ABSTRACT
It has long been observed that diseases of the basal ganglia result in disorders of
movement, both hypo- and hyperkinetic. An understanding of the anatomy, physiology,
and neurochemistry of the component structures of the basal ganglia has greatly facilitated
our understanding of control of movement in both health and disease. The direct-indirect
pathway model developed in the late 1980s described two parallel channels of neuronal
information converging to influence the output nuclei of the basal ganglia. According
to this model, alterations in levels of excitation or inhibition produce changes in
the absolute level of neuronal activity in the target structures and can be used to
explain a number of observations from both laboratory and clinical settings. This
model greatly aided our understanding of basal ganglia function and has contributed
to the development of new therapies for movement disorders. However, there are a number
of findings which are not satisfactorily explained, and a higher level of complexity
of basal ganglia function is clearly implicated. Additional anatomically defined projections
may serve as internal autoregulatory loops connecting external pathways. These are
taken into account in a recently developed model and may help elucidate some of the
contradictory evidence from both laboratory experiments and clinical results of neurosurgical
interventions.
KEYWORD
Basal ganglia - models - movement disorders
