reactivation in immunocompromised patients. Most commonly associated with natalizumab (Tysabri), fingolimod (Gilenya), dimethyl fumarate (Tecfidera), ocrelizumab (Ocrevus). JC antibody index should be monitored q6 months in natalizumab patients. High-risk patients (high JC index + >2 years on natalizumab) should consider switching therapy. The lecture case study (slide 149) specifically tests: ocrelizumab → PML = 'destruction of oligodendrocytes by the JC Virus.'

Q23. [MS / MG]  Answer: B

Myasthenia gravis (MG): chronic autoimmune NMJ disease, AChR antibodies (most common), MuSK Ab, LRP4 Ab. Key features: FATIGABLE weakness (worsens with use, improves with rest), ptosis/diplopia most common, PUPIL SPARING (distinguishes from CN III palsy), intact reflexes and sensation (pure motor NMJ). Ice pack test: applying ice to ptotic eye for 2 minutes IMPROVES ptosis. First-line outpatient: PYRIDOSTIGMINE (acetylcholinesterase inhibitor) — treats symptoms especially ocular. Thymectomy in AChR+ generalized MG. Myasthenic crisis (respiratory failure): IVIg or plasma exchange.

Q24. [MS / MG]  Answer: B

NMOSD differs from MS in that it predominantly affects the OPTIC NERVES and SPINAL CORD (longitudinally extensive transverse myelitis = ≥3 vertebral segments). Caused by antibodies against AQUAPORIN-4 (water channel in astrocytes). Test: serum AQP4-IgG (or MOG-IgG). NMOSD attacks tend to be more severe than MS. No periventricular white matter lesions (distinguishes from MS). Treatment targets the underlying antibody-mediated autoimmunity (rituximab, eculizumab). Distinct pathophysiology from MS — some MS treatments may WORSEN NMOSD.

Q25. [Spinal Cord]  Answer: B

Brown-Séquard syndrome: hemisection of the cord (penetrating injury most common). IPSILATERAL: motor loss (CST) + proprioception/vibration loss (dorsal column). CONTRALATERAL: pain/temperature loss (STT decussates). Best prognosis of incomplete SCIs. Central cord treatment pearl from the final outline: 'REPERFUSE THE SPINAL CORD' — maintain MAP >85 mmHg in acute SCI to ensure adequate spinal cord perfusion pressure. High-dose steroids (methylprednisolone) are controversial but may be used in acute SCI.

Q26. [Spinal Cord]  Answer: B

Central cord syndrome: MOST COMMON incomplete SCI. Caused by HYPEREXTENSION in elderly patients with pre-existing cervical stenosis. UE weakness > LE weakness (medial corticospinal fibers — cervical — are more centrally located than LE fibers). Also some pain/temperature loss (central STT). Treatment: reperfuse the spinal cord (MAP >85 mmHg) + surgical decompression when indicated. Best prognosis for ambulation recovery among incomplete SCIs.

Q27. [Spinal Cord]  Answer: B

Cauda equina syndrome (CES): compression of nerve roots below the conus medullaris. Most common cause: herniated disc. Classic: back pain → bilateral leg weakness + SADDLE ANESTHESIA + urinary RETENTION (PVR >100mL is red flag) + bowel/bladder/sexual dysfunction. Physical: LOWER motor neuron signs (areflexia, hypotonia), absent rectal tone, absent bulbocavernosus reflex. MRI LUMBAR SPINE = gold standard. SURGICAL EMERGENCY: decompression within 48 hours to prevent permanent neurologic damage.

Q28. [Spinal Cord]  Answer: B

Spinal epidural abscess: risk factors = IV drug use + diabetes (most common). S. aureus = most common organism. Classic triad: midline BACK PAIN + FEVER + NEUROLOGIC DEFICITS. Once deficits appear → PARALYSIS within 24 hours. Requires HIGH clinical suspicion. MRI WITH CONTRAST = imaging of choice, followed by needle aspiration. ESR >30 and CRP >10 support diagnosis. Treatment: SURGICAL EVACUATION (majority) + IV antibiotics 4-8 weeks. S. aureus → penicillin or 1st/2nd-gen cephalosporins; MRSA → vancomycin.

Q29. [Spinal Cord]  Answer: B

Spinal stenosis: narrowing of the spinal canal causing NEUROGENIC CLAUDICATION — pain, weakness, and numbness with walking/standing that is relieved by sitting, leaning forward, or lying down (flexion opens the canal). It is NOT an emergency. CES: acute compression of multiple cauda equina nerve roots causing saddle anesthesia + urinary retention (hallmark) + bowel/sexual dysfunction = SURGICAL EMERGENCY. Any patient with new urinary retention + saddle anesthesia + bilateral leg deficits = MRI immediately + emergent neurosurgical consultation.

