AMC MCQ (CAT) neurology questions

In any patient presenting with sudden focal neurological deficit within the thrombolysis/thrombectomy window, the first priority is urgent non-contrast CT brain to exclude haemorrhage, performed in parallel with stroke team activation so that reperfusion therapy is not delayed. Time is brain: eTG and Australian stroke guidelines recommend door-to-CT times of under 25 minutes for suspected acute stroke. Blood pressure lowering, antiplatelet therapy and further imaging decisions all depend on the CT result and specialist assessment. MRI is more sensitive for early ischaemia but is slower to access and not the first-line investigation in the acute pathway.

• A. Carotid imaging is part of secondary work-up, not the immediate next step in a time-critical presentation.
• B. MRI is not the first-line acute investigation; it is slower to obtain and non-contrast CT is sufficient to exclude haemorrhage before treatment decisions.
• D. Blood pressure is not lowered pre-emptively before imaging; aggressive lowering may worsen penumbral perfusion and is only indicated in specific circumstances (e.g. before thrombolysis if above threshold, or in haemorrhage).
• E. Aspirin should not be given until haemorrhage has been excluded on CT.

Proximal large vessel occlusion (such as M1 middle cerebral artery) with a disabling deficit and a large volume of salvageable brain tissue is an indication for mechanical thrombectomy, which should proceed without delay even after thrombolysis has been given. Endovascular therapy significantly improves functional outcomes when performed within 24 hours of onset in appropriately selected patients, with the greatest benefit seen when performed early. Thrombolysis and thrombectomy are complementary, not alternatives, in eligible patients. Anticoagulation has no role in the acute phase of large vessel occlusive stroke and hemicraniectomy is reserved for malignant oedema, not as an initial intervention.

• A. Therapeutic anticoagulation is not indicated in the acute management of ischaemic stroke and increases haemorrhagic risk.
• B. Decompressive hemicraniectomy is reserved for malignant cerebral oedema with mass effect, not as first-line treatment of large vessel occlusion.
• C. Supportive care alone is insufficient when a proximal occlusion amenable to clot retrieval has been identified.
• D. Repeat imaging at 24 hours would delay definitive treatment of a large vessel occlusion that is amenable to intervention now.

This patient has had a transient ischaemic attack with high-risk features (age over 60, diabetes, hypertension, motor and speech symptoms lasting more than 10 minutes), placing her at high short-term risk of stroke. Australian guidelines recommend that patients with suspected TIA, particularly those with high-risk features, be assessed urgently as an emergency, ideally within 24 hours, with brain and vascular imaging to guide secondary prevention, as the risk of stroke is highest in the first 48 hours after a TIA. Outpatient or routine referral pathways are unsafe given this early risk window. Starting aspirin alone without urgent specialist assessment and imaging is insufficient, as it does not identify the underlying cause or address the need for timely intervention.

• A. Driving advice alone is inadequate; urgent medical assessment and imaging are required first.
• B. A two-week delay is unsafe given the high short-term risk of stroke after a high-risk TIA.
• D. Starting antiplatelet therapy without urgent same-day specialist assessment and imaging does not address the need to identify and manage the underlying cause within the high-risk window.
• E. Routine referral within a month is unsafe; high-risk TIA requires assessment within 24 hours.

This presentation, fluent but nonsensical speech with impaired comprehension and lack of awareness of the deficit, is classic for Wernicke's (receptive) aphasia, which localises to the posterior superior temporal gyrus of the dominant hemisphere, typically the left in right-handed individuals. This region is responsible for language comprehension, and its damage disrupts the ability to understand spoken and written language while sparing the motor programming of speech, producing fluent but meaningless output. Broca's area lesions produce non-fluent, effortful speech with relatively preserved comprehension, the opposite pattern. Right hemisphere lesions in right-handed patients typically spare language function, as language is lateralised to the left hemisphere in the vast majority of right-handed people.

• A. In a right-handed individual, language is lateralised to the left hemisphere, so a right-sided lesion would not typically cause aphasia.
• B. This region corresponds to Broca's area, which produces non-fluent, effortful speech with relatively preserved comprehension, not this fluent, comprehension-impaired pattern.
• C. Isolated damage to the arcuate fasciculus causes conduction aphasia, with fluent speech and impaired repetition but relatively preserved comprehension.
• D. Language is left-lateralised in right-handed individuals, so this right hemisphere region is not responsible for this deficit.

This combination of crossed sensory loss (ipsilateral facial, contralateral body pain and temperature loss), ipsilateral Horner's syndrome, and ipsilateral bulbar signs (dysphagia, hoarseness, diminished gag) with preserved limb strength is the classic presentation of lateral medullary (Wallenberg) syndrome, typically due to occlusion of the posterior inferior cerebellar artery or vertebral artery. The pattern reflects involvement of the spinothalamic tract, descending sympathetic fibres, and nucleus ambiguus within the lateral medulla, while the corticospinal tracts, which run more medially, are spared, explaining the preserved motor power. Medial medullary syndrome characteristically causes contralateral limb weakness and does not produce this sensory and bulbar pattern. Pontine and cerebellar haemorrhage typically present with additional long tract or cerebellar signs rather than this specific crossed pattern.

• B. Medial medullary infarction causes contralateral limb weakness and tongue deviation, with sparing of the lateral structures responsible for this patient's findings.
• C. Pontine haemorrhage typically causes bilateral long tract signs, pinpoint pupils and often reduced consciousness, not this specific crossed sensory and bulbar pattern.
• D. Cerebellar haemorrhage typically causes limb and gait ataxia with signs of raised intracranial pressure, not this crossed sensory loss and bulbar pattern.
• E. Anterior spinal artery occlusion in the medulla produces a different pattern involving motor and dorsal column pathways, not these lateral medullary findings.

For a moderate ischaemic stroke with newly diagnosed atrial fibrillation, current guidelines recommend delaying initiation of anticoagulation for approximately 7 to 10 days after stroke onset, to reduce the risk of haemorrhagic transformation into the evolving infarct while still providing timely protection against early recurrent cardioembolic stroke. Very early anticoagulation, particularly with heparin bridging, increases the risk of haemorrhagic transformation without proven benefit and is not recommended. Excessively delaying anticoagulation for weeks to months leaves the patient unprotected against recurrent embolic stroke during a period of elevated risk. The timing is generally guided by infarct size and haemorrhagic risk rather than degree of neurological recovery, with larger infarcts warranting longer delay.

• A. Anticoagulation timing is guided by infarct size and haemorrhagic risk rather than waiting for full neurological recovery, and 3 months is an unnecessarily long delay.
• B. Delaying for a full 4 weeks leaves the patient unnecessarily unprotected against recurrent cardioembolic stroke during a period of elevated risk.
• D. Anticoagulation started within hours to days of a moderate stroke carries a significant risk of haemorrhagic transformation of the infarct.
• E. Heparin bridging immediately after stroke increases the risk of haemorrhagic transformation and is not recommended in this setting.

