1991; 71:60-67.PHYS THER. George E Stelmach and James G PhillipsGanglia

Limb Movement and the Basal−−Movement Disorders

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Movement Science Series

Movement Disorders-Limb Movement and the Basal Ganglia

The primay concern of this article is to review experimental methods that may lead to a better understanding of the functional role of the basal ganglia in the control of movement. Two models of basal ganglia impaimzent are considered, Parkinson's disease and Huntington's disease. The review focuses primarily on akinesia and bradykinesia because they are key abnormalities of basal ganglia dysfunction. In general, through electromyography and kinematic analysis of movement, it may be possible to characterize specific movement disorders. Specifi- cally, if damage sustained by the central nervous system is traced to a certain structure, it may provide insight on the extent of involvement and functional role of that structure in the control of mouement. Much of the data reviewed suggests that the basal ganglia may play a specific role in the initiation and regulation of force control. [Stelmach GE, Phillips JG. Mouementdisorders: limb movement and the basal ganglia. Phys Ther. 1991; 71:60-67.]

Key Words: Basal ganglia; Huntington chorea; Kinesiologylbiomechanics, gen- eral; Movement control; Parkinson disease.

Movement Disorders and Motor Control

One method of attaining inferences about the role of a brain structure in the control of movement is the associ- ation of that structure with impair- ments of function. Such association may take place through brain imag- ing' or pharmacologically.2 For exam- ple, in Huntington's disease, there is enhanced activity in the dopaminergic system,' whereas in Parkinson's dis- ease, there is a loss of dopaminergic cells in the substantia nigra, such that

patients respond to dopamine ago- nists therapy.2 However, inferences about basal ganglia function are dif- ficult to interpret because the basal ganglia mediate between higher and lower brain structures, receiving, for example, inputs from cortical areas and the substantia nigra and innervat- ing thalamic and midbrain nuclei.3

Damage to structures such as the basal ganglia, cerebellum, o r frontal cortex may interfere with smooth execution of movement. Deficits in functioning may indicate the role a

G Stelmach, PhD, PT, is Professor of Exercise Science, Exercise and Sport Research Institute, Psy- chobiology Section, Arizona State University, Tempe, AZ 85287 (USA). He was Director, Motor Behavior Laboratory, and Professor, Depanment of Physical Education and Dance, School of Educa- tion, University of Wisconsin-Madison, 2000 Observatory Dr, Madison, WI, when this anicle was written. Address all correspondence to Dr Stelmach.

J Phillips PhD, is Senior Tutor, Psychology Depanment, Monash University, Clayton, Victoria 3168, Australia.

George E Stelmach James G PhlllIps

structure normally plays in the con- trol of movement. Careful consider- ation, however, must be given to a number of factors before making an attempt at identification of func- tional loss.*,5 Observed disruption of function could result from any of the following: (1) natural age- related decline, (2) deficits in higher cognitive processes (eg, de- pression, dementia), (3) side effects of drug therapy (eg, dyskinesia, con- fusion), (4) biomechanical changes (eg, rigidity, body mass), and (5) deficits in the coordination of movement (eg, preparatory pro- cesses, feedback guidance). Given the number of possible causes of functional disruption, expertise is required of researchers in the areas of neurology, physiology, psychol- ogy, and experimental methodology.

This research was supported by NIH Grant NS17431.

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Assessment of Functional Loss

A number of techniques are currently used in the assessment and identifica- tion of functional losses in patients with basal ganglia impairment. Reaction-time paradigms, electromy- ography (EMG), and kinematic analy- sis may be used to examine deficits in the control of movement. Such tech- niques attempt to document how movement in patients deviates from normal movement. The assessment of functional loss, therefore, requires an understanding of normal functioning.

