This is a general survey of the question, to which extent clinical biochemistry can contribute to an understanding of epileptic symptomatology. The subject will be subdivided into two main items: (i) epilepsy in general; (ii) myoclonus epilepsy (Unverricht-Lundborg's disease).
EPILEPSY IN GENERALThe pertinent literature comprises reports on biochemical changes in naturally occurring human epilepsy as well as in convulsive conditions experimentally induced by one of the various techniques.Many of these studies provide extremely controversial information. Some results have never been confirmed and stand as isolated observations. Thus, Rieder (30) andMall (23) have tested body fluids from epileptic patients for the possible presence of toxic substances which could modify the formation of cobwebs. Elliott (9) has studied alterations in the guanidine content of the serum and Altea (1) has investigated the lecithinolytic activity of serum.This type of study essentially aimed at ascribing epileptic seizures to a toxic factor. Other authors (5,22,29) have searched for abnormalities in the carbohydrate metabolism but the results are not unequivocal. This is also true for observations on the cholesterol content of the serum (29), for urinary excretion of sulphates (25,26), for studies on acetylcholine and cholinesterase (4, 5, 24) and for the investigations of Ferroni and Indovina (22) concerning copper in the blood.The following discussion, however, will be limited to studies on electrolyte metabolism, protein metabolism and amino-acid metabolism, because these seem to be the only ones which have provided useful information. It should be stressed, however, that this information offers no definite solution to the problem raised.
Electrolyte distributionUnder this heading we will discuss various reports concerning the distribution of