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Epilepsy & antiepileptics flashcards

26 high-yield MRCP Part 1 cards from the Intellect Medicos Neurology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. Under current UK (MHRA) restrictions, what is first-line for generalised tonic-clonic seizures in a newly diagnosed patient under 55?

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    Lamotrigine or levetiracetam.

    Why? Valproate is very effective but is teratogenic and may affect fertility. Since 2024 it must not be started in anyone under 55 unless two specialists agree.

  2. MHRA (2024): valproate must not be started in anyone younger than ______ years unless two specialists independently document that no other treatment is effective or tolerated.

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    55

    Why? Valproate causes major malformations and neurodevelopmental disorders in exposed babies, and there are concerns about male fertility. Men already taking it do not need a second specialist sign-off (MHRA Feb 2025) but should use effective contraception during treatment and for 3 months after stopping.

  3. MHRA (2024): valproate must not be started in anyone younger than 55 years unless ______ independently document that no other treatment is effective or tolerated.

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    two specialists

    Why? Valproate causes major malformations and neurodevelopmental disorders in exposed babies, and there are concerns about male fertility. Men already taking it do not need a second specialist sign-off (MHRA Feb 2025) but should use effective contraception during treatment and for 3 months after stopping.

  4. What is first-line drug treatment for focal seizures?

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    Lamotrigine or levetiracetam.

    Why? Both are effective for focal epilepsy and safer in pregnancy than older drugs.

  5. What is the first-line drug for absence seizures?

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    Ethosuximide.

    Why? Ethosuximide blocks T-type calcium channels in the thalamus, which drive the 3 Hz spike-and-wave discharges.

  6. What is the first-line drug for myoclonic seizures (e.g. juvenile myoclonic epilepsy)?

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    Levetiracetam.

    Why? Levetiracetam works across generalised seizure types and avoids valproate restrictions.

  7. Status epilepticus in hospital with IV access: what is the first-line drug?

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    IV lorazepam, repeated once after 5-10 minutes if seizures continue.

    Why? Benzodiazepines boost GABA-A inhibition and stop most seizures quickly. Status is a seizure of 5 minutes or more, or repeated seizures without recovery.

  8. What is first-line treatment for status epilepticus in the community (no IV access)?

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    Buccal midazolam (or rectal diazepam).

    Why? Both can be given without IV access by carers or paramedics.

  9. Status epilepticus continues after two doses of benzodiazepine. Name the second-line IV options.

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    IV levetiracetam, IV phenytoin or IV sodium valproate.

    Why? This is established status. NICE does not rank the three, but notes levetiracetam may be quicker to give with fewer adverse effects. If they fail, third-line options under expert guidance are phenobarbital or general anaesthesia.

  10. What is the most important serious adverse effect to warn about when starting lamotrigine?

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    Skin rash progressing to Stevens-Johnson syndrome.

    Why? Rash risk is highest early in treatment, so the dose is increased slowly.

  11. Which electrolyte abnormality is classically caused by carbamazepine, and by what mechanism?

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    Hyponatraemia, via SIADH.

    Why? Carbamazepine and oxcarbazepine increase ADH effect. They can also cause agranulocytosis, aplastic anaemia and SJS.

  12. A woman on carbamazepine wants the combined oral contraceptive. What is the problem?

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    Carbamazepine is a hepatic enzyme inducer and reduces contraceptive effectiveness.

    Why? CYP3A4 induction speeds up oestrogen and progestogen metabolism. Phenytoin, phenobarbital and topiramate (at higher doses) do the same.

  13. What folic acid dose is recommended for a woman with epilepsy on antiepileptics planning pregnancy?

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    Folic acid 5 mg daily, started before conception and continued in early pregnancy.

    Why? Antiepileptics raise the risk of neural tube defects. The high dose lowers that risk.

  14. Which two antiepileptics are regarded as the safer options in pregnancy?

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    Lamotrigine and levetiracetam.

    Why? They carry the lowest malformation risk among commonly used antiepileptics.

  15. Infantile spasms (West syndrome) with hypsarrhythmia on EEG in a child with tuberous sclerosis: what is the drug of choice?

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    Vigabatrin.

    Why? NICE offers vigabatrin alone first-line for spasms due to tuberous sclerosis, adding prednisolone if no response after 1 week. For other causes, NICE offers high-dose oral prednisolone plus vigabatrin.

  16. What is the mechanism of action of levetiracetam?

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    It binds the synaptic vesicle protein SV2A, modulating neurotransmitter release.

    Why? It has few drug interactions. Key adverse effects are irritability, mood change and depression.

  17. What is the mechanism of action of lamotrigine?

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    Blocks voltage-gated sodium channels, reducing glutamate release.

    Why? Stabilising neuronal membranes reduces repetitive firing. It is broad-spectrum and relatively safe in pregnancy.

  18. Topiramate can cause ______, weight loss, paraesthesia and metabolic acidosis, partly through carbonic anhydrase inhibition.

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    kidney stones

    Why? Topiramate blocks sodium channels, enhances GABA, inhibits carbonic anhydrase and reduces glutamate activity. Zonisamide shares the stone and acidosis risk.

  19. Topiramate can cause kidney stones, weight loss, paraesthesia and ______, partly through carbonic anhydrase inhibition.

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    metabolic acidosis

    Why? Topiramate blocks sodium channels, enhances GABA, inhibits carbonic anhydrase and reduces glutamate activity. Zonisamide shares the stone and acidosis risk.

  20. Name three classic adverse effects of long-term phenytoin.

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    Any three: gingival hyperplasia, hirsutism, coarse facies, peripheral neuropathy, folate-deficiency megaloblastic anaemia, osteomalacia.

    Why? Phenytoin is a sodium-channel blocker and a hepatic enzyme inducer, so it also causes many drug interactions.

  21. Why can a small increase in phenytoin dose cause toxicity?

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    Its metabolism saturates at therapeutic levels (zero-order kinetics), so plasma levels rise disproportionately.

    Why? Toxicity causes nystagmus, ataxia, slurred speech and confusion. Plasma levels guide dosing.

  22. Name three adverse effects of sodium valproate other than teratogenicity.

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    Any three: weight gain, hair loss, tremor, hepatotoxicity, pancreatitis, thrombocytopenia, hyperammonaemic encephalopathy, parkinsonism.

    Why? Valproate is also a hepatic enzyme inhibitor, so it raises levels of drugs such as lamotrigine.

  23. Before starting carbamazepine in a patient of Han Chinese or Thai origin, which genetic test is advised, and why?

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    HLA-B*1502, because it strongly predicts carbamazepine-induced Stevens-Johnson syndrome.

    Why? Carriers should not be given carbamazepine unless there is no alternative.

  24. What EEG pattern is characteristic of childhood absence seizures?

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    Bilateral, symmetrical 3 Hz spike-and-wave discharges.

    Why? Hyperventilation in clinic often provokes an absence and the EEG pattern.

  25. DVLA group 1: after a first unprovoked seizure, stop driving for ______ if MRI and EEG show no relevant abnormality; with established epilepsy, driving is allowed once seizure-free for 12 months.

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    6 months

    Why? The patient must tell the DVLA. A first seizure with an abnormal MRI or EEG means 12 months off driving.

  26. DVLA group 1: after a first unprovoked seizure, stop driving for 6 months if MRI and EEG show no relevant abnormality; with established epilepsy, driving is allowed once seizure-free for ______.

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    12 months

    Why? The patient must tell the DVLA. A first seizure with an abnormal MRI or EEG means 12 months off driving.

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