Basal Ganglia and Movement Disorders | Neurology

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Basal Ganglia and Movement Disorders | Neurology

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The basal ganglia are organized to facilitate voluntary movements and to inhibit competing movements that might interfere with the desired movement. Dysfunction of these circuits can lead to movement disorders that are characterized by impaired voluntary movement, the presence of involuntary movements, or both. Current models of basal ganglia function and dysfunction have played an important role in advancing knowledge about the pathophysiology of movement disorders, but they have not contained elements sufficiently specific to allow for understanding the fundamental differences among different involuntary movements, including chorea, dystonia, and tics. A new model is presented here, building on existing models and data to encompass hypotheses of the fundamental pathophysiologic mechanisms underlying chorea, dystonia, and tics.

During the past 15 years, there has been substantial progress in understanding the pathophysiology of movement disorders related to basal ganglia dysfunction. Much of this progress can be attributed to the influential hypotheses of Albin et al1 and DeLong.2 If the success of a model is measured by the amount of research it stimulates, these schemes have been extraordinarily successful. In simple terms, these models propose that hypokinetic movement disorders (eg, parkinsonism) can be distinguished from hyperkinetic movement disorders (eg, chorea and dystonia) based on the magnitude and pattern of the basal ganglia output neurons in the globus pallidus pars interna (GPi) and substantia nigra pars reticulata (SNpr).3 Basal ganglia output neurons inhibit the motor thalamus and the midbrain extrapyramidal area; their role has been proposed to be analogous to a braking mechanism such that increased activity inhibits and decreased activity facilitates motor pattern generators in the cerebral cortex and brainstem.4 The inputs to the GPi and SNpr from the striatum and subthalamic nucleus (STN) are organized anatomically and physiologically such that the striatum provides a specific, focused, context-dependent inhibition, while the STN provides a less specific, divergent excitation. Because the output from the GPi and SNpr is inhibitory, this organization translates to a focused facilitation and surround inhibition of motor mechanisms in thalamocortical and brainstem circuits. The function of this organization is to selectively facilitate desired movements and to inhibit potentially competing movements.
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