IM20.1-5 | Seizure Disorders — Practice Quiz

Correct. ILAE 2014 criteria define epilepsy as (1) at least two unprovoked seizures more than 24 hours apart, (2) one unprovoked seizure with a recurrence risk of at least 60% over the next 10 years (e.g., lesional epilepsy, remote symptomatic aetiology), or (3) diagnosis of an epilepsy syndrome. A single first unprovoked seizure without a high-risk structural or EEG finding does not meet criteria — long-term AED therapy is not routinely started.

Epilepsy (ILAE 2014) = at least two unprovoked seizures (more than 24 hours apart), OR one unprovoked seizure with at least 60% ten-year recurrence risk, OR an epilepsy syndrome diagnosis. A first-ever generalised tonic-clonic seizure by itself does not equal epilepsy.

ILAE 2014 defines epilepsy as two or more unprovoked seizures OR one unprovoked seizure with a recurrence risk of at least 60% over 10 years. Duration of the seizure and the presence of post-ictal confusion do not themselves satisfy the definition. Full investigation is always warranted after a first seizure.

Correct. Under ILAE 2017, seizures beginning in one hemisphere that subsequently evolve to involve both hemispheres and produce bilateral tonic-clonic activity are classified as 'focal to bilateral tonic-clonic seizures.' This replaces the older term 'secondarily generalised seizure.' The focal onset component is classified by awareness (aware or impaired awareness) and motor features before the bilateral spread.

ILAE 2017 classification: Focal onset (aware or impaired awareness) — Generalised onset — Unknown onset. A seizure beginning focally that spreads to both hemispheres = focal to bilateral tonic-clonic seizure (old term: secondarily generalised). This distinction has direct AED implications.

A seizure that starts in one hemisphere and then spreads to involve both hemispheres is a focal to bilateral tonic-clonic seizure under ILAE 2017 — not a primarily generalised onset seizure. The focal onset is the defining feature, even though the motor manifestation becomes bilateral.

Correct. This presentation is consistent with childhood absence epilepsy with co-occurring generalised tonic-clonic seizures — a generalised epilepsy syndrome. Sodium valproate is the first-line agent for absence seizures with GTCS; ethosuximide is effective for pure absence but does not protect against GTCS and should be combined with valproate when GTCS are present. Carbamazepine and phenytoin are contraindicated in generalised epilepsies with absence or myoclonic features — they can worsen absence and myoclonus by exacerbating the 3 Hz discharges.

AED selection by seizure type: valproate is broad-spectrum (absence + GTCS + myoclonic). Carbamazepine and phenytoin are CONTRAINDICATED in absence epilepsy and juvenile myoclonic epilepsy — they aggravate these seizure types. Ethosuximide targets absence only; add valproate when GTCS coexist.

Carbamazepine and phenytoin are sodium channel blockers that are effective in focal epilepsies but contraindicated in generalised epilepsy syndromes involving absence or myoclonic seizures — they worsen these seizure types. Valproate (broad-spectrum) is the first-line choice here; ethosuximide targets absence but does not prevent GTCS.

Correct. Valproate carries the highest teratogenic risk of all commonly used AEDs: neural tube defects (1–2%), orofacial clefts, cardiac malformations, and neurodevelopmental delay. It should ideally be avoided in women of childbearing potential; if unavoidable (as in JME where alternatives may be less effective), the lowest effective dose plus high-dose folic acid (5 mg/day) pre-conception and through the first trimester is mandatory. Carbamazepine is CONTRAINDICATED in JME (worsens myoclonic seizures) and is NOT a safer alternative here.

Valproate teratogenicity: highest among AEDs (neural tube defects 1–2%, neurodevelopmental delay). Avoid in women of childbearing potential where possible. If essential, use lowest effective dose + folic acid 5 mg/day pre-conception. NEVER switch a JME patient to carbamazepine — it worsens myoclonus.

Valproate has the highest teratogenic risk among AEDs, causing neural tube defects, cardiac malformations, and neurodevelopmental delay. Carbamazepine is contraindicated in JME — it worsens myoclonic seizures. Pre-conception counselling, high-dose folic acid (5 mg/day), and consideration of lamotrigine (less effective for myoclonus in JME) are essential.

Correct. A seizure lasting 5 minutes or longer meets the operational definition of status epilepticus. Benzodiazepines are the first-line treatment: IV lorazepam (0.1 mg/kg, maximum 4 mg) or IV diazepam (0.15–0.2 mg/kg, maximum 10 mg). These should be given immediately — delay beyond 5 minutes significantly increases drug resistance and neuronal injury. IV phenytoin is a second-line agent used if benzodiazepines fail, not first-line.

Status epilepticus definition: seizure ≥5 minutes. First-line = benzodiazepine (IV lorazepam preferred; or IV diazepam). Give within 5 minutes of SE onset. If no IV access: midazolam IM or buccal. Second-line: IV valproate, phenytoin/fosphenytoin, or levetiracetam. Third-line: anaesthesia (propofol/midazolam/thiopental) if two AEDs fail.

A seizure lasting 5 minutes or more = status epilepticus; immediate benzodiazepine is first-line therapy (IV lorazepam 0.1 mg/kg or IV diazepam 0.15–0.2 mg/kg). Do not wait. Phenytoin is second-line (after benzodiazepine failure). Levetiracetam is also second-line. Time-to-drug is the most critical determinant of outcome.

