12. The Basal Ganglia
Revised August 8, 2007
The objectives of this chapter are to:
- Describe basal ganglia anatomy and blood supply.
- Describe the pathways through which the basal ganglia affect motor function.
I. BASAL GANGLIA ANATOMY
A group of brain nuclei are known collectively as the basal ganglia (fig 12a). The basal ganglia that are studied in this chapter are the caudate nucleus (#4766), the putamen (#4752), the globus pallidus (#4753), the subthalamic nucleus (#4809), and the substantia nigra (#4810). The motor components of the basal ganglia make up the extrapyramidal motor system, a term that is sometimes still used clinically.
Diseases of the basal ganglia cause movement disorders. Movement disorders are diseases characterized by hypokinesia (inhibition of intentional movement) and/or hyperkinesia (abnormal involuntary movements such as tremor and writhing movements). Basal ganglia diseases include such well-known diseases as Parkinson's disease (hypokinetic) (video) and Huntington's disease (hyperkinetic) (video). However, not all movement disorders are due to dysfunction of the basal ganglia.
An axial (horizontal) section offers a panoramic view of the general shapes and relations of the caudate nucleus, putamen, and globus pallidus with each other and with the lateral ventricle and internal capsule (fig 12b). A coronal view through the frontal horn shows the relationships of the head of the caudate (#6475) and the anterior part of the putamen (#6474) to the anterior limb of the internal capsule and the frontal horn. Note that the head of the caudate nucleus bulges into the frontal horn of the lateral ventricle (#6475).
The putamen and caudate nucleus are developmentally a single nuclear mass that is divided by the internal capsule, but with gray matter bridges still connecting them (#6428, fig 12d). Because of this appearance, the putamen and caudate nucleus together are known as the dorsal striatum ("striped"). In Huntington's disease, atrophy of the striatum causes flattening of the caudate nucleus where it bulges into the lateral ventricle (#5686).
The putamen and globus pallidus together are known as the lentiform nucleus (lenticular nucleus) (#6297). This name was given to them because of their lens shape as seen in axial (horizontal) sections.
II. BASAL GANGLIA PATHWAYS
The principal source of striatal afferents is the cerebral cortex. The sensorimotor cortex (#4323) projects primarily to the putamen. What is the course of these ipsilateral corticostriate fibers? Other significant striatal afferents come from the substantia nigra, pars compacta, which is the pigmented part of the substantia nigra (#5256). Degeneration of these of these dopamine-containing nigrostriatal axons is linked to the genesis of Parkinson's disease (#5523), in which degeneration of the cell bodies leads to loss of pigmentation of the substantia nigra (#41958).
The putamen and the caudate nucleus send most of their axons, respectively, to the globus pallidus (dorsal pallidum) and the substantia nigra, pars reticulata (the non-pigmented part of the substantia nigra). The globus pallidus has an internal segment and an external segment, fig 12e, and focuses its activity on two areas: (A) It projects to the thalamus (#6594), and (B) It has reciprocal connections with the subthalamic nucleus (#6496).
A. Pallidal projections to the thalamus
To reach the thalamus, the pallidothalamic fibers have to get from one side of the internal capsule to the other.
[They either go directly across the capsule or swing under it. The axons that penetrate the capsule form the fasciculus lenticularis (#8310). The axons that go around it are known as the ansa lenticularis (#4639, fig 12e). These axons are named "lenticularis" because the pallidum and putamen together are known as the lentiform nucleus, as noted above. This name was given to them because of their lens shape as seen in horizontal sections (#6297).]
The chief destination of the pallidothalamic fibers that influence movement is the anterior part of the ventral lateral nucleus (VLa) of the thalamus (#6491), also called the ventral oral nucleus (VO) in humans. The pallidal efferents end in a different (anterior) part of VL than the fibers from the cerebellum.
VLa sends axons through the internal capsule primarily to the supplementary motor area (fig 12f), which is on the medial surface of the frontal lobe rostral (anterior) to the paracentral lobule . The supplementary motor area is interconnected with Brodmann's area 4 (the precentral gyrus (#4321) and the adjacent anterior part of the paracentral lobule). In this way, the basal ganglia affect the activity of the corticospinal tract (#42050). Surgical lesions of the thalamus are sometimes made to ameliorate movement disorders. If the movement disorder is on the right side of the body, which side of the thalamus would be the surgical target?
B. Pallidal connections with the subthalamic nucleus
The globus pallidus (#8395) and subthalamic nucleus (#8405) are reciprocally connected. Lesions of the subthalamic nucleus, usually due to vascular disease, produce rapid, ballistic movements of the opposite side of the body (hemiballismus ). Why is the opposite side affected? What is meant by the term "disinhibition"?
III. BLOOD SUPPLY TO THE BASAL GANGLIA
The blood supply to the basal ganglia comes primarily from the middle cerebral artery (#4796), in particular, the lenticulostriate branches, seen on a postmortem frontal angiogram in #9811, and as small holes in a gross horizontal specimen in #5631. These narrow lenticulostriate vessels are a frequent site of cerebral hemorrhage in people with uncontrolled hypertension. Such events can be fatal (#10865). Small infarcts produced by occlusion of these small vessels are called lacunar infarcts (lacunes) and may be asymptomatic, discovered incidentally at autopsy (#11219) or on CT or MRI. However, lacunes in the basal ganglia may cause movement disorders.
- Hemiballismus from vascular accident
- Hemichorea from moyamoya a rare progressive vascular disorder involving the basal ganglia
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