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Physiology of epilepsia partialis continua and subcortical mechanisms of status epilepticus

Epilepsia partialis continua (EPC), a continuous seizure type (Engel and International League Against Epilepsy (ILAE), 2001), was defined by Obeso et al. (1985) as ‘‘Spontaneous regular or irregular clonic twitching of cerebral cortical origin, sometimes aggravated by action or sensory stimuli, confined to one part of the body, and continuing for hours, days or weeks.’’ Cockerell et al. (1996), however, used the less restrictive definition of ‘‘Continuous muscle jerks of cortical origin,’’ which no longer implied a constant expression of jerks in a fixed somatic area, and highlighted the reflex component in relation to the aggravating role of action or sensory stimuli. Biraben and Chauvel (1997) maintained that the definition of EPC should be restricted to local and elementary motor signs, whether or not associated with spreading seizures. However, the notion of epileptic discharges that remain restricted to a narrow cortical—or corticothalamic—sector, without propagation, over a long period of time, is now challenged by descriptions of disorders characterized by continuous rhythmic muscle jerks, arising from abnormal excitation involving extensive areas of the sensorimotor cortex (Guerrini et al., 1996; Grosse et al., 2003). We will see in brief the main conditions that may be accompanied by EPC and what is known about the pathophysiology of EPC, and we will try to formulate a comprehensive definition of EPC.