The basal ganglia and cerebellum are large collections of nuclei that modify movement on a minute-to-minute basis. Motor cortex sends information to both, and both structures send information right back to cortex via the thalamus. (Remember, to get to cortex you must go through thalamus.) The output of the cerebellum is excitatory, while the basal ganglia are inhibitory. The balance between these two systems allows for smooth, coordinated movement, and a disturbance in either system will show up as movement disorders.

A. The basal ganglia:

What are the basal ganglia? The name is confusing, as generally a ganglion is a collection of cell bodies outside the central nervous system. Blame the early anatomists. The basal ganglia are a collection of nuclei deep to the white matter of cerebral cortex. The name includes: caudate, putamen, nucleus accumbens, globus pallidus, substantia nigra, subthalamic nucleus, and historically the claustrum and the amygdala. However, the claustrum and the amygdala do not really deal with movement, nor are they interconnected with the rest of the basal ganglia, so they have been dropped from this section. Other groupings you may hear are the striatum (caudate + putamen + nucleus accumbens), the corpus striatum (striatum + globus pallidus), or the lenticular nucleus (putamen + globus pallidus), but these groupings obviously get confusing very quickly, so we will try to avoid them.

The anatomy of these structures should be a review from the "coronal and horizontal sections" lab. Here once again are the basal ganglia as they appear when stained for myelin:

rostral section:

middle section:

caudal section:

An alternate stain is the acetylcholinesterase (AChE) stain. This technique stains for the enzyme that degrades acetylcholine (ACh), a major neurotransmitter. Areas which use ACh generally stain darkly. Here is a section through monkey brain, stained for AChE.

You can see that the caudate and putamen are stained, while the globus pallidus remains fairly pale. This emphasizes their different functions and connections. And those are...?

B. Different functions and connections:

The relationships between the nuclei of the basal ganglia are by no means completely understood. When dealing with the brain, you may sometimes be tempted to think that everything is connected to everything else. Take heart, some fairly simple generalizations and schematics can be drawn.

The caudate and putamen receive most of the input from cerebral cortex; in this sense they are the doorway into the basal ganglia. There are some regional differences: for example, medial caudate and nucleus accumbens receive their input from frontal cortex and limbic areas, and are implicated more in thinking and schizophrenia than in moving and motion disorders. The caudate and putamen are reciprocally interconnected with the substantia nigra, but send most of their output to the globus pallidus (see diagram below).

The substantia nigra can be divided into two parts: the substantia nigra pars compacta (SNpc) and the substantia nigra pars reticulata (SNpr). The SNpc receives input from the caudate and putamen, and sends information right back. The SNpr also receives input from the caudate and putamen, but sends it outside the basal ganglia to control head and eye movements. The SNpc is the more famous of the two, as it produces dopamine, which is critical for normal movement. The SNpc degenerates in Parkinson's disease, but the condition can be treated by giving oral dopamine precursors.

The globus pallidus can also be divided into two parts: the globus pallidus externa (GPe) and the globus pallidus interna (GPi). Both receive input from the caudate and putamen, and both are in communication with the subthalamic nucleus. It is the GPi, however, that sends the major inhibitory output from the basal ganglia back to thalamus. The GPi also sends a few projections to an area of midbrain (the PPPA), presumably to assist in postural control.

This schematic summarizes the connections of the basal ganglia as described above.

Although there are many different neurotransmitters used within the basal ganglia (principally ACh, GABA, and dopamine), the overall effect on thalamus is inhibitory. The function of the basal ganglia is often described in terms of a "brake hypothesis". To sit still, you must put the brakes on all movements except those reflexes that maintain an upright posture. To move, you must apply a brake to some postural reflexes, and release the brake on voluntary movement. In such a complicated system, it is apparent that small disturbances can throw the whole system out of whack, often in unpredictable ways. The deficits tend to fall into one of two categories: the presence of extraneous unwanted movements or an absence or difficulty with intended movements.

C. Lesions of the basal ganglia:

Lesions in specific nuclei tend to produce characteristic deficits. One well-known disorder is Parkinson's disease, which is the slow and steady loss of dopaminergic neurons in SNpc. An instant Parkinson-like syndrome will result if these neurons are damaged. This happened several years ago to an unfortunate group of people who took some home-brewed Demerol in search of a high. It was contaminated by a very nasty byproduct, MPTP ,which selectively zapped the SNpc neurons. The three symptoms usually associated with Parkinson's are tremor, rigidity, and bradykinesia. The tremor is most apparent at rest. Rigidity is a result of simultaneous contraction of flexors and extensors, which tends to lock up the limbs. Bradykinesia, or "slow movement", is a difficulty initiating voluntary movement, as though the brake cannot be released.

Huntington's disease, or chorea, is a hereditary disease of unwanted movements