PLAB 1 (UKMLA AKT) neurology questions

Any patient with suspected acute stroke must have an urgent non-contrast CT head to exclude intracranial haemorrhage before any antiplatelet or thrombolytic therapy is given, since these would be dangerous if the stroke were haemorrhagic. CT is widely available, fast, and sufficiently sensitive for acute haemorrhage, making it the first-line imaging modality in the hyperacute setting. Thrombolysis can only be considered once haemorrhage has been excluded and the patient meets eligibility criteria within the licensed time window.

• A. Aggressive blood pressure lowering is not indicated before determining stroke type and is avoided in acute ischaemic stroke unless very high or thrombolysis is planned.
• B. Alteplase cannot be given until a CT has confirmed an ischaemic stroke without haemorrhage.
• C. MRI is not the first-line emergency investigation; CT is faster and more readily available in the acute setting.
• D. Aspirin must not be given until haemorrhage has been excluded by CT.

The ROSIER score assigns points for the presence of asymmetric facial weakness, arm weakness, leg weakness, speech disturbance and visual field defect, while subtracting points for loss of consciousness, seizure activity or hypoglycaemia, since these suggest an alternative diagnosis. A score greater than zero makes stroke likely and warrants urgent further assessment. In this patient, the presence of facial and arm weakness with normal glucose (excluding hypoglycaemia as a mimic) supports stroke as the likely diagnosis.

• A. Loss of consciousness subtracts points, counteracting the positive scoring from a visual field defect.
• B. Seizure activity subtracts points on the ROSIER scale and suggests an alternative diagnosis.
• C. Loss of consciousness subtracts points on the ROSIER scale, making stroke less likely.
• E. Normal glucose alone does not score points; it is relevant only to exclude hypoglycaemia as a stroke mimic.

Thrombolysis with alteplase is contraindicated in patients on warfarin with an INR above 1.7, because the combination substantially increases the risk of intracranial and systemic haemorrhage. An INR of 2.5 exceeds this threshold, so alteplase must be withheld regardless of the time window or haemorrhage-negative CT. Mechanical thrombectomy may still be considered if the patient meets criteria, as it does not carry the same bleeding risk from anticoagulation.

• A. Correcting the INR with vitamin K takes too long to be useful within the thrombolysis time window and is not standard practice for this indication.
• B. There is no dose adjustment of alteplase for anticoagulated patients; the therapy is simply contraindicated above the INR threshold.
• C. An INR of 2.5 is above the safe threshold and makes thrombolysis unsafe due to bleeding risk.
• D. Fresh frozen plasma is not routinely used to rapidly reverse warfarin for the purpose of enabling thrombolysis within the time-critical window.

Lacunar strokes result from occlusion of small perforating arteries and classically present with one of: pure motor hemiparesis, pure sensory loss, sensorimotor stroke, or ataxic hemiparesis, without cortical signs such as dysphasia, neglect or visual field defects. This patient's isolated, equal motor deficit affecting face, arm and leg with preserved higher cortical function is typical of pure motor lacunar stroke. Total and partial anterior circulation strokes require cortical features such as dysphasia, neglect or homonymous hemianopia, which are absent here.

• A. Partial anterior circulation stroke requires at least one cortical feature such as dysphasia or neglect, which this patient lacks.
• B. Posterior circulation stroke typically presents with cranial nerve palsies, cerebellar signs, or bilateral deficits, not an isolated unilateral motor deficit.
• D. Total anterior circulation stroke requires all three of higher cortical dysfunction, homonymous hemianopia, and contralateral motor/sensory deficit, none of which beyond motor deficit are present.
• E. Watershed infarct is not a Bamford classification category and typically presents with proximal limb weakness from hypoperfusion, not a classic lacunar syndrome.

Patients with crescendo TIA (two or more episodes within a week) are treated as high risk regardless of ABCD2 score and require urgent specialist assessment within 24 hours of symptom onset, along with immediate aspirin 300 mg unless contraindicated. This reflects the significant short-term risk of subsequent stroke, which is highest in the days following a TIA. Specialist assessment includes further risk stratification, brain and vascular imaging as appropriate, and initiation of secondary prevention.

• A. Reassurance without specialist review is inappropriate given the high short-term stroke risk after crescendo TIA.
• B. Carotid Doppler within a week is too slow; crescendo TIA requires same-day specialist assessment, not community imaging alone.
• C. MRI referral within a week is too slow for a patient with crescendo TIA, who needs same-day specialist review.
• E. A 7-day assessment window is appropriate only for lower-risk, single TIA episodes beyond 1 week, not crescendo TIA.

Following ischaemic stroke without atrial fibrillation, clopidogrel is recommended first-line for long-term secondary prevention because it is at least as effective as aspirin combined with dipyridamole but better tolerated. High-intensity statin therapy (such as atorvastatin 20-80 mg) is also started regardless of baseline cholesterol level to reduce recurrent vascular events. Carotid Doppler imaging should also be arranged if the stroke is in the anterior circulation territory, to assess for significant carotid stenosis amenable to endarterectomy.

• A. Aspirin and dipyridamole combined is reserved for patients who cannot tolerate clopidogrel, not first-line therapy.
• C. Warfarin is indicated for secondary prevention only when there is an underlying indication such as atrial fibrillation, not for all ischaemic strokes.
• D. Fibrate therapy is not standard secondary stroke prevention; high-intensity statin is indicated instead.
• E. Dipyridamole alone is not first-line, and low-intensity statin does not provide adequate secondary prevention benefit.

In haemorrhagic stroke, anticoagulation must be reversed urgently to limit haematoma expansion; for warfarin-associated intracerebral haemorrhage, this is done with prothrombin complex concentrate and intravenous vitamin K. Antiplatelet agents and thrombolytics are absolutely contraindicated because they would worsen bleeding. Supportive care, blood pressure control and neurosurgical assessment for evacuation or management of raised intracranial pressure are also required, but the most immediate life-saving step is anticoagulation reversal.

