Advances in the Understanding of Neural Mechanisms in Movement Disorders
Relatively little is known about how various primary pathologies within the basal ganglia manifest themselves in the appearance of movement disorders. For example, both Parkinson’s disease and Huntington’s disease are characterised by dysfunction of the striatum. In the case of Parkinson’s disease, loss of the ascending dopamine systems results in disordered striatal activity, whereas in Huntington’s disease, parts of the striatum degenerate. It is implicitly assumed that the abnormal movements result from the disordered striatal activity acting on lower motor centres, presumably via the intermediary of the thalamus and its connections with the cortex. However, the pathophysiological processes by which the abnormal striatal output acts upon the intervening basal ganglia nuclei are yet to be defined. In an attempt to address these issues we have developed primate models of a spectrum of movement disorders and then attempted to both elucidate the neural circuitry which is responsible for mediating them and to define the underlying characteristic changes in neural activity in each of the affected basal ganglia nuclei.
KeywordsTardive Dyskinesia Excitatory Amino Acid Globus Pallidus Subthalamic Nucleus Kynurenic Acid
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