Membership of the Royal College of Physicians (MRCP UK) Neurology Flashcards

24 sample cards from the Neurology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. List common causes of a predominantly sensory peripheral neuropathy (glove-and-stocking).

   Diabetes mellitus, alcohol, vitamin $B_{12}$ deficiency, chronic kidney disease, drugs (e.g. isoniazid, chemotherapy), and amyloidosis.

2. Describe the pathophysiology and antibody of myasthenia gravis.

   Autoantibodies against the postsynaptic nicotinic acetylcholine receptor (anti-AChR in ~85%; anti-MuSK in some seronegative cases), causing fatigable weakness worse with activity. Associated with thymic hyperplasia/thymoma.

3. How is myasthenia gravis treated, and what defines a myasthenic crisis?

   Symptomatic: pyridostigmine (acetylcholinesterase inhibitor). Immunosuppression: prednisolone, azathioprine; thymectomy if thymoma. Myasthenic crisis = respiratory failure requiring ventilation; treat with IVIG/plasma exchange.

4. Contrast Lambert-Eaton myasthenic syndrome with myasthenia gravis.

   LEMS: antibodies to presynaptic voltage-gated calcium channels (P/Q-type), associated with small-cell lung cancer; weakness improves with repeated use (incremental response on repetitive nerve stimulation), with hyporeflexia and autonomic features. MG: postsynaptic AChR antibodies, fatigable weakness worsening with use.

5. What is the inheritance, key clinical signs and pathognomonic feature of Duchenne muscular dystrophy?

   X-linked recessive (dystrophin gene). Proximal weakness, calf pseudohypertrophy, Gowers' sign, and markedly elevated creatine kinase. Onset in early childhood; wheelchair-bound by adolescence.

6. Name the four main clinical patterns of motor neurone disease and the most common type.

   Amyotrophic lateral sclerosis (most common; mixed UMN + LMN), progressive bulbar palsy, progressive muscular atrophy (LMN only), and primary lateral sclerosis (UMN only). Sensory and eye movements are spared.

7. What drug modestly prolongs survival in motor neurone disease, and how?

   Riluzole, a glutamate antagonist (inhibits glutamate release), prolongs survival by approximately 3 months. Non-invasive ventilation also improves survival and quality of life.

8. State the cardinal motor features and core pathology of Parkinson's disease.

   Bradykinesia, resting (pill-rolling) tremor, and rigidity (cogwheel), typically asymmetrical with postural instability. Pathology: loss of dopaminergic neurones in the substantia nigra pars compacta with Lewy bodies ($\alpha$-synuclein).

9. Compare the 'Parkinson-plus' syndromes: PSP, MSA and corticobasal degeneration by a distinguishing feature each.

   Progressive supranuclear palsy: vertical gaze palsy and early falls. Multiple system atrophy: early autonomic dysfunction (postural hypotension, bladder) + cerebellar signs. Corticobasal degeneration: asymmetric apraxia and 'alien limb' phenomenon.

10. What is the first-line treatment for Parkinson's disease with motor symptoms affecting quality of life, and a key long-term complication?

    Levodopa (combined with a peripheral dopa-decarboxylase inhibitor, e.g. co-careldopa). Long-term: motor fluctuations ('wearing off', 'on-off') and dyskinesias.

11. Distinguish essential tremor from Parkinsonian tremor.

    Essential tremor: postural/action tremor (6–12 Hz), bilateral, improves with alcohol, often family history, worse with arms outstretched; treated with propranolol/primidone. Parkinsonian tremor: resting tremor (4–6 Hz), asymmetric, improves with action.

12. What is the genetics and characteristic movement disorder of Huntington's disease?

    Autosomal dominant CAG trinucleotide repeat expansion in the huntingtin (HTT) gene on chromosome 4, showing anticipation. Causes chorea, plus cognitive decline and psychiatric features; treat chorea with tetrabenazine.