• B. Clopidogrel is an antiplatelet agent and is contraindicated in haemorrhagic stroke; the priority is reversing anticoagulation first.
• C. Alteplase is absolutely contraindicated in haemorrhagic stroke as it would markedly worsen the bleed.
• D. Heparin is an anticoagulant and would worsen the haemorrhage; anticoagulation must be reversed, not added.
• E. Aspirin is contraindicated in haemorrhagic stroke as it would worsen bleeding.

Giant cell arteritis carries a risk of sudden irreversible visual loss due to ischaemic optic neuropathy, so treatment must never be delayed for biopsy confirmation. Current guidance recommends starting high-dose glucocorticoids (typically prednisolone 40-60 mg daily) immediately on clinical suspicion, with biopsy performed within days afterwards as steroids do not significantly affect histology for about two weeks. Jaw claudication, scalp tenderness and a markedly raised ESR in a patient over 50 years are classic features supporting the diagnosis. Delaying treatment risks irreversible blindness, which steroids can prevent if started promptly.

• A. Aspirin has no proven role in preventing visual loss in this condition and is not a substitute for steroids.
• B. Delaying treatment risks irreversible visual loss and is not recommended while awaiting biopsy.
• D. Imaging is not required before starting urgent treatment and would cause harmful delay.
• E. Amitriptyline treats neuropathic pain, not the underlying vasculitis, and does not prevent visual loss.

Idiopathic intracranial hypertension typically affects obese women of reproductive age and presents with headache worse on lying down, pulsatile tinnitus, visual disturbance and papilloedema. Diagnosis requires a raised CSF opening pressure above 25 cmH2O with normal CSF composition, normal neuroimaging, and no other identifiable cause of raised intracranial pressure. The normal CT head and normal CSF constituents help exclude structural lesions and infection. Management includes weight loss, acetazolamide, and monitoring of visual fields to prevent permanent visual loss.

• A. Migraine with aura does not cause papilloedema or a raised opening pressure.
• B. Bacterial meningitis causes fever, neck stiffness and abnormal CSF with pleocytosis, none of which are present.
• C. Venous sinus thrombosis should be excluded with venography before diagnosing idiopathic intracranial hypertension, but the normal CSF composition and typical demographic make this less likely here.
• D. Posterior reversible encephalopathy syndrome is associated with severe hypertension or eclampsia and causes seizures and cortical blindness, not isolated papilloedema with normal imaging.

New-onset headache in a patient over 50 years, early morning headache with vomiting, and headache worsened by coughing or straining are red flag features suggestive of raised intracranial pressure from a space-occupying lesion. These features warrant urgent neuroimaging, typically CT head, to exclude an intracranial mass, even when examination including fundoscopy is normal, as papilloedema may be absent early on. Prompt imaging allows timely diagnosis and treatment of conditions such as a brain tumour. Waiting or treating empirically risks delayed diagnosis of a serious underlying cause.

• A. Amitriptyline is used for chronic tension-type headache or migraine prevention, not appropriate until serious pathology is excluded.
• C. Electroencephalography assesses seizure activity, not the structural cause suggested by these red flag symptoms.
• D. Reassurance and delayed review are inappropriate given multiple red flag features requiring urgent investigation.
• E. Propranolol is used for migraine prophylaxis, which is not the likely diagnosis given these red flag features.

According to the Resuscitation Council UK and Status Epilepticus guidance, if seizures continue despite an initial benzodiazepine dose, a second dose of benzodiazepine (intravenous lorazepam 4 mg, or diazepam if lorazepam unavailable) should be given, provided at least 10 minutes have passed and airway, breathing and circulation are being supported. Second-line agents such as intravenous phenytoin, levetiracetam, or valproate are reserved for seizures persisting after two doses of benzodiazepine (established status epilepticus). General anaesthesia with rapid sequence induction is reserved for refractory status epilepticus unresponsive to second-line agents. Since only one benzodiazepine dose has been given here, the next step is a further benzodiazepine dose with IV access now available.

• A. Intravenous access is now available, so the intravenous route is preferred over repeating the rectal route.
• B. Rapid sequence induction is reserved for refractory status epilepticus unresponsive to first- and second-line drugs.
• C. Phenytoin is a second-line agent used after two doses of benzodiazepine have failed, not before a repeat benzodiazepine dose.
• E. Levetiracetam is a second-line agent used after benzodiazepines have failed, not as the immediate next step.

Lateral tongue biting and a prolonged postictal period of confusion lasting many minutes are highly specific features favouring a true epileptic seizure over syncope or a psychogenic non-epileptic seizure. Syncope, whether vasovagal or cardiac, typically causes rapid recovery of orientation within seconds to a couple of minutes once cerebral perfusion is restored, without prolonged postictal confusion. Psychogenic non-epileptic seizures may show more variable, often asynchronous movements and typically lack lateral tongue biting or significant postictal confusion. Back pain can occur from forceful muscle contraction during a tonic-clonic seizure, further supporting this diagnosis.

• A. Vasovagal syncope causes rapid recovery of consciousness and does not typically cause tongue biting or prolonged postictal confusion.
• B. Cardiac syncope also causes rapid recovery once circulation is restored and would not typically cause lateral tongue biting.
• C. A transient ischaemic attack does not cause convulsive movements or loss of consciousness in this way.
• D. Psychogenic non-epileptic seizures typically lack lateral tongue biting and prolonged true postictal confusion.

Temporal lobe focal seizures classically produce an aura of déjà vu or other altered perception, followed by automatisms such as lip-smacking, chewing, or fumbling with objects or clothing, with impaired awareness but not complete loss of consciousness. These automatisms and the preceding experiential aura localise the seizure focus to the temporal lobe, often involving mesial structures such as the hippocampus or amygdala. Postictal amnesia for the event is also typical. Frontal lobe seizures more commonly cause brief motor features such as hypermotor activity or asymmetric tonic posturing rather than déjà vu and oroalimentary automatisms.

• A. Absence seizures cause brief staring spells without aura or automatisms and typically occur in children.
• C. Generalised tonic-clonic seizures involve loss of consciousness with convulsive motor activity, not an isolated aura with automatisms.
• D. A panic attack does not typically cause lip-smacking automatisms or impaired responsiveness with amnesia for the event.
• E. Frontal lobe seizures typically present with brief, often bizarre motor activity or tonic posturing rather than déjà vu and oroalimentary automatisms.

