IM20.1-5 | Seizure Disorders — Graded Quiz

Correct. Lateral tongue biting has a specificity of approximately 95% for epileptic seizures — it is virtually pathognomonic. It occurs because the forceful jaw contraction during the tonic phase drives the lateral tongue between the molars. Tip-of-tongue biting can occur in syncope; lateral tongue biting does not. Urinary incontinence, post-ictal confusion, and GTCS motor activity are all consistent with epileptic seizures but also occur in syncope with convulsive movements and in psychogenic non-epileptic attacks, making them less specific.

Lateral tongue biting: specificity ~95% for epileptic seizures — virtually pathognomonic. Never occurs in psychogenic non-epileptic attacks. Tip-of-tongue biting can occur in syncope. Use this as an anchor feature when differentiating epileptic seizures from mimics in an acute setting.

Lateral tongue biting (specifically lateral, not tip) has about 95% specificity for epileptic seizures. Urinary incontinence can occur in syncope; post-ictal confusion may also follow prolonged syncope; GTCS-type movements occur in psychogenic non-epileptic attacks. Lateral tongue biting is the most specific single feature.

Correct. The clinical features — behavioural arrest, automatisms (lip-smacking, hand-picking), impaired awareness (confirmed by post-ictal confusion and the described automatisms occurring without normal response), with focal temporal EEG onset and hippocampal sclerosis — fulfil the ILAE 2017 classification of focal onset impaired awareness seizure. The old term was 'complex partial seizure.' Awareness is classified as impaired because the patient is not aware and responsive during the episode. Absence seizures are generalised, brief (5–20 s), and lack post-ictal confusion.

Focal onset impaired awareness seizure (old term: complex partial seizure) = focal onset + impaired awareness during the event + often automatisms + post-ictal confusion. Contrast with absence: generalised 3 Hz spike-wave, very brief, no post-ictal confusion. Hippocampal sclerosis is the most common structural cause of focal temporal lobe epilepsy.

Behavioural arrest with automatisms and post-ictal confusion arising from a focal temporal onset (EEG) with hippocampal sclerosis = focal onset impaired awareness seizure (ILAE 2017). Absence seizures are generalised (3 Hz spike-wave), brief (5–20 s), and have no post-ictal confusion — these features are absent here.

Correct. Carbamazepine is metabolised primarily by CYP3A4 to its active metabolite carbamazepine-10,11-epoxide. Fluconazole is a potent CYP3A4 inhibitor. Co-administration raises carbamazepine (and its active epoxide) plasma levels, causing dose-related toxicity. The classic triad of carbamazepine toxicity is diplopia, nystagmus, and ataxia — exactly the features here. Management is to stop or dose-reduce the offending agent and check plasma carbamazepine levels.

Carbamazepine toxicity signs: diplopia + nystagmus + ataxia (dose-related). CYP3A4 inhibitors (azoles, macrolides, verapamil, grapefruit) raise carbamazepine levels. CYP3A4 inducers (rifampicin, phenytoin, phenobarbitone) lower levels. Always check interactions before co-prescribing.

Fluconazole is a potent CYP3A4 inhibitor, not an inducer. It raises carbamazepine plasma levels → dose-related toxicity (diplopia, nystagmus, ataxia). The key principle: azole antifungals (fluconazole, ketoconazole, itraconazole) are CYP3A4 inhibitors — always check for interactions with CYP3A4-metabolised drugs.

Correct. Phenytoin is a potent inducer of CYP2C9, which is the main enzyme responsible for S-warfarin metabolism (the more potent enantiomer). Increased CYP2C9 activity accelerates warfarin clearance, lowering plasma levels and reducing anticoagulation. This patient's INR has fallen below the therapeutic range for a mechanical mitral valve (2.5–3.5), putting her at risk of prosthetic valve thrombosis. Warfarin dose adjustment with frequent INR monitoring is mandatory, or an alternative AED with fewer CYP interactions (e.g., levetiracetam) should be considered.

Phenytoin + warfarin = CYP2C9 induction → lower INR → thromboembolism risk. Carbamazepine has the same effect. Valproate INHIBITS warfarin metabolism (raises INR). Levetiracetam and lamotrigine have minimal P450 interactions — preferred when complex drug interactions must be avoided.

