MCCQE Part I neurology questions

This patient has a confirmed large vessel occlusion (M1 segment of the middle cerebral artery) with a favorable ASPECTS score and a large mismatch between infarct core and penumbra on perfusion imaging, meeting criteria for mechanical thrombectomy up to 24 hours from last known well in selected patients. Thrombectomy for anterior circulation LVO within this extended window relies on imaging-based selection (core-penumbra mismatch) rather than time alone, per current Canadian and international stroke guidelines. IV alteplase should still be given if within its own eligibility window, but thrombectomy is the definitive management for LVO. Anticoagulation and hemicraniectomy are not indicated here, and carotid endarterectomy addresses extracranial disease, not an intracranial M1 occlusion.

• A. Alteplase alone is insufficient for a confirmed large vessel occlusion with a large salvageable penumbra; it should be combined with thrombectomy when eligible, not used alone as the definitive step.
• B. Endarterectomy treats carotid artery disease, not an M1 occlusion, and is not an acute intervention for this presentation.
• C. Heparin is not indicated in acute ischemic stroke and does not address the occlusion.
• D. Hemicraniectomy is reserved for malignant edema with impending herniation, not initial management of LVO.

Non-contrast CT of the head is the fastest and most widely available imaging study to exclude intracranial hemorrhage before administering alteplase, and it is the standard first investigation in all acute stroke protocols. CT is highly sensitive for acute hemorrhage and can be performed within minutes, which is critical given the narrow time window for thrombolysis. MRI is more sensitive for early ischemic changes but takes longer to perform and is not necessary to exclude hemorrhage before treatment. Carotid ultrasound and echocardiography are useful for determining stroke etiology but play no role in the acute decision to thrombolyse. Lumbar puncture is reserved for suspected subarachnoid hemorrhage with a negative CT or suspected infection, not for routine acute stroke evaluation.

• A. Lumbar puncture is not indicated in this presentation and could be dangerous if there is elevated intracranial pressure.
• B. Echocardiography investigates a cardioembolic source but has no role in the immediate exclusion of hemorrhage.
• D. MRI is more sensitive but too slow for the acute thrombolysis decision and is not required to rule out hemorrhage.
• E. Carotid ultrasound evaluates extracranial stenosis and does not assess for hemorrhage or guide the acute thrombolysis decision.

Pure motor hemiparesis with a lesion localized to the internal capsule is the classic lacunar syndrome, caused by occlusion of small, deep penetrating arteries (lenticulostriate branches) due to chronic hypertension and diabetes. The underlying pathology is lipohyalinosis, a degenerative process in small vessel walls characterized by hyaline thickening and narrowing of the lumen, distinct from the large-vessel atherosclerosis seen in carotid disease. Lacunar infarcts typically present with isolated motor or sensory deficits without cortical signs like aphasia, neglect, or visual field loss because the small lesion spares the cortex. Cardioembolism and carotid atherosclerotic embolism typically cause cortical infarcts with larger territories and additional cortical signs. Berry aneurysm rupture causes subarachnoid hemorrhage, not ischemic infarct, and vasculitis is a rare cause unrelated to this classic hypertensive small vessel pattern.

• A. Berry aneurysm rupture causes subarachnoid hemorrhage, presenting with sudden severe headache, not an ischemic capsular infarct.
• B. Carotid bifurcation emboli typically cause cortical MCA territory infarcts with cortical signs, not isolated small deep lacunar lesions.
• C. Vasculitis is an uncommon cause of stroke and would not be the most likely mechanism in a patient with classic vascular risk factors and a typical lacunar syndrome.
• D. Cardioembolic strokes usually produce larger cortical infarcts with features like aphasia or neglect, not pure motor lacunar syndromes.

An ABCD2 score of 5 places this patient in the high-risk category for recurrent stroke within the next 48 hours to 7 days, warranting urgent same-day evaluation including brain imaging (CT or MRI) and vascular imaging (carotid Doppler or CT angiography) to identify a treatable source such as carotid stenosis or atrial fibrillation. Canadian stroke best practice guidelines recommend that high-risk TIA patients be assessed within 24 hours in a stroke prevention clinic or emergency department rather than waiting weeks for outpatient follow-up. Rapid identification of a treatable etiology allows timely initiation of secondary prevention, including antiplatelet therapy, statins, and possible carotid endarterectomy if significant stenosis is found. Delaying imaging or follow-up for weeks exposes the patient to unacceptable risk of a disabling stroke during the highest-risk period.

• A. Scheduling MRI in 2 weeks is too delayed for a high-risk TIA; imaging and vascular workup should occur the same day.
• B. Admission without imaging delays identification of a treatable cause and does not align with urgent same-day imaging protocols.
• C. Waiting 4 to 6 weeks for neurology follow-up is far too long for a high ABCD2 score; this delay carries substantial stroke risk.
• D. Starting aspirin without urgent imaging misses the chance to identify and treat a high-grade carotid stenosis or cardioembolic source promptly.

For symptomatic patients with ipsilateral carotid stenosis of 70-99%, carotid endarterectomy performed within 2 weeks of the triggering event provides the greatest reduction in stroke recurrence, as the benefit of surgery is highest when performed early after symptom onset. This patient has a clearly symptomatic TIA referable to the stenotic carotid artery and is a good surgical candidate given his functional independence and absence of major comorbidities. Current guidelines favor endarterectomy over stenting in most patients, particularly older patients, due to lower periprocedural stroke risk with surgery. Delaying intervention for months significantly reduces its benefit because the highest risk of recurrent stroke occurs in the weeks immediately following the index event. Indefinite medical therapy alone is inferior to endarterectomy for this degree of symptomatic stenosis.

• A. Repeating ultrasound in 3 months delays necessary intervention during the highest-risk period for stroke recurrence.
• B. Medical therapy alone is inferior to endarterectomy for symptomatic stenosis of 70% or greater; dual antiplatelet therapy also increases bleeding risk if used long term.
• D. Stenting is generally reserved for patients at high surgical risk or with contraindications to surgery, not as a strategy to wait for further progression.
• E. Delaying surgery for 6 months eliminates most of the benefit, since recurrent stroke risk is highest in the early weeks after the TIA.

