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Neuropsychological data collected from two groups of patients with idiopathic Parkinson's disease (n = 50, 159) were analysed to investigate the association between presenting motor symptoms determined from retrospective chart review and the risk of cognitive impairment. Presenting motor symptoms were abstracted from the medical records and coded by type, location, and laterality. Longitudinal data on changes in the maximum speed of voluntary arm movements were available for a subsample of patients. Bilateral (v unilateral) presentation was associated with an increased risk of cognitive impairment an average of nine years after onset of disease as measured by memory tests and the mini-mental state examination. A higher rate of decline of arm movement speed was also predictive of greater memory dysfunction. The type, side (left v right), and location (lower v upper extremity) of the presenting symptoms were not, however, consistently associated with the risk of cognitive impairment later in the course of the disease.

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Sixty patients with Parkinson's disease were administered a battery of neuropsychological tests. Using regression data from a matched normal control sample, age- and education-residualized test scores were obtained for the patients. Three clusters of patients were identified: those with both verbal memory and visuospatial reasoning disorders (n = 24), those with memory impairment only (n = 17) and those with normal intellectual function (n = 12). Analysis of variance and planned comparisons (Newman-Keuls) were performed to detect group differences. No difference on 9 memory measures were found between the 2 memory-impaired groups. However, these groups differed significantly on all memory measures from the group with normal function. The 2 memory-impaired groups also differed significantly from each other on all 7 measures of visuospatial reasoning. The group with memory loss only was significantly younger than the group with both visuospatial and memory impairment and also demonstrated less bradykinesia. Otherwise, there were no group differences in the severity of motor signs, disease duration or duration of levodopa therapy. These findings support a different etiology for motor and intellectual deficits in Parkinson's disease.

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Histopathologic studies of the cerebral cortex, hippocampus, and three subcortical nuclei were performed in four patients with Parkinson's disease whose mental status had been evaluated by neuropsychologic testing. Clinicopathologic correlations suggest that dementia with marked visuospatial disturbance as well as severe aphasia may be associated with severe neuronal loss in subcortical nuclei, without significant numbers of plaques or tangles in the hippocampus and cerebral cortex. Furthermore, memory loss may not be consistently related to neuronal loss in the nucleus basalis of Meynert, particularly in non-Lewy body parkinsonism.

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The outcomes of two different 12-week exercise programs were assessed by machine measurements of motor signs, tests of grip strength, motor coordination and speed, and neurophysiologic determinations of long-latency stretch responses in two groups of Parkinson patients matched for age, sex and stage of disease. The programs tested included an exercise program developed by the United Parkinson Foundation and a program of upper body karate training. Outcomes of these programs were similar. The majority of patients in both groups showed improvements in gait, tremor, grip strength and motor coordination on tasks requiring fine control. In one task involving whole body coordination there was a decline in function, while muscle rigidity was unchanged. The findings suggest that exercise is a useful adjunct to pharmacologic therapy.

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We studied 60 patients with idiopathic Parkinson disease with motor and neuropsychologic tests to ascertain whether the severity of motor symptoms was associated with the degree of neuropsychologic deficity. Significant correlations were found between the severity of brady kinesia and impaired performance on tests assessing visual-spatial reasoning and psychomotor speed. More severe tremor was associated with better performance on a spatial orientation memory test. There relationships remained when age, age at onset, and self-rated depression were controlled. The findings suggested that cognitive impairment may result from the same subcortical lesions that cause motor symptoms.

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An extensive set of neuropsychological measures was administered to 60 Parkinson's disease patients and age-, sex-, and education-matched controls in order to investigate the nature and prevalence of the cognitive deficit in the disease. Parkinsonian patients performed significantly poorer on all measures with the exception of tests for apraxia and object recognition, and on a test of vocabulary knowledge. Discriminant analysis of the test data revealed that over 93% of patients are impaired relative to matched controls, but that assigning a prevalence rate for dementia in the disease may be difficult due to the continuous distribution of cognitive deficits.

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Experiments were performed in 18 normal subjects to estimate the time course of changes in the gains of pathways mediating short- and long-latency responses to muscle stretch during the transition from a maintained posture against a steady load to a rapid ballistic movement. Subjects were instructed to rapidly flex or extend their forearm in response to a tone from an initial position of 90 degree of elbow flexion. Torque pulses stretching the biceps muscle were applied to the forearm at 8 different times before and after the signal to initiate the movement, and the gains of short- and long-latency pathways were estimated from averages of rectified biceps EMG activity for 20 trials at each time interval between the onsets of the tone and torque pulse. The findings demonstrate that changes in the magnitude of long-latency responses (M2, M3) occur during the period between the onset of the auditory signal and the voluntary motor response. However, the magnitude of the short-latency response (M1) remains unchanged until after the onset of voluntary motor activity. The differences in the timing of short- and long-latency stretch responses suggests that activity in long-latency pathways may play an important preparatory role in facilitating the transition from posture to movement.

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Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.

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A method for measuring head tremor and rotation in spasmodic torticollis using specially devised instrument is described in detail. Repeated measurements in ten patients with spasmodic torticollis have revealed this method to be consistently reproducible regarding both the rotation and tremor of the head. Analysis of the tremor recordings from these patients reveals basically two types of head tremor, (a) a regular tremor varying in rate from 4 to 7 cycles per second and (b) an irregular tremor which varies in frequency as well as amplitude at different times of recording. This method provides quantitative data regarding the two outstanding features of spasmodic torticollis, viz: head rotation and head tremor, and is especially suited for comparing clinical response to various forms of treatment as well as studying the natural history of this disease.

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