Following a first unprovoked seizure, DVLA rules require a group 1 licence holder to stop driving and notify the DVLA. If investigations (including EEG and imaging) are normal and there is no further seizure, driving may resume after 6 seizure-free months, at the DVLA's discretion. It is the patient's legal responsibility to inform the DVLA, though the doctor should advise them of this duty and document the advice given. Group 2 (HGV/bus) licences have much stricter rules, typically requiring 5 years seizure-free off medication.

• A. A normal MRI alone does not override the mandatory 6-month seizure-free period required by DVLA guidance.
• C. Permanent surrender is not required after a single first seizure with normal investigations.
• D. The duty to inform DVLA arises immediately after the seizure, not only after a recurrence.
• E. Absence of warning symptoms does not exempt a patient from the notification requirement or the seizure-free period.

Carbamazepine is a potent inducer of hepatic cytochrome P450 enzymes, which accelerates the metabolism of both oestrogen and progestogen components of combined oral contraceptives, lowering their serum levels and reducing contraceptive efficacy. This manifests clinically as breakthrough bleeding and an increased risk of unintended pregnancy. Women on enzyme-inducing antiepileptics should be advised to use additional or alternative contraception, such as a copper intrauterine device, or a method unaffected by enzyme induction. The combined pill and progestogen-only pill are not considered reliable first-line choices for women taking enzyme-inducing drugs.

• A. The interaction is hepatic metabolic induction, not a reduction in gut absorption.
• B. There is no direct endometrial toxicity; the bleeding reflects reduced circulating hormone levels from increased metabolism.
• C. Carbamazepine is an enzyme inducer, not an inhibitor, and inhibition would raise rather than lower hormone levels.
• E. Protein-binding displacement is not the mechanism underlying this well-recognised interaction.

Lamotrigine is considered one of the safer antiepileptic drugs in women of childbearing potential, with a lower risk of major congenital malformations and neurodevelopmental problems compared with sodium valproate. It is also effective monotherapy for focal epilepsy. Sodium valproate is associated with significant risks of neural tube defects and long-term neurodevelopmental impairment and is contraindicated in women who could become pregnant unless no other effective treatment is available, under a pregnancy prevention programme. Phenytoin and topiramate also carry teratogenic risks and are not preferred first-line choices in this context.

• A. Primidone carries teratogenic risk and is not a first-line choice for focal epilepsy in women planning pregnancy.
• B. Phenytoin is associated with fetal hydantoin syndrome and is not first-line in women planning pregnancy.
• D. Sodium valproate carries a high risk of neural tube defects and neurodevelopmental disorders and should be avoided in women of childbearing potential.
• E. Topiramate is associated with oral clefts and low birth weight and is not preferred in this context.

A simple febrile seizure is generalised, lasts less than 15 minutes, does not recur within 24 hours, and is followed by complete recovery, as in this case. Children with a simple febrile seizure who have returned to their normal neurological baseline and have no signs of serious underlying infection do not require routine EEG or neuroimaging, as these do not alter management and simple febrile seizures do not indicate epilepsy. Management is supportive, with parental education on fever control, safety-netting advice, and reassurance that the recurrence risk is around one in three but the risk of subsequent epilepsy is only slightly above the general population. Investigations such as lumbar puncture are reserved for children with signs suggesting meningitis or encephalitis.

• A. EEG is not indicated after a simple febrile seizure with full recovery and a normal examination.
• B. Prophylactic antiepileptic treatment is not indicated after a single simple febrile seizure.
• C. Lumbar puncture is reserved for children with signs of meningism, reduced consciousness, or other red flags, none of which are present here.
• E. CT imaging is not routinely required for a simple febrile seizure with a normal neurological examination.

Early morning headache that improves on standing, vomiting without preceding nausea, and bilateral papilloedema with loss of venous pulsation are classic features of raised intracranial pressure. Overnight recumbency and the lower cerebral venous outflow when lying flat exacerbate intracranial pressure, explaining the diurnal pattern of worse symptoms on waking. This presentation warrants urgent neuroimaging to look for a space-occupying lesion such as a tumour, abscess, or haematoma. Papilloedema results from impaired axoplasmic flow in the optic nerve secondary to raised pressure transmitted along the optic nerve sheath.

• A. Cluster headache causes severe unilateral periorbital pain with autonomic features, not papilloedema or this diurnal headache pattern.
• B. Temporal arteritis typically occurs in older patients with scalp tenderness, jaw claudication, and a raised ESR, not this pattern of symptoms.
• D. Migraine does not typically cause papilloedema or loss of venous pulsation and usually presents with unilateral throbbing headache and aura.
• E. Intracranial hypotension causes postural headache that worsens on standing, the opposite pattern to this case, and does not cause papilloedema.

Focal neurological signs and papilloedema raise concern for a space-occupying lesion and raised intracranial pressure, in which lumbar puncture carries a significant risk of precipitating cerebral or cerebellar herniation (coning) due to the pressure gradient created between the cranial and spinal compartments. Current guidance mandates CT imaging before lumbar puncture whenever there are focal neurological signs, papilloedema, reduced consciousness, or other features suggesting raised intracranial pressure. If imaging reveals a mass lesion, lumbar puncture should be avoided and the patient referred urgently to neurosurgery. This safety step takes priority over moving directly to CSF analysis.

• B. Antibiotics may be appropriate if meningitis is suspected, but imaging to exclude a mass lesion is still required before lumbar puncture when focal signs are present.
• C. Lumbar puncture in the presence of papilloedema and focal signs risks herniation and must not be done before imaging has excluded a mass lesion.
• D. Imaging guidance does not eliminate the risk of herniation caused by the pressure gradient; CT must be done first regardless of technique.
• E. Mannitol is not given empirically before basic imaging and does not substitute for excluding a structural lesion first.