In cardioembolic stroke due to atrial fibrillation, anticoagulation is typically delayed to reduce the risk of hemorrhagic transformation while still preventing early recurrent embolism. For a moderate-sized infarct without hemorrhage, starting a direct oral anticoagulant around day 3 to 7 after confirming no hemorrhagic transformation on repeat or follow-up imaging balances these risks. Very early initiation (within 48 hours) increases hemorrhagic transformation risk, especially with larger infarcts, while excessive delay increases recurrent stroke risk. Bridging with heparin is not recommended in this setting, and antiplatelet therapy alone is inferior to anticoagulation for stroke prevention in atrial fibrillation.

• A. Antiplatelet therapy alone is inferior to anticoagulation for secondary stroke prevention in atrial fibrillation.
• C. Heparin bridging before oral anticoagulation is not supported by current guidelines in this setting.
• D. Immediate anticoagulation raises the risk of hemorrhagic transformation in a sizeable fresh infarct.
• E. A 4-week delay is excessive for a moderate infarct and unnecessarily raises recurrent embolic stroke risk.

A sudden, maximal-intensity headache (thunderclap headache) described as the worst of one's life, especially triggered by exertion and accompanied by meningismus, is classic for subarachnoid hemorrhage until proven otherwise. Aneurysmal rupture is the most common cause of spontaneous subarachnoid hemorrhage and often presents this way. Migraine typically has a more gradual onset over minutes to hours and lacks neck stiffness. Bacterial meningitis usually presents with fever and a more subacute course. Reversible cerebral vasoconstriction syndrome can cause thunderclap headache but is far less common and is a diagnosis of exclusion after subarachnoid hemorrhage is ruled out.

• A. Migraine headaches build up gradually rather than reaching maximal severity within seconds to minutes.
• B. Cervicogenic headache does not typically reach maximal intensity instantly or present as the worst headache of life.
• C. This is a less common cause of thunderclap headache and must be considered only after excluding subarachnoid hemorrhage.
• D. Bacterial meningitis typically presents with fever and a more progressive course rather than sudden maximal headache.

When a high-quality non-contrast CT performed within 6 to 24 hours of symptom onset is read as normal by an experienced radiologist, current guidelines still recommend lumbar puncture to assess for xanthochromia, as CT sensitivity, while very high in the first 6 hours, is not absolute, particularly as more time elapses. Xanthochromia on spectrophotometry reliably distinguishes true subarachnoid hemorrhage from a traumatic lumbar puncture. CT angiography is used to identify an aneurysm once subarachnoid hemorrhage is confirmed, not as the initial test to rule it out when CT is negative. MRI and EEG do not have adequate sensitivity or specificity for this purpose in the acute setting.

• B. CT angiography identifies a bleeding source after subarachnoid hemorrhage is confirmed, not as the screening test when CT is negative.
• C. EEG has no role in diagnosing subarachnoid hemorrhage.
• D. MRI is not the standard next step and is less sensitive than lumbar puncture with spectrophotometry for detecting subarachnoid blood after CT is negative.
• E. Repeating CT does not add diagnostic value when clinical suspicion remains high after an adequate initial negative CT.

Delayed cerebral ischemia due to vasospasm typically occurs between days 4 and 14 after aneurysmal subarachnoid hemorrhage and presents with new focal deficits or altered consciousness, as in this case. Nimodipine is given prophylactically to reduce the incidence and severity of vasospasm-related ischemic injury, though it does not eliminate the risk. The normal blood pressure and absence of new hemorrhage or hydrocephalus on CT make hypotension, rebleeding, and obstructive hydrocephalus unlikely explanations. While seizure is a differential consideration, the clinical context and timing make vasospasm the most likely diagnosis, and further workup typically includes transcranial Doppler or CT angiography.

• A. CT shows no hydrocephalus, excluding this as the cause.
• B. CT shows no new hemorrhage, making rebleeding unlikely.
• D. The clinical timing and absence of described seizure activity make vasospasm more likely than a postictal state.
• E. Her blood pressure is normal, making hypotension an unlikely cause of her new deficits.

In acute intracerebral hemorrhage with significantly elevated blood pressure, current evidence and guidelines support careful intravenous titration to a target systolic blood pressure of approximately 140 mmHg to reduce hematoma expansion while avoiding hypoperfusion. Labetalol or nicardipine, given as intravenous infusions with close monitoring, allow smooth, controlled reduction rather than precipitous drops. Withholding treatment risks ongoing hematoma expansion, while rapid uncontrolled lowering with sublingual agents like nifedipine can cause dangerous swings in cerebral perfusion pressure. Mannitol addresses elevated intracranial pressure but does not substitute for blood pressure control, and oral therapy is inappropriate in this emergent, high-acuity setting.

• A. Oral therapy is too slow and unreliable for this acute, high-risk presentation.
• B. Untreated severe hypertension increases the risk of ongoing hematoma expansion and worse outcomes.
• D. Mannitol treats elevated intracranial pressure but does not address the need for controlled blood pressure reduction.
• E. Sublingual nifedipine causes an unpredictable, rapid drop in blood pressure that can compromise cerebral perfusion.

Migraine with aura is characterized by fully reversible visual, sensory, or speech disturbances that develop gradually over 5 to 60 minutes and precede or accompany a migraine headache. The described positive visual phenomenon (zigzag lines) evolving gradually, followed by a unilateral throbbing headache lasting hours with nausea and photophobia, fits the International Classification of Headache Disorders criteria for migraine with aura. Tension-type headache is typically bilateral, pressing, and without aura. Cluster headache is strictly unilateral, periorbital, and associated with autonomic features, occurring in bouts. Transient ischemic attack and seizure typically have an abrupt onset or different evolution and lack the characteristic migrainous headache pattern.

• A. TIA symptoms typically have abrupt onset and do not gradually evolve over 20 minutes in this stereotyped positive visual pattern.
• B. Seizures usually have a more abrupt onset and different evolution, and do not typically precede a classic migrainous headache pattern.
• D. Tension-type headache lacks aura and the migrainous features described, such as throbbing quality and nausea.
• E. Cluster headache is typically much shorter, strictly unilateral periorbital, and associated with autonomic symptoms like lacrimation or rhinorrhea.

Medication overuse headache is diagnosed when a patient with a pre-existing primary headache disorder develops headache on 15 or more days per month in the setting of regular overuse of acute headache medications (combination analgesics or opioids on 10 or more days per month, or simple analgesics on 15 or more days per month) for over 3 months. This patient's escalating use of an opioid-combination analgesic on 20 days per month closely parallels the increase in headache frequency, strongly implicating medication overuse. Management requires withdrawal of the overused medication along with initiation of migraine prophylaxis. This diagnosis is important because continued analgesic use perpetuates the cycle of headache chronification.

