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MRCP PART 1 · NEUROLOGY

Neurology questions
for MRCP Part 1.

Clinora has 343 neurology single best answer questions covering 334 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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FREE SAMPLE QUESTIONS

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Question 1Transient ischaemic attackEasy

A 67-year-old man develops sudden right arm weakness and expressive dysphasia lasting 20 minutes. He is now asymptomatic. Capillary glucose is normal, there is no head injury or bleeding history, and intracranial haemorrhage is not suspected. What is the most appropriate immediate management?

  1. AGive aspirin 300 mg now and arrange specialist assessment within 24 hours
  2. BCalculate an ABCD2 score and refer only if the score is high
  3. CWithhold antiplatelet treatment until outpatient brain MRI is completed
  4. DStart therapeutic low-molecular-weight heparin while awaiting carotid imaging
  5. EReassure him and arrange a routine neurology appointment within six weeks
Show answer and explanation

Answer: A Give aspirin 300 mg now and arrange specialist assessment within 24 hours

Sudden right arm weakness and expressive dysphasia that resolves completely within 20 minutes is a suspected TIA in the left carotid territory. The risk of stroke is highest in the first few days, so speed matters. NICE NG128 recommends aspirin 300 mg immediately, unless there is a contraindication: a bleeding disorder, anticoagulation, or suspicion of intracranial haemorrhage, in which case imaging comes first. It also recommends referral for specialist assessment within 24 hours of symptom onset. NICE advises against using risk scores such as ABCD2 to decide who is seen urgently, because everyone with a suspected TIA should be seen within 24 hours. The specialist assessment usually includes MRI (diffusion-weighted imaging), urgent carotid imaging, ECG and rhythm monitoring for atrial fibrillation, and vascular risk factors. Secondary prevention follows: antiplatelet therapy, statin, blood pressure control, and carotid endarterectomy if there is significant symptomatic stenosis. He should not drive for at least 1 month.

Key clue
A sudden focal neurological deficit has completely resolved and haemorrhage is not suspected.
What it means
This is a suspected TIA requiring immediate secondary prevention and urgent assessment.
What to do
Give aspirin 300 mg immediately and arrange specialist assessment within 24 hours.

Why the other options are less appropriate

  • B NICE advises against using ABCD2 to decide urgency. Everyone with a suspected TIA should be seen within 24 hours.
  • C Haemorrhage is not suspected, so aspirin should not wait for an outpatient MRI.
  • D Therapeutic heparin is not routine treatment for TIA. It risks bleeding without proven benefit unless there is another indication.
  • E A routine appointment at 6 weeks misses the period when the risk of stroke is highest.

Source: NICE NG128: Stroke and transient ischaemic attack in over 16s — recommendations 1.1.4 to 1.1.6

Question 2Wake-up strokeHard

A 64-year-old man awakens with aphasia and right hemiparesis. He was last known well 9 hours ago. Non-enhanced CT excludes haemorrhage; CT angiography shows a proximal left middle cerebral artery occlusion. He was previously independent. What is the most appropriate next step?

  1. AExclude reperfusion because the exact symptom-onset time is unknown
  2. BGive routine intravenous thrombolysis solely because the deficit was noticed on waking
  3. CObtain urgent perfusion or diffusion imaging and refer for imaging-selected reperfusion
  4. DStart aspirin and postpone vascular treatment until a 24-hour repeat scan
  5. EUse the admission NIHSS score alone to decide whether thrombectomy is appropriate
Show answer and explanation

Answer: C Obtain urgent perfusion or diffusion imaging and refer for imaging-selected reperfusion

In a wake-up stroke, onset is timed from when he was last known well, here 9 hours ago. That is outside the standard thrombolysis window, but not outside treatment. CT angiography shows a proximal anterior-circulation occlusion, so NICE NG128 supports thrombectomy between 6 and 24 hours after he was last known well. It applies when perfusion CT or diffusion-weighted MRI shows a small core of established infarction and a larger area of salvageable brain, and he was functionally independent before. Advanced imaging therefore decides treatment, not the clock alone. Refer urgently to the thrombectomy centre while the imaging is done or reviewed. Some services also give thrombolysis to selected wake-up strokes, within 4.5 hours of waking, when MRI shows a diffusion–FLAIR mismatch. That is an imaging decision, not an automatic one. Aspirin is held until haemorrhage is excluded after any reperfusion treatment.