The combination of hypertension, bradycardia, and irregular respiration is Cushing's triad, a late and ominous sign of critically raised intracranial pressure, usually from an expanding intracranial haematoma or oedema causing brainstem compression. Rising intracranial pressure reduces cerebral perfusion, triggering a reflex rise in systemic blood pressure (the Cushing reflex) mediated by the sympathetic nervous system to maintain cerebral perfusion pressure; this hypertension then causes a baroreceptor-mediated reflex bradycardia, while brainstem compression disrupts the normal respiratory pattern. This presentation indicates impending brainstem herniation and requires immediate senior neurosurgical and anaesthetic involvement. Hypovolaemic and neurogenic shock both cause hypotension rather than hypertension, distinguishing them from this picture.

• A. Hypovolaemic shock causes hypotension and tachycardia, the opposite of the hypertension and bradycardia seen here.
• C. Neurogenic shock from spinal cord injury causes hypotension and bradycardia, not hypertension.
• D. There is no indication of cardiac ischaemia, and this pattern is a recognised late sign of raised intracranial pressure after head trauma.
• E. A vasovagal response causes hypotension and bradycardia, not hypertension, and would not explain the declining conscious level.

This presentation, a lucid interval following initial loss of consciousness and subsequent rapid deterioration with a dilating pupil, is classic for an extradural (epidural) haematoma, most often caused by a temporal bone fracture lacerating the middle meningeal artery. On CT, extradural haematomas appear as biconvex, lens-shaped hyperdense collections that are limited by cranial suture lines, because the blood collects between the skull and the tightly adherent dura, which is anchored at the sutures. The ipsilateral dilated pupil reflects compression of the third cranial nerve from uncal herniation as the haematoma expands, indicating a neurosurgical emergency requiring urgent evacuation.

• A. A crescent-shaped collection crossing suture lines describes a subdural haematoma, which classically follows venous bleeding and a more gradual course.
• C. Subarachnoid blood outlining the basal cisterns is typical of subarachnoid haemorrhage, usually from aneurysm rupture, not this traumatic lucid-interval picture.
• D. Diffuse oedema suggests diffuse axonal injury or global hypoxic injury, not the focal lucid-interval presentation described here.
• E. Scattered punctate haemorrhages at the grey-white junction are typical of diffuse axonal injury, not a biconvex arterial bleed.

Nocturnal paraesthesia of the thumb, index and middle fingers with a positive Tinel's sign (tapping over the wrist reproducing tingling) and Phalen's sign (symptoms on sustained wrist flexion) is classic for carpal tunnel syndrome, caused by compression of the median nerve within the carpal tunnel. Palmar sensation is typically preserved because the palmar cutaneous branch of the median nerve arises proximal to the carpal tunnel and is unaffected. Thenar muscle weakness, particularly of thumb abduction (abductor pollicis brevis), reflects motor involvement in more advanced disease. Initial management is a wrist splint and local corticosteroid injection, with surgical decompression reserved for refractory or severe cases.

• A. Cervical radiculopathy would typically cause neck pain and symptoms not reproduced by wrist-specific provocation tests.
• B. Ulnar nerve entrapment affects the little and ring fingers, not the thumb, index and middle fingers.
• C. Thoracic outlet syndrome causes diffuse arm symptoms often with vascular signs, not isolated nocturnal median nerve distribution symptoms.
• E. De Quervain's tenosynovitis causes pain over the radial wrist with a positive Finkelstein's test, not sensory symptoms in a median nerve distribution.

Sensory loss confined to the little finger and medial half of the ring finger, with involvement of the dorsal hand surface, localises to the ulnar nerve rather than a nerve root, because root lesions typically spare the dorsal hand in a nerve-specific pattern and affect a broader dermatomal distribution. Clawing of the ring and little fingers results from unopposed action of the long extensors with weakness of the ulnar-innervated lumbricals to these digits. Reproduction of symptoms by tapping over the medial epicondyle (a positive Tinel's sign at the elbow) localises the lesion to the cubital tunnel, the most common site of ulnar nerve entrapment. Management includes activity modification and avoiding prolonged elbow flexion, with surgical decompression considered if conservative measures fail.

• A. Klumpke's palsy affects the whole hand including median and ulnar distributions, usually with a history of brachial plexus traction injury.
• C. A median nerve lesion at the wrist affects the thumb, index, middle and half of the ring finger, not the ulnar distribution described.
• D. A radial nerve lesion at the spiral groove causes wrist drop with sensory loss over the dorsum of the hand, not clawing of the ring and little fingers.
• E. A C8 root lesion would involve the dorsal and palmar forearm in a dermatomal pattern and typically affects wrist and finger extensors, not an isolated ulnar hand pattern.

The radial nerve runs in close contact with the humerus in the spiral (radial) groove, making it particularly vulnerable to injury in mid-shaft humeral fractures. Damage here produces wrist drop due to paralysis of the wrist and finger extensors, along with sensory loss over the dorsal first web space, the area supplied by the superficial branch of the radial nerve. Triceps function is preserved because the branches to triceps arise proximal to the spiral groove. Most such injuries are neuropraxias that recover spontaneously over weeks to months with conservative management and splinting.

• A. Ulnar nerve injury causes clawing of the ring and little fingers with sensory loss over the medial hand, not wrist drop.
• C. Axillary nerve injury causes deltoid weakness and sensory loss over the lateral shoulder (regimental badge area), not wrist drop.
• D. Median nerve injury would cause weakness of forearm pronation and thumb opposition, not wrist extension loss.
• E. Posterior interosseous nerve injury causes finger drop with preserved wrist extension and no sensory loss, as it is a purely motor branch.

The common peroneal (fibular) nerve winds superficially around the neck of the fibula, making it vulnerable to compression or injury at this site, such as with a fibular neck fracture, tight plaster casts, or habitual leg crossing. Injury produces foot drop from paralysis of ankle dorsiflexion (tibialis anterior) and eversion (peroneus longus and brevis), with sensory loss over the dorsum of the foot and lateral lower leg supplied by its superficial and deep branches. Plantarflexion and inversion, supplied by the tibial nerve, and the ankle jerk reflex, mediated by the tibial nerve via S1/S2, remain normal, which helps distinguish this from a more proximal sciatic nerve lesion. Management is usually conservative with an ankle-foot orthosis and physiotherapy, as most cases resolve as the neuropraxia recovers.