• A. Idiopathic intracranial hypertension typically presents with papilledema and visual symptoms, which are absent here.
• B. This diagnosis would not explain the clear temporal relationship between increased combination analgesic use and headache chronification.
• C. New daily persistent headache begins acutely without a prior episodic headache history and is not explained by medication use.
• E. Trigeminal autonomic cephalalgias feature unilateral pain with cranial autonomic symptoms, not a bilateral pressure headache pattern.

This patient's presentation of severe, strictly unilateral periorbital pain with ipsilateral autonomic features (conjunctival injection, tearing, ptosis, miosis), occurring in bouts with restlessness, is classic for cluster headache. High-flow oxygen (typically 100% at 12-15 L/min via non-rebreather mask for 15-20 minutes) is first-line abortive therapy for acute cluster attacks and provides rapid relief in most patients. Subcutaneous or intranasal triptans are the other first-line acute option. Oxygen therapy is preferred in this setting because it has a rapid onset, is safe, and can be used even with multiple daily attacks.

• A. Corticosteroids may be used as a short-term bridge prophylaxis in cluster headache but are not the acute abortive treatment of choice for an individual attack.
• B. Propranolol is not used for cluster headache; verapamil is the preferred prophylactic agent for this condition.
• D. Topiramate is not a standard treatment for cluster headache, which is instead usually managed with verapamil for prevention.
• E. Intramuscular ketorolac is not an effective or guideline-recommended treatment for acute cluster headache attacks.

Tension-type headache characteristically presents with bilateral, pressing or tightening (non-pulsatile) pain of mild to moderate intensity that does not worsen with routine physical activity and is not associated with nausea, vomiting, photophobia, or phonophobia. This contrasts with migraine, which is typically unilateral, pulsatile, moderate to severe, aggravated by activity, and accompanied by nausea and/or photophobia and phonophobia. This patient's clinical picture fits all the typical features of tension-type headache rather than migraine. Tension-type headache is the most common primary headache disorder and is generally managed with simple analgesics and lifestyle measures.

• A. Migraine with aura requires transient neurological aura symptoms preceding or accompanying the headache, which are absent in this case.
• C. Hemicrania continua is a strictly unilateral, continuous headache with autonomic features, which does not match this patient's bilateral, non-autonomic presentation.
• D. Cluster headache presents with severe unilateral periorbital pain and ipsilateral autonomic features, not a bilateral band-like ache.
• E. Migraine without aura requires features such as unilateral location, pulsatile quality, aggravation by activity, or associated nausea/photophobia/phonophobia, none of which are present here.

This patient's presentation is a classic thunderclap headache (maximal intensity within one minute) with neck stiffness, which is a red flag requiring urgent investigation to rule out subarachnoid hemorrhage. Non-contrast CT of the head is the first-line investigation and has very high sensitivity for detecting subarachnoid hemorrhage when performed within 6 hours of symptom onset. If CT is negative but clinical suspicion remains, a lumbar puncture should follow to look for xanthochromia or red blood cells. Immediate imaging is essential because untreated subarachnoid hemorrhage carries a high risk of rebleeding and death.

• A. A thunderclap headache with meningismus requires urgent same-day evaluation, not delayed outpatient referral.
• C. Lumbar puncture should generally follow a non-contrast CT, not precede it, both to assess for hemorrhage and avoid risks related to raised intracranial pressure.
• D. MRI is not the first-line test in the acute setting for suspected subarachnoid hemorrhage; CT is faster, more available emergently, and highly sensitive early.
• E. Empiric migraine treatment is inappropriate and dangerous without first excluding a life-threatening secondary cause given the thunderclap onset.

This patient has idiopathic intracranial hypertension (pseudotumor cerebri), supported by her risk factor of obesity, typical headache pattern, pulsatile tinnitus, papilledema, elevated opening pressure with normal cerebrospinal fluid composition, and normal imaging aside from an empty sella. The most feared complication of idiopathic intracranial hypertension is progressive, irreversible visual loss from chronic papilledema causing optic nerve damage, which is why serial visual field testing and ophthalmologic monitoring are essential. Treatment includes weight loss, acetazolamide, and in refractory cases with progressive visual loss, surgical interventions such as optic nerve sheath fenestration or cerebrospinal fluid shunting. Visual field constriction, as seen in this patient, is an early warning sign requiring close follow-up and often escalation of therapy.

• A. Hydrocephalus with cognitive decline is not a recognized complication of idiopathic intracranial hypertension, which has normal ventricular size on imaging.
• C. Transtentorial herniation is not a typical risk in idiopathic intracranial hypertension, which does not usually cause a mass effect or midline shift.
• D. Idiopathic intracranial hypertension is not an infectious process, so bacterial meningitis is not a related complication.
• E. Cerebral venous sinus thrombosis is an important condition to exclude as a secondary cause of raised intracranial pressure but is not a complication arising from idiopathic intracranial hypertension itself.

This patient's presentation of new temporal headache, jaw claudication, temporal artery tenderness with a diminished pulse, and markedly elevated erythrocyte sedimentation rate is highly suggestive of giant cell arteritis. Because this condition carries a significant risk of sudden, irreversible vision loss from ophthalmic artery involvement, high-dose glucocorticoids (typically oral prednisone 40-60 mg daily) should be started immediately on clinical suspicion, without waiting for biopsy confirmation. Temporal artery biopsy should still be arranged promptly, ideally within 1-2 weeks of starting steroids, as the histological changes typically persist for this period despite treatment. Early steroid initiation is a widely endorsed guideline recommendation given the time-sensitive risk to vision.

• B. Delaying steroids until biopsy confirmation risks permanent vision loss and is not recommended given the urgency of this diagnosis.
• C. Low-dose acetylsalicylic acid alone does not treat the underlying vasculitis and would not prevent vision loss.
• D. Methotrexate is sometimes used as a steroid-sparing agent in refractory or relapsing disease, but it is not appropriate as initial monotherapy in acute presentation.
• E. Imaging is not required before initiating urgent treatment when the clinical picture and inflammatory markers strongly suggest giant cell arteritis.

