Basal ganglia structure and function

Basal Ganglia

The control of motor movement progresses from mastery of gross movement to fine motor control as humans develop (Wilson, 2013). This progression depends on the maturation of the extrapyramidal motor system, followed by the maturation of the pyramidal motor system. The extrapyramidal motor system incorporates multiple areas of the brain that are involved in controlling gross motor movements, including the cerebellum and basal ganglia. The cerebellum functions to coordinate muscle movement in response to sensory stimuli generated by muscles, tendons, the reticular formation, and the vestibular system. By comparison, the role of the basal ganglia in regulating muscle movement is still being investigated. In general terms, the basal ganglia serve as an information relay center for various centers within the cerebral cortex; however, researchers seem to agree that one of the functions of the basal ganglia is to inhibit muscle movements before they can begin.

Researchers have also found evidence to support a role for the basal ganglia in regulating diverse cognitive functions, including procedural memory, habit formation, skill learning, attention, perception, language, planning, syllogistic reasoning, and solving math problems (Stocco, Lebiere, and Anderson, 2010). This essay will examine the many roles of the basal ganglia as revealed through disease etiology, symptomology, and treatments.

Disorders of the Basal Ganglia

A number of disorders can develop when the basal ganglia are injured or diseased. The heritable disease Huntington's is believed to be caused by elevated dopamine activity in the basal ganglia, resulting in involuntary muscle movement (Wilson, 2013). This is consistent with the theory that the basal ganglia are involved in controlling muscle movements before they start. There is no cure for Huntington's, but during the early stages of the disease antipsychotic medications that lower dopamine levels have proven beneficial. Drugs that impact the glutaminergic and gabanergic neurotransmitter systems are currently being tested by researchers for the ability to control symptoms during later stages of the disease.

Consistent with a cognitive role separate from motor control, patients with Huntinton's disease are unable to adapt to wearing prism goggles (reviewed by Stocco, Lebiere, and Anderson, 2010). The inability to acquire complex sensorimotor skills like this reveals a deficit in nondeclaritive memory. Additional support comes the finding that Huntington's patients are unable to unconsciously learn a hidden sequence during a probabilistic classification task. Deficits in the ability to access different forms of working memory have also been found.

Parkinson's disease is a disorder linked to the destruction of dopaminergic neurons in the substantia nigra within the basal ganglia (Wilson, 2013). The symptoms, based on the above theory, would therefore result in too much control of motor movements. The symptoms of Parkinson's include muscle tremor, unsteadiness, loss of balance, and in more advanced stages of disease muscle rigidity and incomplete muscle movements. Possible causes include environmental toxins, such as street drugs, pesticides, and first generation antipsychotics. The only accepted treatment for early stage disease is L-dopa, which is a dopamine precursor capable of crossing the blood-brain barrier. Unfortunately, the side-effects can be debilitating and its use is therefore limited and no treatment currently exists for the more advanced stages of disease.

Parkinson's patients reveal cognitive deficits similar to those found in patients with Huntington's disease (reviewed by Stocco, Lebiere, and Anderson, 2010). These include nondeclaritive and working memory deficits, although L-dopa administration can improve working memory. When Parkinson's patients with mild to moderate disease were challenged with a probabilistic category task, they performed significantly worse than healthy controls (Shohamy, Myers, Onlaor, and Gluck, 2004). Performance improved over time for both patients and controls, but patients always performed worse in the task; however, on the first of three days of testing the difference was not statistically significant. The authors discovered that the learning strategies employed by patients and controls were essentially the same on the first day, but only the controls began to rely on a more complex strategy during the next two days of testing. Parkinson's patients were therefore unable to acquire a multi-cue strategy required for optimal performance on the task and continued to rely on a single-cue strategy.