Key clue
Wake-up deficit, last known well 9 hours ago, proximal anterior-circulation occlusion and no haemorrhage.
What it means
Late-window reperfusion eligibility depends on advanced imaging evidence of salvageable tissue.
What to do
Obtain urgent perfusion or diffusion imaging and refer immediately for imaging-selected reperfusion.

Why the other options are less appropriate

  • A An unknown onset time does not rule out reperfusion. Imaging can show salvageable brain up to 24 hours after last known well.
  • B He is 9 hours from last known well. Thrombolysis cannot be given simply because the deficit was found on waking; it needs imaging selection.
  • D Waiting 24 hours with aspirin loses salvageable brain while the occlusion stays untreated.
  • E NIHSS shows how severe the deficit is, but not how large the infarct core is or how much tissue can be saved.

Source: NICE NG128: Stroke and transient ischaemic attack in over 16s — thrombectomy recommendation 1.4.6

Question 3Secondary prevention after ischaemic strokeMedium

A 66-year-old woman has recovered from a non-cardioembolic ischaemic stroke. Prolonged rhythm monitoring shows no atrial fibrillation, echocardiography shows no cardiac thrombus, and there is no other indication for anticoagulation. Which long-term prevention strategy is most appropriate?

  1. AUse antiplatelet therapy with intensive management of lipids, blood pressure and lifestyle risk
  2. BUse warfarin routinely because all previous strokes require anticoagulation
  3. CCombine long-term aspirin, clopidogrel and warfarin for maximal protection
  4. DStop antithrombotic therapy once the neurological deficit has resolved
  5. EUse anticoagulation alone and defer management of vascular risk factors
Show answer and explanation

Answer: A Use antiplatelet therapy with intensive management of lipids, blood pressure and lifestyle risk

Once atrial fibrillation, cardiac thrombus and any other reason for anticoagulation have been excluded, recurrence after ischaemic stroke is driven by platelet-mediated atherothrombosis and small-vessel disease. Long-term prevention is therefore antiplatelet therapy combined with intensive control of risk factors. The 2023 National Clinical Guideline for Stroke recommends clopidogrel 75 mg daily as first-line long-term treatment. If clopidogrel is not tolerated, aspirin with modified-release dipyridamole is used, or aspirin alone. For blood pressure, it advises a target systolic pressure below 130 mmHg for most people (with a less strict target in severe bilateral carotid stenosis). For lipids, it advises a high-intensity statin, aiming for LDL cholesterol below 1.8 mmol/L, with ezetimibe or other therapy added if needed. Lifestyle measures include stopping smoking, regular exercise, a healthy diet, moderating alcohol, and managing weight and diabetes. Anticoagulation in people without AF increases bleeding without reducing recurrence.

Key clue
Ischaemic stroke has no atrial fibrillation, cardiac thrombus or other anticoagulation indication.
What it means
This is a non-cardioembolic secondary-prevention setting.
What to do
Use antiplatelet therapy plus comprehensive vascular-risk reduction.

Why the other options are less appropriate

  • B Warfarin has no advantage over antiplatelet therapy in non-cardioembolic stroke and causes more bleeding, including intracranial haemorrhage.
  • C Long-term triple antithrombotic therapy greatly increases bleeding with no proven benefit. Dual antiplatelet therapy is used only briefly after minor stroke.
  • D Recovery of the deficit does not remove the vascular risk. Recurrence risk is highest early but continues long term.
  • E Anticoagulation is not indicated, and putting off risk-factor control would leave the main drivers of recurrence untreated.

