UKMLA Neurology Essentials: Stroke, Seizures, Headache

Neurology is the specialty most UKMLA candidates quietly dread, and it is the specialty where strong pattern recognition yields the biggest exam-day payoff. The AKT tests neurology heavily because acute neurological emergencies (stroke, status epilepticus, meningitis, subarachnoid haemorrhage) are high-stakes F1-relevant decisions, and because chronic neurological conditions (Parkinson's, dementia, migraine, epilepsy) thread through every primary-care stem.

A typical 200-question AKT paper contains 20–30 neurology stems — roughly 12–15% of the total. They cluster around four topic blocks: acute cerebrovascular events, seizures and epilepsy, headache differential, and movement/cognitive disorders. Each block has a short list of can't-miss diagnoses, tight time-critical thresholds, and specific stem cues that discriminate between them. Drill the four blocks and you convert a feared specialty into a reliable mark cluster.

This masterclass walks through the highest-yield neurology content for the 2026 AKT, aligned to NICE/RCP stroke guidance, the updated 2022 NICE epilepsy guideline (NG217), and the GMC content map. Each section closes with the specific question patterns the AKT uses and the common distractors that catch candidates out.

Table of contents

1. Why neurology carries exam weight
2. Acute stroke — FAST, CT, thrombolysis
3. Ischaemic vs haemorrhagic stroke
4. TIA — the updated pathway
5. Subarachnoid haemorrhage
6. First fit — workup and safety-netting
7. Status epilepticus
8. Epilepsy drug choice (NG217)
9. Headache red flags
10. Tension headache, migraine, cluster
11. Giant cell arteritis
12. Parkinson's disease
13. Dementia subtypes
14. Cognitive screening and reversible causes
15. Common AKT question patterns
16. FAQ

1. Why neurology carries exam weight

The GMC content map includes "altered consciousness", "headache", "limb weakness", "seizures", "confusion", and "tremor" as core presentations — all direct neurology. Between them they appear in roughly 25–30 AKT stems. The remaining 5–10 neurology-adjacent stems come from pharmacology (antiepileptic drug choice, Parkinson's drug side-effects), emergency medicine (stroke thrombolysis window, status epilepticus algorithm), and clinical ethics (capacity, end-of-life decisions in dementia).

Candidates lose neurology marks most often from three errors: missing the stroke thrombolysis window (or picking aspirin-first instead of thrombolysis-eligible), misclassifying headache red flags, and confusing Parkinson's with the atypical Parkinsonian syndromes. Each is preventable with targeted drilling.

Your target: 70%+ subscore on neurology Q-bank filters. Pair this post with the emergency presentations masterclass for the stroke and status epilepticus emergency framing.

2. Acute stroke — FAST, CT, thrombolysis

Recognition (pre-hospital): FAST — Face droop, Arm weakness, Speech disturbance, Time to call 999.

In hospital: ROSIER score (Recognition of Stroke in the Emergency Room) stratifies likelihood. Positive score plus clinical suspicion triggers the stroke pathway.

Immediate assessment:

1. ABCDE.
2. Glucose — hypoglycaemia is a stroke mimic.
3. NIH Stroke Scale (NIHSS) for severity documentation.
4. CT head within 1 hour of arrival — primary goal is to exclude haemorrhage. Ischaemic stroke may appear normal early; haemorrhage is hyperdense immediately.

Ischaemic stroke — time-critical thresholds:

• IV alteplase (thrombolysis): within 4.5 hours of symptom onset OR within 4.5 hours of last-known-well if wake-up stroke with imaging-based eligibility. Contraindications: recent haemorrhage, major surgery, anticoagulation, BP >185/110 uncontrolled.
• Mechanical thrombectomy: up to 6 hours routinely; up to 24 hours in large-vessel occlusion with favourable imaging (DAWN/DEFUSE criteria). Thrombectomy is offered in addition to thrombolysis if both indicated.
• Aspirin 300 mg OD for 2 weeks then clopidogrel 75 mg OD lifelong.