Reaction-time paradigms have been used to assess the preparatory pro- cesses in patients with movement disorders. In general terms, reaction- time studies can provide strong indi- cations of whether there are pre- movement abnormalities. In particular, response latencies have been used as an index of diaculty in movement preparation. Researchers reason that disproportionate difficulty in preparing movement parameters should be evident from longer re- sponse latencies."' Reaction-time par- adigms have been used to examine whether patients with movement dis- orders are slower than control sub- jects when given an opportunity to plan movements, choose among re- sponse alternatives, and use advance information.

Electromyography has been used to examine the voluntary movement of patients with a variety of movement disordersH,9 and is typically used to determine whether observed move- ment deficits are attributable to disor- dered force control (eg, scaling the magnitude and duration of EMG). Normal ballistic movement is pre- sented by a triphasic (agonist, antago- nist, agonist) pattern of muscle activ- ity." Patients with movement disorders often exhibit disruptions of this pat- tern, which, if studied, may contribute to our understanding of the brain's role in the organization of move- ment.1° For example, in comparing similar movements, patients with Par- kinson's disease require a number of cycles of agonist-antagonist activity, suggesting that the basal ganglia have

a role in facilitating movement.11~12 In contrast, patients with cerebellar defi- cits exhibit problems with the dura- tion of activity of agonist o r antagonist muscles, which suggests that pans of the cerebellum have a role in deter- mining the end points of movement.8

Electromyography has also been used to describe the involuntary move- ments of patients with various move- ment disorders.13 The involuntary movement accompanying Tourette's syndrome has been shown to have a normal triphasic pattern. The involun- tary movement seen in Huntington's disease, however, presents a variety of possible patterns of activity, ranging from tonic activation, to co-contrac- tion, to triphasic patterns of activa- tion.14 Application of EMG techniques ultimately may be useful in the differ- ential diagnosis of movement disorders.l3

Kinematic analyses may provide indi- cators of disruptions in normal motor coordination resulting from deficits in movement preparation and in muscle activation. Kinematic analysis has tended to be descriptive in its applica- tion. It permits thorough, microscopic inspection of the spatial and temporal characteristics of a movement in rela- tion to joint segments. Because it is important to establish the precise ways in which the movement trajecto- ries of patients with movement disor- ders differ from those of healthy sub- jects, indexes have been derived to describe the efficiency of movement trajectories. An optimum trajectory benveen initiation and termination of movement has only one cycle of ac- celeration and deceleration.l5 The movement of patients with Parkin- son's disease and cerebellar disorders tends to be irregular and asymmetri- cal. For example, Stelmach and Wor- ringhaml6 and Teulings and Stel- mach17 have shown that parkinsonian patients do not have precise control over their movement trajectories.

Parklnson9s Dlsease and Basal Ganglla Functlon

Parkinson's disease significantly im- pairs a patient's quality of life. Without

medication, or during on-off phases of therapy, there are dramatic incapaci- tating changes in motor control. Par- kinson's disease often produces akinetic and bradykinetic symptoms, resulting in problems performing dis- crete movements as well as sequences of rhythm. For example, handwriting tends to be slower and smaller in patients with Parkinson's disease.5 During rhythmic movement, move- ments tend to be reduced in size and/or duration, causing a hastening (festination) of movement.5

The damage associated with Parkin- son's disease tends to be localized to a loss of the dopaminergic cells in the substantia nigra that project to the basal ganglia.lH This loss disrupts basal ganglia function. Thus, Parkin- son's disease provides a model for making inferences about the motor functions of the basal ganglia. The basal ganglia are a collection of sub- cortical nuclei consisting of the cau- date, putamen, external and internal segments of the globus pallidus, sub- thalamic nucleus, and pars compacta and pars reticulata of the substantia nigra.lg

Generally, patients with Parkinson's disease initially present unilateral symptoms, but exhibit bilateral symp- toms as the disease progresses.5 Prob- lems with postural reflexes and gait arise at still later stages20 The four cardinal symptoms associated with Parkinson's disease are (1) akine- sia-a difficulty in initiation of move- ment, (2) bradykinesia-a slowness in execution of movement, (3) rigidi- ty-a resistance to the passive stretch of muscles, and (4) tremor-a trem- bling or shaking at rest of about 4 to 5.5 Hz. In addition, they have marked changes in gait and posture.

