Mechanisms of anticonvulsant drug action

Abstract

The mechanisms by which the clinically effective anticonvulsant drugs act include effects on neurotransmitter action, effects on repetitive neuronal firing mechanisms, effects on neuronal networks, and effects on neuronal ionic transport. The combination of effects possessed by each individual agent along with its pharmacokinetic properties determine the usefulness of each agent. Phenytoin, carbamazepine and phenobarbital are effective in generalized tonic-clonic and partial epilepsies. Phenytoin exerts important effects on neuronal sodium and calcium ion transport, reduces repetitive firing, reduces excitation in neuronal networks of the brainstem reticular formation, and produces some decrease in the effect of the inhibitory transmitter, gamma-aminobutyric acid (GABA). Carbamazepine blocks repetitive firing mechanisms, reduces excitation in neuronal networks with some effect on sodium and potassium ion transport, and has effects on the actions of norepinephrine, adenosine and perhaps acetylcholine. Phenobarbital enhances the action of GABA with some reduction of repetitive firing and reduces excitation in reticular formation neuronal networks.

Treatment of Infantile Spasms with High‐Dosage Vitamin B6

“…The synthesis of the inhibitory neurotransmitter GABA is carried out by a pyridoxal phosphate-dependent enzyme, glutamic acid decarboxylase. Other drugs used for treatment of infantile spasms also enhance the inhibitory effect of GABA (Macdonald et al, 1979;Faingold and Browning, 1987). Moreover, the concentration of GABA in CSF was lowest in children with infantile spasms, when compared with other forms of epilepsy.…”