Q30. [Dementia]  Answer: B

Vascular dementia: decline in function due to cerebrovascular events. Key features: ABRUPT onset of symptoms (following stroke), symptoms vary by location/size/number of infarcts, MRI shows infarcts. Risk factors = cardiovascular risk factors (HTN, DM, smoking, dyslipidemia). Treatment: manage vascular risk factors (aspirin, statins, BP control). Memory loss is LESS prominent than in Alzheimer's. Cognitive impairment often includes motor dysfunction, urinary incontinence, and sensory changes — depending on infarct location.

Q31. [Dementia]  Answer: B

CRITICAL TIMING DISTINCTION: Dementia with Lewy Bodies (DLB): COGNITIVE DECLINE comes FIRST (at least 1 year before extrapyramidal symptoms). Pathophysiology: alpha-synuclein aggregation (Lewy bodies) in basal ganglia. Features: fluctuating cognition, vivid visual hallucinations (early), extrapyramidal signs (come later). Parkinson's Disease Dementia (PDD): PARKINSON'S MOTOR SYMPTOMS come FIRST (at least 1 year before cognitive decline). Both: cholinesterase inhibitors first-line. For psychosis in DLB/PDD: quetiapine or pimavanserin — AVOID typical antipsychotics (worsen parkinsonism).

Q32. [Dementia]  Answer: B

Frontotemporal dementia (FTD): spectrum of syndromes involving degeneration of the FRONTAL and TEMPORAL lobes. KEY DISTINGUISHING FEATURES: YOUNGER age of onset (45-65), significant behavioral and language deterioration (vs memory loss in AD). Two subtypes: (1) Behavioral variant: sexual disinhibition, verbal disinhibition, loss of empathy, decline in social cues. (2) Language variant: temporal lobe dysfunction (speech/comprehension). Pathophysiology: TAU protein deposition, astrocytosis, microvacuole formation. No cure; treat behavioral symptoms with mood stabilizers.

Q33. [Dementia]  Answer: B

Normal pressure hydrocephalus (NPH): classic TRIAD = 'wet, wobbly, and wacky' — Gait instability (magnetic gait, small shuffling steps), Urinary incontinence, Cognitive decline. MRI: ENLARGED VENTRICLES out of proportion to cortical atrophy (unlike cerebral atrophy where both are enlarged). DIAGNOSTIC: improvement in GAIT after large-volume LP (tap test, 30-50mL CSF). TREATMENT: ventriculoperitoneal (VP) shunt. NPH is a REVERSIBLE cause of dementia/parkinsonism — critical not to miss.

Q34. [Motor Neuron Disease]  Answer: B

ALS (amyotrophic lateral sclerosis): BOTH UMN signs (hyperreflexia, spasticity, Babinski) AND LMN signs (fasciculations, atrophy, hyporeflexia) in the SAME patient with INTACT SENSATION. EMG: fibrillations + positive sharp waves. Average survival 2-4 years; 10% live to 10 years; 90% idiopathic. Treatment: riluzole, edaravone, tofersen (slow progression); BiPAP, PEG tube, speech therapy, early palliative care. PLS = UPPER MOTOR NEURON ONLY (no fasciculations, no atrophy, no LMN signs) — many patients live normal lifespan but become very disabled.

Q35. [Motor Neuron Disease]  Answer: B

Primary Lateral Sclerosis (PLS): UPPER MOTOR NEURON ONLY disease. Slowly progressive spasticity and clumsiness starting in one leg, progressing over months to DECADES. Dysarthria, dysphagia. NO fasciculations, NO atrophy, NO LMN signs. Sensory exam NORMAL. Idiopathic. No cure. Many patients live a NORMAL LIFESPAN but become significantly debilitated (requires careful prognostic counseling). Distinguished from ALS by absence of LMN signs. Breathing and bladder rarely affected (distinguishes from CES).

Q36. [Syncope]  Answer: B

POTS = orthostatic INTOLERANCE + excessive TACHYCARDIA (HR increase ≥30 bpm in adults, ≥40 in adolescents) WITHOUT orthostatic HYPOTENSION. Within 10 minutes of standing. Onset often follows viral illness, trauma, surgery, or pregnancy. Treatment: non-pharmacologic FIRST — 8-12g salt/day, 2-3L fluid/day, compression garments, gradual exercise, avoid caffeine/alcohol. Pharmacologic: fludrocortisone, midodrine, beta-blockers, ivabradine. Tilt table testing is definitive. Fludrocortisone = mineralocorticoid → ↑ sodium/water retention → ↑ plasma volume → reduces compensatory tachycardia.