In Ontario, physicians have a mandatory legal duty under the Highway Traffic Act to report patients who have a condition that may impair their ability to drive safely, including a first unprovoked seizure, to the Ministry of Transportation. Most Canadian provinces require a minimum seizure-free period (commonly 6 to 12 months, depending on seizure type and etiology) before driving privileges for a private licence can be reinstated. This reporting duty exists independent of the ongoing diagnostic workup and overrides patient confidentiality in the interest of public safety. Deferring the report or allowing continued driving pending investigations breaches this legal obligation and places the public at risk.

• A. Reporting is mandatory at the time of the seizure, not deferred until investigations are complete.
• C. There is no provision for a partial restriction to highway driving only; the seizure must be reported for a full driving assessment.
• D. Reporting is required after the first unprovoked seizure, not only after a recurrence.
• E. Continuing to drive pending investigations violates the mandatory reporting duty and risks public safety.

Valproic acid carries the highest risk among antiepileptic drugs for major congenital malformations (neural tube defects, cardiac and craniofacial anomalies) and for neurodevelopmental impairment, including lower IQ and autism spectrum disorder, even at doses considered therapeutic. Current guidelines, including those followed in Canadian practice, recommend avoiding valproate in women of childbearing potential unless no other effective alternative exists, after a specialist discussion of risks. Lamotrigine and levetiracetam have substantially lower teratogenic risk profiles and are preferred first-line options for women who may become pregnant. Folic acid supplementation, contraception, dose minimization, or anomaly screening do not eliminate valproate's disproportionate teratogenic risk and do not substitute for choosing a safer agent when one is available.

• B. Relying on contraception does not address the unplanned pregnancy risk given inconsistent use, and a safer drug alternative should be chosen instead.
• C. Folic acid supplementation reduces some neural tube defect risk generally but does not offset valproate's uniquely high teratogenic and neurodevelopmental risk.
• D. Even at low doses, valproate carries disproportionately higher teratogenic risk compared with alternative antiepileptics.
• E. Planning for anomaly screening after conception does not prevent the malformation risk; a safer agent should be chosen before pregnancy occurs.

Nystagmus, ataxia, and dysarthria are the classic triad of phenytoin toxicity, which follows a dose-dependent progression: nystagmus appears first, followed by ataxia, and then dysarthria and altered mental status at higher levels. The elevated serum level of 32 mg/L confirms toxicity in this patient who took extra doses to compensate for missed ones. Because phenytoin exhibits zero-order (saturation) kinetics at higher concentrations, small dose increases above the therapeutic range can cause disproportionate rises in serum level, making careful dose titration and monitoring essential. Management involves holding or reducing the dose and rechecking levels rather than treating for an alternative diagnosis.

• A. Wernicke encephalopathy classically presents with confusion, ophthalmoplegia, and ataxia in the setting of thiamine deficiency, not an elevated phenytoin level after dose errors.
• B. A cerebellar stroke would not explain the markedly elevated phenytoin level and typically has an acute focal onset rather than a gradual presentation tied to dosing changes.
• D. Multiple sclerosis relapse does not explain the elevated drug level and is not suggested by this acute presentation in a patient without a prior MS diagnosis.
• E. There is no history of benzodiazepine use, and the elevated phenytoin level directly explains the clinical picture.

A simple febrile seizure is defined as a generalized seizure lasting less than 15 minutes, occurring once in a 24-hour period, in a neurologically normal child aged 6 months to 5 years without CNS infection or prior afebrile seizures. This child meets all these criteria, so no neuroimaging, EEG, or lumbar puncture is routinely required, and the child can be discharged with reassurance and fever management education for the parents. A complex febrile seizure (prolonged over 15 minutes, focal features, or recurrence within 24 hours) raises concern and may prompt further evaluation. Lumbar puncture is reserved for signs suggesting meningitis, incomplete immunization, or infants under 12 months with insufficient Hib/pneumococcal vaccination, none of which apply here.

• A. EEG is not indicated for a simple febrile seizure as it does not change management or predict future epilepsy risk in this setting.
• B. This seizure meets all criteria for a simple febrile seizure, so it is not classified as complex and neuroimaging is unnecessary.
• D. The seizure is febrile (occurred with fever), not afebrile, and the presentation meets simple febrile seizure criteria rather than warranting admission.
• E. Lumbar puncture is reserved for signs of meningitis or incomplete immunization status, not required for a simple febrile seizure in this well-appearing child.

Psychogenic nonepileptic seizures (PNES) are characterized by prolonged duration (often over 2 minutes), asynchronous or out-of-phase limb movements, pelvic thrusting, forced eye closure with resistance to opening, retained partial recall, and absence of true postictal confusion, all of which are present here. The definitive diagnostic finding is normal EEG recorded during the actual clinical event on video-EEG monitoring, confirming no cortical epileptiform correlate. True epileptic seizures, including focal seizures with secondary generalization, typically show stereotyped, synchronous motor activity with EEG correlate and are followed by postictal confusion. PNES requires a multidisciplinary approach involving neurology and psychiatry, often related to underlying psychological trauma as suggested in this patient's history.

• A. Absence status epilepticus presents with impaired consciousness and characteristic generalized epileptiform discharges on EEG, not normal EEG with thrashing movements.
• B. Nocturnal frontal lobe seizures occur during sleep with brief hypermotor or tonic activity and would show epileptiform correlates, unlike this case.
• D. Focal epileptic seizures would show an EEG correlate during the event and typically produce more stereotyped, synchronous movements with postictal confusion.
• E. Frontal lobe epilepsy seizures are typically brief, stereotyped, and show an EEG or semiological correlate, unlike this normal EEG during a prolonged asynchronous event.

Alcohol withdrawal seizures classically occur 6 to 48 hours after the last drink, consistent with this patient's timeline, and result from unmasked neuronal hyperexcitability due to downregulation of inhibitory GABA-A receptors and upregulation of excitatory NMDA receptors during chronic alcohol exposure. Benzodiazepines, which potentiate GABA-A receptor activity, are first-line for both treating the acute seizure and preventing further withdrawal seizures or progression to delirium tremens. Phenytoin and other antiepileptics are not effective for alcohol withdrawal seizures because the mechanism is not related to sodium channel pathology. Delirium tremens, characterized by hallucinations, severe autonomic instability, and confusion, typically occurs 48 to 96 hours after cessation and is not yet present here; antipsychotics are not first-line and can lower seizure threshold.