A sudden, severe, maximal-at-onset ('thunderclap') headache triggered by exertion, accompanied by photophobia, vomiting and meningism, is the classic presentation of subarachnoid haemorrhage, most commonly from a ruptured intracranial aneurysm. The absence of fever argues against infective meningitis. The combination of abrupt onset and meningism from blood irritating the meninges is the key clinical clue distinguishing this from primary headache disorders. Urgent non-contrast CT brain is the first investigation.

• A. Venous sinus thrombosis usually causes a headache that evolves over days with signs of raised intracranial pressure rather than sudden onset.
• B. Fever is typically present and onset is usually more gradual over hours rather than instantaneous.
• C. Cervicogenic headache is typically unilateral, related to neck movement, and lacks the abrupt thunderclap onset and meningism described.
• D. Migraine headache builds up over minutes to hours and is not classically described as reaching maximal intensity within a minute.

Todd's paresis is a transient, post-ictal focal weakness that follows a focal seizure, typically resolving gradually over minutes to hours, and is well recognised in patients with a structural brain lesion such as this woman's prior meningioma resection site acting as an epileptogenic focus. The preceding focal motor jerking and post-ictal confusion, followed by weakness that improves progressively rather than remaining static or worsening, favours a post-seizure phenomenon over an acute vascular event. Ischaemic stroke and TIA typically present with sudden deficit without preceding convulsive movements, and the gradual improvement pattern here is atypical for infarction. Normal blood glucose excludes a hypoglycaemic cause.

• A. Ischaemic stroke causes sudden deficit without preceding focal jerking, and typically does not show gradual improvement over the following hour.
• B. Hemiplegic migraine classically involves aura symptoms with headache, not preceding focal motor seizure activity and post-ictal confusion.
• D. TIA deficits resolve within minutes without a preceding seizure and without the post-ictal confusion described.
• E. Blood glucose of 5.8 mmol/L is normal, excluding hypoglycaemia as the cause of the weakness.

For a patient in status epilepticus with intravenous access already established, intravenous benzodiazepine such as lorazepam is the first-line treatment, acting rapidly via potentiation of GABA-A receptor-mediated inhibition to terminate seizure activity. If seizures persist despite an adequate benzodiazepine dose, a second-line intravenous antiepileptic such as phenytoin, levetiracetam or sodium valproate is given to achieve longer-term seizure control. Rectal diazepam is reserved for situations where intravenous access is unavailable, which does not apply here. General anaesthesia is reserved for refractory status epilepticus that fails to respond to first- and second-line agents.

• B. Phenytoin is a second-line agent used after an adequate trial of benzodiazepine has failed to terminate the seizure.
• C. Induction of general anaesthesia is reserved for refractory status epilepticus unresponsive to first- and second-line therapy.
• D. Levetiracetam is a second-line agent given after benzodiazepine treatment has been tried, not as the initial step.
• E. Rectal diazepam is used when intravenous access is unavailable; this patient already has intravenous access established.

Childhood absence epilepsy classically presents with brief staring episodes with abrupt onset and offset, no post-ictal confusion, and the characteristic EEG finding is generalised 3 Hz spike-and-wave discharges, often precipitated by hyperventilation. Sodium valproate (or ethosuximide, particularly favoured in girls of childbearing potential due to valproate's teratogenicity, though valproate remains a standard first-line choice in guidelines) is effective first-line therapy targeting the thalamocortical circuits involved in absence seizures. Carbamazepine and other sodium channel-blocking drugs can worsen absence seizures and are contraindicated. Hypsarrhythmia is characteristic of infantile spasms (West syndrome), an entirely different epileptic encephalopathy of infancy.

• B. Hypsarrhythmia is seen in infantile spasms (West syndrome) in infancy, not childhood absence epilepsy.
• C. Focal temporal sharp waves suggest focal epilepsy, not generalised absence seizures, and carbamazepine can worsen absence seizures.
• D. Generalised polyspike discharges are more typical of juvenile myoclonic epilepsy, and lamotrigine is not the first-line choice for absence seizures.
• E. The EEG in childhood absence epilepsy is characteristically abnormal during episodes, and treatment is required due to the frequency of seizures and risk to learning.

Sodium valproate is associated with a high risk of major congenital malformations (neural tube defects, cardiac and limb defects) and a dose-dependent risk of neurodevelopmental impairment including autism spectrum disorder, affecting up to 30-40% of exposed children. Australian guidelines (TGA and eTG) recommend that valproate should only be used in women of childbearing potential if other treatments are ineffective or not tolerated, and only with highly effective contraception and informed discussion of risks, reviewed annually. Abruptly stopping or switching an effective antiepileptic without a planned transition risks seizure recurrence, which carries its own harms. The correct approach balances seizure control with pregnancy risk through counselling and reliable contraception, not unilateral cessation or switching.

• A. This is false reassurance; there is no safe dose of valproate in pregnancy regarding teratogenicity.
• B. Switching antiepileptics abruptly without specialist input risks breakthrough seizures and is not the immediate priority.
• C. Abrupt cessation without a seizure management plan risks status epilepticus and is not guideline-recommended.
• D. This fails to address the unreliable contraception and ongoing teratogenic risk, which requires active discussion now.

Carbamazepine is a potent inducer of cytochrome P450 enzymes, particularly CYP3A4, which increases the hepatic metabolism of both the oestrogen and progestogen components of combined oral contraceptives, substantially reducing their efficacy. Women on enzyme-inducing antiepileptics should be advised to use a non-hormonal method (such as a copper intrauterine device) or a method less affected by enzyme induction, such as the levonorgestrel or copper IUD, as recommended by eTG and the Australian Immunisation Handbook-aligned contraception guidance. The progestogen-only pill is also significantly affected by enzyme induction and is not considered reliable in this setting. Timing of pill intake relative to carbamazepine dosing does not mitigate this pharmacokinetic interaction.

• B. Carbamazepine induces rather than inhibits hepatic metabolism, so oestrogen levels fall rather than rise.
• C. This ignores the well-documented enzyme-inducing effect of carbamazepine on contraceptive steroid metabolism.
• D. The progestogen-only pill is also unreliable with enzyme-inducing antiepileptics due to increased progestogen clearance.
• E. The interaction is pharmacokinetic via enzyme induction, not dependent on dosing intervals between the two medications.

This presentation is consistent with a simple febrile convulsion: generalised, lasting under 15 minutes, occurring once in 24 hours, in a child aged 6 months to 6 years, with a normal neurological examination and no red flags such as meningism, prolonged or focal seizure activity, or recent antibiotic use masking meningitis. Simple febrile convulsions are benign and self-limiting, and management focuses on identifying and treating the source of fever, with reassurance and safety-netting advice for parents. Neuroimaging, lumbar puncture and EEG are reserved for atypical presentations, complex febrile seizures, or signs suggesting central nervous system infection, none of which are present here. Routine anticonvulsant prophylaxis is not recommended for simple febrile convulsions.