Q37. [Syncope]  Answer: B

Vasovagal syncope: most common cause of syncope. Reflex-mediated (sudden ↓HR and ↓BP) from emotional stress, pain, prolonged standing, dehydration, heat. Classic PRODROME: pallor, lightheadedness, tunnel vision, nausea, diaphoresis. Complete and rapid recovery with full return to baseline. Patients may TWITCH during the episode (mimics seizure — important differential). Immediate treatment: SUPINE position. Long-term: AVOID TRIGGERS. ECG is the only universally required test per ACEP. Vasovagal = benign prognosis.

Q38. [Syncope]  Answer: B

Cardiac syncope carries the WORST prognosis of all syncope types. Red flags: sudden onset WITHOUT prodrome, EXERTIONAL, older age, family history of sudden cardiac death, structural heart disease. CHESS mnemonic for high-risk: Cardiac hx/CHF, Hematocrit <30%, ECG changes, SOB, SBP <90. QT-BRIDE for high-risk ECG patterns: QT prolongation, Brugada, Right heart strain, Ischemic changes, Delta waves (WPW), HCM. Deadly syncope mimics (Rule of 15): SAH, MI, PE, aortic dissection, AAA, ectopic pregnancy. ECG = only universally required test (ACEP).

Q39. [POTS / CRPS / Phantom Pain]  Answer: B

CRPS (complex regional pain syndrome): small fiber nerve damage causing DISPROPORTIONATE, intense pain with sensory, motor, and autonomic abnormalities in the affected limb. 90% occur after fracture/trauma/surgery. Budapest Criteria: (1) continuing pain disproportionate to the inciting event, (2) ≥1 symptom in all 4 categories (sensory, vasomotor, sudomotor/edema, motor/trophic), (3) no other diagnosis explains symptoms. MAINSTAY TREATMENT: PHYSIOTHERAPY + PSYCHOTHERAPY (multidisciplinary). Additional: neuromodulation, NSAIDs, anticonvulsants (pregabalin), ketamine, opioids. Amputation only for severe refractory cases.

Q40. [POTS / CRPS / Phantom Pain]  Answer: B

Phantom limb pain: perception of pain in an AMPUTATED limb. Nerve connections remain intact even though the limb is absent. Symptoms: burning, aching, stabbing, itching, throbbing. Diagnosis is CLINICAL after excluding residual limb causes (infection, poor blood flow, tight prosthetic). Key non-pharmacologic: MIRROR THERAPY — visual feedback of the intact limb tricks the brain into perceiving movement of the phantom limb, reducing pain. Also: virtual reality, TENS, spinal cord stimulation, mindfulness. Pharmacologic: NSAIDs, acetaminophen, antidepressants, ASMs, topical analgesics.

Q41. [Headaches]  Answer: C

Cluster headache: SEVERE unilateral periorbital pain lasting 15-180 minutes with IPSILATERAL autonomic features (conjunctival injection, tearing, ptosis, rhinorrhea, miosis). KEY DIFFERENTIATOR: patients PACE and cannot lie still (opposite of migraine where patients want to lie in a dark room). Attacks occur in clusters at the same time daily. Triggers: alcohol, cigarettes, nitrites, head trauma. RESCUE: INHALED 100% OXYGEN (12-15L/min via non-rebreather) is most common; also SQ sumatriptan and intranasal zolmitriptan. PREVENTION: high-dose verapamil.

Q42. [Headaches]  Answer: B

Migraine with aura (visual aura = 'squiggly lines'). DSM criteria for migraine without aura: ≥5 attacks, 4-72 hours, ≥2 of (unilateral/pulsating/moderate-severe/aggravated by activity), plus nausea/vomiting OR photophobia/phonophobia. PREVENTIVE therapy (≥4-6 migraine days/month): beta-blockers (propranolol, metoprolol), anticonvulsants (topiramate), CGRP inhibitors (injectable form), TCAs (amitriptyline), SNRIs (venlafaxine), onabotulinumtoxin A (chronic migraine). RESCUE/ABORTIVE: NSAIDs + triptans (rizatriptan, sumatriptan) + CGRP inhibitors (oral form).