• A. This presentation at 30 hours without hallucinations or severe confusion is not yet delirium tremens, and antipsychotics are not first-line and may lower seizure threshold.
• B. There are no signs of liver failure or asterixis suggesting hepatic encephalopathy in this presentation.
• D. Phenytoin and other standard antiepileptics are ineffective for preventing or treating alcohol withdrawal seizures because the underlying mechanism involves GABA and NMDA receptor changes, not targeted by these drugs.
• E. There is no evidence of ophthalmoplegia, confusion, or ataxia to suggest Wernicke encephalopathy, though thiamine should still be given as routine prophylaxis in alcohol use disorder.

Asymmetric onset of bradykinesia, rest tremor, and cogwheel rigidity in an older adult, with preserved reflexes and no early postural instability or cognitive decline, is classic for idiopathic Parkinson disease. The asymmetry at onset is a key clinical clue that helps distinguish it from atypical parkinsonian syndromes, which tend to present more symmetrically and with additional early features (falls, autonomic failure, eye movement abnormalities). Diagnosis remains clinical, based on bradykinesia plus rest tremor or rigidity, with a good response to dopaminergic therapy supporting the diagnosis. Micrographia and reduced arm swing are classic early signs reflecting bradykinesia.

• B. Corticobasal degeneration presents with markedly asymmetric rigidity, apraxia, and alien limb phenomenon, which are absent here.
• C. Multiple system atrophy features early autonomic failure, cerebellar signs, or symmetric parkinsonism poorly responsive to levodopa.
• D. Progressive supranuclear palsy presents with early falls, vertical gaze palsy, and symmetric axial rigidity, not seen here.
• E. Normal pressure hydrocephalus presents with the triad of gait disturbance, urinary incontinence, and cognitive decline, not a unilateral rest tremor.

As Parkinson disease progresses, nigrostriatal neurons progressively lose their capacity to store and buffer dopamine, so striatal dopamine levels increasingly mirror the pulsatile pharmacokinetics of oral levodopa rather than being smoothed out. This leads to a narrowing therapeutic window: wearing-off (end-of-dose deterioration) and peak-dose dyskinesias (choreiform, dystonic movements at peak drug levels). This is the pathophysiologic basis of long-term levodopa-induced motor fluctuations, which affect the majority of patients after 5-10 years of therapy. Management includes dose fractionation, extended-release or adjunctive agents (MAO-B inhibitors, COMT inhibitors), or advanced therapies in refractory cases.

• B. Levodopa motor fluctuations arise centrally from disease progression, not from altered hepatic clearance of the drug.
• C. Levodopa does not provoke a clinically significant antibody-mediated response; this is not a recognized mechanism.
• D. Cholinergic neuron loss is implicated in Parkinson disease-related cognitive decline, not in motor fluctuations.
• E. Alpha-synuclein pathology in autonomic ganglia underlies dysautonomia in Parkinson disease, not dyskinesia from levodopa therapy.

Drug-induced parkinsonism results from blockade of postsynaptic D2 dopamine receptors in the striatum by antipsychotic medications, functionally reducing dopaminergic transmission without destroying dopaminergic neurons. This produces bradykinesia and rigidity that are typically symmetric and lack the classic asymmetric rest tremor of idiopathic Parkinson disease, as seen in this patient. Onset is temporally linked to starting or increasing the offending drug, and symptoms improve with dose reduction, discontinuation, or switching to an agent with lower D2 affinity. Distinguishing this from idiopathic Parkinson disease is important because the underlying nigrostriatal neurons are structurally intact and the condition is reversible.

• A. There is no autoimmune destruction of basal ganglia neurons in drug-induced parkinsonism; the receptors remain intact but blocked.
• B. Lewy body accumulation is the pathological hallmark of idiopathic Parkinson disease and dementia with Lewy bodies, not drug-induced parkinsonism.
• C. Acetylcholinesterase inhibition increases cholinergic activity and is unrelated to antipsychotic-induced extrapyramidal symptoms, which result from dopamine blockade.
• E. Nigrostriatal neuronal degeneration is the mechanism of idiopathic Parkinson disease, not drug-induced parkinsonism, which is a functional receptor blockade.

Restless legs syndrome is strongly associated with iron deficiency, as iron is a cofactor for tyrosine hydroxylase in dopamine synthesis within the central nervous system, and low brain iron stores are implicated in its pathophysiology. Serum ferritin is the most appropriate initial investigation in any patient presenting with restless legs syndrome, particularly when risk factors for iron deficiency are present, such as heavy menstrual bleeding and a vegetarian diet in this patient. A ferritin level below approximately 75 mcg/L warrants iron supplementation, which can significantly improve symptoms. Nerve conduction studies, polysomnography, B12 levels, and spinal imaging are not first-line investigations unless an alternative diagnosis such as peripheral neuropathy or radiculopathy is suspected based on examination findings.

• A. Polysomnography is used to evaluate for periodic limb movements of sleep or other sleep disorders, but is not the first investigation when the clinical diagnosis of restless legs syndrome is already apparent.
• B. Nerve conduction studies would be indicated if examination suggested peripheral neuropathy, which is not supported by her normal sensory and motor examination.
• C. Vitamin B12 deficiency can cause neuropathic symptoms but is not the primary association with restless legs syndrome; her normal examination makes neuropathy less likely.
• E. Lumbosacral MRI would be considered if there were findings suggesting radiculopathy or myelopathy, which are absent on her normal neurologic examination.

This patient meets the 2017 McDonald criteria for multiple sclerosis: she has had two clinically distinct episodes (dissemination in time by history) and lesions in at least two of the typical MS locations, periventricular, juxtacortical, and spinal cord (dissemination in space), with CSF-specific oligoclonal bands providing additional supportive evidence that can substitute for radiologic dissemination in time when only one clinical attack has occurred. The lesions are non-enhancing, consistent with lesions of different ages reflecting separate inflammatory episodes rather than a single monophasic process. Oligoclonal bands restricted to CSF reflect intrathecal immunoglobulin synthesis and are found in roughly 90% of MS patients, supporting the diagnosis. This presentation, with resolving sensory and motor deficits in a young woman, is classic for a relapsing-remitting course.

