A 28-year-old woman with juvenile myoclonic epilepsy is started on valproate. The drug's most important mechanism relevant to myoclonic seizures involves:
- A Blockade of voltage-gated sodium channels at high frequencies
- B Enhancement of GABA-mediated inhibition through multiple mechanisms including GABA transaminase inhibition ✓
- C Blockade of T-type calcium channels in thalamic relay neurons
- D NMDA receptor antagonism reducing excitatory neurotransmission
Explanation
Valproate has multiple mechanisms including inhibition of GABA transaminase (increasing GABA levels), inhibition of voltage-gated Na+ channels, and some T-type Ca²⁺ channel blockade. For myoclonic seizures specifically, enhancement of GABAergic inhibition is the primary relevant mechanism since myoclonus involves cortical hyperexcitability. Ethosuximide targets T-type Ca²⁺ channels for absence seizures, while carbamazepine mainly blocks Na+ channels and is NOT used in myoclonic epilepsy (may worsen it).
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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