Q43. [Headaches]  Answer: B

THUNDERCLAP headache = 'worst headache of life' with sudden onset = SUBARACHNOID HEMORRHAGE until proven otherwise. SAH: spontaneous (aneurysm, AVM) or traumatic. CT head is initially performed but may be NEGATIVE in 5-10% of SAH cases (especially if done >6 hours after onset). A NEGATIVE CT does NOT rule out SAH — LUMBAR PUNCTURE is mandatory to look for XANTHOCHROMIA (yellow CSF from breakdown of RBCs). SAH red flags: thunderclap onset, worst ever, neck stiffness, photophobia, vomiting, loss of consciousness. Treatment: emergent neurosurgical consultation (coiling or clipping).

Q44. [Headaches]  Answer: B

Trigeminal neuralgia (TGN): intermittent attacks of severe, electric shock-like FACIAL PAIN along the trigeminal nerve distribution (CN V), unilateral. TRIGGERS: touch, eating, talking, brushing teeth, cold, shaving, sneezing. Severe, paroxysmal, lasting seconds. Diagnosis is CLINICAL but all patients require MRI ± MRA to rule out vascular compression or mass. First-line: ANTICONVULSANTS — carbamazepine or oxcarbazepine. Second-line: gabapentin, lamotrigine, baclofen. Surgical: radiofrequency ablation, microvascular decompression, gamma knife.

Q45. [Meningitis / Encephalitis]  Answer: B

Bacterial meningitis classic triad: headache + HIGH FEVER + NECK STIFFNESS ± AMS, photophobia, petechial rash (meningococcemia). CSF: ELEVATED NEUTROPHILS (PMNs), VERY ELEVATED protein, LOW glucose. N. meningitidis = most common in ADOLESCENTS (college dorms, military). S. pneumoniae = most common in ADULTS. The lecture case (slide 156) matches: adolescent + petechial rash + PMN-predominant CSF = N. meningitidis. Empiric treatment: CEFTRIAXONE + VANCOMYCIN ±ampicillin (age >50 or immunocompromised — covers Listeria). Treat rapidly — do not wait for cultures.

Q46. [Meningitis / Encephalitis]  Answer: B

CSF differentiation (HIGH-YIELD): Bacterial meningitis: PMN (neutrophil) predominance, VERY elevated protein, LOW glucose (bacteria consume glucose), elevated opening pressure. Viral meningitis: LYMPHOCYTE predominance, mildly elevated protein, NORMAL glucose, normal-to-slightly elevated pressure. Fungal: elevated opening pressure, elevated protein, LOW glucose, variable cells. Key: LOW CSF glucose = bacterial or fungal. NORMAL CSF glucose = viral. Acyclovir if HSV suspected (even before results). Ceftriaxone + vancomycin if bacterial suspected.

Q47. [Meningitis / Encephalitis]  Answer: B

Viral encephalitis: BRAIN INFLAMMATION (vs meningitis = meningeal inflammation). Features: fever + headache + ALTERED MENTAL STATUS + seizures + focal neurologic deficits. MRI: temporal and frontal lobe inflammation. CSF: lymphocytic pleocytosis, elevated protein, NORMAL glucose. HSV 1 and 2 are the MOST COMMON causes of viral encephalitis. TREATMENT: ACYCLOVIR EMPIRICALLY while awaiting viral serology — start immediately (even before confirmation). Temporal lobe involvement = HSV until proven otherwise. Encephalitis = brain; Meningitis = meninges. AMS distinguishes encephalitis from meningitis.

Q48. [Hydrocephalus]  Answer: B

NPH is a COMMUNICATING hydrocephalus (CSF flows between ventricles but absorption is impaired). TRIAD: gait instability ('wet, wobbly, wacky'), cognitive decline, urinary incontinence. MRI: enlarged ventricles WITHOUT proportional cortical atrophy. TAP TEST (LP with 30-50mL CSF removal): gait IMPROVEMENT is diagnostic. Treatment: VP shunt. Obstructive hydrocephalus: CSF blocked BETWEEN ventricles (non-communicating); most common cause = tumor. Treatment: remove tumor or third ventriculostomy. Hypersecretory: overproduction by papilloma; treat with choroid plexus coagulation.

Q49. [Hydrocephalus]  Answer: B

IIH (idiopathic intracranial hypertension, pseudotumor cerebri): increased ICP with no identifiable cause. Risk factors: obese women (9/10 cases) aged 20-50, recent significant weight gain, CKD, lupus, iron deficiency. Symptoms: pulsatile tinnitus, headache, diplopia (CN VI palsy most common), visual changes, PAPILLEDEMA (key finding). MRI: normal (no mass, no hydrocephalus). LP: opening pressure >25 cmH2O with otherwise normal CSF. First-line: WEIGHT REDUCTION + ACETAZOLAMIDE (reduces CSF production). Escalation: topiramate, optic nerve sheath fenestration, CSF shunting, venous sinus stenting.