• A. Lumbar puncture is unnecessary without signs of meningism, altered consciousness or other red flags.
• B. Prophylactic anticonvulsants are not recommended for an isolated simple febrile convulsion.
• C. CT brain is not indicated for a simple febrile convulsion with a normal neurological examination.
• D. EEG monitoring is not indicated for a typical simple febrile convulsion.

Eye closure during the event with active resistance to passive eyelid opening is one of the most specific and reliable clinical signs distinguishing psychogenic non-epileptic seizures from epileptic seizures, as epileptic seizures typically occur with eyes open and show no voluntary resistance to examination. While prolonged duration, asynchronous movements, preserved memory of the event, stress triggers and absence of tongue biting or incontinence are all suggestive features, they are individually less specific and can occur in some epileptic seizure types, particularly frontal lobe seizures. Normal oxygen saturation and immediate recall further support a non-epileptic event but are supportive rather than the single most discriminating sign. Video-EEG telemetry remains the gold standard for definitive diagnosis when clinical features are equivocal.

• A. Stress triggers can also precede genuine epileptic seizures and are not specific to psychogenic events.
• B. Many epileptic seizures, especially focal seizures, do not involve tongue biting or incontinence, making this a non-specific finding.
• D. Asynchronous movements are suggestive but can occasionally be seen in frontal lobe epileptic seizures.
• E. Some epileptic seizures, particularly frontal lobe seizures, can also be prolonged, making duration alone less discriminating.

This history is characteristic of migraine with aura, with a gradually evolving visual aura lasting 5-60 minutes followed by migrainous headache, meeting International Classification of Headache Disorders criteria. Triptans such as sumatriptan are the first-line acute therapy for moderate to severe migraine and should be taken at the onset of the headache phase rather than during the aura, as triptans have not been shown to prevent or reduce aura and early administration during the aura does not improve efficacy and may increase exposure without benefit. Ergotamine is largely obsolete due to a less favourable side effect and interaction profile compared with triptans. Opioid-containing analgesics such as paracetamol-codeine are discouraged for migraine due to risk of medication overuse headache and limited efficacy, and antiemetics alone do not address the headache itself.

• A. Ergotamine is no longer recommended as first-line therapy due to a worse adverse effect profile compared with triptans.
• C. An antiemetic alone does not adequately treat the headache component of the migraine attack.
• D. Triptans are not more effective when taken during the aura phase and current guidelines recommend administration at headache onset.
• E. Opioid-containing analgesics are not first-line for migraine and carry a higher risk of medication overuse headache.

Medication overuse headache occurs when headache is present on 15 or more days per month in a patient with a pre-existing primary headache disorder who regularly overuses acute symptomatic medication, in this case opioid-containing analgesics used on more than 10 days per month for over 3 months. The characteristic pattern is a dull, often bilateral headache that paradoxically worsens in frequency and becomes less responsive to treatment despite, or because of, increasing analgesic use. Management involves gradual withdrawal of the overused medication along with appropriate migraine prophylaxis, as eTG recommends avoiding opioid-containing analgesics for headache due to their high potential to cause this condition. Chronic migraine is a relevant differential but the clear temporal relationship with escalating codeine-containing analgesic use points specifically to medication overuse headache.

• A. Cluster headache presents with severe unilateral periorbital pain with autonomic features, not a dull bilateral pressure pattern.
• B. New daily persistent headache begins abruptly without a preceding episodic pattern or medication overuse, unlike this case.
• D. Tension-type headache does not typically show this pattern of progressive worsening linked to analgesic overuse.
• E. Chronic migraine alone does not explain the clear pattern of worsening frequency driven by escalating opioid analgesic use.

This presentation is typical of cluster headache: strictly unilateral periorbital pain with ipsilateral autonomic features (lacrimation, ptosis, conjunctival injection) and restlessness, occurring in a cluster bout. High-flow 100% oxygen at 12-15 L/min via non-rebreather mask for 15-20 minutes is first-line acute treatment and aborts most attacks within minutes. Subcutaneous or nasal triptans are the alternative acute option if oxygen is unavailable. Preventive agents such as verapamil are used for the cluster period but do not treat the acute attack.

• A. Simple analgesics are ineffective for cluster headache given its short, severe, time-limited nature.
• B. Antiemetics are not first-line acute therapy for cluster headache.
• C. Propranolol is a migraine preventive, not an acute cluster headache treatment, and is not first-line cluster prophylaxis.
• D. Corticosteroids may be used as a short bridging prophylactic course but do not abort an acute attack already in progress.

Tension-type headache is characterised by bilateral, pressing or tightening (non-pulsatile) pain of mild to moderate intensity that is not aggravated by routine physical activity, and lacks the nausea/vomiting and photophobia/phonophobia seen in migraine. This distribution and quality, rather than frequency or duration alone, is the key discriminating feature from migraine, which is typically unilateral, pulsatile, aggravated by activity, and accompanied by autonomic or sensory symptoms. Most people with migraine do not have aura, so its absence does not distinguish the two conditions. A normal examination is expected in both primary headache disorders.

• A. A normal neurological examination is expected in both tension-type headache and migraine and does not help differentiate them.
• C. High frequency headaches can occur in both tension-type headache and chronic migraine, so frequency alone does not discriminate.
• D. Duration overlaps considerably between tension-type headache and migraine and is not the discriminating feature.
• E. Most migraine sufferers never experience aura, so its absence is not specific for tension-type headache.

This history of new temporal headache, jaw claudication and polymyalgic symptoms in a woman over 50 is highly suggestive of giant cell arteritis, which carries a significant risk of irreversible visual loss from ophthalmic artery involvement. Treatment with high-dose glucocorticoids (prednisolone, typically 40-60 mg/day) should be started immediately on clinical suspicion, without waiting for biopsy confirmation, because biopsy changes can persist for one to two weeks after starting steroids. ESR and CRP should be checked urgently to support the diagnosis, and temporal artery biopsy arranged promptly to confirm it. Delaying treatment risks permanent blindness.

• A. Treatment must not be delayed for biopsy results because of the risk of sudden irreversible vision loss.
• B. A two-week wait for specialist review is unsafe given the imminent risk of vision loss; treatment must start immediately.
• D. Aspirin alone does not treat the underlying vasculitis and a one-week delay risks blindness.
• E. MRI is not the diagnostic test of choice and deferring steroids risks permanent visual loss.