• A. Sciatic nerve palsy would additionally impair plantarflexion, inversion and the ankle jerk, since it supplies the tibial division as well.
• B. Tibial nerve palsy causes weakness of plantarflexion and inversion with loss of the ankle jerk, the opposite pattern to that described.
• C. Deep peroneal nerve palsy alone would spare eversion and the lateral calf sensory loss, which are supplied by the superficial branch.
• E. An L4 root lesion would also affect knee extension and the knee jerk reflex, not isolated to foot drop with this sensory pattern.

Pain radiating from the back down the posterior leg to the lateral foot, reproduced by straight leg raising (which stretches the sciatic nerve roots), together with reduced ankle plantarflexion power and a diminished ankle jerk, localises to an S1 radiculopathy, most commonly caused by an L5/S1 disc prolapse. The straight leg raise test is positive when leg pain is reproduced below 60 degrees of elevation, reflecting tension on an irritated lumbosacral nerve root. Most episodes of sciatica from disc prolapse are managed conservatively with analgesia, advice to stay active and physiotherapy, as the majority resolve within weeks to months. Red flag features such as saddle anaesthesia, bilateral symptoms or urinary retention would mandate urgent imaging to exclude cauda equina syndrome.

• B. An L4 radiculopathy would cause weakness of knee extension and a reduced knee jerk, with sensory loss over the anterior thigh and medial leg, not this pattern.
• C. Piriformis syndrome causes buttock pain radiating down the leg but does not typically cause reflex loss or motor weakness.
• D. Meralgia paraesthetica causes sensory symptoms over the anterolateral thigh only, without motor weakness or a positive straight leg raise.
• E. Diabetic peripheral neuropathy causes symmetrical distal sensory loss, not a unilateral radicular pattern with a positive straight leg raise.

Saddle anaesthesia, bilateral lower limb weakness, urinary retention with a significant post-void residual, and reduced anal tone are red flag features of cauda equina syndrome, a surgical emergency caused by compression of the lumbosacral nerve roots below the level of the spinal cord. Emergency MRI of the whole spine is required immediately, as delayed diagnosis and decompression beyond 24 to 48 hours significantly worsens the chance of recovering bladder, bowel and sexual function. Plain X-ray and nerve conduction studies do not adequately visualise soft tissue compression of the nerve roots and would delay definitive management. Urinary retention must be managed alongside, not instead of, urgent investigation of the underlying cause.

• A. Managing urinary retention alone ignores the need for urgent imaging and neurosurgical assessment to prevent permanent neurological damage.
• B. Nerve conduction studies take time to arrange and do not assess acute compressive lesions of the cauda equina.
• D. Plain X-ray does not visualise the spinal canal or nerve roots and is inadequate to diagnose or exclude cauda equina syndrome.
• E. Cauda equina syndrome is a surgical emergency requiring immediate imaging, not a routine or urgent outpatient appointment within two weeks.

Guillain-Barré syndrome classically shows albuminocytological dissociation on lumbar puncture: a raised protein concentration with a normal or only mildly raised white cell count. This reflects inflammation and increased permeability of nerve roots without significant meningeal cellular infiltration. The preceding diarrhoeal illness (often Campylobacter jejuni) is a recognised trigger through molecular mimicry. Nerve conduction studies showing demyelinating features support the diagnosis alongside the clinical picture of ascending symmetrical weakness with areflexia.

• A. A markedly raised white cell count suggests bacterial or viral meningitis rather than Guillain-Barré syndrome.
• C. Low glucose with pleocytosis is typical of bacterial meningitis, not Guillain-Barré syndrome.
• D. Oligoclonal bands restricted to the CSF are characteristic of multiple sclerosis, not Guillain-Barré syndrome.
• E. Xanthochromia and red cells suggest subarachnoid haemorrhage, which does not fit this presentation.

In Guillain-Barré syndrome, respiratory muscle weakness can progress rapidly and lead to ventilatory failure before oxygen saturation or blood gases become abnormal, because hypoxia is a late sign. Regular bedside spirometry measuring forced vital capacity (FVC) is the recommended way to monitor respiratory function, with a falling trend or FVC below approximately 15-20 mL/kg prompting consideration of escalation to intensive care and possible ventilatory support. Pulse oximetry and blood gases are useful adjuncts but lag behind the earliest signs of neuromuscular respiratory failure. Peak flow mainly reflects airway calibre rather than global respiratory muscle strength.

• A. Peak expiratory flow is more a measure of airway obstruction and is less reliable than FVC for neuromuscular weakness.
• B. Chest radiography does not assess respiratory muscle strength and will not detect impending ventilatory failure.
• C. Arterial blood gases typically remain normal until respiratory failure is advanced, so they do not detect deterioration early.
• D. Pulse oximetry remains normal until late in neuromuscular respiratory failure and is not sensitive enough alone.

The history of fatigable ptosis and diplopia worsening with sustained activity and improving with rest is characteristic of myasthenia gravis, an autoimmune disorder affecting the neuromuscular junction. Most cases are caused by antibodies against the postsynaptic acetylcholine receptor, which reduce effective neuromuscular transmission and cause progressive fatigue of repeatedly used muscles. Testing for acetylcholine receptor antibodies is the key diagnostic investigation, supported where needed by electromyography showing decremental response on repetitive nerve stimulation. A CT chest is also performed to look for an associated thymoma.

• A. Anti-Jo-1 antibodies are associated with antisynthetase syndrome and polymyositis, not myasthenia gravis.
• C. Anti-Hu antibodies are a paraneoplastic marker associated with sensory neuronopathy and encephalomyelitis, not typical myasthenia.
• D. Anti-dsDNA antibodies are associated with systemic lupus erythematosus, not fatigable neuromuscular weakness.
• E. Anti-GQ1b antibodies are associated with Miller Fisher syndrome, a variant of Guillain-Barré syndrome.