• A. Susac syndrome involves the triad of encephalopathy, branch retinal artery occlusions, and sensorineural hearing loss, none of which are present here.
• C. Acute disseminated encephalomyelitis is a monophasic illness, usually post-infectious, with widespread lesions and encephalopathy, inconsistent with this patient's two distinct relapsing episodes.
• D. Neuromyelitis osteomyelitis spectrum disorder typically causes severe longitudinally extensive spinal cord lesions or bilateral optic neuritis and is associated with aquaporin-4 antibodies, not the pattern seen here.
• E. CNS vasculitis typically presents with systemic inflammatory features, infarct-pattern lesions, and abnormal vessel imaging, not discrete demyelinating lesions with CSF-specific oligoclonal bands.

The finding described is a relative afferent pupillary defect (Marcus Gunn pupil), which occurs when optic nerve inflammation in one eye, as in this patient's left optic neuritis, reduces the afferent visual signal reaching the midbrain from that eye compared with the healthy eye. When light is swung to the affected eye, the weaker afferent signal results in less pupillary constriction than expected, which appears as paradoxical dilation relative to the preceding consensual constriction. The efferent pupillary pathway (cranial nerve III and its parasympathetic fibers) is intact bilaterally, which is why direct and consensual responses are preserved when testing the unaffected eye. This finding, combined with painful unilateral vision loss and disc swelling in a young woman, is characteristic of optic neuritis, a common presenting feature of multiple sclerosis.

• A. Horner syndrome causes a small (miotic) pupil with ptosis and anhidrosis due to sympathetic denervation, not the dilation seen with the swinging light test here.
• B. The efferent parasympathetic pathway is intact in optic neuritis; the defect lies in the afferent (sensory) limb of the pupillary light reflex, not the efferent limb.
• C. A tonic pupil results from ciliary ganglion damage causing a pupil that reacts slowly to light with light-near dissociation, which is a different mechanism from the relative afferent pupillary defect described.
• D. Oculomotor nerve compression would cause a fixed, dilated pupil with impaired direct and consensual responses and typically ptosis and ophthalmoplegia, not the swinging flashlight pattern described.

Acute MS relapses causing functionally significant symptoms, such as optic neuritis with visual loss, are treated with high-dose intravenous corticosteroids (methylprednisolone 1 g daily for 3 to 5 days), which hastens recovery by reducing inflammation and blood-brain barrier disruption at the site of demyelination, though it does not alter long-term disability. Low-dose oral steroids are not of proven benefit and may worsen outcomes in optic neuritis. Disease-modifying therapies like natalizumab are used for long-term relapse prevention, not acute treatment. Plasma exchange is reserved for steroid-refractory relapses.

• A. Low-dose oral corticosteroids are not an effective treatment for acute optic neuritis and may increase recurrence risk.
• B. Functionally significant relapses such as vision loss warrant treatment to hasten recovery, not observation.
• C. Plasma exchange is reserved for relapses that fail to respond to high-dose corticosteroids.
• E. Natalizumab is a maintenance disease-modifying therapy, not an acute relapse treatment.

Disease-modifying therapies in relapsing-remitting MS aim to reduce relapse frequency and the development of new or enlarging lesions on MRI, which correlates with reduced disability accumulation over time. These agents work through various immunomodulatory mechanisms but do not repair existing demyelination or axonal loss that has already occurred. Corticosteroids remain the treatment for acute relapses regardless of DMT use. While early effective DMT use may reduce the likelihood of progression, it cannot guarantee prevention in every patient since conversion to secondary progressive MS can still occur.

• A. Patients on DMTs may still experience relapses requiring corticosteroid treatment.
• B. DMTs are immunomodulatory and do not reverse established axonal or myelin damage.
• C. No current therapy cures the underlying autoimmune process in MS.
• E. DMTs reduce but do not guarantee prevention of conversion to progressive disease in every patient.

Guillain-Barré syndrome following Campylobacter jejuni enteritis is classically explained by molecular mimicry: antibodies generated against the bacterium's lipooligosaccharide cross-react with gangliosides (such as GM1 and GD1a) on peripheral nerve myelin and axons, triggering an autoimmune attack. This mechanism underlies the acute inflammatory demyelinating or axonal neuropathy seen in GBS, including the areflexia and ascending weakness described. There is no direct bacterial invasion of nerves; the mechanism is immune-mediated, not infectious or toxin-mediated.

• A. GBS is not caused by viral reactivation in dorsal root ganglia; that mechanism describes herpes zoster.
• B. Vasculitic immune complex deposition describes a different mechanism of neuropathy, not classic post-infectious GBS.
• C. GBS is immune-mediated, not due to direct bacterial invasion of nerve tissue.
• E. Toxin-mediated neuromuscular blockade describes botulism, not GBS.

A declining FVC approaching or below 20 mL/kg (or an absolute value under 15-20 mL/kg), rapid progression of weakness, bulbar involvement, or autonomic instability are indications for ICU transfer in GBS because of the risk of impending respiratory failure requiring mechanical ventilation. Oxygen saturation and respiratory rate are insensitive late markers and can remain normal until the patient is close to decompensating, so FVC trend is the key bedside parameter to follow. Oxygen therapy alone does not address the underlying neuromuscular respiratory failure and may mask hypoventilation by maintaining saturation.

• A. There is no indication of infection; antibiotics are not indicated based on these findings.
• B. Discharge is inappropriate given rapidly progressive weakness and a declining FVC indicating respiratory compromise.
• D. Supplemental oxygen does not treat neuromuscular respiratory failure and normal saturation can falsely reassure while ventilatory failure progresses.
• E. A falling FVC in a patient with rapidly progressive weakness warrants immediate escalation, not delayed repeat testing.

Intravenous immunoglobulin (IVIG) or plasma exchange are equally effective first-line treatments for Guillain-Barré syndrome in patients who are unable to walk independently or have significant functional impairment, and should be started as soon as possible after diagnosis, ideally within 2 weeks of symptom onset. IVIG works by modulating the immune response, including saturation of Fc receptors and neutralization of pathogenic antibodies. Corticosteroids have not been shown to improve outcomes in GBS and are not recommended. Combining IVIG and plasma exchange does not confer additional benefit over either alone.

• A. Pyridostigmine is used to improve neuromuscular transmission in myasthenia gravis, not GBS.
• B. Interferon beta-1a is a disease-modifying therapy for multiple sclerosis, not GBS.
• C. Azathioprine is a chronic immunosuppressant used in conditions like myasthenia gravis or CIDP, not acute GBS.
• D. Corticosteroids, unlike in CIDP, have not shown benefit in acute GBS and are not recommended.

