[Treatment of epilepsy: where are we today?]

The modern treatment of epilepsy has improved considerably in all three pillars. More than a century has passed, however, since Sir Charles Locock introduced the bromides in 1857 and Sir Victor Horsely pioneered epilepsy surgery in 1886 (18). In drug therapy, the 'classic AED' of the last decades, i.e. phenobarbital (Hauptmann, 1912) and phenytoin (Putnam and Merrit, 1938) are being largely displaced by valproate (Meunir, 1963) and carbamazepine (Lorge, 1963). Only ethosuximide (Zimmermann, 1951) has continued to maintain its position in 3/s spikewave-absence epilepsy, in particular in the USA (28, 29). Although it is an excellent drug against absences, it has the unpleasant property that it may induce GM seizures and should therefore be combined with a so-called 'GM protector' (mostly phenobarbital). For this reason ethosuximide has been relegated to second place in Europe by valproate. Thus, the decision as to which AED should be employed at the outset has been simplified considerably: actually, with valproate as the drug of first choice, which displays a very broad spectrum of action, we are on the right track for virtually all forms of epilepsy, perhaps with the exception of focal epilepsy (11). Especially in the event of focal epilepsy of temporal origin we employ carbamazepine as the preparation of first choice. In some countries (Denmark), because of the less severe side effects, oxcarbazepine is already preferred (Mogens Dam, personal communication). Considerable experience and knowledge are still required, however, when resistance has developed to traditionally applied classic monotherapy. Here, the range of further treatment can also be greatly extended by the availability of the 'new AED'. A generally accepted protocol for the replacement of one preparation with another first- or second-choice drug and, above all, for the 'right' combination with third-choice preparations can as yet not be compiled. What we need here is the expert epileptologist who has experience with 'theoretically useful' combinations and has an insight into the interactions occurring with such combinations. For several specific epileptic syndromes the 'Königsteiner Working Group of German-Speaking Epileptologists' has given clear and binding recommendations for AED therapy (e.g. for benign juvenile myoclonic epilepsy--Janz syndrome). This working group has also made recommendations for the necessary clinical and laboratory controls in AED therapy with potentially severe side effects (e.g. valproate therapy in high-risk children), which were published and/or are being published and discussed in the 'Epilepsie-Blätter' of the German League against Epilepsy (4). Despite all advances in drug therapy, the number of epilepsy patients not satisfactorily treatable with drug therapy has not been dramatically reduced statistically, so that the other two pillars of epilepsy therapy, i.e. epileptic surgery and behavioural therapy, continue to be very important.