This study tested the hypothesis that the slowing seen in parkinsonism includes cognitive as well as motoric components. The sample consisted of 20 nondemented parkinsonian patients, group matched to 16 normals by age, education, and verbal IQ. Each group was divided into young (64 and under) and old (65 and over) subsets. The Sternberg character classification paradigm was used to measure the speed and accuracy of one cognitive function, short term memory scanning. Following a logarithmic transformation of the reaction time data, scanning speed was found to be increased, but only for the elderly patients (p = .01). Scanning accuracy was normal for both patient groups. These findings suggest that at least one cognitive function, the scanning of elements held in short term memory, is slowed in parkinsonism. This mnemonic slowing, like bradykinesia, is seen primarily in elderly parkinsonian patients. It is not readily explained as a motor phenomenon, as part of a generalized mnemonic or intellectual deficit, or as an artifact secondary to periodic extreme reaction times. The term bradyphrenia, used in early descriptions of parkinsonism, may be an apt descriptor of this deficit.

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A theory is proposed suggesting that 2 separate striatal nerve cell populations exist, one dopamine facilitated and one dopamine inhibited. The abnormal movements in Huntington’s chorea are due to an exaggerated or altered facilitatory effect of normal amounts of dopamine acting upon altered striatal neurons.

Acquired hepatocerebral degeneration (AHCD) is a well-defined clinical and neuropathological entity associated with various types of chronic liver disease, and usually related to portal-systemic shunting. Various movement disorders, including choreoathetosis, are commonly seen in AHCD. The frequent neuropathological finding of neuronal degeneration in the striatum (caudate nuclei and putamens) suggested that choreoathetotic movements in AHCD might be caused by dopamine hypersensitivity in striatal receptor sites and that treatment of such movement disorders might be effected by known striatal dopamine-blocking agents of proven benefit in similar movement disorders, e. g. Huntington’s chorea. A patient with documented post-necrotic cirrhosis and portal hypertension who had had a successful portacaval shunt developed signs of AHCD with choreoathetotic movements of the tongue, face, and mouth (linguo-facio-buccal dyskinesia); he was treated with haloperidol, a striatal dopamine-blocking agent, with prompt and sustained cessation of his dyskinesia. Evidence of a normal baseline central dopamine content and of central dopamine blockade after administration of haloperidol was obtained. The implications of these findings and of similar findings in other movement disorders regarding the role of neuro-transmitting agents in the normal individual and in various disease states are discussed, and therapeutic considerations are presented.