This presentation with papilloedema, postural headache, pulsatile tinnitus and obesity in a young woman is characteristic of idiopathic intracranial hypertension. Neuroimaging with MRI brain and MR venography is required first to exclude a structural lesion or venous sinus thrombosis as secondary causes of raised intracranial pressure. Once these are excluded, lumbar puncture with manometry confirms the diagnosis by demonstrating an elevated opening pressure (greater than 25 cmH2O) with normal cerebrospinal fluid composition. Performing lumbar puncture before imaging risks missing a mass lesion or herniation risk.

• A. Inflammatory markers are not relevant to the diagnosis of idiopathic intracranial hypertension.
• B. Temporal artery imaging is used to investigate giant cell arteritis, which does not fit this clinical picture.
• D. CT brain alone has lower sensitivity for detecting venous sinus thrombosis and subtle structural causes than MRI with venography.
• E. EEG assesses electrical brain activity and has no role in diagnosing raised intracranial pressure.

A thunderclap headache reaching maximum severity within one minute, especially the worst headache of a patient's life with new onset in middle age, is a red flag requiring urgent exclusion of subarachnoid haemorrhage. Non-contrast CT brain performed within six hours of symptom onset has very high sensitivity for detecting subarachnoid blood and is the first-line investigation. If CT is negative but clinical suspicion remains, lumbar puncture performed at least six to twelve hours after onset is used to look for xanthochromia. Delaying investigation risks missing a ruptured aneurysm with high mortality from rebleeding.

• B. A one-week delay for outpatient imaging is unsafe given the risk of aneurysmal rebleeding in the interim.
• C. Discharging a patient with thunderclap headache without imaging risks missing a life-threatening subarachnoid haemorrhage.
• D. Thunderclap headache is a neurosurgical emergency until proven otherwise; symptomatic treatment without urgent imaging is inappropriate.
• E. Lumbar puncture should follow, not precede, CT imaging to first exclude a mass effect or haemorrhage visible on CT.

The combination of asymmetric resting tremor, rigidity with cogwheeling, bradykinesia (reduced arm swing, slow turning, hypomimia) and shortened stride length is the classic clinical triad of Parkinson's disease. Asymmetric onset is a key feature that helps distinguish idiopathic Parkinson's disease from other parkinsonian syndromes, which tend to present more symmetrically. Essential tremor is typically a postural or kinetic tremor that improves at rest, the opposite pattern seen here. Diagnosis remains clinical, based on bradykinesia plus either rigidity or resting tremor.

• A. Normal pressure hydrocephalus classically presents with the triad of gait disturbance, urinary incontinence and cognitive decline, without resting tremor or cogwheel rigidity.
• B. There is no history of exposure to dopamine-blocking medication, and drug-induced parkinsonism is typically symmetric.
• C. Essential tremor is a postural/kinetic tremor absent at rest, which contrasts with the resting tremor described here.
• D. Progressive supranuclear palsy presents with early postural instability, falls and vertical gaze palsy, not the asymmetric tremor-predominant picture described.

Long-term levodopa therapy is associated with motor fluctuations, including the wearing-off phenomenon in which the clinical benefit of each dose shortens over time, causing return of parkinsonian symptoms before the next dose. Peak-dose dyskinesias are involuntary choreiform or dystonic movements that occur when striatal dopamine levels are highest, reflecting pulsatile stimulation of denervated dopamine receptors. Together these fluctuations reflect the narrowing therapeutic window that develops with long-term levodopa use and advancing disease. Management options include fractionating doses, adding a COMT inhibitor or dopamine agonist, or extended-release formulations.

• A. This patient has Parkinson's disease, not essential tremor, and the description is of dyskinesia rather than tremor progression.
• B. Restless legs syndrome causes an urge to move the legs, typically worse in the evening and at rest, not dose-linked dyskinesia.
• C. Drug-induced parkinsonism describes new parkinsonian features caused by dopamine-blocking drugs, not fluctuating response to levodopa in a patient with established Parkinson's disease.
• D. Serotonin syndrome presents with hyperthermia, clonus, agitation and autonomic instability, not dose-related motor fluctuation.

Metoclopramide is a dopamine D2 receptor antagonist that crosses the blood-brain barrier and can block dopamine receptors in the nigrostriatal pathway, producing drug-induced parkinsonism. This typically presents with symmetrical bradykinesia, rigidity and tremor developing over days to weeks after starting the offending drug, in contrast to the asymmetric onset of idiopathic Parkinson's disease. Other common culprits include typical and some atypical antipsychotics. The condition is usually reversible over weeks to months after stopping the causative agent.

• A. Small vessel ischaemic disease causes vascular parkinsonism, typically with a lower-body predominant gait disorder, not the pattern following metoclopramide exposure here.
• B. Lewy body accumulation is characteristic of idiopathic Parkinson's disease and dementia with Lewy bodies, not drug-induced parkinsonism.
• D. Neuronal degeneration in the substantia nigra is the mechanism of idiopathic Parkinson's disease, not drug-induced parkinsonism.
• E. Excessive dopaminergic stimulation would cause dyskinesia or psychosis, not parkinsonism, and is not the mechanism of a dopamine antagonist.

Essential tremor is a bilateral, largely symmetric postural and kinetic tremor affecting the hands, worsened by action (holding, writing) and improved by rest, alcohol and beta-blockers. It is often familial (autosomal dominant inheritance in many cases) and occurs without bradykinesia, rigidity or gait disturbance, unlike Parkinson's disease where tremor is classically asymmetric, present at rest, and accompanied by other parkinsonian signs. The alcohol responsiveness and action-predominant pattern described here are classic clinical clues that distinguish essential tremor from parkinsonian tremor.

• B. Parkinson's disease tremor is typically a resting, pill-rolling tremor that improves with action, and is usually accompanied by bradykinesia, rigidity or gait change, none of which are present here.
• C. Cerebellar tremor is a low-frequency intention tremor that worsens on reaching a target and is usually accompanied by ataxia or dysmetria, not described here.
• D. There is no history of exposure to antipsychotics, metoclopramide or other dopamine-blocking agents to suggest a drug cause.
• E. Physiological tremor is a fine, low-amplitude tremor seen in anxiety, thyrotoxicosis or caffeine use and does not typically run in families or respond dramatically to alcohol.

Huntington's disease is caused by an autosomal dominant CAG trinucleotide repeat expansion in the HTT gene on chromosome 4. Each offspring of an affected parent has an independent 50% chance of inheriting the mutant allele, regardless of sex, because one copy from the affected parent is passed on. The disease shows age-dependent penetrance, with most carriers developing symptoms in mid-adulthood, and repeat length can expand further with paternal transmission (genetic instability), sometimes causing earlier onset in the next generation (anticipation). Pre-symptomatic genetic counselling and testing should be offered with appropriate psychological support given the implications for employment, insurance and family planning.