Fluoroquinolones such as ciprofloxacin can precipitate myasthenic crisis by impairing neuromuscular transmission, and this patient's hypoxia, tachypnea, poor cough, and neck flexor weakness indicate impending respiratory failure requiring urgent ICU transfer for close monitoring and potential mechanical ventilation. Increasing pyridostigmine is not appropriate in impending respiratory failure, as excess cholinergic stimulation can worsen secretions and does not substitute for securing the airway. The priority is airway and ventilatory assessment and support before addressing the precipitating medication.

• A. Bronchodilators do not address neuromuscular respiratory failure and delaying escalation risks further decompensation.
• B. Adjusting cholinergic medication does not address the urgent risk of respiratory failure and may worsen secretions through excess cholinergic effect.
• D. While the offending antibiotic should eventually be stopped, ward-level observation is inadequate given signs of impending respiratory failure.
• E. Atropine treats cholinergic excess (muscarinic side effects), not the neuromuscular weakness of myasthenic crisis.

This presentation of nocturnal paresthesia and sensory loss confined to the median nerve distribution (thumb, index, and middle fingers), with a positive Tinel sign at the wrist, is classic for carpal tunnel syndrome, which is common in pregnancy due to fluid retention and soft tissue swelling causing median nerve compression at the wrist; it is also associated with hypothyroidism, diabetes, and acromegaly. Cervical radiculopathy typically presents with neck pain and a dermatomal pattern not isolated to the median nerve distribution. Thenar weakness or atrophy may develop in more severe or chronic cases but is not required for diagnosis.

• B. Ulnar neuropathy at the elbow causes sensory loss in the fourth and fifth digits, not the thumb through middle finger.
• C. Thoracic outlet syndrome typically causes symptoms in an ulnar or diffuse distribution with possible vascular signs, not isolated median nerve sensory loss at the wrist.
• D. De Quervain tenosynovitis causes pain over the radial wrist with thumb movement, not numbness in a median nerve sensory distribution.
• E. C6 radiculopathy typically involves neck pain radiating down the arm and may include the thumb but usually also affects the forearm in a dermatomal pattern, and lacks a positive Tinel sign at the wrist.

Bell palsy is an idiopathic, unilateral lower motor neuron facial palsy affecting the forehead, eye closure, and lower face equally, because the facial nerve nucleus and nerve itself are affected distal to the point where upper facial muscles receive bilateral cortical innervation. In contrast, a central (upper motor neuron) lesion such as stroke spares the forehead because those muscles retain bilateral cortical input. The absence of vesicles, other cranial neuropathies, or limb findings argues against Ramsay Hunt syndrome, Guillain-Barré syndrome, or demyelinating disease. Bell palsy is a diagnosis of exclusion based on this classic pattern.

• A. A lacunar stroke causing facial weakness would typically spare the forehead due to bilateral cortical innervation of the upper face.
• C. Guillain-Barré syndrome typically causes ascending symmetric limb weakness and areflexia, not isolated unilateral facial palsy.
• D. Ramsay Hunt syndrome is caused by varicella-zoster reactivation and presents with a vesicular rash in the ear canal or on the pinna, which is absent here.
• E. Multiple sclerosis would typically present with other neurologic findings such as optic neuritis or limb symptoms, and isolated facial palsy is not typical.

This patient's presentation of saddle anesthesia, urinary retention, and bilateral leg weakness with sciatica is classic for cauda equina syndrome, a surgical emergency caused by compression of the lumbosacral nerve roots below the conus medullaris. Urgent MRI of the lumbosacral spine is required without delay to confirm the diagnosis and identify the compressive lesion, most commonly a large central disc herniation, so that emergency surgical decompression can be arranged before permanent neurologic damage occurs. Delay in imaging and surgery beyond 24-48 hours is associated with worse outcomes for bladder and bowel function.

• A. Lumbar puncture is not indicated and could be harmful if there is a mass lesion causing compression.
• C. Nerve conduction studies take time to arrange and do not identify the compressive lesion; they have no role in this emergency.
• D. Plain radiographs do not visualize soft tissue or nerve root compression and are inadequate to diagnose cauda equina syndrome.
• E. Outpatient management is inappropriate and dangerous given red flag signs requiring emergency evaluation and likely surgery.

This presentation of back pain, progressive bilateral leg weakness, a sensory level, and new bladder involvement in a patient with known metastatic cancer is highly suggestive of malignant spinal cord compression, an oncologic emergency. Immediate intravenous dexamethasone should be given to reduce vasogenic edema around the tumour and preserve neurologic function, followed by urgent MRI of the entire spine to localize the lesion and guide definitive treatment with radiation therapy or surgical decompression. Delay in treatment increases the risk of irreversible paraplegia and permanent sphincter dysfunction.

• B. Lumbar puncture does not diagnose cord compression and may be unsafe in this setting.
• C. Imaging is required before radiation to confirm the level and extent of compression and guide the treatment field.
• D. Outpatient imaging introduces unacceptable delay in a patient with rapidly progressive neurologic deficits.
• E. Bisphosphonates and physiotherapy do not address the acute cord compression and delay necessary emergency treatment.

Anterior cord syndrome results from infarction in the territory of the anterior spinal artery, which supplies the corticospinal and spinothalamic tracts while sparing the dorsal columns supplied by the posterior spinal arteries. This produces bilateral motor weakness and loss of pain and temperature sensation below the lesion, with preservation of vibration and proprioception, exactly as seen in this patient. It is classically precipitated by hypotension or aortic surgery compromising spinal cord perfusion. Posterior cord syndrome, in contrast, selectively impairs vibration and proprioception with preserved motor and pain/temperature function.

• A. Complete transverse myelitis would cause loss of all sensory modalities below the lesion, including vibration and proprioception, which are preserved here.
• C. Posterior cord syndrome causes loss of vibration and proprioception with preserved motor function and pain/temperature sensation, the opposite of this presentation.
• D. Brown-Séquard syndrome results from cord hemisection and causes ipsilateral motor and dorsal column loss with contralateral pain/temperature loss, not bilateral symmetric findings.
• E. Central cord syndrome typically causes greater weakness in the upper limbs than the lower limbs, often after hyperextension injury in an older patient.