Q50. [Intracranial Hemorrhage]  Answer: B

EDH: classic 'lucid interval' → rapid deterioration from middle meningeal artery laceration (temporal bone fracture). CT: BICONVEX (lens-shaped), does NOT cross suture lines (dura is firmly attached at suture lines). Fixed dilated pupil IPSILATERAL to lesion (CN III compression from uncal herniation). CONTRALATERAL hemiparesis. EMERGENT SURGICAL EVACUATION = neurosurgical emergency. Excellent prognosis if detected and treated EARLY. SDH = crescent-shaped, CROSSES suture lines (bridging veins), associated with elderly/anticoagulated patients.

Q51. [Intracranial Hemorrhage]  Answer: B

Subdural hematoma (SDH): blood in SUBDURAL space, crescent-shaped, CROSSES suture lines (bridging veins). Risk: elderly, anticoagulated, alcoholics (brain atrophy stretches bridging veins). ACUTE SDH: hyperdense (bright white) on CT — blood is fresh. CHRONIC SDH: hypodense (dark, similar to CSF) on CT — occurs >3 weeks after injury, from repeat small bleeds/rebleeds. Presentation: gradual onset lethargy, confusion, headache. Treatment: neurosurgery consultation (conservative vs. surgical based on size and clinical status).

Q52. [Intracranial Hemorrhage]  Answer: B

SAH: spontaneous bleeding into the SUBARACHNOID SPACE. Most common cause: RUPTURED CEREBRAL ANEURYSM. 'Worst headache of life' + thunderclap onset = SAH until proven otherwise. CT: NEGATIVE in 5-10% of cases (sensitivity decreases after 6-12 hours). LP: XANTHOCHROMIA (yellow CSF from bilirubin from RBC breakdown) confirms SAH when CT is negative. Treatment: emergent neurosurgical consultation → endovascular COILING (preferred) or surgical CLIPPING. Nimodipine for vasospasm prevention (ONLY for aneurysmal SAH — NOT traumatic SAH). SAH = second most common cause of spontaneous intracranial hemorrhage after hypertensive ICH.

Q53. [Stroke / Hemorrhage]  Answer: B

TIA (transient ischemic attack): short-lived neurologic deficits with COMPLETE RESOLUTION, no infarct on imaging. NOT a benign diagnosis — 15% of patients have a STROKE within 90 days (especially in first 48 hours). Always obtain CT head first to RULE OUT HEMORRHAGE before antiplatelet therapy. Then MRI brain (DWI) for subtle ischemia. Complete evaluation: vessel imaging (CTA/MRA), cardiac ECHO, ECG (Afib), labs. Treatment: DUAL antiplatelet therapy for 21 days (aspirin + clopidogrel) for high-risk TIA (ABCD2 score). Address vascular risk factors.

Q54. [Cranial Nerve Palsy]  Answer: B

Bell's palsy: spontaneous unilateral PERIPHERAL CN VII palsy, usually post-viral. KEY DISTINCTION: UPPER AND LOWER face affected (including forehead wrinkle inability) = PERIPHERAL (LMN) CN VII lesion. CENTRAL (UMN) lesion (stroke): FOREHEAD IS SPARED (because upper face has bilateral cortical representation). Additional features: hyperacusis, loss of taste (anterior 2/3), decreased lacrimation. Treatment: CORTICOSTEROIDS within 72 hours (prednisone 60mg x 5 days then taper) ± antivirals (valacyclovir in severe cases). Supportive: artificial tears, eye taping at night. Ramsay Hunt syndrome: same presentation but caused by herpes ZOSTER (vesicles in ear canal).

Q55. [Parkinson's Disease]  Answer: B

Parkinson's disease clinical diagnosis (BRADYKINESIA is required criterion). First-line: LEVODOPA/CARBIDOPA — carbidopa inhibits peripheral conversion of levodopa, allowing more to reach the brain. PD hallucinations: quetiapine (least dopamine blockade) or PIMAVANSERIN (Nuplazid, FDA-approved for PD psychosis — serotonin antagonist, no dopamine blockade). AVOID haloperidol, risperidone, olanzapine (block dopamine → dramatically worsen parkinsonism). Patients die from COMPLICATIONS (aspiration pneumonia, falls) not from the disease itself. Life expectancy: 6-25 years after diagnosis.

