A NEURAL MODEL OF BASAL GANGLIA-THALAMOCORTICAL RELATIONS IN NORMAL AND PARKINSONIAN MOVEMENT

Anatomical, neurophysiological, and neurochemical evidence supports th e notion of parallel basal ganglia-thalamocortical motor systems. We d eveloped a neural network model for the functioning of these systems d uring normal and parkinsonian movement. Parkinson's disease (PD), whic h results predominantly from nigrostriatal pathway damage, is used as a window to examine basal ganglia function. Simulations of dopamine de pletion produce motor impairments consistent with motor deficits obser ved in PD that suggest the basal ganglia play a role in motor initiati on and execution, and sequencing of motor programs. Stereotaxic lesion s in the model's globus pallidus and subthalamic nucleus suggest that these lesions, although reducing some PD symptoms, may constrain the r epertoire of available movements. It is proposed that paradoxical obse rvations of basal ganglia responses reported in the literature may res ult from regional functional neuronal specialization, and the non-unif orm distributions of neurochemicals in the basal ganglia. It is hypoth esized that dopamine depletion produces smaller-than-normal pallidotha lamic gating signals that prevent rescalability of these signals to co ntrol variable movement speed, and that in PD can produce smaller-than -normal movement amplitudes.