## Mechanism of Action of Antiepileptic Drugs ### Correct Statements **Key Point:** Phenytoin blocks voltage-gated Na⁺ channels and prolongs the inactivation state, stabilizing the neuronal membrane and raising the seizure threshold [cite:KD Tripathi 8e Ch 12]. **Key Point:** Valproic acid increases GABA synthesis by inhibiting GABA transaminase (the enzyme that catabolizes GABA), thereby increasing inhibitory neurotransmission [cite:KD Tripathi 8e Ch 12]. **Key Point:** Ethosuximide blocks T-type (low-voltage-activated) calcium channels in the thalamus, particularly effective in absence seizures [cite:Harrison 21e Ch 369]. ### The Incorrect Statement **High-Yield:** Lamotrigine does NOT enhance GABA release by blocking presynaptic sodium channels. Instead, lamotrigine: - Blocks voltage-gated sodium channels (similar to phenytoin) - Inhibits glutamate release (reduces excitatory neurotransmission) - Does NOT primarily work through GABA enhancement The distractor conflates lamotrigine's sodium channel blockade with a false GABA-enhancing mechanism. ### Summary Table | Drug | Primary Mechanism | Secondary Mechanism | | --- | --- | --- | | Phenytoin | Na⁺ channel blockade | Prolongs inactivation | | Valproic acid | ↑ GABA synthesis | Blocks Na⁺ channels | | Lamotrigine | Na⁺ channel blockade | ↓ Glutamate release | | Ethosuximide | T-type Ca²⁺ blockade | Thalamic-specific | **Clinical Pearl:** Lamotrigine is broad-spectrum (generalized and focal seizures) because it reduces both excitatory and inhibitory neurotransmission; ethosuximide is narrow-spectrum (absence only) because it targets thalamic oscillations.
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