Haemorrhagic stroke:

• Reverse anticoagulation urgently (PCC + vitamin K for warfarin; andexanet/PCC for DOACs; idarucizumab for dabigatran).
• BP control: target SBP <140 mmHg within 6 hours of spontaneous ICH (INTERACT-3 trial; updated guidance reinforces earlier aggressive control).
• Neurosurgical referral for posterior fossa bleeds, significant mass effect, or hydrocephalus.
• No thrombolysis or antiplatelets.

Secondary prevention:

• Clopidogrel 75 mg OD lifelong (ischaemic).
• Atorvastatin 80 mg OD.
• BP control — target <130/80 in most.
• DOAC for AF-related stroke.
• Carotid endarterectomy if >50% stenosis and symptomatic within 2 weeks.
• Lifestyle: smoking cessation, diet, exercise.

AKT question pattern. Patient presents 2.5 hours after right-sided weakness and dysphasia. CT excludes bleed. Next step? IV alteplase. Distractor: start aspirin first (wrong — thrombolysis first if eligible; aspirin given 24 hours post-thrombolysis).

3. Ischaemic vs haemorrhagic stroke

Clinical features overlap, so CT is always required to distinguish.

Features suggestive of haemorrhage (but not definitive):

• Sudden severe headache
• Vomiting at onset
• Rapidly decreasing consciousness
• Seizures at onset
• Very high blood pressure (>220 mmHg systolic)

Features more typical of ischaemia:

• Focal deficit without headache or vomiting
• AF history
• Stepwise progression (lacunar)
• Normal consciousness initially

Stroke syndromes by vessel (Bamford/Oxford classification):

• TACS (total anterior circulation stroke): all three of — unilateral weakness (face/arm/leg), higher cerebral dysfunction (dysphasia, neglect), homonymous hemianopia. Highest mortality.
• PACS (partial anterior): two of the three TACS features.
• LACS (lacunar): pure motor, pure sensory, sensorimotor, or ataxic hemiparesis. No higher cortical signs.
• POCS (posterior circulation): brainstem/cerebellar signs — vertigo, ataxia, cranial nerve palsies, isolated homonymous hemianopia.

AKT question pattern. Patient with sudden right hemiplegia, dysphasia, and right homonymous hemianopia. Syndrome? TACS. Vessel? Left MCA.

4. TIA — the updated pathway

Current NICE guidance (NG128) simplified the TIA pathway in 2019 and it's been consolidated since.

Definition. Transient (<24 hours, usually minutes) focal neurological symptoms from vascular cause.

Management:

1. Aspirin 300 mg immediately (unless contraindicated).
2. Specialist TIA clinic assessment within 24 hours if symptoms ≤7 days ago.
3. Within 7 days if symptoms >7 days ago.
4. MRI with diffusion-weighted imaging preferred over CT.
5. Carotid Doppler within 24 hours if carotid territory symptoms.
6. Echocardiogram if cardioembolic suspicion.

ABCD² score historically used but NICE no longer requires it — all suspected TIAs get urgent specialist review. Recognise the score for exam purposes:

• Age ≥60 — 1
• BP ≥140/90 — 1
• Clinical: unilateral weakness (2), speech disturbance without weakness (1)
• Duration ≥60 min (2), 10–59 min (1)
• Diabetes — 1

Higher scores historically triggered same-day review; current guidance is universal urgent review.

Secondary prevention identical to ischaemic stroke: clopidogrel 75 mg, statin, BP control, DOAC if AF, carotid endarterectomy if stenosis >50%.

AKT question pattern. Patient had 20 minutes of left arm weakness yesterday. First action? Aspirin 300 mg + urgent TIA clinic within 24 hours.

5. Subarachnoid haemorrhage

Presentation. Sudden severe "thunderclap" headache, peak within seconds ("worst headache of life"). May have neck stiffness, photophobia, vomiting, reduced GCS, seizures. Focal signs depend on aneurysm location.

Causes. 85% saccular aneurysm rupture. Others: AVM, trauma, idiopathic perimesencephalic.

Risk factors. Smoking, hypertension, family history, ADPKD, connective tissue disease (Ehlers-Danlos, Marfan's).