Aminoglycosides such as gentamicin impair neuromuscular transmission by reducing presynaptic acetylcholine release and can precipitate a myasthenic crisis in patients with myasthenia gravis. This presents with rapidly worsening bulbar and respiratory muscle weakness, as seen in this patient, and may require urgent ventilatory support. Other drugs that can worsen myasthenia include beta-blockers, certain antiarrhythmics, magnesium, and some fluoroquinolones. Avoiding these agents and recognising early signs of crisis is essential in managing patients with myasthenia gravis who require treatment for intercurrent illness.

• A. Nitrofurantoin does not have a recognised significant effect on neuromuscular junction function.
• B. Cefalexin, a cephalosporin, is not known to significantly worsen myasthenia gravis.
• D. Amoxicillin is not strongly associated with worsening of neuromuscular transmission in myasthenia gravis.
• E. Co-trimoxazole is not a classic precipitant of myasthenic crisis, unlike aminoglycosides.

Lambert-Eaton myasthenic syndrome is caused by antibodies against presynaptic voltage-gated calcium channels, impairing acetylcholine release at the neuromuscular junction. It characteristically causes proximal limb weakness that improves transiently with repeated muscle use (post-exercise facilitation) and is strongly associated with small cell lung cancer, which should be excluded in any smoker presenting with this pattern. Autonomic features such as dry mouth are common. Unlike myasthenia gravis, where fatigability worsens with repeated use, the weakness and reflexes in Lambert-Eaton syndrome characteristically improve with sustained contraction before fatiguing further later.

• A. Multifocal motor neuropathy causes asymmetric distal motor weakness, not proximal weakness improving with activity.
• B. Myasthenia gravis causes fatigable weakness that worsens, rather than transiently improves, with repeated muscle use.
• C. Polymyositis causes proximal weakness but is not associated with reflex facilitation or strong lung cancer association in this pattern.
• E. Guillain-Barré syndrome causes ascending weakness with progressive areflexia, not improvement with exercise.

This boy demonstrates Gower's sign, using his hands to push up from the floor because of proximal pelvic girdle weakness, together with calf pseudohypertrophy and a markedly raised creatine kinase, which together are characteristic of Duchenne muscular dystrophy. It is caused by X-linked recessive mutations in the dystrophin gene, leading to progressive muscle degeneration, and typically presents between ages 2 and 5 years with loss of ambulation usually by early teenage years, consistent with the family history of an affected maternal uncle. Becker muscular dystrophy has a similar but milder and later-onset phenotype due to partially functional dystrophin.

• A. Congenital myotonic dystrophy presents with hypotonia and feeding difficulties in infancy, with myotonia rather than this pattern of proximal weakness.
• B. Spinal muscular atrophy typically presents with hypotonia and lower motor neurone signs without markedly raised creatine kinase.
• C. Becker muscular dystrophy has a similar but later-onset and more slowly progressive course, not matching this early severe presentation.
• D. Limb-girdle muscular dystrophy is usually autosomal in inheritance and presents later, not matching the X-linked family history.

Parkinson's disease is primarily a clinical diagnosis, based on the presence of bradykinesia plus at least one of resting tremor, rigidity or postural instability, typically asymmetric at onset, as seen in this patient with unilateral tremor, rigidity and reduced arm swing. NICE guidance recommends that patients with suspected parkinsonism are referred to a specialist for assessment, but imaging such as DAT-SPECT is reserved for cases where the diagnosis is uncertain, for example to distinguish Parkinson's disease from essential tremor, rather than being required in every patient. A dramatic and sustained response to levodopa supports the diagnosis but is not required to make it, and a lack of complete resolution does not exclude Parkinson's disease.

• A. DAT-SPECT is reserved for diagnostic uncertainty, not used routinely in every patient with a classic clinical presentation.
• C. Routine MRI is not required for a classic presentation of idiopathic Parkinson's disease and is mainly used to exclude other causes if atypical features are present.
• D. Diagnosis does not require complete symptom resolution with levodopa; partial or good response supports but is not mandatory for diagnosis.
• E. Caeruloplasmin is used to screen for Wilson's disease, which typically presents at a younger age, not as the first-line test here.

With long-term levodopa therapy, the duration of benefit from each dose shortens (wearing-off) as striatal dopamine storage capacity declines, so motor control becomes dependent on fluctuating plasma levodopa levels. Peak-dose dyskinesias (choreiform or dystonic involuntary movements) occur when plasma levodopa concentration peaks, reflecting pulsatile stimulation of dopamine receptors. Both wearing-off and dyskinesia together are classic late motor complications of chronic levodopa treatment, distinct from the disease itself. Management options include fractionating doses, adding a COMT inhibitor or MAO-B inhibitor, or using modified-release preparations.

• B. Disease progression alone would not explain the clear temporal relationship between dosing and symptom pattern.
• C. Multiple system atrophy features additional autonomic and cerebellar signs, not described here.
• D. There is no new drug history given to suggest drug-induced parkinsonism.
• E. Psychosis presents with hallucinations or delusions, not motor fluctuations.

This presentation, a bilateral postural and action tremor that improves with alcohol, has a family history, and occurs without parkinsonian features, is typical of essential tremor. First-line pharmacological treatment is a non-selective beta-blocker such as propranolol, which reduces tremor amplitude via beta-adrenergic blockade of peripheral and central tremor pathways. Primidone is an alternative first-line agent, particularly if beta-blockade is contraindicated. Levodopa and dopamine agonists are used for Parkinson's disease, which this patient does not have.

• A. Co-beneldopa treats Parkinson's disease, which features resting tremor and bradykinesia, not postural tremor.
• B. Anticholinergics such as trihexyphenidyl are used for drug-induced parkinsonism or dystonia, not essential tremor.
• C. Clonazepam is not first-line therapy for essential tremor and carries dependence risk.
• D. Dopamine agonists are used for Parkinson's disease, not essential tremor.

