Motor Functions and Movement Programs

Given the motor symptoms of Huntington's and Parkinson's diseases and the major involvement of the basal ganglia in these disorders, the involvement of the basal ganglia in movement has been taken for granted. Huntington's disease is an autosomal-dominant genetic disorder characterized by choreiform movements (i.e., involuntary movements that resemble segments of voluntary movements). In the early stages of Huntington's disease, cell loss is obvious in the head of the caudate nucleus, but as the disease progresses cell loss becomes obvious in other parts of the basal ganglia and in the cerebral cortex, most conspicuously in the frontal lobe. Dopamine antagonists have been used to treat symptoms of Hunting-ton's disease. Hemiballismus is also a disorder in which abnormal involuntary movements occur on one side of the body. Ballism represents the more forceful, or violent, form of involuntary movement. Discrete lesions of the subthalamic nucleus cause hemiballis-mus. Parkinson's disease is characterized by resting tremors, difficulty or slowness in initiating voluntary movements (bradykinesia), rigidity, and gait disturbance. Parkinson's disease is caused by loss of midbrain dopamine neurons (the pars compacta of the substantia nigra and the ventral tegmental area), particularly those projecting to the motor portions of the striatum. Theoretical explanations of the involvement of the basal ganglia in movement as far back as Bucy's (1942) paper attempt to explain the symptoms of one or more of these disorders by involvement of the basal ganglia motor loops.

Because of the involvement of the striatum and the subthalamic nucleus in disorders exhibiting involuntary movements (Huntington's disease and hemibal-lismus, respectively), the indirect basal ganglia loop involving projections from the striatum to the lateral globus pallidus, from the lateral globus pallidus to the subthalamic nucleus, and from the subthalamic nucleus to the medial globus pallidus has frequently been assigned the function of suppressing unwanted movements. One interesting facet of Huntington's versus Parkinson's disease is that the effects of the former can be mitigated with dopamine antagonists, whereas the effects of the latter can be mitigated with a dopamine precursor. These differences in response to dopami-nergic agents, as well as the differences in motor symptoms (involuntary movements in Huntington's disease and bradykinesia in Parkinson's disease), have been related to the different phenomena affecting the indirect loop. The loss of striatal neurons influencing the indirect loop in the case of Huntington's disease prevents this loop from suppressing unwanted movements. The loss of inhibitory effects of dopamine on striatal neurons projecting into the indirect loop is purported to cause so much suppression of movement in the case of Parkinson's disease that it is difficult to switch to new movements. Rigidity in both Hunting-ton's and Parkinson's diseases has been related to effects on the direct loop (loss of striatal neurons projecting to the medial globus pallidus in Hunting-ton's disease and loss of dopaminergic excitation of these same neurons in Parkinson's disease). In their seminal 1986 work, Penny and Young gave detailed treatment to these differences.

In a recent review, Jueptner and Weiller described their work regarding functional neuroimaging of the basal ganglia and cerebellum. They concluded that the basal ganglia are involved in the selection of movements, whereas the cerebellum processes sensory information and integrates it with movement. The concept of movement selection is consistent with the suggestion that the basal ganglia enhance desired movements while suppressing unwanted movements.

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