Introduction

Epileptic activity involving the sensorimotor cortex can be associated with a wide spectrum of motor manifestations, such as clonic or tonic phenomena, paresis (Penfield & Jasper, 1954; Fisher, 1978; Globus et al., 1982; Tinuper et al., 1987; Lee & Lerner, 1990; Primavera et al., 1993; So, 1995), epileptic negative myoclonus (Tassinari, 1981; Guerrini et al., 1993; Tassinari et al., 1995; Noachtar et al., 1997), apraxia (Neville & Boyd, 1995; Maquet et al., 1995), ataxia (Bennett et al., 1982; Dalla Bernardina et al., 1989), and motor neglect (Galletti et al., 1992; Guerrini et al., 1993). Neurophysiological investigations and, more recently, functional imaging studies have provided a growing amount of data that have proved extremely useful for diagnostic purposes and for pathophysiological speculations. However, the understanding of the mechanisms underlying the different clinical events associated with paroxysmal activity in the sensorimotor cortex is still incomplete. Excitatory or disinhibitory neuronal mechanisms as well as hypersynchronous inhibitory phenomena may play a role (Engel, 1995), as suggested by the finding that ‘interictal’ spike-and-wave discharges (SW) involving a specific cortical area can disrupt its physiological functions (Shewmon & Erwin, 1988a, b, c; 1989).

In the present chapter, we will focus on those types of motor dysfunction resulting from epileptic activity in the sensorimotor cortex, characterized clinically by an altered execution of a motor task or by the inability to perform it, such as epileptic negative myoclonus (ENM), partial atonic seizures (PAS), and syndromes resulting from frequent paroxysmal activity in the sensorimotor cortex.