ANTICONVULSANTS are drugs used to treat convulsions of various types, for instance, in drug or chemical poisoning, e.g. chlorpromazine, diazepam. However, these anticonvulsants are not necessarily effective or suitable for epilepsy.

In practice, the antiepileptic drugs are the more used, especially for prolonged treatment, and these agents have extensive usage in preventing the occurrence of epileptic seizures. The drug of choice depends on the type and severity of the epilepsy. For tonic-clonic seizures (Grand Mai) as part of a syndrome of primary generalized epilepsy the drugs of choice are carbamazepine and phenytoin. For absence seizures (Petit Mai), sodium valproate and ethosuximide. For myoclonic seizures, sodium valproate, clonazepam and ethosuximide. For other types of seizure, such as atypical absence, atonic and tonic seizures (often in childhood), phenytoin, sodium valproate, clonazepam, phenobarbitone, or ethosuximide are valuable. These all appear to work by stabilizing membranes and decreasing excitability, though with differing profiles of activity and mechanisms of action.

Phenobarbitone, though a barbiturate, is more of an anticonvulsant than expected from its sedative actions, and it resembles phenytoin. They appear to work by an interaction with the modulatory site of the GABAA receptor and thereby enhance GABA’s neuronal inhibitory action. Carbamazepine has an interesting, but a little understood mechanism of action, whereby it stabilizes unstable neurons (working, for instance, against trigeminal neuralgia).

Vigabatrin is an analogue of GABA that irreversibly inhibits the enzyme GABA transaminase which degrades endogenous GABA, thereby having an inhibitory action within the brain. It may be effective in generalized clonic-tonic seizures unresponsive to other drugs. Sodium valproate seems to have a number of actions, such as inhibition of GABA transaminase, it may induce glutamic acid decarboxylase, and some actions in closing sodium channels.