Specific Mechanisms of Selected Anticonvulsants

The specific mechanism of actions by which certain selected anticonvulsants dicussed in this chapter are enumerated below  

It is found to exert its action on the motor cortex where it stabilizes the neuronal membrane and thereby inhibits the spread of the seizure discharge. Present evidence also suggests that it limits high frequency repititive firing by blocking Na -channels in a use and frequency dependent fashion. Besides, it enhances Ca- binding to the phospholipids present in neuronal membranes. 

In fact, these effects collectively give rise to a more stable membrane configuration. Importantly, these critical findings are found to be in perfect harmony with the glaring and supportive fact that its most easily demonstrated characteristic features are by virtue of its ability to limit the development of maximal seizure activity and also to minimize the virtual extension of the seizure phenomenon from the active focus. Interestingly, both of these splendid features in phenytoin are very much related to the clinical usefulness beyond any reasonable doubt. 

It is N-dealkylated and /)flra-hydroxylated in vivo. However, the N-dealkyl metabolite is most presumably the active compound it is similarly metabolized by ara-hydroxylation, and the resulting hydroxyl function undergoes conjugation subsequently. 

This particular drug substance is used against not-so-specific seizures, but invariably on an adjunctive basis on account of its low potency. In a broader perspective, such anticonvulsants which are not completely branched on the appropriate C-atom are of definite lower potency than their rather more fully-branched structural analogues. 

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