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  • Updated 11.21.2020
  • Released 04.04.2001
  • Expires For CME 11.21.2023

Basal ganglia: functional anatomy and neuropharmacology

Introduction

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. 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

Although the basal ganglia was first recognized in the 17th century by English anatomist Thomas Willis, our current view of the associated circuitry started evolving in the 1950s. The models for the “direct and indirect pathways” emerged in the 1990s, and our understanding of the basal ganglia pathways have built upon, expanded, and challenged this perspective. This understanding has been challenging because disorders associated with basal ganglia pathology have 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. Observations from experiments in nonhuman primates using transneuronal tracing with the use of neurotropic viruses, such as rabies virus, have also contributed to the understanding of basal ganglia circuitry. 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 (172).

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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