Basal ganglia: functional anatomy and neuropharmacology

Brent Bluett DO (Dr. Bluett of the Cleveland Clinic Nevada Lou Ruvo Center for Brain Health has no relevant financial relationships to disclose.)
Ryan R Walsh MD PhD (Dr. Walsh of Lou Ruvo Center for Brain Health and Lerner College of Medicine of Case Western Reserve University received a consulting fee from Lundbeck.)
Joseph Jankovic MD, editor. (Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, received research funding from Allergan, Allon, Ceregene, Chelsea, EMD Serono, Impax, Ipsen, Lundbeck, Medtronic, Merz, and Teva, and compensation for his services as a consultant or an advisory committee member by Allergan, Auspex, EMD Serono, Lundbeck, Merz, Neurocrine Biosciences, and Teva.)
Originally released April 4, 2001; last updated November 5, 2015; expires November 5, 2018

Overview

The authors describe the functional anatomy of the basal ganglia, with an emphasis on extensions of the standard “rate” model that have evolved recently. They also describe basal ganglia physiology including changes observed in pathologic states, highlighting Parkinson disease in particular. Finally, potential mechanisms of basal ganglia function and dysfunction are discussed.

Key points

 

• The basal ganglia are a set of subcortical gray matter structures historically associated with motor function but that also are involved in critical cognitive and limbic functions.

 

• Emerging evidence suggests that the functional anatomy of the basal ganglia may not be fully accounted for in the standard “rate” model.

 

• Parkinson disease is characterized by consistent changes in basal ganglia physiology, including changes in firing rates, firing patterns, synchronization, and oscillatory activity. Changes in other disease states are less well characterized but evident.

 

• Advances in functional imaging and deep brain stimulation continue to improve our understanding of basal ganglia networks.

 

• Despite much progress, a comprehensive model of basal ganglia function that fully explains its normal and pathologic function remains elusive.

Historical note and terminology

Disorders associated with basal ganglia pathology historically presented a puzzle for conventional clinicopathologic correlations. Unlike other CNS subsystems, such as the cerebellum and its connections where motor deficits are often similar regardless of the anatomic locus of pathologies, lesions of distinct basal ganglia subregions cause qualitatively different clinical syndromes. The best example is the contrast between the paucity of spontaneous movement associated with parkinsonism and the excess involuntary movements associated with the chorea-athetosis-ballism spectrum. Some crude correlations based on gross pathology were possible (Table 1), but an integrated understanding of the bases for the diverse phenomena associated with basal ganglia pathology is continuing to emerge.

Many investigators have contributed to an improved understanding of the basal ganglia. Particularly important in the context of understanding the bases for the phenomenology of common movement disorders are: considerably improved understanding of basal ganglia anatomy and physiology, good animal models of parkinsonism, and a large body of clinical research. Electrophysiological studies of patients undergoing deep brain stimulation for treatment of movement disorders, and advances in diffusion tensor imaging are valuable adjuncts to basic science investigations of basal ganglia physiology.

Table 1. Localization of Pathology within the Basal Ganglia

Clinical phenomenon

Localization

Chorea-athetosis-ballism
Parkinson disease
Dystonia

Striatum or subthalamic nucleus
Substantia nigra-nigrostriatal projection
Pallidum

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