Ethosuximide — Absence Epilepsy
Figure 1 — Drugs That Treat vs. Worsen Absence (Gemini)
Ethosuximide
T-Type Calcium Channel Blocker
- First-line for pure childhood absence epilepsy
- Blocks T-type calcium channels in thalamic relay neurons
- No efficacy against tonic-clonic or myoclonic seizures
- Use valproate instead when absence coexists with other seizure types
Newer Agents
Levetiracetam
- Synaptic vesicle protein 2A modulator
- NOT sodium, calcium, or gamma-aminobutyric acid
- No cytochrome P450 interactions
- Key adverse effect: irritability, aggression (behavioral, not sedation)
- Preferred in pregnancy
Topiramate
- Multiple mechanisms including carbonic anhydrase inhibition
- Cognitive impairment ("Dopamax") — dose-limiting
- Weight loss (used therapeutically)
- Kidney stones from carbonic anhydrase inhibition
- Teratogenicity — cleft palate and lip
Gabapentin / Pregabalin
- Alpha-2-delta subunit of voltage-gated calcium channels
- NOT gamma-aminobutyric acid receptor agonists — name is misleading
- Gabapentin: focal seizures, neuropathic pain; worsens absence
- Pregabalin: same + fibromyalgia, generalized anxiety disorder; Schedule V
Gabapentin vs. Pregabalin
Figure 2 — Gabapentin vs. Pregabalin Comparison (Gemini)
High-Yield Trap — Gabapentin and Pregabalin
Despite their names, gabapentin and pregabalin are NOT gamma-aminobutyric acid receptor agonists. They bind the alpha-2-delta subunit of voltage-gated calcium channels. A question asking which drug acts at gamma-aminobutyric acid receptors should never have gabapentin or pregabalin as the answer.