Since the first descriptions at the end of the last century of a ‘peculiar form of cortical epilepsy’ (Kojewnikow, 1895), there has been much written about what we now term epilepsia partialis continua (EPC). This initial description of ‘localized continuous clonic jerks’, intermingled in these cases with more typical spreading focal motor seizures of the Jacksonian type (Taylor, 1931), has been followed by numerous other case reports and series. There has been much debate concerning the most appropriate definition, and what pathophysiological mechanisms under-lie this particular movement disorder. Now, over a century later, although much progress has been made, there are still many unanswered questions. This chapter will start by considering the definition and mechanisms underlying EPC, followed by a review of the current clinical literature in terms of etiologies, diagnosis, prognosis and treatment.
EPC is undoubtedly rare. The only study from which epidemiological data can be inferred is that of Cockerell et al. (1996), which identified 40 cases in the United Kingdom over a 1-year period. This suggests an estimated minimum prevalence of less than 1 in a million, so most neurologists will have little if any clinical experience of the condition. The most frequent cause of EPC is Rasmussen's encephalitis (Rasmussen et al., 1958; Andermann, 1991), accounting for 20–50% of EPC cases and predominantly affecting children (Dereux, 1955; Lohler & Peters, 1974; Cockerell et al., 1996).