This presentation, fever, neck stiffness, photophobia and a non-blanching rash, is classic for meningococcal meningitis with septicaemia, a medical emergency. Empirical IV antibiotics (ceftriaxone) should be given immediately without waiting for lumbar puncture or imaging, since any delay increases mortality, and IV dexamethasone is added in suspected bacterial meningitis to reduce neurological complications, though it should be withheld or used cautiously if septic shock or meningococcal sepsis with rash dominates the picture per local protocol. Lumbar puncture and CT head can be performed after antibiotics if there are no contraindications, but must never delay treatment. Blood cultures should be taken ideally before antibiotics if this causes no delay.

• A. Oral antibiotics and outpatient management are inappropriate for a life-threatening presentation requiring immediate IV treatment and admission.
• C. Lumbar puncture should never delay empirical antibiotic treatment in suspected bacterial meningitis.
• D. Imaging should not delay antibiotic administration in a patient with signs of meningococcal sepsis.
• E. Aciclovir is used for suspected herpes encephalitis, not for this presentation with a purpuric rash suggesting meningococcal disease.

In suspected meningococcal disease with a non-blanching rash in the community, UK guidance recommends giving a single dose of IM (or IV if access is available) benzylpenicillin immediately before transfer to hospital, unless there is a clear history of anaphylaxis to penicillin, because early antibiotics reduce mortality from fulminant meningococcal sepsis. This should not delay emergency transfer by ambulance (999) to hospital for definitive management including blood cultures and further IV antibiotics. Oral antibiotics are inadequate for this severity of illness, and waiting for signs of reduced consciousness or for hospital-based cultures before treating would dangerously delay care.

• B. Benzylpenicillin should be given now, not held back until deterioration occurs.
• C. Oral antibiotics do not achieve adequate tissue levels quickly enough for suspected meningococcal sepsis, and transfer should be emergency, not routine.
• D. Antibiotics must not be delayed for diagnostic tests when meningococcal disease is suspected in the community.
• E. Symptomatic treatment alone is inappropriate and dangerously delays definitive care for a life-threatening emergency.

Viral meningitis typically produces a CSF lymphocytic pleocytosis (predominantly lymphocytes), mildly to moderately raised protein, and a normal or near-normal CSF-to-plasma glucose ratio, consistent with this patient's results (CSF glucose is more than two-thirds of plasma glucose). Acute bacterial meningitis classically shows a neutrophil-predominant pleocytosis, markedly raised protein, and low CSF glucose (CSF:plasma ratio typically below 0.4) due to bacterial glucose consumption. Tuberculous meningitis typically shows a lymphocytic pleocytosis with very high protein and markedly low glucose, usually with a more insidious subacute course. Subarachnoid haemorrhage would show red cells or xanthochromia rather than a predominantly lymphocytic picture.

• A. Bacterial meningitis would show a neutrophil-predominant pleocytosis with markedly reduced CSF glucose, not seen here.
• B. Tuberculous meningitis typically causes a very low CSF glucose and higher protein, with a longer prodrome.
• C. Subarachnoid haemorrhage would show xanthochromia and red blood cells on CSF analysis, not a lymphocytic pleocytosis.
• E. Fungal meningitis typically causes a low CSF glucose and occurs mainly in immunocompromised patients, not matching this normal glucose ratio.

Fever, acute behavioural change, seizures and MRI findings of asymmetric temporal and insular lobe signal change are highly suggestive of herpes simplex encephalitis, caused by HSV-1 reactivation with a predilection for the temporal lobes. Treatment with IV aciclovir should be started empirically as soon as encephalitis is suspected, without waiting for CSF PCR confirmation, because delayed treatment significantly worsens morbidity and mortality. Diagnosis is later confirmed with CSF HSV PCR, but initiation of antiviral therapy should not be delayed pending results. Oral valaciclovir does not achieve adequate CNS levels for this severe infection, and antibiotics are not effective against a viral cause.

• A. Steroids alone do not treat the underlying viral infection and are not first-line management here.
• B. Oral antiviral therapy does not achieve sufficient CNS penetration for severe encephalitis, which requires IV treatment.
• D. Benzylpenicillin has no activity against herpes simplex virus.
• E. Ceftriaxone treats bacterial meningitis, not viral encephalitis, which is suggested by the temporal lobe MRI changes.

This patient has two clinically distinct episodes of neurological dysfunction separated in time (18 months apart) and space (optic nerve, then facial sensory pathway), fulfilling the McDonald criteria for dissemination in time and space. The periventricular lesions oriented perpendicular to the ventricles (Dawson fingers) and CSF-restricted oligoclonal bands are classic supportive findings. This clinical and radiological pattern is diagnostic of relapsing-remitting multiple sclerosis. Optic neuritis is a common presenting feature of MS.

• B. CNS vasculitis typically presents with headache, stroke-like episodes and systemic inflammatory markers, not this classic relapsing demyelinating pattern.
• C. CIDP affects the peripheral nervous system with motor and sensory polyneuropathy, not the central nervous system.
• D. NMOSD typically causes more severe, bilateral optic neuritis and longitudinally extensive spinal cord lesions, with aquaporin-4 antibodies usually present.
• E. ADEM is typically a monophasic post-infectious illness in children with encephalopathy, not a relapsing course in an adult.

This is an acute relapse of multiple sclerosis with new objective neurological deficits (leg weakness, sixth nerve palsy) and no evidence of an alternative cause such as infection. NICE guidance recommends high-dose intravenous methylprednisolone (usually 1g daily for 3-5 days) to speed recovery from an acute relapse, after excluding infection. Disease-modifying therapies such as interferon, fingolimod and natalizumab are used to reduce future relapse frequency and are initiated by a specialist neurologist, not during acute management by a foundation doctor. Plasma exchange is reserved for severe relapses refractory to steroids.

• A. Natalizumab is a disease-modifying therapy requiring specialist initiation and monitoring, not used for acute relapses.
• B. Plasma exchange is reserved for severe relapses that fail to respond to corticosteroids, not first-line treatment.
• D. Fingolimod is a disease-modifying therapy for relapse prevention, not acute relapse management.
• E. Interferon beta-1a is a disease-modifying therapy for relapse prevention, not acute treatment, and requires specialist initiation.