Phenytoin induces CYP2C9 (the principal enzyme metabolising S-warfarin) — accelerating warfarin clearance and reducing INR. A mechanical mitral valve requires INR 2.5–3.5; an INR of 1.4 = severe under-anticoagulation = risk of valve thrombosis. Levetiracetam does not have this interaction and is preferred when INR stability is critical.

Correct. AED withdrawal can be considered after 2–5 years of seizure freedom in adults. The decision must be individualised based on risk factors for relapse: abnormal EEG, structural (symptomatic) aetiology, focal onset seizures, prior treatment failure requiring multiple drugs, and JME (which typically requires lifelong therapy). If withdrawal is attempted, it must be gradual (over months), and the patient must be counselled about seizure recurrence risk and its implications (driving, occupation, safety).

AED withdrawal: consider after 2–5 seizure-free years. High relapse risk: abnormal EEG, structural aetiology, focal onset, JME (lifelong therapy in most). Taper gradually over months. Reinstate driving restrictions during taper period. Decision is always individualised and shared with the patient.

AED withdrawal is possible after 2–5 seizure-free years, but must be individualised. High relapse-risk features: abnormal EEG, structural cause, focal seizures, JME, prior drug failure. JME typically requires lifelong therapy. Withdrawal must be gradual; counsel about driving restrictions during and after taper.

Correct. Self-limited epilepsy with centrotemporal spikes (SLECTS, formerly BECTS — benign epilepsy of childhood with centrotemporal spikes) is the most common childhood focal epilepsy syndrome. Hallmarks: unilateral facial/arm focal seizures (often sleep-related), centrotemporal spikes on EEG activated by sleep, normal MRI, normal neurological development. Almost all children (90%+) achieve spontaneous remission by age 16 without AED therapy or with minimal treatment. Lennox-Gastaut has slow spike-wave and a poor prognosis; JME presents in adolescents with morning myoclonus; Dravet is characterised by febrile hemiclonic seizures in infancy.

SLECTS (formerly BECTS): age 4–12, unilateral centrofacial/arm motor seizures, centrotemporal spikes activated by sleep EEG, normal MRI, normal intellect. Prognosis excellent — spontaneous remission by 16 in >90%. Many need no AEDs; if treating, low-dose carbamazepine or levetiracetam. JME is lifelong; Lennox-Gastaut has poor prognosis.

SLECTS (formerly BECTS) presents in school-age children with focal motor seizures (face/arm/leg) often nocturnal, centrotemporal spikes on sleep EEG, and normal MRI. It has an excellent prognosis — spontaneous remission by age 14–16 in over 90% of children. This distinguishes it from structural and genetic generalised epilepsies with poor prognosis.

Correct. Post-stroke seizures occurring within 7 days are classified as 'early' (acute symptomatic/provoked) and carry a lower recurrence risk — long-term AEDs are not routinely initiated. Seizures occurring more than 7 days after stroke are 'late' (unprovoked in the context of the remote injury) and carry a substantially higher recurrence risk (approximately 70%+ over 5 years), meeting ILAE criteria for epilepsy on the basis of high recurrence risk. Long-term AED therapy is generally warranted. Levetiracetam or lamotrigine are preferred in this age group due to better tolerability.

Post-stroke epilepsy: early (within 7 days) = acute symptomatic, lower recurrence risk, AED not routinely needed long-term; late (after 7 days) = high recurrence risk (~70%), meets ILAE criteria, long-term AED indicated. Preferred AEDs in elderly: levetiracetam or lamotrigine (fewer interactions, better tolerability).

Early post-stroke seizures (within 7 days) = acute symptomatic (provoked); late seizures (after 7 days) = high recurrence risk = meet ILAE epilepsy criteria = long-term AED indicated. Levetiracetam and lamotrigine are preferred in elderly post-stroke patients over older enzyme-inducing AEDs (phenytoin, carbamazepine) due to better tolerability and fewer drug interactions.

Correct. During a generalised tonic-clonic seizure in pregnancy, maternal hypoxia and lactic acidosis caused by the convulsion can rapidly produce fetal hypoxia and acidosis. Even though the seizure has stopped and maternal SpO2 is 96%, fetal distress can be present — continuous fetal heart rate monitoring is required immediately. Supplemental oxygen, left lateral positioning to avoid aortocaval compression, and early obstetric review are essential. Teratogenicity is a pre-conception concern and irrelevant for a 20-week established pregnancy; seizure-related fetal hypoxia is the acute risk.