Q56. [Parkinson's Disease]  Answer: B

Atypical parkinsonism (Multiple System Atrophy, Progressive Supranuclear Palsy, Corticobasal Degeneration): symptoms similar to PD (tremors, bradykinesia, rigidity) but with ADDITIONAL features and QUICKER progression. CRITICAL PEARL: exogenous dopamine (levodopa) does NOT help in atypical parkinsonism because the pathology involves protein buildup in multiple brain regions, not just dopamine neuron depletion in the substantia nigra. MSA: autonomic failure + parkinsonism + cerebellar ataxia. Treatment: treat the underlying disease. Drug-induced parkinsonism: bilateral onset, temporal relationship to medication, DaTScan normal.

Q57. [Parkinson's Disease]  Answer: B

Wilson's disease: autosomal recessive disorder preventing copper removal → accumulates in liver, brain, eyes. KAYSER-FLEISCHER RINGS (copper deposits in Descemet membrane of cornea — visible on slit-lamp) are pathognomonic. Neurologic: dystonia, tremor, ataxia, dysarthria, parkinsonism. Labs: LOW ceruloplasmin, ELEVATED 24-hour urine copper. Treatment: copper CHELATION with penicillamine or trientine; ZINC blocks intestinal copper absorption. Liver transplant for severe hepatic disease. ALWAYS in the differential for movement disorders in young patients.

Q58. [Neurologic Exam]  Answer: B

CN VII (facial nerve): LMN lesion affects BOTH upper AND lower face (including forehead wrinkle and eye closure). UMN (central/stroke) lesion: FOREHEAD IS SPARED because upper face has bilateral cortical representation. Test: raise eyebrows, wrinkle forehead, close eyes tightly, show teeth, puff cheeks. If forehead involved = LMN (peripheral) = Bell's palsy territory. If forehead SPARED = UMN (central stroke). Additional CN VII functions: taste (anterior 2/3 tongue), lacrimation, salivation. Hyperacusis = stapedius muscle paralysis.

Q59. [Neurologic Exam]  Answer: C

Reflex levels (high-yield mnemonic): S1-S2 = Achilles ('1-2 Buckle My Shoe'); L3-L4 = Patellar knee jerk ('3-4 Shut the Door'); C5-C6 = Biceps AND Brachioradialis ('5-6 Pick Up Sticks'); C7-C8 = Triceps ('7-8 Shut the Gate'). Graded 0-4+ with 2+ being normal. Hyperreflexia (3-4+) = UMN lesion. Hyporeflexia/areflexia (0-1+) = LMN lesion or peripheral neuropathy. When performing DTR exam: use distraction, compare sides, grade each reflex.

Q60. [Neurologic Exam]  Answer: B

ROMBERG TEST: Patient stands with feet together, eyes open (uses vision + proprioception + vestibular). Then eyes CLOSED (removes vision → relies only on proprioception + vestibular). POSITIVE Romberg (sways/falls with eyes closed) = SENSORY ATAXIA (proprioceptive deficit, posterior column disease, peripheral neuropathy). CEREBELLAR ataxia: patient is UNSTABLE with BOTH eyes open AND closed (cerebellum doesn't need visual input for coordination). Key: Romberg positive = sensory problem (posterior column or peripheral neuropathy). Romberg negative but ataxia = cerebellar.

Q61. [Neurologic Exam]  Answer: B

PRONATOR DRIFT: Patient holds arms extended, palms up, eyes closed. A normal arm maintains position. If one arm DRIFTS DOWN and PRONATES → subtle CORTICOSPINAL TRACT (UMN) weakness on that side. This is a sensitive test for mild hemiparesis not obvious on standard strength testing. The pronation occurs because flexor tone overrides extensor tone when the corticospinal tract is compromised. Document: 'Pronator drift positive on the right, suggesting subtle right corticospinal tract dysfunction.' Key exam pearl: drift to one side after eye closure = pyramidal tract involvement ipsilateral to the drift.

Q62. [Peripheral Neuropathy]  Answer: B

Diabetic peripheral neuropathy (DPN): most common peripheral neuropathy. SENSORY + MOTOR + AUTONOMIC neuropathy. Glove-stocking distribution, worst distally. Annual screening for ALL diabetic patients. AUTONOMIC involvement: orthostatic hypotension, gastroparesis, bladder dysfunction, anhidrosis, sexual dysfunction. FDA-approved for painful DPN: DULOXETINE (Cymbalta — SNRI) and PREGABALIN (Lyrica — calcium channel alpha-2-delta ligand). Gabapentin is commonly used off-label. Glycemic control is the most important preventive measure. Non-healing wounds → amputation risk.