This patient has clinical features of metastatic spinal cord compression: progressive back pain, bilateral leg weakness, a sensory level and bladder dysfunction in a patient with known malignancy. NICE guidance recommends immediate administration of dexamethasone (typically 16mg daily with gastric protection) to reduce cord oedema, and urgent MRI of the whole spine within 24 hours to confirm the diagnosis, localise the lesion and guide definitive treatment such as radiotherapy or surgery. This is a neurosurgical and oncological emergency, and any delay risks permanent paraplegia. Treatment should not wait for oncology referral or imaging results.

• A. Outpatient imaging is far too slow; suspected cord compression requires MRI within 24 hours.
• B. Plain X-ray has poor sensitivity for cord compression and is not the investigation of choice.
• C. Delaying assessment risks irreversible paralysis; this is a spinal emergency requiring immediate action.
• D. Oncology referral is appropriate once the diagnosis is confirmed, but immediate steroids and imaging must not be delayed.

This patient has a combination of dorsal column signs (loss of vibration and proprioception) and corticospinal tract signs (brisk reflexes, extensor plantars) alongside a peripheral neuropathy and macrocytic anaemia, classic for subacute combined degeneration of the spinal cord due to vitamin B12 deficiency. B12 is required for myelin synthesis, and deficiency causes demyelination of the dorsal columns and lateral corticospinal tracts, combined with a peripheral neuropathy. A vegan diet is a recognised risk factor for B12 deficiency due to lack of dietary animal products. Diagnosis is confirmed by low serum B12 and treated with intramuscular hydroxocobalamin.

• A. Autoimmune peripheral nerve demyelination describes Guillain-Barre syndrome or CIDP, which do not typically cause combined upper and lower motor neurone signs with macrocytic anaemia.
• B. Folate deficiency causes macrocytic anaemia but does not cause the combined dorsal column and corticospinal tract signs seen here.
• C. Copper deficiency can mimic B12 deficiency but is far less common and not suggested by the macrocytic anaemia here.
• E. Cervical cord compression would not explain the macrocytic anaemia or symmetric peripheral sensory loss.

This patient has Brown-Sequard syndrome caused by hemisection of the spinal cord, classically from a penetrating injury such as a stab wound. Ipsilateral weakness and loss of vibration and proprioception occur because the corticospinal and dorsal column fibres have not yet decussated at the level of injury. Contralateral loss of pain and temperature occurs because the spinothalamic tract fibres have already crossed near their entry level, so damage on one side affects sensation on the opposite side below the lesion. This dissociated sensory pattern with crossed findings is the hallmark of cord hemisection.

• B. Complete transection would cause bilateral loss of all sensory and motor function below the lesion, not this crossed pattern.
• C. Posterior cord syndrome causes bilateral loss of proprioception and vibration with preserved motor and pain sensation, not this asymmetric pattern.
• D. Central cord syndrome typically causes greater weakness in the arms than legs with a cape-like sensory loss, not this crossed hemisection pattern.
• E. Anterior spinal artery occlusion causes bilateral loss of pain, temperature and motor function with sparing of dorsal columns, not a unilateral pattern.

This patient has syringomyelia, a fluid-filled cavity (syrinx) within the central spinal cord, commonly associated with Chiari malformation. The expanding syrinx damages the decussating spinothalamic fibres crossing near the central canal before they ascend, causing loss of pain and temperature sensation in a cape-like or shawl-like distribution over the shoulders and arms. Dorsal column function, carried in separate posterior tracts, is preserved, so light touch, vibration and proprioception remain intact. This dissociated sensory loss pattern is the clinical hallmark of a central cord lesion such as a syrinx.

• A. Diabetic peripheral neuropathy typically causes a symmetric glove-and-stocking pattern affecting the distal extremities, not a shawl distribution over the shoulders.
• C. Multiple sclerosis causes varied patterns of sensory and motor loss depending on lesion location, not this specific cape-like dissociated sensory loss.
• D. Guillain-Barre syndrome causes ascending symmetric weakness and sensory loss affecting all modalities, not a dissociated cape-like pattern.
• E. Anterior spinal artery occlusion causes bilateral loss of pain and temperature below the lesion level, not a localised cape distribution with a syrinx history.

This woman has an acute onset of confusion over hours to days, in the context of a precipitating illness (urinary tract infection), with fluctuating attention and visual hallucinations, all consistent with delirium. Her previous baseline of independent functioning argues strongly against an underlying dementia as the primary problem. Delirium is typically reversible once the underlying cause, such as infection, is treated, whereas dementia has an insidious onset over months to years with a progressive, usually non-fluctuating course. Acute confusion in an elderly patient should always prompt a search for a precipitating medical cause.

• A. Lewy body dementia can cause visual hallucinations and fluctuating cognition but develops gradually over time, unlike this acute single-day onset with an infective trigger.
• C. Vascular dementia typically has a stepwise decline associated with cerebrovascular events, not an acute fluctuating course triggered by infection.
• D. Frontotemporal dementia presents with gradual personality and behavioural change over years, not acute confusion triggered by infection.
• E. Alzheimer's disease has an insidious onset over months to years with progressive decline, not acute onset over days.

NICE guidance recommends acetylcholinesterase inhibitors such as donepezil, galantamine or rivastigmine as first-line pharmacological treatment for mild to moderate Alzheimer's disease. Donepezil is the most commonly used first-line agent because it is taken once daily and has a favourable side effect profile. These drugs work by inhibiting the breakdown of acetylcholine, increasing cholinergic transmission to partially compensate for the cholinergic neuronal loss characteristic of Alzheimer's disease. Memantine, an NMDA receptor antagonist, is reserved for moderate to severe disease or when acetylcholinesterase inhibitors are contraindicated or not tolerated.

• A. Rivastigmine is an acetylcholinesterase inhibitor and a reasonable alternative, but donepezil is more commonly used first-line due to its once-daily dosing and side effect profile.
• B. Sertraline is an antidepressant and has no role in treating the cognitive symptoms of Alzheimer's disease itself.
• D. Risperidone is an antipsychotic used cautiously for severe behavioural disturbance in dementia, not first-line treatment of cognitive symptoms.
• E. Memantine is reserved for moderate to severe Alzheimer's disease, not first-line treatment of mild disease.