Overview
Clinical Meaning
Seizures arise from hypersynchronous neuronal discharges due to imbalance between excitatory and inhibitory neurotransmission.
FNP
FNP
Seizures arise from hypersynchronous neuronal discharges due to imbalance between excitatory and inhibitory neurotransmission. Glutamate (excitatory) acts on NMDA, AMPA, and kainate receptors to depolarize neurons. GABA (inhibitory) acts on GABA-A (chloride channel hyperpolarization) and GABA-B (potassium conductance) receptors. The paroxysmal depolarization shift (PDS) is the cellular hallmark: a sustained calcium-dependent depolarization followed by burst firing. When inhibition fails, the PDS propagates creating hypersynchronous discharge. Ion channelopathies play central roles: gain-of-function sodium channel mutations (SCN1A in Dravet syndrome), loss-of-function potassium channel mutations, and GABA-A receptor mutations. Antiseizure medications target these mechanisms: sodium channel blockers (carbamazepine, phenytoin, lamotrigine), GABA enhancers (benzodiazepines increase frequency, barbiturates increase duration of chloride channel opening), T-type calcium channel blockers (ethosuximide for absence), SV2A modulators (levetiracetam), and glutamate antagonists (perampanel blocks AMPA).
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