Q63. [Peripheral Neuropathy]  Answer: B

GBS (AIDP = acute inflammatory demyelinating polyradiculoneuropathy): ascending symmetric weakness, AREFLEXIA, post-infectious (Campylobacter jejuni most common; GI or respiratory illness 1-6 weeks prior). Babinski ABSENT (LMN disease — no UMN signs). AUTONOMIC: tachycardia, labile BP, anhidrosis. MOST FEARED COMPLICATION: respiratory failure in 25% (monitor FVC serially — intubate if FVC <20mL/kg or NIF worse than -25 cmH2O). Treatment: IVIg 2g/kg over 5 days OR plasma exchange. STEROIDS NOT effective in GBS. Miller Fisher variant: ataxia + areflexia + ophthalmoplegia.

Q64. [Basal Ganglia]  Answer: B

Basal ganglia dopamine dual role: dopamine ACTIVATES the DIRECT pathway (net: increased movement) AND INHIBITS the INDIRECT pathway (net: decreased movement). Result: dopamine = net PRO-MOVEMENT. In PD: SNc pars compacta loses dopamine neurons → BOTH pathway effects are lost → NET EFFECT: too much inhibition of thalamus → DECREASED movement (bradykinesia, rigidity, tremor). In Huntington's: GABA degeneration of striatal neurons → indirect pathway disinhibited → INCREASED uncontrolled movement (chorea). DBS targets subthalamic nucleus (PD) to block this excessive inhibition.

Q65. [Eye Anatomy]  Answer: B

CN III palsy: PTOSIS (levator palpebrae superioris) + eye deviated DOWN and OUT (unopposed CN IV/VI) + PUPIL DILATED and non-reactive (parasympathetic fibers run on outside of CN III are compressed first). Causes: ischemic (diabetes/hypertension = most common overall) OR posterior communicating artery aneurysm (compresses CN III externally). PUPIL-INVOLVING CN III palsy = PComm aneurysm until PROVEN otherwise — EMERGENT imaging required. Pupil-SPARING CN III palsy = more likely ischemic (diabetes/HTN). Test: accommodation, EOMs (H pattern), swinging light test.

Q66. [Vascular Disorders]  Answer: B

Ischemic stroke treatment window: tPA (alteplase) within 3 hours (up to 4.5 hours if meeting criteria: age <80, no prior CVA+DM, NIHSS <25, not on anticoagulants, <1/3 MCA territory). Goal: tPA within 45 MINUTES of ED arrival. ONLY required lab BEFORE tPA: FINGERSTICK GLUCOSE (hypoglycemia mimics stroke). tPA contraindications: prior ICH, ischemic stroke <3 months, active bleeding, BP >185/110, platelets <100k, DOAC use <48 hours. NIHSS score on admission = strong predictor of prognosis. Mechanical thrombectomy for large vessel occlusion up to 24 hours.

Q67. [Vascular Disorders]  Answer: B

Intracerebral (intraparenchymal) hemorrhage: bleeding INTO brain parenchyma. Most common cause: HYPERTENSION (#1), followed by alcohol abuse and smoking. Common locations: basal ganglia, cerebral lobes, brainstem, cerebellum. CT head (no contrast) = GOLD STANDARD — blood appears bright white acutely. BP management: GRADUALLY decrease to 150/90 mmHg (NOT rapid drop — risks ischemia). Preferred agents: LABETALOL or NICARDIPINE. Reverse anticoagulation if applicable. Prognosis: poor — 30-50% mortality. Only 20% of survivors achieve independence.

Q68. [Vascular Disorders]  Answer: B

Unruptured aneurysm: management depends on SIZE (small <3mm usually watch; large >7mm usually intervene), LOCATION, and patient factors. Serial MRA/CTA imaging for surveillance. Treatment options: endovascular coiling (preferred) or surgical clipping or stenting. RUPTURED aneurysm (SAH): CT head w/o contrast FIRST (gold standard for acute blood). If CT NEGATIVE → LP (xanthochromia confirms SAH when CT negative). THEN CTA or MRA for aneurysm localization. Angiography for definitive pre-surgical planning. SAH treatment: emergent neurosurgery + NIMODIPINE for vasospasm prevention.