Investigation:

1. CT head (non-contrast) within 6 hours — sensitivity ~98% in first 6 hours, drops after.
2. If CT negative but clinical suspicion remains → lumbar puncture at ≥12 hours from onset to look for xanthochromia (yellow CSF from bilirubin).
3. CT angiogram to identify aneurysm.

Management:

• Bed rest, analgesia, antiemetics.
• Nimodipine 60 mg 4-hourly PO for 21 days — reduces vasospasm-related delayed cerebral ischaemia.
• BP control to <160 systolic.
• Neurosurgical/interventional neuroradiology referral for definitive treatment — endovascular coiling (first-line) or surgical clipping.
• Treat hydrocephalus with EVD if needed.

Complications. Rebleed, vasospasm, hydrocephalus, hyponatraemia (SIADH or cerebral salt wasting), seizures.

AKT question pattern. Sudden thunderclap headache, neck stiffness, CT negative at 18 hours. Next step? Lumbar puncture to look for xanthochromia.

6. First fit — workup and safety-netting

Definition. First unprovoked seizure (≠ epilepsy; epilepsy is diagnosed after 2+ unprovoked seizures or one seizure + high recurrence risk).

History — key to rule out mimics:

• Syncope: prodrome (dizziness, pallor, sweating), rapid recovery, no post-ictal confusion.
• Non-epileptic attack disorder (NEAD): eyes closed, asynchronous movements, pelvic thrusting, pre-existing trauma/psychiatric history, normal ECG during event.
• Cardiac arrhythmia: sudden collapse, no prodrome.
• Hypoglycaemia: risk factors, pre-event symptoms.

Examination. Neurological + cardiovascular full examination.

Investigations:

• Blood glucose — mandatory.
• U&Es, calcium, magnesium — correct electrolytes.
• 12-lead ECG — exclude long QT, Brugada, arrhythmias.
• CT head if traumatic, focal signs, or suspected organic cause.
• Outpatient EEG (within 2 weeks) — low yield but may guide recurrence risk.
• MRI brain — outpatient, all new-onset unprovoked seizures.
• Neurology referral within 2 weeks.

Safety-netting for the patient:

• Do not drive — must inform DVLA. First seizure without structural cause: 6 months off driving (Group 1); 5 years off Group 2.
• Avoid swimming alone, heights, dangerous machinery.
• Shower rather than bath.
• Supervision around young children.

Treatment. First seizure with low recurrence risk (normal MRI, normal EEG) — typically no AED. High-risk features (structural lesion, abnormal EEG, clear epileptic features) — start AED after neurology review.

AKT question pattern. First unprovoked seizure in 22-year-old, normal examination. Next steps? ECG + electrolytes + glucose, urgent neurology clinic within 2 weeks, no driving, safety-netting advice.

7. Status epilepticus

Definition (operational). Seizure ≥5 minutes OR ≥2 seizures without recovery between (updated from old 30-minute definition).

Management algorithm:

Time 0–5 min:

• ABCDE.
• Lay on side, protect airway.
• High-flow O₂.
• IV access, bloods (glucose, electrolytes, AED levels, toxicology).
• Glucose — correct hypoglycaemia.

Time 5–10 min — first-line benzodiazepine:

• IV lorazepam 4 mg (may repeat once after 10 min if still seizing).
• If no IV access: buccal midazolam 10 mg OR rectal diazepam 10 mg.

Time 10–20 min — if still seizing, second-line:

• IV levetiracetam 60 mg/kg (max 4.5 g) — increasingly first choice in 2022 NICE (NG217) update.
• OR IV sodium valproate 40 mg/kg (max 3 g) — avoid in women of childbearing potential.
• OR IV phenytoin 20 mg/kg (historical choice; requires cardiac monitoring).

Time 20–30 min — refractory status:

• ICU for general anaesthesia (propofol or thiopental) + intubation.
• Continuous EEG monitoring.

After seizure stops:

• Identify cause: electrolyte derangement, infection, drug withdrawal, missed AED, structural lesion, toxicity.
• CT head if not already done.
• LP if CNS infection suspected.
• Neurology input.