Subacute combined degeneration results from vitamin B12 deficiency impairing methylation reactions required for myelin synthesis, leading to demyelination of the dorsal columns and lateral corticospinal tracts of the spinal cord. Dorsal column involvement explains the loss of vibration and position sense with a positive Romberg sign, while corticospinal tract involvement explains the extensor plantar responses (upper motor neuron sign). Concurrent peripheral neuropathy from B12 deficiency can cause absent ankle reflexes, producing a mixed picture of upper and lower motor neuron findings. Treatment with parenteral vitamin B12 can halt or partially reverse the deficits if started promptly.

• A. Isolated peripheral axonal loss would not explain the extensor plantar responses, which indicate corticospinal tract involvement.
• B. Neuromuscular junction pathology, as in myasthenia gravis, causes fatigable weakness without sensory loss or upper motor neuron signs.
• D. Anterior horn cell demyelination is not the mechanism of B12-related myelopathy and would cause pure lower motor neuron signs.
• E. Anterior spinal artery infarction would cause loss of pain/temperature with preserved dorsal column function, the opposite of this patient's findings.

Alzheimer disease is a clinical diagnosis made after excluding reversible and other neurodegenerative causes in a patient with insidious, progressive amnestic decline affecting memory and visuospatial function, with preserved alertness and no focal neurologic signs. Screening labs (TSH, B12, calcium, CBC) are normal, ruling out common reversible metabolic causes, and CT shows only atrophy without structural lesion, stroke, or hydrocephalus. The gradual, amnestic-predominant course distinguishes it from the other options, which typically have distinguishing early features (stepwise decline, behavioural change, parkinsonism/hallucinations, rapid progression). This pattern matches standard diagnostic criteria for probable Alzheimer disease.

• B. Vascular dementia typically shows a stepwise decline with vascular risk factors and corresponding infarcts on imaging, not seen here.
• C. Creutzfeldt-Jakob disease causes rapidly progressive dementia over weeks to months with myoclonus, inconsistent with an 18-month indolent course.
• D. Dementia with Lewy bodies features early visual hallucinations, parkinsonism, and fluctuating cognition, none of which are described.
• E. Frontotemporal dementia presents earlier with behavioural or language changes, not primarily memory loss, and relative memory sparing early on.

The triad of gait disturbance (typically the earliest and most prominent feature), urinary incontinence, and cognitive decline, combined with ventriculomegaly disproportionate to cortical atrophy on imaging, is characteristic of normal pressure hydrocephalus. The gait is classically wide-based and shuffling (magnetic gait) rather than the narrow-based, festinating gait with rigidity and tremor seen in parkinsonism. NPH is important to recognize because gait and cognitive symptoms may improve with ventriculoperitoneal shunting, unlike most other dementia syndromes. A high-volume lumbar puncture or extended CSF drainage trial is often used to support the diagnosis before shunting.

• A. Vascular dementia shows a stepwise decline with focal deficits and corresponding infarcts, not ventriculomegaly with this triad.
• B. Parkinson disease presents with resting tremor, rigidity, and bradykinesia, with gait disturbance appearing later, not the presenting symptom with incontinence.
• C. Progressive supranuclear palsy causes early falls with vertical gaze palsy and axial rigidity, not the triad described here.
• E. Alzheimer disease presents primarily with memory impairment early on, with gait and urinary symptoms occurring late if at all.

Delirium is characterized by an acute onset, fluctuating course, and inattention, often triggered by an underlying medical illness such as infection, as seen here with fever and tachycardia from a urinary tract infection. This patient had normal baseline cognition before admission, distinguishing this presentation from a dementia, which develops insidiously over months to years and does not typically fluctuate hour to hour. Delirium is a medical emergency requiring identification and treatment of the underlying cause, as it is often reversible. Dementias are chronic, progressive conditions that do not present acutely in a previously cognitively intact patient over 48 hours.

• A. Frontotemporal dementia presents with gradual behavioural or language changes over months to years, not acute onset confusion.
• B. Dementia with Lewy bodies does feature fluctuating cognition but develops gradually with parkinsonism and hallucinations, not an acute onset over 2 days.
• D. Vascular dementia follows a stepwise decline related to cerebrovascular events, not an acute fluctuating course tied to an infection.
• E. Alzheimer disease develops insidiously over years and does not present as an acute fluctuating confusional state in a previously intact patient.

Herpes simplex encephalitis classically presents with fever, altered mental status, and focal seizures, often with temporal lobe involvement, and is a neurological emergency because delayed treatment increases mortality and morbidity. Empiric IV acyclovir should be started immediately once HSE is suspected clinically, without waiting for confirmatory PCR results, because treatment delay worsens outcomes while acyclovir has a favourable safety profile. CSF HSV PCR is the diagnostic test of choice and should be sent in parallel with starting therapy, not used to decide whether to start it. Imaging (preferably MRI, which is more sensitive than CT for temporal lobe changes) supports the workup but should not delay empiric treatment.

• B. MRI is more sensitive than CT for HSE but obtaining it should not delay starting empiric acyclovir.
• C. Waiting for PCR results before treating increases the risk of death and permanent neurological damage; treatment should not be delayed.
• D. This combination targets bacterial meningitis but does not cover HSV, which is the leading clinical concern given the focal seizures and lymphocytic pleocytosis.
• E. Seizure control alone does not address the underlying infection and omits antiviral therapy, which is essential in suspected HSE.

Progressive headache worse in the morning, a new focal deficit (pronator drift and upgoing plantar response), and papilledema strongly suggest a space-occupying intracranial lesion, most likely a brain tumor, causing raised intracranial pressure. MRI with contrast is the imaging modality of choice because it offers superior soft-tissue resolution and sensitivity for detecting and characterizing mass lesions, including small or posterior fossa tumors that CT may miss. CT without contrast can be used when MRI is unavailable or contraindicated, but it is less sensitive and should not be the first choice when a tumor is suspected and MRI is accessible. Lumbar puncture is contraindicated here because papilledema and focal signs raise concern for a mass lesion, and LP risks herniation if intracranial pressure is elevated.

• A. CT without contrast is less sensitive than MRI for detecting and characterizing brain tumors and is reserved for situations where MRI is unavailable or contraindicated.
• B. Carotid duplex evaluates extracranial vascular disease and is not indicated for a presentation suggesting a space-occupying intracranial lesion.
• D. Lumbar puncture is contraindicated before imaging in a patient with papilledema and focal neurological signs because of the risk of brain herniation.
• E. EEG evaluates electrical seizure activity and has no role in diagnosing a structural mass lesion causing focal deficits and raised intracranial pressure.