Another broad perspective on the result of focal damage in the basal ganglia was afforded by Bhatia and Marsden, who reviewed 240 cases based on CT and MRI in which there were lesions in the caudate, putamen, and globus pallidus associated with movement abnormalities. Dystonia was the most common finding, and chorea and parkinsonism were infrequent. It was also notable that a common associated behavioral abnormality was abulia (apathy and loss of initiative), in those with caudate lesions. The deficiencies of this type of case analysis (i.e., the crudeness of early imaging studies obtained without regard to the temporal aspects of the clinical disorder), conceded by the authors, are obvious. We nonetheless find it surprising that choreoathetosis was not more frequent. Needed are detailed anatomic (postmortem) studies of cases in which the disturbances of function were stable for many months or years. However, restating the comments above, there is no consistent association between any type of movement disorder and a particular location in the basal ganglia.
As a prelude to the next section, Table 4-3 summarizes the clinicopathologic correlations of extrapyramidal movement disorders that are accepted by most neurologists; it must be emphasized, however, that there is still some uncertainty as to the finer details.
In broad terms, all motor disorders consist of functional deficits (or negative symptoms) and conversely, excessive motor activity (positive symptoms), the latter being ascribed to the release or disinhibition of the activity of undamaged parts of the motor system. When diseases of the basal ganglia are analyzed along these lines, bradykinesia, hypokinesia, and loss of normal postural reflexes stand out as the primary negative symptoms, and tremor, rigidity, and the involuntary dyskinetic movements of chorea, athetosis, ballismus and dystonia, as the positive ones. Disorders of phonation, articulation, and locomotion due to basal ganglia disease are more difficult to classify. In some instances this group of signs is clearly a consequence of rigidity and postural disorders, whereas in others, where rigidity is slight or negligible, they seem to represent primary deficiencies. The changes in gait related to diseases of the basal ganglia are the result of both fundamental alterations in tone and posture as well as disruption of the more inherent control of walking by the extrapyramidal system. Psychological stress and anxiety generally worsen the abnormal movements in extrapyramidal syndromes, just as relaxation improves them. A role for the basal ganglia in cognitive function and abnormal behavior is hinted at provocatively in Parkinson disease, progressive supranuclear palsy, Tourette syndrome, and other processes, as summarized by Ring and Serra-Mestres. Slowness in thinking (bradyphrenia) in some of these disorders was alluded to earlier, but is inconsistent. Again, it would be an oversimplification to assign primary importance to the presence of depression, dementia, psychosis, and other disturbances in disease of the basal ganglia or to view changes in these structures as proximate causes of obsessive-compulsive and other behavioral disorders; rather, a role as part of a larger circuitry is likely. All that can be stated is that the basal ganglia modulate complex behavior, but the precise nature of their effect is not known at this time.