AKT question pattern. Patient seizing for 8 minutes. IV access established. First drug? IV lorazepam 4 mg.

8. Epilepsy drug choice (NG217)

The 2022 NICE epilepsy update (NG217) restructured first-line AED choices. Key 2026-testable changes:

Focal epilepsy (first-line):

• Lamotrigine OR levetiracetam (equal first-line).

Generalised tonic-clonic epilepsy:

• Sodium valproate first-line in men and women unable to have children.
• Lamotrigine or levetiracetam first-line in women of childbearing potential.

Absence epilepsy:

• Ethosuximide first-line.
• Sodium valproate second-line (men/post-childbearing only).

Myoclonic epilepsy:

• Sodium valproate first-line (men/post-childbearing).
• Levetiracetam in women of childbearing potential.

Women of childbearing potential — valproate restrictions:

• Valproate is contraindicated unless the woman is on the Pregnancy Prevention Programme (PPP).
• Even with PPP, use only if no alternative.
• Effective contraception mandatory.
• Annual risk-acknowledgement form.
• Teratogenic risk: ~10% major malformation, ~30–40% neurodevelopmental impact in utero.

Driving rules (Group 1, car):

• Seizure-free 12 months → can drive.
• Seizures during sleep only for ≥3 years → can drive.
• Withdrawal from AEDs: must not drive during withdrawal and for 6 months after last dose.

AKT question pattern. 28-year-old woman with generalised tonic-clonic epilepsy, planning pregnancy. First-line AED? Lamotrigine or levetiracetam (not valproate). Distractor: carbamazepine (outdated; lamotrigine now preferred).

9. Headache red flags

Headache is common; missing a sinister cause is examined. The red flags mnemonic "SNOOP":

• Systemic symptoms (fever, weight loss, immunocompromise, cancer history)
• Neurologic signs or symptoms (focal deficits, seizures, altered cognition)
• Onset sudden (thunderclap)
• Older age (new headache >50 years — think GCA, malignancy)
• Pattern change (new headache type, progressively worsening)

Additional red flags:

• Headache worse lying down, worse with Valsalva, nocturnal → raised ICP (mass, hydrocephalus, venous sinus thrombosis).
• Postural (worse standing) → low-pressure headache (post-LP, CSF leak).
• Temporal tenderness + jaw claudication + visual symptoms + age >50 → GCA.
• Associated with eye pain + red eye + nausea → acute angle-closure glaucoma.
• Pregnancy/postpartum → pre-eclampsia, cerebral venous sinus thrombosis.
• Associated with reduced consciousness or vomiting → raised ICP, meningitis, SAH.

Any red flag triggers urgent imaging (CT/MRI) and specialist review.

AKT question pattern. 68-year-old with new-onset temporal headache + jaw claudication + blurred vision. Next step? Start high-dose prednisolone (60 mg OD) immediately; check ESR/CRP; temporal artery biopsy within 2 weeks. Do not delay steroids.

10. Tension headache, migraine, cluster

Tension-type headache. Bilateral, band-like, non-pulsatile, mild-moderate severity, no autonomic features. Not aggravated by activity. Management: paracetamol, NSAIDs, stress management. Avoid opioids and avoid medication overuse (>15 days/month analgesic use).

Migraine (without aura). Unilateral, pulsating, moderate-severe, 4–72 hours, associated nausea/vomiting, photophobia, phonophobia. Aggravated by activity. POUND mnemonic: Pulsating, Over 4 hours, Unilateral, Nausea, Disabling.

Migraine (with aura). Aura = focal neurological symptoms preceding headache by ≤60 minutes. Visual (most common — zigzag lines, scotoma), sensory (paraesthesia), speech, motor (hemiplegic migraine — rare, familial).

Migraine management:

• Acute: triptan (sumatriptan 50 mg PO or 6 mg SC) + NSAID (naproxen 500 mg) + antiemetic (metoclopramide). Avoid ergotamine (old, more side effects).
• Prophylaxis (if ≥4 migraines/month or disabling): propranolol 80–160 mg OD first-line; topiramate second-line (avoid in pregnancy — teratogenic); amitriptyline third-line.
• CGRP antagonists (erenumab, fremanezumab, galcanezumab) — specialist, for refractory chronic migraine.
• Botulinum toxin for chronic migraine (≥15 headache days/month) as specialist option.