• A. Huntington's disease is autosomal, located on chromosome 4, not X-linked, so risk does not depend on the child's sex.
• B. A 25% risk would apply to an autosomal recessive condition with two carrier parents, not an autosomal dominant disorder with one affected parent.
• C. Huntington's disease does not skip generations; it is fully penetrant with age, so a carrier will eventually develop disease if they live long enough.
• E. Penetrance is not sex-limited in Huntington's disease; both sons and daughters who inherit the expanded allele are at equal risk of developing symptoms, and not every carrier necessarily develops symptoms before being affected by an unrelated cause of death.

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. Current guidelines recommend checking serum ferritin in all patients with restless legs syndrome, and iron replacement is first-line treatment when ferritin is below approximately 75 µg/L, as this may resolve or substantially improve symptoms without the need for dopaminergic drugs. This patient's microcytic anaemia and menorrhagia point to a treatable iron deficiency cause that should be addressed before considering medication. Non-pharmacological measures (good sleep hygiene, avoiding caffeine) are also recommended alongside correcting iron stores.

• A. Dopamine agonists such as pramipexole are used for moderate-to-severe restless legs syndrome once reversible causes like iron deficiency have been excluded or treated, not as a first step bypassing investigation.
• B. Venous Doppler ultrasound is used to investigate suspected deep venous disease or chronic venous insufficiency, which does not produce the classic evening dysaesthesia relieved by movement described here.
• C. Clonazepam is a second-line option for refractory restless legs syndrome and should not be started before correcting an underlying treatable cause such as iron deficiency.
• E. Nerve conduction studies are used to assess peripheral neuropathy, which does not characteristically cause an urge to move relieved by movement and worsening in the evening; the normal neurological examination here does not suggest neuropathy.

The length-dependent, symmetric stocking distribution of sensory loss with absent ankle reflexes and preserved strength in a patient with long-standing poorly controlled diabetes is typical of distal symmetric diabetic peripheral neuropathy, the most common form of diabetic neuropathy. Management focuses on optimising glycaemic control to slow progression, annual foot examination including monofilament and vibration testing, and patient education on daily foot inspection, appropriate footwear and avoiding thermal or mechanical injury because of reduced protective sensation. Palpable pulses argue against a significant vascular contribution to his symptoms. Early recognition and foot care education are key to preventing ulceration and amputation.

• A. Metformin-associated B12 deficiency can cause a sensory neuropathy, but the chronicity, symmetry and clear association with long-standing poorly controlled diabetes make diabetic peripheral neuropathy the most likely diagnosis here.
• B. Radiculopathy typically causes asymmetric, dermatomal sensory loss often with associated back pain or radicular leg pain, not a symmetric stocking distribution.
• C. Guillain-Barré syndrome causes a rapidly progressive ascending weakness over days to weeks, not a gradual onset of sensory symptoms over a year with preserved strength.
• E. Peripheral arterial disease would be expected to cause claudication, reduced or absent pulses, or trophic skin changes; this patient has palpable pulses and no ischaemic features.

Respiratory failure in Guillain-Barré syndrome results from progressive weakness of the diaphragm and intercostal muscles, and can develop rapidly even while oxygen saturation remains normal, because hypoxaemia is a late sign. Serial bedside spirometry measuring forced vital capacity is the key monitoring tool; a falling FVC (classically below 15-20 mL/kg or a rapid downward trend), neck flexor weakness, and symptoms such as breathlessness lying flat or difficulty completing sentences are indications for urgent intensive care unit assessment and consideration of elective intubation before a crisis occurs. Waiting for SpO2 to fall or for blood gas results risks a sudden respiratory arrest, since CO2 retention and hypoxaemia occur late after significant respiratory muscle weakness has already developed.

• A. Her symptoms and signs (orthopnoea, poor breath-counting, accessory muscle use, inability to lift her head) indicate significant respiratory muscle weakness requiring urgent action, not reassurance.
• C. An arterial blood gas may be part of assessment but should not delay urgent FVC measurement and ICU review, as gas exchange abnormalities occur late in neuromuscular respiratory failure.
• D. Intravenous fluids do not address neuromuscular respiratory failure and delaying appropriate monitoring and ICU review by 24 hours risks a respiratory arrest.
• E. There is no clinical indication of aspiration pneumonia such as fever, crackles or infiltrate; antibiotics are not the priority intervention here.

Fatigable ptosis and diplopia that worsen with sustained activity and improve with rest, along with fatigable limb weakness and normal sensation, are classic for myasthenia gravis, a disorder of neuromuscular transmission caused by autoantibodies against the postsynaptic acetylcholine receptor in most cases. Acetylcholine receptor antibody testing is the most appropriate initial serological test, as it is positive in the majority of patients with generalised myasthenia gravis and is both sensitive and widely available. Anti-MuSK antibodies are tested in acetylcholine receptor antibody-negative patients as a second step, not as the initial test. Electrophysiological studies such as repetitive nerve stimulation or single-fibre electromyography can support the diagnosis but antibody testing is the key initial diagnostic test in this clinical picture.

• B. Creatine kinase is usually normal in myasthenia gravis, as it is a disorder of neuromuscular transmission rather than a primary muscle disease.
• C. Nerve conduction studies assess peripheral nerve function and are not the most useful initial test for a neuromuscular junction disorder presenting with fatigable weakness.
• D. Anti-MuSK antibody testing is reserved for patients who test negative for acetylcholine receptor antibodies, not as the first-line test.
• E. Anti-Jo-1 antibodies are associated with antisynthetase syndrome and inflammatory myopathy with features such as muscle pain and interstitial lung disease, not fatigable ocular and bulbar weakness.

Aminoglycosides such as gentamicin impair neuromuscular transmission by inhibiting presynaptic release of acetylcholine and reducing postsynaptic sensitivity to acetylcholine, which can precipitate or worsen a myasthenic crisis in patients with underlying neuromuscular junction disease. This drug class, along with other agents such as macrolides, fluoroquinolones and magnesium, should be avoided or used with extreme caution in myasthenia gravis, and alternative antibiotics should be chosen when infection requires treatment. This patient's acute deterioration with bulbar and respiratory symptoms shortly after starting gentamicin requires urgent reassessment of ventilatory status, cessation of the offending drug, and consideration of ICU-level care and crisis treatment such as intravenous immunoglobulin or plasma exchange. Recognising high-risk drugs is essential to preventing iatrogenic myasthenic crisis.

• A. Aminoglycosides do not destroy acetylcholine receptors; the underlying autoimmune destruction of receptors is a separate, chronic process unrelated to the acute drug effect.
• B. Gentamicin's interaction with myasthenia gravis is pharmacodynamic at the neuromuscular junction, not due to altering renal clearance of pyridostigmine.
• D. There is no evidence that gentamicin increases acetylcholine receptor antibody production; its effect is a direct pharmacological impairment of neuromuscular transmission, which can occur within hours, too rapid for an antibody-mediated flare.
• E. Gentamicin precipitates myasthenic crisis through a neuromuscular junction mechanism, not by causing a demyelinating peripheral neuropathy such as that seen in Guillain-Barré syndrome.

