Abstract
Insights into the structure and function of the basal ganglia and their role in the pathophysiology of movement disorders resulted in the 1980s in the development of testable models of hypokinetic and hyperkinetic movement disorders. Further refinement in the 1990s resulted from continued research in animal models and the addition of physiological recordings of neuronal activity in humans undergoing functional neurosurgical procedures (1–7). These models have gained considerable practical value, guiding the development of new pharmacologic and surgical treatments, but, in their current form, more and more insufficiencies of these simplified schemes are becoming apparent. In the following chapter we discuss both models, as well as some of the most important criticisms.
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References
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Wichmann, T., Vitek, J.L. (2003). Physiology of the Basal Ganglia and Pathophysiology of Movement Disorders. In: Tarsy, D., Vitek, J.L., Lozano, A.M. (eds) Surgical Treatment of Parkinson’s Disease and Other Movement Disorders. Current Clinical Neurology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-312-5_1
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