Q69. [Red Flags]  Answer: B

Headache RED FLAGS (SNOOP4): Systemic symptoms/disease (fever, weight loss, HIV/cancer), Neurologic symptoms (focal deficits, AMS), Onset sudden/thunderclap, age >50 new headache, Pattern change from prior headaches, Postural component, Precipitated by Valsalva/exertion, Progressive worsening. MOST URGENT: thunderclap 'worst headache of life' = SAH until proven otherwise. Other red flags: new headache in cancer patient (metastasis), headache waking from sleep, headache in elderly without prior history, headache with fever and neck stiffness (meningitis/encephalitis). Neuroimaging NOT indicated in patients with recurrent headaches that match a primary headache pattern, normal neuro exam, and no red flags.

Q70. [Red Flags]  Answer: B

Brain tumor red flags: history of systemic cancer (most likely metastatic), progressive/worsening headache, new focal neurologic deficits, seizures in a middle-aged or older patient without prior epilepsy, personality change, papilledema (elevated ICP). GRAY-WHITE JUNCTION: characteristic location for METASTATIC disease (vascular transition zone where tumor emboli lodge). Primary GBM: irregular ring-enhancing single mass in cortex. Meningioma: dural-based, enhancing. In a cancer patient, assume brain mets until proven otherwise. Most common source: lung > breast > colon > kidney > melanoma.

Q71. [Integration]  Answer: B

Subacute combined degeneration (SCD): posterior AND lateral (corticospinal) column demyelination from VITAMIN B12 DEFICIENCY. Combined syndrome: posterior column signs (loss of vibration/proprioception/sensory ataxia) + UMN signs (hyperreflexia, Babinski) + peripheral neuropathy (areflexia if severe). Macrocytosis = clue. Causes: pernicious anemia, strict veganism, GI malabsorption, long-term metformin. Lhermitte's sign (electric shock with neck flexion) can occur. Diagnosis: serum B12, methylmalonic acid, homocysteine. Treatment: B12 replacement (IM if malabsorption). Also listed as a cause of Lhermitte's sign in Week 4.

Q72. [Integration]  Answer: B

Lambert-Eaton myasthenic syndrome (LEMS): autoimmune NMJ disease (presynaptic VGCC antibodies). 50-70% associated with SMALL CELL LUNG CANCER — LEMS may be the FIRST symptom. Key: proximal weakness that IMPROVES with REPEATED use (facilitation — opposite of MG which worsens with use). AUTONOMIC symptoms: dry mouth, orthostatic hypotension, constipation, SLUGGISH PUPILS (sympathetic/parasympathetic involvement — helps distinguish from other NMJ diseases). EMG: INCREMENTING response with high-frequency stimulation. Treatment: treat the primary tumor; symptoms improve after malignancy removal; 3,4-diaminopyridine for symptoms.

Q73. [Integration]  Answer: B

Prion disease (Creutzfeldt-Jakob Disease = most common prion disease in humans): RAPID progressive cognitive decline + myoclonus + periodic sharp waves on EEG + elevated 14-3-3 protein in CSF + cortical ribboning on MRI DWI. Onset typically >60 years (sporadic CJD = 85%). No cure — supportive care with early hospice. Death within months of symptom onset. CJD variants: vCJD (younger patients, exposure to BSE/mad cow disease, 'florid plaques'); Kuru (ritualistic cannibalism, New Guinea). Genetic counseling for family members if inherited form.

Q74. [Integration]  Answer: B

Meningococcemia (N. meningitidis): gram-negative diplococcus transmitted via aerosolized secretions. High-risk: college students (dorms), military personnel, complement-deficient patients. Classic: fever + severe headache + neck stiffness + PETECHIAL/PURPURIC RASH (meningococcemia). TREAT IMMEDIATELY — do NOT wait for LP. Ceftriaxone 2g IV/IM + vancomycin + ±dexamethasone (before first antibiotic dose). PUBLIC HEALTH: CHEMOPROPHYLAXIS for all close contacts (rifampin, ceftriaxone, or ciprofloxacin) within 24 hours. DROPLET precautions. Meningococcal VACCINE (3 types available in the US for age >10) — primary prevention.

Q75. [Integration]  Answer: B

Botulism: Clostridium botulinum toxin blocks PRESYNAPTIC acetylcholine RELEASE at the NMJ. DESCENDING paralysis (starts with cranial nerves → works downward — opposite of GBS which ascends). Pupil involvement (fixed, dilated) — important differentiator from MG (MG spares pupils). AUTONOMIC features: constipation, urinary retention, dry mouth, absent gag reflex. Sources: home-canned/preserved foods (food-borne), wound (IV drug use), infant botulism (honey). TREATMENT: heptavalent botulinum antitoxin (HBAT) + supportive care (respiratory support). Early recognition is critical — respiratory failure can develop rapidly. No benefit from anticholinesterases.