Source: National Clinical Guideline for Stroke — Long-term management and secondary prevention

Question 4Cerebral venous sinus thrombosisMedium

A 32-year-old woman, 10 days postpartum, develops progressive headache, a focal seizure and papilloedema. CT shows a small haemorrhagic parasagittal venous infarct. Which approach is most appropriate?

  1. APerform lumbar puncture immediately and discharge if cerebrospinal fluid is normal
  2. BAvoid anticoagulation permanently because the infarct contains haemorrhage
  3. CTreat as primary migraine and review after six weeks
  4. DObtain CT or MR venography and start therapeutic anticoagulation unless specifically contraindicated
  5. EGive aspirin alone because venous thrombosis is managed like arterial TIA
Show answer and explanation

Answer: D Obtain CT or MR venography and start therapeutic anticoagulation unless specifically contraindicated

She has three clues pointing to cerebral venous sinus thrombosis. She is postpartum, which is a prothrombotic state. She has a progressive headache with papilloedema, showing raised intracranial pressure. She has a seizure with a haemorrhagic parasagittal infarct, typical of superior sagittal sinus occlusion. Plain CT is often normal or shows only indirect signs. CT or MR venography confirms that the sinus is blocked. D-dimer can be normal, so it should not be used to rule this out. The National Clinical Guideline for Stroke recommends full-dose anticoagulation, starting with heparin and then oral anticoagulation. It applies even when the infarct has bled, because the bleeding is caused by venous congestion and anticoagulation relieves it. Oral treatment usually continues for 3 to 12 months. While she is breastfeeding, LMWH and warfarin are suitable, but DOACs are generally avoided. Treat the seizure with an antiseizure medicine. If she gets worse despite anticoagulation, consider endovascular treatment or decompressive surgery.

Key clue
Postpartum progressive headache, seizure, papilloedema and a haemorrhagic parasagittal infarct.
What it means
These features indicate cerebral venous sinus thrombosis rather than primary arterial stroke.
What to do
Confirm with CT or MR venography and anticoagulate therapeutically unless contraindicated.

Why the other options are less appropriate

  • A Papilloedema with a mass lesion makes lumbar puncture unsafe before imaging. Normal CSF would not exclude venous thrombosis anyway.
  • B Bleeding into a venous infarct is caused by venous congestion. Anticoagulation treats that cause and is still recommended.
  • C A focal seizure, papilloedema and a haemorrhagic infarct are red flags. They need urgent imaging, not a migraine diagnosis.
  • E Aspirin is not an established treatment for venous thrombosis. This is a venous clot, not an arterial TIA.

Source: National Clinical Guideline for Stroke — Acute care: cerebral venous thrombosis

Question 5Migraine with auraEasy

A 24-year-old woman sees a shimmering zigzag line that gradually expands across both visual fields over 20 minutes. It resolves completely and is followed by unilateral throbbing headache, photophobia and nausea. Neurological examination is normal. What is the most likely diagnosis?

  1. AMigraine with typical aura
  2. BRetinal artery occlusion
  3. COccipital intracerebral haemorrhage
  4. DTransient ischaemic attack
  5. EAcute angle-closure glaucoma
Show answer and explanation

Answer: A Migraine with typical aura

The key clue is a positive visual phenomenon, a shimmering zigzag line, that spreads gradually over minutes and resolves completely before a typical migraine headache. This reflects cortical spreading depression, a slow wave of neuronal depolarisation moving across the occipital cortex at a few millimetres per minute, which explains the gradual march of symptoms. Involvement of both visual fields indicates a cortical rather than a retinal cause. NICE CG150 describes typical aura as fully reversible visual, sensory and/or speech symptoms that develop gradually, with each symptom lasting at least 5 minutes and no more than 60 minutes. Motor weakness, double vision, visual symptoms in one eye only, poor balance or reduced consciousness are atypical and need further assessment. For acute treatment NICE recommends an oral triptan combined with an NSAID or paracetamol, and propranolol or topiramate for prevention; topiramate needs a pregnancy prevention programme. Migraine with aura is a contraindication to combined hormonal contraception (UKMEC 4) because of increased stroke risk.

