Antiepileptic drugs are administered to prevent or decrease (in intensity and frequency) seizures or their equivalents (loss or impairment of consciousness, behavioral and autonomic disorders, other) that occur periodically in different forms of epilepsy.
The mechanism of action of such drugs is not clear enough, since in most cases the etiology of epilepsy is unknown. One of the possible mechanisms is a reduction in neuronal excitability in the epileptogenic focus. However, most antiepileptic drugs have a predominantly inhibitory effect on the spread of the pathological impulses.
It is likely that the primary reactions, underlying the mechanism of action of the antiepileptic drugs, occur on the level of neuronal membranes. There is evidence that some antiepileptic drugs block sodium channels (phenytoin, carbamazepine), and others - activate GABA system (phenobarbital, benzodiazepines, sodium valproate). It has also been shown that the blockade of T-type calcium channels is one of the mechanisms leading to the reduction in seizure activity. Ethosuximide, trimethadione and partly, valproate act via this mechanism. Drugs that suppress the stimulating effect of the glutamatergic system, are also of interest. Blockers of different subtypes of glutamate receptors (topiramate) and drugs that reduce glutamate release from the presynaptic terminals (for example, lamotrigine) are very useful. Each of these groups is characterized by a certain range of antiepileptic action.
Inhibition of synaptic transmission by antiepileptic drugs can be related both to inhibition of neuronal excitation and to intensification of inhibitory effects (for example, from inhibitory neurons' stimulation).
There are several convulsive and non-convulsive forms of epilepsy, each one of which is characterized by a special clinical presentation and certain changes in the EEG (the latter has especially high diagnostic significance). There are grand mal1