Epilepsy: some epidemiological aspects

The epilepsies have been subject to effective chemical control for a good half century longer than the functional psychoses. Phenobarbitone, which was preceded by over 50 years by bromides, came into use in 1913, dilantin in 1938. Perhaps this early advent of successful pharmacological control of the epilepsies, as compared with that of the functional psychoses, damped epidemiological research into the subject. We venture that there is less epidemiological knowledge about the distribution and aetiology of the epilepsies than about the psychoses. This neglect of the epidemiology of seizure disorders has left fallow a most intriguing psychiatric issue, namely, the association of temporal lobe epilepsy with psychiatric disorders, and with schizophrenia in particular. We shall concern ourselves here with the more general epidemiological background of the epilepsies. Anticonvulsants permit the control of seizures in 60-80% of epileptic patients (Rodin, 1972). After a 20-year follow-up, some 70 % of patients have been found free of seizures for 5 years (Annegers et al. 1979). Still, as a recent review in this journal suggested, long-term use of anticonvulsants may produce mental deterioration (Trimble & Reynolds, 1976). Experiments on preweanling and postweanling rats also suggest, alarmingly, that phenobarbitone given during the brain growth spurt, or even during the subsequent deceleration, retards brain growth and disturbs behaviour (Diaz et al. 1977; Diaz & Schain, 1977). In addition, many persons with seizures go undiagnosed and untreated or improperly medicated. A recent report has drawn attention to under-medication and overmedication that is widespread and substantial in certain institutionalized settings (Murphy & D'Souza, 1977). Primary prevention is surely what we must aim for in the long run an aim which can only be achieved by a search for causes. This goal is ambitious. At present, about 70 % of seizures identified in population surveys are ascribed to unknown causes (Hauser, 1978). Even this figure is an underestimate, since the environmental and genetic 'causes' often cited are best treated as hypothetical rather than established. The search for causes begins with a quest for variations in the frequency of the disorder. Since 1950, at least 36 surveys whether concerned exclusively with seizure disorders in particular or with neurological disorders in general have been conducted in various settings around the world (see bibliography). Fourteen of these deal exclusively with infants and children. Worldwide, the reported incidence rates of the epilepsies for all ages combined range from 0-173 per 1000 in Niigata City, Japan (Sato, 1964) to 1 per 1000 in Australia (Crombie et al. 1960). Within England itself, the reported rates vary from 0-30 per 1000 in Carlisle (Brewis et al. 1966) to 0-73 per 1000 in 14 general practices in southeast England (Pond et al. 1960). Prevalence rates for all ages combined range from 1-50 per 1000, again in Niigata City, Japan (Sato, 1964), to 20 per 1000 among the Wapogoro tribe in Tanzania (Jilek & Jilek-Aall, 1970). In England, prevalence rates have varied from 3-33 (Logan & Cushion, 1958) to 7-90 per 1000 (Pond et al. 1960). For many conditions true variation of this order is not beyond the limits of credibility, but the data to hand for the epilepsies conflate the contributions of research methods and those of morbidity. Studies employ non-comparable definitions, a variety of ways of finding and ascertaining cases, and different measures of frequency. At one extreme, Hauser & Kurland (1975) restrict epilepsy to recurrent seizures occurring in the absence of identifiable cause. At the other extreme, Gudmundsson (1966) includes isolated afebrile seizures, and Pond et al. (1960) include febrile seizures as well. Inclusion of isolated and/or febrile seizures can inflate estimates of incidence or prevalence anywhere from 1-7 (Hauser & Kurland, 1975) to 37 times (Lessell et al. 1962). Most surveys rely on medical