Key clue
A positive binocular visual symptom gradually spreads, fully resolves and precedes migraine headache.
What it means
The tempo and positive reversible symptom are typical of cortical migraine aura.
What to do
Diagnose migraine with typical aura.

Why the other options are less appropriate

  • B Retinal artery occlusion causes sudden, painless, monocular loss of vision that does not spread gradually or resolve fully within minutes.
  • C Occipital haemorrhage causes a sudden, persistent field defect with headache, not a gradually spreading scintillation that resolves completely.
  • D TIA causes sudden negative symptoms such as field loss, rather than positive symptoms that spread gradually over 20 minutes.
  • E Angle-closure glaucoma causes a painful red eye, haloes and reduced acuity in one eye, not binocular spreading zigzags.

Source: NICE CG150: Headaches in over 12s — diagnosis of migraine with aura

That is 5 of 343. Carry on with neurology in the practice bank, with progress tracking, flashcards and timed sessions.

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Topics covered

Show all 334 neurology topics
  • A concerning trend in inspiratory pressure
  • A reversible stroke mimic at first contact
  • Absence seizures with other generalised seizure types
  • Absence seizures with other seizure types
  • Acclimatisation when initiating planned NIV in MND
  • Acoustic neuroma presentation
  • Acute disseminated encephalomyelitis
  • Acute ischaemic stroke
  • Acute levodopa challenge as a diagnostic shortcut
  • Acute transverse myelitis
  • Acute vertigo without cochlear symptoms
  • Acute vestibular syndrome
  • Adult-onset dystonia
  • Advance planning at a respiratory transition
  • Alexia without agraphia
  • Alice in Wonderland syndrome
  • Alien hand syndrome
  • Alzheimer disease treatment
  • Ambulatory EEG for unresolved diagnostic uncertainty
  • An emergency steroid supply for unassessed future MS relapses
  • An individualised NIV trial with severe bulbar impairment
  • Aneurysmal subarachnoid haemorrhage
  • Anterior cerebral artery infarction
  • Anterior spinal artery syndrome
  • Anti-NMDA receptor encephalitis with teratoma
  • Anti-NMDA-receptor encephalitis
  • Antipsychotic that worsens motor disease
  • Antiseizure medicine withdrawal
  • Antiseizure titration in an older adult
  • Aspirin after acute ischaemic stroke
  • Assessing response to CGRP migraine prevention
  • Atypical migraine aura with motor weakness
  • Autonomic dysreflexia from catheter obstruction
  • Avoiding an ergot-derived initial Parkinson treatment
  • Balint syndrome
  • Behavioural-variant frontotemporal dementia
  • Benign paroxysmal positional vertigo
  • Benign positional vertigo
  • Blood pressure before intravenous thrombolysis
  • Blood pressure in intracerebral haemorrhage
  • Bone health after long-term antiseizure treatment
  • Bone health during long-term antiseizure treatment
  • Botulinum toxin for chronic migraine
  • Botulism
  • Brain abscess
  • Breastfeeding while using an antiseizure medicine
  • Brief stereotyped sensory spells and epilepsy assessment
  • Brown-Séquard syndrome
  • CAA-related transient focal neurological episodes
  • CADASIL
  • CANVAS
  • CANVAS syndrome
  • Carpal tunnel syndrome
  • Cauda equina syndrome
  • Cenobamate sequencing
  • Central facial weakness
  • Cerebral amyloid angiopathy
  • Cerebral venous sinus thrombosis
  • Cerebrotendinous xanthomatosis
  • Cervical artery dissection
  • Charcot–Marie–Tooth disease type 1A
  • Childhood absence epilepsy
