From the internal pallidum, two bundles of fibers reach the thalamus—the ansa lenticularis and the fasciculus lenticularis. The ansa sweeps around the internal capsule; the fasciculus traverses the internal capsule in a number of small fascicles and then continues medially and caudally to join the ansa in the prerubral field. Both of these fiber bundles join the thalamic fasciculus, which then contains not only the pallidothalamic projections but also mesothalamic, rubrothalamic, and dentatothalamic ones. These projections are directed to separate targets in the ventrolateral nucleus of the thalamus and to a lesser extent in the ventral anterior and intralaminar thalamic nuclei. The centromedian nucleus of the intralaminar group projects back to the putamen and, via the parafascicular nucleus, to the caudate. A major projection from the ventral thalamic nuclei to the ipsilateral premotor cortex completes the large cortical–striatal–pallidal–thalamic–cortical motor loop, with conservation of the somatotopic arrangement of motor fibers, again emphasizing the nexus of motor control at the thalamic nuclei.
Newer observations have made it apparent that there are a number of parallel basal ganglionic–cortical circuits. These circuits run parallel to the premotor pathway but remain separate anatomically and physiologically. At least five such anatomic connections have been described, each projecting to different portions of the frontal lobe: (1) the prototypical motor circuit, converging on the premotor cortex; (2) the ocular motor circuit, projecting onto the frontal eye fields; two prefrontal circuits: (3) one ending in the dorsolateral prefrontal and (4) the other on the lateral orbitofrontal cortex; and (5) a limbic circuit that projects to the anterior cingulate and medial orbitofrontal cortex.
An additional and essential feature of basal ganglionic structure is the nonequivalence of all parts of the striatum. Particular cell types and zones of cells within this structure appear to mediate different aspects of motor control and to utilize specific neurochemical transmitters, as detailed below under “Pharmacologic Considerations” (see also Albin et al and DeLong). This specialization has taken on further importance with the observation that specific cell types are destroyed preferentially in degenerative diseases such as Huntington chorea.
In simplest physiologic terms, Denny-Brown and Yanagisawa, who studied the effects of ablation of individual extrapyramidal structures in monkeys, concluded that the basal ganglia function as a kind of clearinghouse where, during an intended or projected movement, one set of activities is facilitated and all other unnecessary ones are suppressed. They used the analogy of the basal ganglia as a brake or switch, the tonic inhibitory (“brake”) action preventing target structures from generating unwanted motor activity and the “switch” function referring to the capacity of the basal ganglia to select which of many available motor programs will be active at any given time. Still other theoretical constructs focus on the role of the basal ganglia in the initiation, sequencing, and modulation of motor activity (“motor programming”). Also, it appears that the basal ganglia participate in the constant priming of the motor system, enabling the rapid execution of motor acts without premeditation—for example, hitting a baseball. In most ways, these conceptualizations restate the same notions of balance and selectivity imparted to all motor actions by the basal ganglia.