13. What is dystonia, and what is the typical management of focal dystonia (e.g. cervical dystonia, blepharospasm)?

    Sustained or intermittent involuntary muscle contractions causing abnormal postures/twisting movements. Focal dystonia is treated first-line with botulinum toxin injections.

14. What are the diagnostic principles (McDonald criteria concept) for multiple sclerosis?

    Demonstration of CNS demyelination disseminated in space and time. MRI shows periventricular, juxtacortical, infratentorial and spinal cord lesions; CSF shows oligoclonal bands (not in serum).

15. Name the classic clinical syndromes of multiple sclerosis (optic neuritis, internuclear ophthalmoplegia, Lhermitte's, Uhthoff's).

    Optic neuritis: painful monocular visual loss with RAPD. Internuclear ophthalmoplegia: impaired adduction + contralateral nystagmus (MLF lesion). Lhermitte's: electric-shock sensation down spine on neck flexion. Uhthoff's: symptoms worsen with heat.

16. How are acute MS relapses and disease-modifying therapy approached?

    Acute relapse: high-dose methylprednisolone (IV or oral) to shorten duration. Long-term: disease-modifying therapies (e.g. beta-interferon, natalizumab, ocrelizumab, dimethyl fumarate) to reduce relapse frequency.

17. What are the typical CSF findings in bacterial versus viral versus tuberculous/fungal meningitis?

    Bacterial: high neutrophils, high protein, low glucose ($<\frac{1}{2}$ serum), cloudy. Viral: lymphocytes, normal/mildly raised protein, normal glucose, clear. TB/fungal: lymphocytes, high protein, low glucose, fibrin web.

18. What is the empirical antibiotic for suspected bacterial meningitis in adults, and the adjunct that reduces complications?

    IV ceftriaxone (add amoxicillin if $>50$ years or immunocompromised, to cover Listeria). Adjunctive dexamethasone reduces neurological complications (especially in pneumococcal meningitis).

19. What is the classic presentation, EEG/MRI finding and treatment of herpes simplex encephalitis?

    Fever, altered mental state, focal seizures and behavioural change. MRI shows temporal lobe involvement; EEG shows periodic lateralised discharges. Treat empirically with IV aciclovir without delay.

20. Compare Alzheimer's disease, vascular dementia, Lewy body dementia and frontotemporal dementia by a hallmark feature each.

    Alzheimer's: insidious memory loss, amyloid plaques + neurofibrillary tau tangles. Vascular: stepwise decline with vascular risk factors. Lewy body: fluctuating cognition, visual hallucinations, parkinsonism, neuroleptic sensitivity. Frontotemporal: early personality/behaviour change or language decline, younger onset.

21. Which dementia treatments are used, and which dementia features make antipsychotics dangerous?

    Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine) for mild–moderate Alzheimer's; memantine (NMDA antagonist) for moderate–severe or as add-on. Antipsychotics cause severe neuroleptic sensitivity reactions in Lewy body dementia.

22. What are the red-flag features and management priority of cauda equina syndrome?

    Bilateral sciatica, saddle anaesthesia, urinary retention/overflow incontinence, faecal incontinence, and reduced anal tone. It is a surgical emergency: urgent MRI whole spine and decompression to prevent permanent deficit.

23. Contrast the clinical features of an anterior cord (anterior spinal artery) syndrome with Brown-Séquard (hemisection) syndrome.

    Anterior cord: bilateral loss of motor function and pain/temperature below the lesion with preserved dorsal column (proprioception/vibration). Brown-Séquard: ipsilateral motor and dorsal column loss, contralateral pain/temperature loss below the lesion.

24. What spinal cord syndrome results from vitamin $B_{12}$ deficiency, and which tracts are affected?

    Subacute combined degeneration of the cord: affects the dorsal columns (loss of proprioception/vibration, sensory ataxia) and lateral corticospinal tracts (UMN weakness, upgoing plantars), often with peripheral neuropathy.

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