Migraine in pregnancy: paracetamol first-line; triptans avoided (specialist decision if needed). Topiramate and valproate contraindicated. Propranolol may be continued for prophylaxis.

Cluster headache. Unilateral, retro-orbital, severe, lasting 15–180 minutes, with autonomic features (ipsilateral lacrimation, rhinorrhoea, conjunctival injection, ptosis, miosis). Episodic clusters over weeks, separated by months of remission. Male > female. Trigger: alcohol.

Cluster management:

• Acute: high-flow 100% O₂ via non-rebreather 15 L/min for 15 min + sumatriptan 6 mg SC.
• Prophylaxis: verapamil first-line (ECG monitoring for PR prolongation); short course of oral steroids as bridging therapy.

AKT question pattern. 35-year-old man with recurring episodes of severe retro-orbital pain with ipsilateral tearing and ptosis. Diagnosis? Cluster headache. Acute treatment? 100% O₂ via non-rebreather + SC sumatriptan.

11. Giant cell arteritis

Presentation. New-onset unilateral temporal headache + scalp tenderness + jaw claudication + visual symptoms (amaurosis fugax, permanent visual loss) + age ≥50. PMR overlap in 50% (shoulder/pelvic girdle stiffness).

Investigations:

• ESR and CRP — usually markedly raised.
• Temporal artery biopsy within 2 weeks of starting steroids. Granulomatous inflammation with giant cells, skip lesions.
• Temporal artery ultrasound (halo sign) — specialist centres.

Management:

• Start prednisolone 40–60 mg OD immediately on clinical suspicion — do not wait for biopsy. Visual loss → IV methylprednisolone 500–1000 mg for 3 days.
• Tapering slowly over 12–24 months; typical total course 1–2 years.
• Bone and stomach protection: bisphosphonate (alendronic acid) + vitamin D + PPI.
• Aspirin 75 mg to reduce ischaemic complications (evidence moderate).
• Monitor ESR/CRP + symptoms for relapse.

AKT question pattern. 70-year-old with new temporal headache, jaw pain on chewing, transient visual loss. First drug? Oral prednisolone 40–60 mg immediately; arrange temporal artery biopsy within 2 weeks. If permanent visual loss → IV methylprednisolone.

12. Parkinson's disease

Cardinal features. Tremor (resting, pill-rolling, 4–6 Hz), Rigidity (cogwheel), Akinesia/bradykinesia, Postural instability (late).

Supporting features: asymmetric onset, micrographia, hypomimia (mask-like face), shuffling gait, reduced arm swing, stooped posture, monotone speech.

Diagnosis. Clinical (UK Brain Bank criteria). DaTscan if diagnostic uncertainty (distinguishes Parkinson's from essential tremor/drug-induced/vascular parkinsonism, not from atypical parkinsonian syndromes).

Drug management (NICE NG71):

• Motor symptoms affecting quality of life → levodopa (with peripheral decarboxylase inhibitor, e.g. co-careldopa, co-beneldopa).
• Motor symptoms not affecting quality of life → dopamine agonist (ropinirole, pramipexole) OR MAO-B inhibitor (rasagiline, selegiline).

Levodopa side effects:

• Dyskinesias (late complication).
• "On-off" phenomenon.
• Wearing off before next dose.
• Impulse control disorders (especially with dopamine agonists — compulsive gambling, hypersexuality; warn patients).
• Hallucinations.

Atypical parkinsonian syndromes (the "Parkinson-plus"):

• Multiple system atrophy (MSA) — early autonomic dysfunction (postural hypotension, urinary incontinence), cerebellar signs, poor levodopa response.
• Progressive supranuclear palsy (PSP) — vertical gaze palsy, early falls, axial rigidity, poor levodopa response.
• Corticobasal degeneration — asymmetric rigidity, apraxia, alien limb.
• Dementia with Lewy bodies — early cognitive fluctuation, visual hallucinations, REM sleep behaviour disorder, marked sensitivity to antipsychotics.

