[Involuntary movements caused by basal ganglia-disorders and their age dependency: introductory remarks].
The basal ganglia modulate voluntary movements involving the neural circuit of the cortex-basal ganglia-thalamus-cortex. The basal ganglia receive all of the afferents at the striatum and project the efferents from two output structures, the medial segment of the globus pallidus and pars reticulata of the substantia nigra. Besides the cortex, the basal ganglia receive inputs from pars compacta of the substantia nigra (SNc) and centromedian nuclei of the thalamus. The afferent from the SNc is the nigrostriatal (NS) dopamine (DA) neuron and has important roles in functional modulation of the basal ganglia. As for efferents, the basal ganglia also have output projections to the superior colliculus and pedunculo-pontine nuclei. In the basal ganglia, the striatum has two efferent pathways; one is the direct projection which projects directly to the output structure and the other is the indirect pathway which projects to the output structures via the lateral segment of the globus pallidus and the subthalamic nuclei, changing synapses at these nuclei. The lesions in the basal ganglia show various movement disorders or involuntary movements depending on their foci. Basal ganglia lesions also develop symptoms age dependently; a certain lesion develops dystonia in younger brains, while revealing parkinsonism in adult or older brains. This age dependency depends on the difference in the course of the functional maturation of each component and pathway of the basal ganglia. At this symposium we tried to show the basic pathophysiologies of age dependency by discussing basal ganglia disorders in children compared to those in adults and referring to the basic science of the basal ganglia.
Segawa
M
M
Segawa Neurological Clinic for Children, Tokyo.
D000328:Adult; D000367:Age Factors; D001480:Basal Ganglia Diseases / Q000150:complications*; D002648:Child; D002675:Child, Preschool; D006801:Humans; D009069:Movement Disorders / Q000209:etiology*