Malfunctions of the basal ganglia cause movement disorders, such as Parkinson's disease and dystonia. Several models have been proposed to explain the pathophysiology of these disorders: (1) firing rate model: activity imbalance between the direct and indirect pathways changes the mean firing rates of the output nuclei of the basal ganglia and induces hypokinetic or hyperkinetic movement disorders; (2) firing pattern model: oscillatory and/or synchronized activity observed in the diseased basal ganglia disturbs information processing in the basal ganglia, resulting in motor symptoms; (3) dynamic activity model: abnormal neuronal modulations through the hyperdirect, direct and indirect pathways interfere with the sequential, dynamic activity changes, and disrupt the balance between the movement-related inhibition and its surrounding excitation in the output nuclei, leading to motor symptoms. In this mini-review, we will critically discuss the three models.
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Nambu et al. (2014) studied this question.
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