Correct. After failure of the initial benzodiazepine dose in status epilepticus, the next step is a second-line IV antiepileptic: IV sodium valproate (20–40 mg/kg at up to 6 mg/kg/min), IV phenytoin/fosphenytoin (20 mg/kg at 50 mg/min), or IV levetiracetam (20–60 mg/kg). These should be initiated promptly — at approximately 10 minutes after the initial benzodiazepine — without waiting for radiological investigation. Imaging is important but must not delay drug treatment in ongoing SE.

SE stepwise management: Benzodiazepine (0–5 min) → Second-line IV AED at 10–20 min (valproate / phenytoin / levetiracetam) → Anaesthesia (propofol / midazolam / thiopental) if seizures persist beyond 30–40 min (refractory SE). Do not delay escalation waiting for imaging.

After benzodiazepine failure in status epilepticus, escalate to a second-line IV AED (valproate, phenytoin/fosphenytoin, or levetiracetam) without delay. Do not wait for imaging — that delays treatment. Oral carbamazepine has no role in acute SE management and is contraindicated in generalised epilepsy.

Correct. Indian Motor Vehicles Act permanently bars people with epilepsy from holding a commercial vehicle licence. For private vehicle driving, standard specialist guidance requires a seizure-free period of at least 1–2 years (with or without AEDs) before resuming, individualised based on seizure type, EEG, and AED status. This patient at 14 months seizure-free on levetiracetam may be close to eligibility for a private licence — exact clearance requires specialist confirmation.

Driving counselling in epilepsy: commercial licence PERMANENTLY barred under Indian MV Act. Private driving: seizure-free period (typically 1–2 years, specialist-guided) before resuming. Must also counsel on swimming alone, heights, operating heavy machinery — all require at least the same seizure-free period.

Indian Motor Vehicles Act permanently disqualifies persons with epilepsy from commercial vehicle licences. For private driving, a specialist-advised seizure-free period (typically 1–2 years) is required before resuming. Being on medication alone does not permit driving — the relevant criterion is absence of seizures.

Correct. The electroclinical constellation here is classic for juvenile myoclonic epilepsy (JME): age of onset in adolescence/early adulthood, bilateral myoclonic jerks predominantly in the morning on awakening, frequent sleep-deprivation trigger, co-occurring GTCS, and irregular polyspike-and-wave discharges on EEG maximal at awakening. JME is a generalised genetic epilepsy syndrome. It requires lifelong AED therapy in most patients; valproate is first-line. Carbamazepine and phenytoin are contraindicated.

JME electroclinical hallmarks: adolescent onset, morning myoclonic jerks on awakening, sleep-deprivation trigger, GTCS, irregular polyspike-and-wave EEG. First-line: valproate (or lamotrigine in women of childbearing potential — note lamotrigine less effective for myoclonus). Carbamazepine and phenytoin are CONTRAINDICATED.

The clinical hallmark of JME is morning myoclonic jerks on awakening, often triggered by sleep deprivation, with irregular polyspike-wave EEG discharges and co-occurring GTCS in adolescence/early adulthood. Valproate is first-line; carbamazepine and phenytoin worsen myoclonus and are contraindicated.

Correct. A first seizure in a middle-aged adult with a focal neurological deficit (Todd's paralysis suggesting focal onset) mandates urgent neuroimaging to exclude a structural cause — stroke, tumour, haemorrhage, or abscess. CT brain without contrast is the most rapidly available modality to exclude haemorrhage or large structural lesion; MRI is preferred electively. EEG is important for classification but not the immediate priority. Lumbar puncture follows imaging if meningitis or encephalitis is suspected. Serum prolactin is an unreliable biomarker and is not routinely recommended.

First seizure workup: urgent CT brain (to exclude haemorrhage/structural lesion) + metabolic screen (glucose, electrolytes, calcium, renal/liver function) + ECG. MRI preferred for elective imaging. EEG after clinical stabilisation. Focal deficit after seizure = Todd's paralysis — lesional cause must be excluded urgently.

A first seizure with a transient focal deficit (Todd's paralysis) in a 55-year-old demands urgent brain imaging to exclude a structural cause — haemorrhage, stroke, or tumour. CT brain is the immediate priority. EEG, LP, and prolactin are important adjuncts but do not replace urgent imaging in this scenario.

Correct. Rifampicin is a potent inducer of hepatic CYP enzymes and UGT glucuronidation pathways, both of which are involved in valproate metabolism. Co-administration can reduce valproate plasma levels significantly, risking seizure breakthrough. Monitoring of serum valproate levels and dose adjustment is required. Isoniazid inhibits CYP2C9/2C19 and can actually reduce carbamazepine and phenytoin clearance (raising levels), but this is not the primary concern with valproate.

Rifampicin (potent CYP inducer) lowers levels of valproate, carbamazepine, phenytoin, and lamotrigine — risks seizure breakthrough. Monitor levels and adjust AED doses. Isoniazid inhibits CYP2C9 — may RAISE phenytoin/carbamazepine levels. Both interactions matter in TB + epilepsy co-management.

Rifampicin is a potent CYP inducer that lowers valproate plasma levels — increasing seizure risk. Monitoring and dose adjustment are required when co-prescribing. This interaction is also critical for phenytoin, carbamazepine, and lamotrigine; rifampicin is the most clinically important enzyme inducer in anti-TB therapy.