  • Chronic subdural haematoma
  • CIDP
  • Cluster headache
  • Cluster headache prevention
  • Cognitive and behavioural assessment in MND
  • Cognitive change at diagnosis may alter care decisions
  • Cognitive stimulation therapy in dementia
  • Cognitive treatment when cholinesterase inhibitors are unsuitable
  • Combining baclofen and gabapentin safely
  • Common peroneal neuropathy
  • Communication support in advanced Parkinson disease
  • Communication support in MND
  • Communication technology must keep pace with progression
  • Comprehensive review in multiple sclerosis
  • Compressive third-nerve palsy
  • Conus medullaris syndrome
  • Convulsion or arrhythmia?
  • Convulsive status epilepticus
  • Correct oxygen delivery for acute cluster headache
  • Cortical tremor
  • Corticobasal syndrome
  • Creutzfeldt–Jakob disease
  • Cross-titrating to an alternative antiseizure medicine
  • Deep brain stimulation when medical control remains adequate
  • Degenerative cervical myelopathy
  • Delayed post-hypoxic leukoencephalopathy
  • Delirium
  • Delivering thrombolysis within a stroke service
  • Dementia with Lewy bodies
  • Diagnosing multiple sclerosis
  • Dissociative seizures
  • Distal sensory symptoms with brisk reflexes
  • Distinguishing emotional lability from depressive illness in MS
  • Dopamine agonist impulse-control disorder
  • Dorsal midbrain syndrome
  • Driving after a first unprovoked seizure
  • Drug-induced parkinsonism
  • Drug-resistant focal epilepsy
  • Dysphagia bulbar red flag
  • Early mobilisation is not maximal mobilisation
  • Early Parkinson disease
  • Epilepsy-protocol MRI after a normal emergency CT
  • Escalating cough assistance in MND
  • Essential tremor
  • Facial palsy eye protection
  • Facioscapulohumeral muscular dystrophy
  • Fampridine for MS mobility
  • First suspected seizure
  • First-line treatment affecting quality of life
  • First-line treatment for isolated absence seizures
  • First-line treatment of convulsive status without IV access
  • First-seizure EEG timing
  • Five-minute convulsion in a resuscitation area
  • Focal epilepsy
  • Focal seizures
  • Focal-seizure monotherapy
  • Foix-Chavany-Marie syndrome
  • Friedreich ataxia
  • Function-limiting MS relapse
  • GBS deterioration
  • Generalised epilepsy
  • Gerstmann syndrome
  • Glossopharyngeal neuralgia
  • Glucose range during acute stroke care
  • Guillain-Barre respiratory monitoring
  • Guillain–Barré syndrome diagnosis
  • Guillain–Barré syndrome treatment
  • Hallucinations in Parkinson disease
  • Hallucinations in Parkinson's disease
  • Hallucinations without distress
  • HINTS central red flag
  • HSV encephalitis
  • Huntington disease
  • Hydrocephalus after intracerebral haemorrhage
  • Hypoactive delirium
  • Hypokalaemic periodic paralysis
  • Idiopathic intracranial hypertension
  • Imaging an established focal epilepsy
  • Imaging when dementia with Lewy bodies is uncertain
  • Immediate imaging in anticoagulated stroke
  • Immediate treatment of suspected TIA
  • Impulse-control disorder from dopamine agonist
  • Ineffective cough in MND
  • Inflammatory myopathy
  • Intracerebral haemorrhage
  • Investigating reversible contributors before symptomatic medication
  • Isaacs syndrome
  • Juvenile myoclonic epilepsy
  • Kennedy disease
  • L5 radiculopathy versus peroneal neuropathy
  • Labyrinthitis hearing loss
  • Lacunar stroke
  • Lambert–Eaton myasthenic syndrome
  • Lambert–Eaton syndrome
  • Lamotrigine monitoring in pregnancy
  • Large-vessel occlusion stroke