Carpal tunnel syndrome is caused by compression of the median nerve within the carpal tunnel, producing nocturnal paraesthesiae and sensory loss in the median distribution (thumb, index, middle and radial half of ring finger) with thenar weakness in more advanced cases. Pregnancy predisposes through fluid retention and soft tissue swelling, which increases carpal tunnel pressure; it typically improves after delivery. Tinel's sign (reproduction of tingling with percussion over the median nerve at the wrist) supports the diagnosis. Other causes to consider include hypothyroidism, diabetes, acromegaly and rheumatoid arthritis, which should be screened for if bilateral or atypical.

• A. De Quervain tenosynovitis causes pain over the radial styloid with a positive Finkelstein test, not sensory loss or nocturnal paraesthesiae.
• B. C6 radiculopathy causes neck pain radiating to the arm and affects the biceps reflex, not an isolated median sensory pattern reproduced by wrist percussion.
• D. Thoracic outlet syndrome typically causes diffuse arm symptoms with vascular features and is not reproduced by percussion at the wrist.
• E. Ulnar neuropathy affects the little finger and medial half of the ring finger, with weakness of finger abduction, not the thumb and index finger.

Subacute combined degeneration occurs due to vitamin B12 deficiency, which causes demyelination of the posterior columns (producing loss of vibration and proprioception with sensory ataxia and a positive Romberg sign) and the corticospinal tracts (producing upper motor neurone signs such as extensor plantar responses), combined with a peripheral neuropathy that abolishes ankle reflexes. Previous gastrectomy predisposes to B12 deficiency by reducing intrinsic factor and acid required for B12 absorption. The combination of upper and lower motor neurone signs with macrocytic anaemia is characteristic, and diagnosis is confirmed with a low serum B12 level, with treatment by intramuscular hydroxocobalamin.

• B. Diabetic peripheral neuropathy causes a distal sensory neuropathy but does not explain the macrocytic anaemia or upper motor neurone signs.
• C. Multiple sclerosis can cause mixed upper and lower motor neurone signs but does not explain the macrocytic anaemia or history of gastrectomy.
• D. Lumbar spinal stenosis causes neurogenic claudication and lower limb symptoms but would not produce extensor plantar responses or macrocytic anaemia.
• E. Folate deficiency causes macrocytic anaemia but does not cause the combined posterior column and corticospinal tract degeneration seen here.

Motor neurone disease is characterised by the combination of upper motor neurone signs (brisk reflexes, extensor plantar response, increased tone, brisk jaw jerk) and lower motor neurone signs (wasting, fasciculations) occurring together in a patient with entirely normal sensory examination, which is a key distinguishing feature from most other neuropathies and myelopathies. Bulbar involvement, as seen here with dysarthria and a brisk jaw jerk, further supports the diagnosis. Diagnosis is clinical, supported by electromyography showing widespread denervation, and management is multidisciplinary with riluzole to modestly slow progression.

• B. Cervical spondylotic myelopathy can cause mixed motor signs but typically also causes sensory symptoms or signs below the lesion and would not explain bulbar signs.
• C. Myasthenia gravis causes fatigable weakness without wasting, fasciculations or upper motor neurone signs.
• D. Chronic inflammatory demyelinating polyneuropathy causes sensorimotor neuropathy with sensory loss and depressed, not brisk, reflexes.
• E. Multifocal motor neuropathy causes pure lower motor neurone weakness without upper motor neurone signs.

In suspected bacterial meningitis with features suggesting meningococcal disease (fever, meningism, petechial rash, tachycardia), empirical intravenous antibiotics (ceftriaxone) must be given immediately, as delay increases mortality and morbidity; blood cultures should be taken beforehand if this does not delay treatment, but antibiotics must never be withheld to await LP or imaging. CT brain before LP is only required if there are specific indications such as reduced consciousness (GCS <13), focal neurological signs, papilloedema, or seizures, none of which are present here. The priority in any patient with suspected bacterial meningitis is immediate antibiotic administration, with LP performed afterward if safe to confirm the diagnosis and guide further therapy.

• A. Waiting for CT before giving antibiotics is inappropriate here as there are no indications for CT (no reduced GCS, focal signs or papilloedema), and this delay risks patient deterioration.
• B. Withholding antibiotics until blood culture results return causes a dangerous delay; blood cultures should be taken quickly but must not delay empirical treatment.
• D. Performing LP before giving antibiotics and waiting for results introduces a dangerous delay in treatment of suspected bacterial meningitis.
• E. Oral amoxicillin and outpatient review are inadequate for suspected bacterial meningitis, which requires immediate intravenous antibiotics and hospital admission.

Chemoprophylaxis for meningococcal disease is recommended for close contacts, defined as those with prolonged close contact in a household-type setting or direct exposure to respiratory or oral secretions in the 7 days before symptom onset, which applies to the housemates sharing drink bottles. Casual contacts such as classmates or lecture attendees without direct secretion exposure do not require prophylaxis. Prophylaxis (commonly rifampicin, ceftriaxone or ciprofloxacin, per eTG) should be given as soon as possible, ideally within 24 hours of diagnosis, rather than waiting for symptoms to develop, since the aim is to prevent secondary cases. Meningococcal disease is a notifiable condition in Australia, and public health units coordinate contact tracing and prophylaxis.

• B. Chemoprophylaxis should be targeted at close contacts, not restricted only to healthcare workers who performed procedures, unless they specifically meet close contact criteria.
• C. Lecture attendees are casual contacts without direct exposure to secretions and do not require chemoprophylaxis.
• D. Prophylaxis is given to prevent secondary cases before symptoms develop, not withheld until contacts become symptomatic.
• E. Chemoprophylaxis should not be delayed for vaccination; it must be given promptly as vaccination takes time to generate immunity and does not replace timely prophylaxis.

Herpes simplex encephalitis classically presents with fever, altered mental state, seizures and focal neurological or cognitive deficits, with MRI showing asymmetric temporal and insular lobe changes and EEG showing periodic lateralised epileptiform discharges, as seen in this patient. Because of the high mortality and morbidity of untreated HSE, empirical intravenous aciclovir must be started immediately on clinical and radiological suspicion, without waiting for CSF PCR confirmation, as PCR may initially be negative early in the illness. CSF should still be sent for PCR to confirm the diagnosis and guide duration of treatment, typically 14-21 days of intravenous therapy.

• A. Waiting for PCR confirmation before starting treatment risks a potentially fatal delay, since early PCR can be falsely negative and treatment should not be withheld on clinical suspicion.
• B. Ceftriaxone and vancomycin treat bacterial meningitis but do not cover herpes simplex virus, which requires aciclovir for this presentation.
• C. Oral valaciclovir has inadequate CNS penetration compared with intravenous aciclovir and outpatient review is inappropriate for a patient with altered consciousness and seizures.
• D. Encephalitis is a medical emergency requiring immediate inpatient treatment, not outpatient imaging follow-up in two weeks.

