New PDF release: Anticonvulsants

By Julius A. Vida (Eds.)

ISBN-10: 0127218408

ISBN-13: 9780127218403

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Phenylethylmalonamide has a half-life of about 40 hours in epileptic patients, and on the basis of animal studies it is a weak anticonvulsant that has the capacity to potentiate the anticonvulsant activity of phénobarbital in concentrations that have no other demonstrable activity (Gallagher and Baumel, 1972). , 1973). The oxidation of primidone to phénobarbital occurs with an enzyme system localized in hepatic microsomes which has all the characteristics of the mixed-function oxidase enzyme system.

These polar metabolites of phénobarbital are excreted by the kidney as such or may be conjugated to glucuronate or sulfate prior to excretion. Phénobarbital is a potent inducing agent for the mixed function oxidase enzyme system, and this forms the basis for some important drug interactions. It should be remembered that most epileptic patients have been exposed to large amounts of various anticonvulsant drugs for many years and may be maximally induced. Consequently, induction is not seen consistently when drugs having this property are administered.

This type of inhibition is unaffected by phenytoin. When multiple interneurons are involved in the inhibitory pathway, the inhibition is polysynaptic. When inhibition originates from axon collaterals of motoneurons synapsing on interneurons called Renshaw cells, which in turn synapse on the same or adjacent motoneurons, it is called recurrent postsynaptic inhibition. In low doses phénobarbital augments monosynaptic responses, and this may be related to a depression of polysynaptic inhibition. The benzodiazepines do not affect postsynaptic inhibition.

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Anticonvulsants by Julius A. Vida (Eds.)


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