  • Late-window thrombectomy selection
  • Lateral medullary syndrome
  • LGI1-antibody encephalitis
  • Limited benefit from accumulating add-on therapy
  • Limited standing balance and rehabilitation in MS
  • Limits on rapid BP lowering in acute haemorrhage
  • Locked-in syndrome
  • Longer taper for a barbiturate antiseizure medicine
  • Magnesium-triggered myasthenic deterioration
  • Malignant middle cerebral artery infarction
  • Malignant middle-cerebral-artery infarction
  • Medication-overuse headache
  • Medicines to avoid in frontotemporal dementia
  • MELAS
  • Memantine in Alzheimer disease
  • Meniere disease triad
  • Metastatic spinal cord compression
  • Migraine
  • Migraine prevention
  • Migraine with aura
  • Miller Fisher syndrome
  • MND cramps after quinine intolerance
  • Modafinil discussion for MS fatigue when pregnancy is planned
  • MOG-antibody-associated disease
  • Mononeuritis multiplex
  • Morvan syndrome
  • Motor neurone disease localisation
  • Motor neurone disease mimic
  • MS fatigue management
  • MS pain caused by positioning and spasticity
  • MS spasticity
  • Multifocal motor neuropathy
  • Multiple system atrophy
  • Myasthenia dysphagia
  • Myasthenia gravis
  • Myasthenic crisis
  • Myelopathic features in apparently stable cervical radiculopathy
  • Myoclonic seizure treatment
  • Myotonic dystrophy type 1
  • Naming a suspected MND diagnosis in the referral
  • Narcolepsy with cataplexy and driving
  • Neurological Whipple disease
  • Neuromyelitis optica spectrum disorder
  • Neuroprotection claims for a Parkinson medicine
  • Neurosarcoidosis
  • New objective signs in a patient with functional neurological disorder
  • NF2-related schwannomatosis
  • NIV needs a home-risk plan, not just a mask
  • Non-convulsive status epilepticus
  • Normal-pressure hydrocephalus
  • Ocular tilt reaction
  • Oligodendroglioma
  • One-and-a-half syndrome
  • Optic chiasm localisation
  • Optic neuritis
  • Oropharyngeal dysphagia stroke
  • Orthostatic hypotension in Parkinson disease
  • Orthostatic tremor
  • Oscillopsia in multiple sclerosis
  • Osmotic demyelination syndrome
  • Otosclerosis pattern
  • Oxygen without hypoxaemia
  • Painful legs and moving toes
  • Palatal tremor
  • Paraneoplastic cerebellar degeneration
  • Parkinson disease
  • Parkinson disease motor complications
  • Parkinsonian syndrome
  • Paroxysmal hemicrania
  • Persistent cognitive problems after reversible contributors are addressed
  • Persistent daytime sleepiness after reversible causes are excluded
  • Persistent drooling after antimuscarinic intolerance
  • Persistent impulse-control disorder after medication adjustment
  • Persistent Parkinson orthostatic symptoms after midodrine intolerance
  • Persistent uncertainty after two EEG methods
  • Personal recurrence risk after a first unprovoked seizure
  • Physiotherapy for Parkinson balance impairment
  • Planned review for epilepsy with a learning disability
  • Posterior reversible encephalopathy syndrome
  • Postpartum reduction after pregnancy-related dose increases
  • Probable autoimmune encephalitis before antibody results
  • Prognosis is not inferred from limb weakness alone
  • Progressive supranuclear palsy
  • Protein redistribution without nutritional deprivation
  • Provocation during EEG requires an informed discussion
  • Pseudo-relapse / Uhthoff phenomenon
  • Pseudo-relapse from infection
  • Psychogenic non-epileptic seizures
  • Psychosis treatment after standard therapy fails in Parkinson disease
