Motor skills in motor disorders: measuring performance changes in tracking and other perceptual-motor tasks.
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Biomedical subjects
Publications and source records attributed to K A Flowers.
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A wide variety of perceptual impairments have been reported in patients with Parkinson's disease (PD) in recent years; the underlying causes of these impairments have been variously attributed to different levels of the visual-cognitive system, from the retina to frontal cortex. Parkinsonian perceptual abnormalities could thus be interpreted as indirectly caused either by 'bottom-up' effects, stemming from dopaminergic dysfunction in the retina, or by 'top-down' effects, stemming from deficits in attention due to disturbances in the striatal-frontal system. Alternatively, a direct visuospatial impairment, perhaps related to the motor symptoms, has been considered. Data on three basic aspects of visual perception (3-D stereo vision, figure-ground discrimination, and pattern perception) which might be expected to give difficulty to PD subjects suffering changes in early processing mechanisms are reported. Visual complexity and the degree of mental manipulation of the material required both varied in different parts of the tests. PD patients were on stable drug regimens. It was found that disease severity interacted with performance: patients with mild PD showed little perceptual abnormality, patients with moderate PD showed only top-down effects, and patients with severe PD showed evidence both of top-down and of bottom-up deficits. Thus it appears that any retinal effects on perception in PD occur only in the advanced stages of the disease; in earlier stages any visual dysfunction probably reflects top-down disturbances from higher levels of the cognitive-behavioural system.
When making discrete aiming movements, patients with Parkinson's disease show greater inherent variability in the endpoints of their movements than do normal subjects. Endpoint variability can be reduced, by moving more slowly, by utilizing visual guidance, and by making small amplitude movements. The greater variability of patients is not a universal finding, but depends on the conditions of movement. For small movements the performance of patients equates to that of controls. For larger movements the results indicate that if sufficient time is available, patients can use visual guidance (if available) to reduce the variability of their movements to the level of normals. Patients can generate fast and/or large amplitude arm movements if required, but they are erratic if made in the dark or over a short duration. Their difficulty lies not so much in the magnitude of muscle force available to them, but rather in an inability to produce it consistently for any given movement attempted. Bradykinesia may in part result from this inherent variability in that parkinsonian patients, in order to maintain accuracy within acceptable limits, are forced to increase the duration of their movements to a level where they can make use of visual guidance. In any event, theoretical explanations for the movement disorder in Parkinson's disease advanced in the literature need to take some account of this increased variability of movement.
Three experiments employing a five-choice button-pressing task tested the ability of Parkinsonian patients to learn and generate sequences of movement, and to switch between alternative sequences at will. It was found that patients could learn and generate individual patterns of movement normally, even complex ones involving an incompatible stimulus-response relationship. They had difficulty, however, in maintaining a sequence if two different ones had been learnt and subjects were required to switch spontaneously from one to the other within a trial. Providing external cues at the start of each sequence to guide the ordering of movements improved the stability of patients' performance. Most errors in sequencing consisted of reverting to the alternative pattern of movement. Parkinsonian subjects thus show an impairment in motor set similar to that found previously in cognitive activity.
Programming and execution of arm movements in Parkinson's disease were investigated in choice and simple reaction time (RT) situations in which subjects made aimed movements at a target. A no-aiming condition was also studied. Reaction time was fractionated using surface EMG recording into premotor (central) and motor (peripheral) components. Premotor RT was found to be greater for parkinsonian patients than normal age-matched controls in the simple RT condition, but not in the choice condition. This effect did not depend on the parameters of the impending movement. Thus, paradoxically, parkinsonian patients were not inherently slower at initiating aiming movements from the starting position, but seemed unable to use advance information concerning motor task demands to speed up movement initiation. For both groups, low velocity movements took longer to initiate than high velocity ones. In the no-aiming condition parkinsonian RTs were markedly shorter than when aiming, but were still significantly longer than control RTs. Motor RT was constant across all conditions and was not different for patient and control subjects. In all conditions, parkinsonian movements were around 37% slower than control movements, and their movement times were more variable, the differences showing up early on in the movement, that is, during the initial ballistic phase. The within-subject variability of movement endpoints was also greater in patients. The motor dysfunction displayed in Parkinson's disease involves a number of components: (1) a basic central problem with simply initiating movements, even when minimal programming is required (no-aiming condition); (2) difficulty in maintaining computed forces for motor programs over time (simple RT condition); (3) a basic slowness of movement (bradykinesia) in all conditions; and (4) increased variability of movement in both time and space, presumably caused by inherent variability in force production.
In two experiments with an Odd-Man-Out choice discrimination task, Parkinsonian subjects had difficulty in alternating between two rules on successive trials. The pattern of errors suggested that the difficulty arises from an instability of cognitive set rather than any loss of reasoning ability, perseveration or increased distractibility.
On four tests of visual recognition memory Parkinsonian patients obtained normal scores, both immediately and after a delay. They also resembled controls closely in nearly all characteristics of memory. Their performance did not correlate with age, motor disability or disease duration. Parkinson's disease does not, therefore, affect this kind of memory.
Four parkinsonian patients who had shown evidence of an impairment of predictive manual control and 4 age-matched normal subjects were tested for the predictive control of eye movements. Subjects tracked a target with their eyes as it moved in either irregular "noise" or regular (predictable) linear ramp or sine waveforms. Eye movements were monitored by electrooculography, and the overall tracking time lag for each condition was determined by cross-correlation. Both normal and parkinsonian subjects showed prediction in eye tracking on the regular waveforms (zero time lag or anticipation of the target track), indicating that (1) the parkinsonian loss of predictive control in manual tasks is not due to defective control of eye movements, and (2) there may be separate predictor mechanisms in the brain for eyes and hands.
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Normal voluntary movements are considered to be of two kinds, or to involve two components, (i) a ballistic or "open-loop" type, which are preprogrammed and executed without reference to current sensory information and (ii) a corrective or "closed-loop" type, whose course or termination are regulated by such information. In a previous paper it was suggested that Parkinsonism disrupted the first kind of movement, but intention tremor did not. In the present paper three experiments designed to test this hypothesis are described. Subjects were tested on an acquisition-tracking task using an oscilloscope display and joystick control, and measurements were made of the duration, velocity and error of their initial movements to acquire the target. Parkinsonian movements were found to be considerably different from normal in that (a) most movements by this group lasted longer than the reaction time for their initiation, as if including some secondary correction in their execution, (b) the rate of movement was not varied for different amplitudes (so keeping the duration fairly constant) as in normal subjects, but rather movements of all amplitudes were made at a constant slow rate, so that duration increased markedly with the larger steps, (c) error increased disproportionately as the velocity of movement increased; in particular any movements completed in one reaction time or less tended to be wildly inaccurate, (d) removing either the target or the response marker from the screen at the beginning of a movement had a significant effect, making it shorter in duration and smaller in amplitude than those usually produced with both markers visible all the time. Parkinsonian subjects showed no improvement in performance with repeated attempts at one movement over a whole sequence, so their deficit appears to be stable even after practice on a known fixed task. These results are interpreted as supporting the hypothesis that Parkinsonism interferes with the generation of accurate ballistic action which are characteristic of normal skilled movement. Tremor subjects in general resembled normal control subjects in their initial acquistion movements, but their accuracy was less with the larger steps.