Bacterial meningitis typically produces a markedly elevated CSF white cell count with neutrophil predominance, high protein, and a low CSF-to-serum glucose ratio (here approximately 0.29, well below the normal ratio of greater than 0.6), reflecting bacterial consumption of glucose and an intense inflammatory response. Viral meningitis usually shows a lymphocyte-predominant pleocytosis with normal or mildly elevated protein and normal glucose. Tuberculous and fungal meningitis typically show a lymphocytic pleocytosis with markedly elevated protein and low glucose, but usually develop over days to weeks rather than acutely, and the neutrophil predominance here is most consistent with acute bacterial infection.

• A. These CSF findings are markedly abnormal, not normal; normal CSF has white cell count less than 5 cells/microL and glucose close to two-thirds of serum glucose.
• C. Tuberculous meningitis usually has a subacute onset over days to weeks with lymphocytic pleocytosis, not an acute neutrophilic picture.
• D. Fungal meningitis typically causes a lymphocytic pleocytosis and usually occurs in immunocompromised patients with a more insidious onset.
• E. Viral meningitis typically shows lymphocytic pleocytosis with normal glucose, not neutrophil predominance with markedly low glucose as seen here.

This presentation of optic neuritis with a prior episode of sensory symptoms separated by time and affecting a different central nervous system location is suggestive of multiple sclerosis. Gadolinium-enhanced MRI of the brain and spinal cord is the key investigation, as it can demonstrate dissemination in space (multiple white matter lesions in characteristic periventricular, juxtacortical, infratentorial or spinal cord locations) and dissemination in time (enhancing and non-enhancing lesions), fulfilling the McDonald criteria. Oligoclonal bands and evoked potentials provide supportive evidence but are not the primary diagnostic test. Aquaporin-4 antibodies are tested when neuromyelitis optica spectrum disorder is suspected, which is less likely given the facial numbness history.

• B. Oligoclonal bands support the diagnosis but are not the first-line confirmatory investigation.
• C. Aquaporin-4 antibody testing is used to investigate neuromyelitis optica spectrum disorder, not typical multiple sclerosis.
• D. CT orbits assesses orbital structures and is not sensitive for demyelinating white matter lesions.
• E. Visual evoked potentials can show delayed conduction but are supportive, not the primary diagnostic test.

Acute, disabling relapses of multiple sclerosis with confirmed new lesion activity are treated with high-dose intravenous methylprednisolone, which shortens the duration and severity of the relapse by reducing inflammation and blood-brain barrier disruption, although it does not alter long-term disability outcomes. Oral corticosteroids are less commonly used and intravenous pulse therapy remains standard for significant relapses. Switching or escalating disease-modifying therapy is a separate decision made after recovery, based on relapse frequency and MRI activity, not as acute relapse treatment. Plasma exchange is reserved for severe relapses that fail to respond to corticosteroids.

• A. Disease-modifying therapy decisions are made after the acute relapse has been managed, not as the immediate treatment.
• B. Simply increasing the current disease-modifying therapy dose does not treat an acute relapse and is not standard practice.
• C. Oral corticosteroids are not the standard first-line treatment for an acute disabling relapse; intravenous pulse therapy is preferred.
• D. Plasma exchange is reserved for relapses refractory to corticosteroids, not first-line therapy.

Weight gain, cold intolerance, bradycardia, dry skin and delayed ankle reflex relaxation are classic features of hypothyroidism, a reversible cause of cognitive impairment that can mimic dementia. Serum thyroid-stimulating hormone is the most appropriate initial test, as an elevated level confirms primary hypothyroidism, which when treated with thyroxine replacement can substantially improve or resolve the cognitive symptoms. Vitamin B12 deficiency should also be excluded in any dementia work-up but does not explain this patient's specific findings of bradycardia and cold intolerance. Imaging and cerebrospinal fluid studies are useful in the broader dementia work-up but are not the priority test given this clinical picture.

• A. MRI brain is part of dementia work-up but does not address the specific clinical features pointing to a metabolic cause.
• B. EEG is not useful for diagnosing hypothyroidism-related cognitive impairment.
• C. Vitamin B12 deficiency does not typically cause bradycardia, cold intolerance or delayed reflex relaxation seen here.
• D. Lumbar puncture is not indicated as the priority investigation given this clinical picture suggestive of hypothyroidism.

The triad of gait disturbance (described as a broad-based, shuffling, magnetic gait), urinary incontinence and cognitive slowing, developing over weeks to months in an older adult, is characteristic of normal pressure hydrocephalus. Gait disturbance is typically the earliest and most prominent feature and often improves most with treatment, which involves ventriculoperitoneal shunting after confirmation with brain imaging showing ventriculomegaly out of proportion to cortical atrophy. Parkinson's disease classically causes a narrow-based shuffling gait with rigidity and tremor rather than early incontinence. Vascular dementia typically presents with stepwise decline and focal deficits related to prior vascular events, and spinal stenosis causes neurogenic claudication without cognitive or urinary symptoms.

• A. Lumbar spinal stenosis causes leg pain with walking and normal cognition and continence, not this triad.
• B. Parkinson's disease typically presents with resting tremor, rigidity and bradykinesia rather than this triad with early incontinence.
• C. Vascular dementia usually shows stepwise decline with focal neurological signs related to vascular events, not this specific triad.
• E. Subdural haematoma usually presents with headache, confusion or focal deficits, often with a history of trauma or anticoagulant use.

Delirium is characterised by acute onset, a fluctuating course, and a core deficit in attention and awareness, often with an identifiable precipitant such as infection, as seen here with the urinary tract infection and fever. Dementia, in contrast, develops insidiously over months to years with relatively preserved attention until late stages. The evening worsening (sundowning) and fluctuating arousal are classic delirium features. Distinguishing the two is essential because delirium is usually reversible once the underlying cause is treated, whereas dementia is a chronic progressive condition.

• B. Gradual functional decline over time is characteristic of dementia rather than an acute confusional state.
• C. Insidious language decline over months suggests a primary progressive dementia process, not delirium.
• D. Delirium typically involves altered level of consciousness or arousal, which is not preserved.
• E. This describes the typical slow progression of dementia, not the acute presentation described.

This patient has clinical features of cauda equina syndrome: bilateral leg weakness, saddle anaesthesia, and urinary retention, which constitutes a neurosurgical emergency. Urgent MRI of the lumbosacral spine is the investigation of choice because it directly visualises the nerve roots, the cauda equina, and any compressive lesion such as a large disc herniation, and it guides immediate surgical decompression. Delay in diagnosis and decompression beyond 24-48 hours significantly worsens the chance of neurological recovery, particularly for bladder and bowel function. Plain X-ray and lumbar puncture do not adequately assess soft tissue or nerve root compression.

