Epilepsy and Seizure Disorders
What to know
Classify each event by semiology and EEG: focal versus generalized, with etiology as genetic, structural, metabolic, infectious, or immune. Recognize syndromes. Childhood absence epilepsy (ages 4–10) shows staring with 3-Hz spike-wave provoked by hyperventilation. Juvenile myoclonic epilepsy presents in adolescence with morning myoclonus, generalized tonic-clonic seizures, and polyspike-wave discharges; it responds to valproate and is lifelong. Benign epilepsy with centrotemporal spikes causes nocturnal facial twitching and hypersalivation and remits. West syndrome is infantile spasms with hypsarrhythmia, treated with ACTH or vigabatrin (vigabatrin first when tuberous sclerosis is present). Lennox-Gastaut has multiple seizure types, slow spike-wave, and drop attacks. Dravet syndrome (SCN1A) begins with prolonged febrile seizures.
Status epilepticus: benzodiazepine first, then fosphenytoin, levetiracetam, or valproate, then anesthetic doses when refractory.
Adverse effects are high-yield: valproate - hepatotoxicity, pancreatitis, hyperammonemia, thrombocytopenia, teratogenicity; carbamazepine - hyponatremia, aplastic anemia, HLA-B*1502 hypersensitivity; lamotrigine - rash, so titrate slowly; vigabatrin - visual field constriction; topiramate and zonisamide - kidney stones.
Traps
Sodium-channel blockers (carbamazepine, oxcarbazepine, phenytoin) worsen absence, myoclonic seizures, and Dravet. Ethosuximide is first-line for pure absence; valproate when absence coexists with generalized tonic-clonic seizures. Simple febrile seizures need no routine EEG, no imaging, and no daily anticonvulsant.
Rule of thumb
Before starting a drug, define the seizure type; the wrong drug for a myoclonic or absence seizure is worse than no drug.