Seizure in pregnancy: immediate risk to fetus = maternal hypoxia + lactic acidosis → fetal hypoxia. Actions: lateral position (aortocaval decompression) + supplemental oxygen + fetal heart rate monitoring + obstetric review. SE in pregnancy requires urgent benzodiazepine — risk of untreated SE far outweighs drug risk.

The immediate concern in a GTCS at 20 weeks gestation is fetal hypoxia from maternal convulsion-associated hypoxia and acidosis. Monitor fetal heart rate, give supplemental oxygen, position left lateral (aortocaval decompression). Teratogenicity is a pre-conception issue; fetal oxygenation is the acute priority.

Correct. This is now refractory status epilepticus — defined as SE that fails to respond to two adequately dosed IV AEDs (in this case, a benzodiazepine and valproate). At this stage, the management protocol requires escalation to general anaesthesia with an anaesthetic agent: IV midazolam infusion (0.2 mg/kg bolus then 0.05–2 mg/kg/hr), IV propofol infusion (1–2 mg/kg bolus then 2–10 mg/kg/hr), or IV thiopental/phenobarbitone. This requires intubation, mechanical ventilation, and continuous EEG monitoring in an ICU setting.

Refractory SE (failed benzodiazepine + second-line IV AED) = anaesthetic agent (propofol/midazolam infusion/thiopental) + intubation + ICU + continuous EEG monitoring. Mortality from prolonged SE is 10–20%; irreversible neuronal injury begins within minutes. Escalate on time, not on hope.

Refractory SE = failure of two adequately dosed IV AEDs. The next step is anaesthetic agent (propofol, midazolam infusion, or thiopental) with intubation and continuous EEG monitoring in ICU. Repeating lorazepam or valproate is not recommended — escalate to third-line therapy. Time and neuronal survival are critical.

Correct. Safety counselling for epilepsy must be specific and empowering, not blanket prohibition. Water safety is the most important point: drowning is the leading cause of accidental death in epilepsy. Never swim alone; always with a supervising adult who knows the seizure history; shower standing rather than bathing in a bathtub. Contact sports with head injury risk should be assessed individually. Sleep deprivation and alcohol should be avoided as they lower the seizure threshold. Unsupervised heights, heavy machinery, and open fires are also risk areas.

Epilepsy lifestyle counselling: water safety first (drowning is #1 accidental death) — never swim alone, shower standing, not bathing. Avoid sleep deprivation and alcohol. Commercial driving barred; private driving after seizure-free period. Heights, open fires, heavy machinery: individual risk assessment. Exercise is beneficial, not prohibited.

Drowning is the leading cause of accidental death in epilepsy. Specific advice: never swim alone or in unsupervised water; shower standing not bathing in tub; avoid sleep deprivation and alcohol (lower seizure threshold); driving per MV Act; heights and heavy machinery with risk assessment. Active exercise is not a trigger and should not be prohibited.

Correct. The clinical features of psychogenic non-epileptic attacks (PNEA) are: prolonged duration (>5 minutes), pelvic thrusting, asynchronous limb movements, eyes tightly shut (resists passive eye opening), emotional precipitants, and — crucially — a completely normal EEG recording during the event (which is diagnostic). The condition is not feigned; it is a genuine dissociative disorder. Management involves non-judgmental disclosure of the diagnosis, psychiatric/psychological referral, and — critically — avoiding unnecessary AED prescribing, which causes drug harm without benefit. Many patients with PNEA have been incorrectly diagnosed with epilepsy and treated with multiple AEDs.

PNEA vs epilepsy: PNEA features — emotional trigger, pelvic thrusting, asynchronous movements, closed eyes resisting opening, prolonged, no post-ictal elevation of prolactin, and NORMAL ictal EEG (gold standard diagnosis). Management: frank disclosure + psychology/psychiatry referral. Avoid AEDs — they do not treat PNEA and cause harm.

PNEA (psychogenic non-epileptic attacks) hallmarks: emotional precipitant, pelvic thrusting, asynchronous movements, eyes closed (resists opening), prolonged duration, and most critically — normal EEG during the attack. Management: non-judgmental disclosure + psychiatric referral. Prescribing AEDs causes harm without benefit. This is a common pitfall in epilepsy practice.