The first surgical attempts to treat tremor and athetosis took place at the end of the 19th century when Horsley removed parts of the motor cortex. This stopped the abnormal movements but invariably caused weakness. It was not until several decades later, when attention was turned to the basal ganglia, that ablative surgeries in various deep nuclei were able to relieve tremor and rigidity without injuring the corticospinal tract and without causing weakness.
Today, movement disorders are understood to result from pathologies involving the basal ganglia and extrapyramidal pathways. Functional loops between the basal ganglia nuclei (the striatum, globus pallidus, substantia nigra, and subthalamic nucleus [STN]) carefully coordinate the appropriate agonist-antagonist balance in the execution of movement. The basal ganglia connect to the thalamus and the motor cortex, which are the primary sensorimotor integrator and the executor of motor activity, respectively. The basal ganglia–thalamocortical circuit, which includes the well-known direct and indirect striatopallidal pathways, helps us understand the functional changes that underlie clinical expressions of various movement pathologies.1,2
Miocinovic S. Beyond the Basal Ganglia: Cortical Effects of Deep Brain Stimulation. JAMA Neurol. 2014;71(1):8–10. doi:10.1001/jamaneurol.2013.4643
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