Abstract

The thalamus, the normal function of which is the relay and control of information flow from the periphery to the cortex (Jones, 1985), has been implicated in the pathogenesis of generalized seizures, particularly the seizures classified as typical absence or petit mal. Thalamic nuclei possess the ability to generate and maintain certain normal rhythms, including the EEG synchronized activity seen during sleep (see Steriade and Llinas, 1988). This property may predispose the thalamus to participate in the generation of abnormal rhythms as well, especially the 3-Hz spike-and-wave (SW) activity seen in petit mal. For example, in children afflicted with petit mal epilepsy, SW occurs with highest frequency during spindle-stage sleep (Kellaway, 1985). Involvement of the thalamus in SW generation has been documented by depth-electrode recording during petit mal seizures that show that thalamic SW discharges may precede those at cortical sites (Spiegel and Wycis, 1950; Williams, 1953). Further evidence supporting the role of the thalamus in the genesis of SW activity comes from the animal models that have been used to study petit mal. For example, in feline generalized penicillin epilepsy (reviewed by Gloor, 1984), SW is observed in both the cortex and thalamus but not at either site when these structures are isolated from one another. In the genetically prone rat model, SW activity is also seen in the thalamus (Vergnes et al., 1987). Whether thalamic activity is responsible for the initiation of such abnormal discharge remains controversial; however, in this genetic model, the leading SW component is sometimes observed within thalamic nuclei, and SW may even appear in the thalamus in isolation (Vergnes et al., 1987). The reverse seems to be true in the feline model of generalized penicillin epilepsy (see Gloor and Fariello, 1988), in which cortical activity may precede thalamic involvement.

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