Petit mal epilepsy and parkinsonian tremor: hypothesis of a common pacemaker

Abstract

Rhythmic oscillation in neuronal systems may serve physiological purposes or may interfere with normal functions of the brain. In disorders of petit mal epilepsy and parkinsonian tremor, centrally and peripherally observable rhythmic patterns are due to network oscillations of thalamocortical cells. This article reviews the afferent mechanisms that might be critically involved in controlling the ionic conductances of thalamic neurons in the behaving organism. We propose that during active behavior the subcortical aminergic and cholinergic inputs to the thalamus act as anti-burst and anti-oscillation mechanisms. We suggest further that the thalamopetal GABAergic inputs (pars reticulata of substantia nigra, entopeduncular nucleus, pallidum) are burst- and oscillation-promoting systems, whose output is controlled by the striatum. Experimental or disease-related decrease of the striatal dopamine levels is hypothesized to increase the efficacy of the GABAergic burst-promoting systems resulting in rhythmic network oscillation of thalamocortical neurons during rest. The recognition of the overlapping neuronal mechanisms in petit mal epilepsy and parkinsonian tremor, and the multistage control of thalamic oscillation suggests that drugs effectively used in petit mal attacks may be effective in levodopa-refractory parkinsonian tremor, and conversely, epileptic patients may benefit from drugs acting on the extrapyramidal system.