Lacosamide, a newer antiepileptic, exerts its unique mechanism of action by:
- A Blocking T-type calcium channels in thalamic relay neurons
- B Potentiating GABA-A receptor-mediated chloride influx at the benzodiazepine site
- C Inhibiting HCN (hyperpolarisation-activated cyclic nucleotide-gated) channels
- D Enhancing slow inactivation of voltage-gated sodium channels without affecting fast inactivation ✓
Explanation
Lacosamide selectively enhances slow inactivation of voltage-gated sodium channels. Unlike carbamazepine and phenytoin (which enhance fast inactivation), lacosamide stabilises channels in the slow-inactivated state — a distinct conformational state that reduces high-frequency neuronal firing while sparing normal low-frequency activity. This makes it effective in focal seizures with minimal effect on normal neurotransmission. Options B–D describe ethosuximide, benzodiazepines, and ivabradine/gabapentinoids respectively.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.