Drug-induced parkinsonism: antipsychotics (typical > atypical), metoclopramide, prochlorperazine. Symmetric and reversible on drug withdrawal. Distinguishable from idiopathic PD by symmetry and drug exposure.

AKT question pattern. Elderly with asymmetric pill-rolling tremor + bradykinesia + rigidity. Diagnosis? Idiopathic Parkinson's. First-line if impacting function? Levodopa/carbidopa.

13. Dementia subtypes

Alzheimer's disease. Insidious cognitive decline, early short-term memory loss, progressive. 60% of dementias. Pathology: amyloid plaques + tau tangles. Treatment: cholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild-moderate; memantine for moderate-severe. Aducanumab/lecanemab — amyloid-targeting monoclonals; access limited in UK.

Vascular dementia. Stepwise decline + vascular risk factors + focal neurological signs. Management: vascular risk factor modification (BP, lipids, antiplatelet, glucose). Cholinesterase inhibitors not routinely indicated (NICE).

Dementia with Lewy bodies. Cognitive fluctuation + visual hallucinations + parkinsonism + REM sleep behaviour disorder. Extreme neuroleptic sensitivity (give antipsychotics with great caution). Cholinesterase inhibitors often effective for both cognition and hallucinations.

Frontotemporal dementia. Early behavioural/personality changes (disinhibition, apathy), early language dysfunction (primary progressive aphasia variants). Younger onset (typically 45–65). Cholinesterase inhibitors not useful; may worsen.

Rapidly progressive dementia. Weeks-to-months decline — consider Creutzfeldt-Jakob disease, autoimmune encephalitis (anti-NMDA, anti-LGI1), viral encephalitis, paraneoplastic syndromes.

14. Cognitive screening and reversible causes

Screening tools:

• AMT (Abbreviated Mental Test) — 10-question bedside.
• 6CIT — alternative bedside tool.
• MMSE (Mini Mental State) — 30-point (now copyrighted; less used).
• MoCA (Montreal Cognitive Assessment) — 30-point; more sensitive for mild impairment and executive dysfunction.
• ACE-III (Addenbrooke's Cognitive Examination) — detailed assessment, specialist use.

Reversible causes to exclude in any new dementia workup:

• B12/folate deficiency.
• Hypothyroidism.
• Hypercalcaemia.
• Hyponatraemia.
• Normal pressure hydrocephalus — triad: dementia + gait disturbance + urinary incontinence ("wet, wobbly, and weird"). CT: dilated ventricles out of proportion to sulcal atrophy. Treatment: VP shunt.
• Chronic subdural haematoma — elderly, falls, anticoagulation; CT head.
• Depression (pseudodementia) — low mood, slowed thinking, often improves with antidepressant.
• Drug toxicity — anticholinergics, benzodiazepines, alcohol.
• Neurosyphilis, HIV — rare but treatable.

Dementia workup minimum: FBC, U&Es, calcium, TFTs, B12/folate, HbA1c, LFTs, ± syphilis/HIV if clinically indicated, CT or MRI head.

AKT question pattern. Older patient + cognitive decline + gait apraxia + urinary incontinence + enlarged ventricles on CT. Diagnosis? Normal pressure hydrocephalus. Treatment? Neurosurgical referral for VP shunt.

15. Common AKT question patterns

Six neurology stem templates recur across AKT papers.

Template 1 — Stroke thrombolysis decision. Stem gives symptom onset time + CT findings + contraindications. Task: thrombolyse, thrombectomise, or aspirin. Mistake: missing the 4.5-hour window or picking aspirin first when thrombolysis is indicated.

Template 2 — Headache red-flag triage. Stem packs red flags; task is to name the diagnosis (SAH, GCA, meningitis, raised ICP). Mistake: failing to act on thunderclap or jaw claudication cues.

Template 3 — Epilepsy drug choice in pregnancy. Woman of childbearing potential with new epilepsy. Task: pick lamotrigine or levetiracetam (not valproate). Mistake: picking valproate for generalised tonic-clonic without reading "woman of childbearing potential".