  • Pure word deafness
  • Quetiapine dose in Parkinson psychosis
  • Radial neuropathy
  • Rapidly progressive gait ataxia over weeks
  • Reconsidering a Parkinson diagnosis as atypical signs emerge
  • Recurrence during an agreed antiseizure taper
  • Refractory convulsive status epilepticus
  • REM sleep behaviour disorder
  • REM sleep behaviour disorder in Parkinson disease
  • Respiratory failure in MND
  • Reviewing apparent failure of first-line epilepsy treatment
  • Riluzole in ALS
  • Rimegepant for acute migraine
  • Rotigotine for persistent nocturnal akinesia
  • Routine CT after resolved TIA
  • Safe withdrawal of ineffective baclofen
  • SAH
  • Second-line oral treatment for MS spasticity
  • Second-line treatment for MS oscillopsia
  • Second-line treatment in convulsive status epilepticus
  • Secondary prevention after ischaemic stroke
  • Sensory neuronopathy
  • Sequential withdrawal from antiseizure polytherapy
  • Severe spasticity despite appropriate oral treatment
  • Sialorrhoea treatment when cognition is impaired
  • Sixth-nerve palsy in raised intracranial pressure
  • Sleep-deprived EEG after a normal routine recording
  • Smoking and multiple-sclerosis progression
  • Spasticity can support transfers
  • Spinal dural arteriovenous fistula
  • Spinal epidural abscess
  • Spontaneous intracranial hypotension
  • Stable hypercapnia in outpatient MND assessment
  • Starting long-term antiseizure treatment
  • Status after two benzodiazepines
  • Steroid regimen for disabling relapse
  • Structural MRI and Parkinson diagnosis
  • Subacute combined degeneration
  • Suboptimal MRI in persisting focal epilepsy
  • Sudden sensorineural hearing loss
  • Sudden sleep episodes and driving
  • Sudden sleep episodes in Parkinson disease
  • SUDEP risk reduction
  • Superficial siderosis
  • Supplement advice in Parkinson disease
  • Susac syndrome with an incomplete presenting triad
  • Suspected bacterial meningitis
  • Suspected epilepsy
  • Swallowing after acute stroke
  • Swallowing safety in Parkinson disease
  • Symptomatic carotid stenosis
  • Symptomatic carotid stenosis below the surgical threshold
  • Syringomyelia
  • Tenacious saliva after treatment for drooling
  • Tension-type headache
  • THC:CBD spray for resistant MS spasticity
  • The normal EEG trap
  • Therapeutic drug monitoring in stable epilepsy
  • Thunderclap headache
  • TIA referral without ABCD2 stratification
  • Time-critical Parkinson medicine in hospital
  • Timing of gastrostomy discussion in MND
  • Tinnitus pulsatile evaluation
  • Topiramate pregnancy-prevention requirements
  • Transient epileptic amnesia
  • Transient ischaemic attack
  • Treating after one unprovoked event
  • Trigeminal neuralgia
  • Trigeminal neuralgia trigger
  • Typical seizure in established epilepsy and unnecessary repeat CT
  • Ulnar neuropathy
  • Unreliable respiratory tests with severe bulbar dysfunction
  • Vaccination advice in multiple sclerosis
  • Valproate initiation safety
  • Vascular dementia
  • Vestibular migraine
  • Vestibular neuritis
  • Vitamin B12 injections for MS fatigue without deficiency
  • Wake-up stroke
  • Warfarin-associated intracerebral haemorrhage
  • Weight loss caused by loss of feeding independence
  • Wernicke encephalopathy
  • Wilson disease
  • Withdrawal after epilepsy surgery
  • Withdrawal strategy for medication-overuse headache
  • Worsening after a sodium-channel agent
  • Worsening over months is not automatically an acute MS relapse

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