• B. Corticosteroids are not standard therapy for disc-related cauda equina syndrome and delay would risk permanent deficit.
• C. Plain X-ray does not visualise soft tissue, nerve roots, or disc material and is inadequate for this emergency.
• D. Lumbar puncture is not indicated here and risks precipitating or worsening cord or nerve root compromise.
• E. Outpatient referral is inappropriate given the risk of permanent neurological and sphincter damage without urgent intervention.

Malignant spinal cord compression is an oncological emergency presenting with back pain, progressive limb weakness, a sensory level, and sphincter disturbance, as seen in this patient with known metastatic prostate cancer. Immediate high-dose corticosteroids (commonly dexamethasone) reduce vasogenic oedema around the tumour and may improve neurological outcome while definitive treatment is arranged. Urgent whole-spine MRI is required because metastases are frequently multifocal and the whole cord must be assessed to plan radiotherapy or surgical decompression. Treatment delay beyond hours can result in permanent paraplegia and loss of sphincter control.

• A. Mobilisation and monitoring delay definitive treatment in a time-critical emergency.
• B. Watchful waiting risks irreversible paraplegia; this presentation requires immediate intervention, not observation.
• D. Oral paracetamol and outpatient planning do not address the acute cord compression and risk permanent paralysis.
• E. Lumbar puncture risks neurological deterioration in cord compression and does not aid diagnosis or treatment.

The S1 nerve root supplies ankle plantarflexion and toe flexion, mediates the ankle (Achilles) reflex, and provides sensation over the lateral foot and little toe. Weakness of plantarflexion with an absent ankle jerk and lateral foot sensory loss, together with a positive straight leg raise test, is the classic pattern of S1 radiculopathy from a lower lumbar disc herniation (typically L5-S1). Accurate root-level examination guides correlation with imaging findings and surgical planning if conservative management fails.

• B. L5 radiculopathy causes weakness of ankle dorsiflexion and great toe extension with sensory loss over the dorsum of the foot, not plantarflexion weakness.
• C. L3 radiculopathy typically causes anterior thigh pain, knee extension weakness, and a reduced knee reflex, not these findings.
• D. L2 radiculopathy involves hip flexion weakness and anterior thigh sensory loss, unrelated to this presentation.
• E. L4 radiculopathy affects knee extension and the knee reflex with sensory loss over the medial lower leg, not matching this pattern.

Cervical spondylotic myelopathy results from chronic degenerative narrowing of the cervical spinal canal causing cord compression, and it typically presents in older adults with a combination of hand clumsiness, gait disturbance, and upper motor neuron signs (hyperreflexia, clonus, spasticity) in the lower limbs. Vibration sense loss reflects posterior column involvement, which is common in myelopathy. The absence of neck pain does not exclude the diagnosis, as many patients present with myelopathic signs without significant pain. MRI of the cervical spine is the investigation of choice to confirm cord compression.

• A. Normal pressure hydrocephalus causes a gait disorder with urinary incontinence and cognitive decline, not hand clumsiness with hyperreflexia.
• C. Amyotrophic lateral sclerosis combines upper and lower motor neuron signs but typically includes bulbar features and does not classically present with isolated posterior column sensory loss.
• D. Parkinson's disease produces bradykinesia, rigidity, and resting tremor rather than upper motor neuron signs and clonus.
• E. Peripheral polyneuropathy causes reduced or absent reflexes and distal sensory loss, not hyperreflexia and clonus.

Extradural haematoma classically follows a direct blow to the temporal region causing laceration of the middle meningeal artery, often associated with an overlying skull fracture. The hallmark presentation is a lucid interval, during which the patient appears neurologically normal after initial loss of consciousness, followed by rapid deterioration in conscious state as the haematoma expands and causes raised intracranial pressure and uncal herniation. The ipsilateral dilated pupil reflects compression of the third cranial nerve, and the contralateral limb weakness reflects compression of the corticospinal tract, both from herniation on the same side as the clot. This presentation requires emergency CT brain and urgent neurosurgical evacuation.

• A. Diffuse axonal injury typically causes immediate and persistent impaired consciousness without a lucid interval.
• B. Subarachnoid haemorrhage classically presents with sudden severe headache and meningism rather than a lucid interval with lateralising signs.
• C. Post-concussive syndrome involves persistent headache, dizziness, and cognitive symptoms without acute pupillary or motor signs of herniation.
• D. Acute subdural haematoma typically causes progressive decline without a classic lucid interval and is more common with cortical vein shearing in the elderly or in high-velocity trauma.

Chronic subdural haematoma classically occurs in elderly patients, particularly those on anticoagulant therapy such as apixaban, often following a seemingly trivial head injury that may be forgotten or minimised. Cerebral atrophy increases the space for the haematoma to expand slowly over weeks, and venous bleeding from bridging veins tends to progress gradually, producing a subacute decline in cognition, drowsiness, and falls, with focal signs such as hemiparesis developing as the clot enlarges. Anticoagulation markedly increases both the risk of bleeding and its rate of expansion, making this diagnosis important to consider in any anticoagulated older adult with cognitive decline after even minor head trauma. Urgent CT brain is required to confirm the diagnosis and guide management, including anticoagulation reversal and neurosurgical referral.

• B. Normal pressure hydrocephalus presents with the triad of gait disturbance, urinary incontinence, and dementia over a longer time course, not focal signs after head trauma.
• C. B12 deficiency causes subacute combined degeneration with sensory ataxia and peripheral neuropathy, not focal hemiparesis and drowsiness after head trauma.
• D. While infection can cause delirium in the elderly, the history of head trauma, anticoagulation, and focal neurological signs point towards a structural intracranial cause.
• E. An ischaemic stroke typically presents with sudden-onset focal deficits rather than a gradual three-week decline in cognition.

The combination of hypertension, bradycardia and irregular respiration (the Cushing reflex) occurs when rising intracranial pressure compresses the brainstem and reduces cerebral perfusion pressure. The brainstem responds with a sympathetically mediated rise in systemic blood pressure to restore cerebral perfusion; the resulting stretch on baroreceptors then produces a vagally mediated reflex bradycardia. Combined with a dilating, fixed pupil and falling GCS, this is a late, ominous sign of impending brainstem herniation and demands immediate action to lower intracranial pressure and arrange urgent neurosurgical review. It is a terminal compensatory mechanism, not a primary cardiovascular or endocrine disorder.

• A. Autonomic dysreflexia causes hypertension and reflex bradycardia but requires a spinal cord lesion with a triggering stimulus below the injury level, not an isolated head injury.
• B. Adrenal insufficiency causes hypotension, not the hypertensive bradycardic pattern seen here.
• D. Hypovolaemic shock produces hypotension and tachycardia, the opposite of the pattern described here.
• E. Neurogenic shock causes hypotension and bradycardia from loss of sympathetic tone, not hypertension.