Lamotrigine is effective in focal and generalised seizures including absence. Its primary mechanism is:
- A Selective blockade of T-type Ca2+ channels in thalamic neurons
- B Use-dependent blockade of voltage-gated Na+ channels AND inhibition of glutamate release ✓
- C Enhancement of GABA-A chloride channel opening frequency
- D Inhibition of carbonic anhydrase reducing neuronal excitability
Explanation
Lamotrigine stabilises the inactivated state of voltage-gated Na+ channels in a use-dependent manner, reducing high-frequency neuronal firing; it also inhibits presynaptic release of glutamate and aspartate. This dual action accounts for its broad-spectrum efficacy across focal, generalised tonic-clonic, and absence seizures. Benzodiazepines and phenobarbital increase GABA-A chloride channel opening frequency; ethosuximide selectively blocks T-type Ca2+ channels; acetazolamide inhibits carbonic anhydrase.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.