Template 4 — Status epilepticus algorithm. Patient seizing X minutes. Task: name the correct drug at the correct stage. Mistake: giving phenytoin at 5 minutes (should be lorazepam first).

Template 5 — Parkinson's vs atypical. Stem describes parkinsonism plus atypical feature (early falls, vertical gaze palsy, autonomic failure, visual hallucinations). Task: name the atypical syndrome (PSP, MSA, DLB). Mistake: calling everything Parkinson's.

Template 6 — Reversible dementia cause. Elderly with cognitive decline + gait + incontinence OR + hypothyroid features OR + chronic anticoagulation + fall. Task: identify NPH, hypothyroidism, or chronic subdural. Mistake: labelling as Alzheimer's without screening for reversibles.

Halfway checkpoint — MLA Prep tags every neurology question by template (stroke window, headache red flag, AED choice, status algorithm, atypical parkinsonism, reversible dementia) with explanations mapped back to the NICE/RCP guideline line it's testing. Start the free diagnostic and see your per-template neurology breakdown.

16. FAQ

How many AKT marks come from neurology? Approximately 20–30 of 200 stems test neurology directly, with 5–10 more touching neuro-pharmacology or neuro-ethics.

Is valproate ever acceptable in women of childbearing potential? Only under the Pregnancy Prevention Programme with effective contraception and annual risk acknowledgement, and only when no alternative works. The AKT default answer for a woman of childbearing potential is not valproate.

What's the difference between "TIA" and "minor stroke"? Former: symptoms fully resolve <24 hours (usually minutes) AND no infarct on imaging. Latter: non-disabling stroke with imaging-confirmed infarct. Management pathway overlaps significantly.

When is thrombectomy offered beyond 6 hours? Up to 24 hours in patients with large-vessel occlusion AND favourable imaging (mismatch between core infarct and penumbra on perfusion CT/MRI, per DAWN/DEFUSE-3). Selected centres.

Do I need to memorise specific migraine triggers? Common ones: stress, skipped meals, menstruation, sleep disruption, specific foods (chocolate, cheese, red wine), COCP. Useful for counselling stems.

What's the first-line anticoagulant for cardioembolic stroke? DOAC (apixaban usual choice) for non-valvular AF. Warfarin only for mechanical valves or severe renal impairment. Start anticoagulation 1–2 weeks post-stroke depending on infarct size.

Are cholinesterase inhibitors used in vascular dementia? Not routinely (NICE). Only if mixed picture with Alzheimer's component. Focus is on vascular risk factor modification.

What's the role of MRI vs CT in stroke workup? CT first (fast, excludes haemorrhage). MRI DWI is more sensitive for small/early ischaemic infarcts and is preferred for TIA characterisation. Posterior circulation strokes often need MRI because CT misses them.

How does MS present on AKT stems? Young adult + relapsing-remitting neurological symptoms separated in time and space. Optic neuritis (painful monocular visual loss with pale disc later), sensory disturbance, Lhermitte's, Uhthoff's (worsening with heat). Diagnosis: MRI brain/spine + CSF oligoclonal bands. Management: disease-modifying therapy (specialist-led). Acute relapse: high-dose IV methylprednisolone.

Is lumbar puncture safe immediately after head trauma with headache? No. If focal signs, reduced GCS, papilloedema, or suspected raised ICP, CT first. LP in raised ICP can precipitate coning.

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Neurology is large but finite. Four topic blocks, six question templates, and a handful of time-critical thresholds — that's the whole surface area. Drill the stroke thrombolysis window, the status epilepticus algorithm, the headache red flags, and the atypical parkinsonism discriminators, and you convert a feared specialty into a reliable 70%+ subscore.

Pair this masterclass with the emergency presentations post for the acute-care framing, the NICE guidelines post for drug-choice alignment, and the content map post for slot-in-the-schedule guidance. The 12-week plan usually places neurology in weeks 4–5.

MLA Prep's neurology module covers all four blocks above with stroke-window drills, NG217-aligned AED stems, and atypical parkinsonism discriminators. Start the free diagnostic to benchmark your subscore, or compare plans for full access.