Marsden21 has suggested that positive symptoms, such as tremor and rigid- ity, are due to the loss of the inhibi- tory influences within the basal gan- glia, but reasons that basal ganglia function may best be understood through examination of the loss of function, that is, the negative symp- toms of akinesia and bradykinesia. Most of the research effort to date has

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been devoted to the study of akinesia and bradykinesia.

Research conducted at the University of Wisconsin-Madison over the past 7 years has been examining functional losses caused by Parkinson's disease. This research has focused on the symptoms of akinesia and bradykine- sia, in particular, mainly because these symptoms have provided information about basal ganglia function21 and because they are thought to be the most debilitating of the symptoms.20

Patients with Parkinson's disease have difficulty in initiating and executing movements that do not seem to be attributable to perceptual impair- ments. Stelmach and associates2' ex- amined the ability to judge distances in patients with Parkinson's disease who do not have dementia and in age-matczhed control subjects. The authors used distance-judging tasks that were systematically varied in per- ceptual and motor difficulty. They found that the patients were not af- fected by variations in the perceptual difficulty of the task, but were affected by variations in the motor require- ments of the task. Thus, the deficits observed in patients with Parkinson's disease appear to be deficits in the control of movement.

Akinesia may be caused by distur- bances in the prepamtion of move- ment. Reaction time, therefore, should be a good index of such an impair- ment. In simple reaction-time tests, because there is no response uncer- tainty, subjects have an opportunity to fully prepare the intended response. In choice reaction-time situations, this is not possible because the response is not known until the imperative stimulus is given. Thus, in contrast to simple reaction time, choice reaction time stresses the subject's ability to select among response alternatives.

Evarts et a123 found in patients with Parkinson's disease substantial delays in simple reaction time without any observed deficit in choice reaction time and interpreted these data to suggest that patients were unable to benefit from the opportunity to pre-

pare the required response. Stelrnach et a17 also found that choice reaction time was not disproportionately de- layed in parkinsonian patients, despite the fact that they clearly demonstrated that patients can use advance informa- tion. Interestingly, Pullman et a12-' re- ported that, although patients' choice reaction times were normal, they increased significantly as current L -dopa levels decreased.

Extending reaction-time paradigms, Stelmach et a17 systematically assessed the ability of patients with Parkinson's disease to prepare components of an arm movement. Patients performed a series of reactions in which precued information provided components of the upcoming movement. The pre- cued information varied between complete and partial information and permitted the patients to prepare movement dimensions such as arm or direction; arm and extent; o r arm, direction, and extent. Although pa- tients took longer than healthy con- trol subjects to prepare movements, and ultimately were slower in execut- ing them, no specific movement di- mension was disproportionately more difficult than another. Patients pre- pared movements at about the same rate as healthy subjects. That is, pa- tients with Parkinson's disease could use advance information. These data are taken as evidence that parkinson- ian patients have no deficit in move- ment planning.

Parkinsonian symptoms such as akine- sia and bradykinesia may indicate problems in accessing and/or activat- ing motor programs. Indeed, patients with Parkinson's disease exhibit defi- cits during the acquisition of skills,25,26 but also benefit from practice. The question is whether these symptoms are the result of problems in access- ing motor plans or programs such that movements cannot be performed in a sequence.

Stelmach et performed an experi- ment in which they varied the num- ber of finger taps required for a se- quence between 1 and 5. Patients with Parkinson's disease and control subjects, at the imperative signal, had

to execute 1, 2, 3, 4, o r 5 taps. This experiment was designed to deter- mine whether parkinsonian patients could program finger-tapping se- quences as well as healthy subjects. The authors observed that the control subjects' reaction time increased as the number of required taps in- creased. This was taken as evidence that the control subjects were pro- gramming the tapping sequence as a whole. In contrast, the parkinsonian patients showed no evidence of in- creasing reaction time with added finger taps. Stelmach et a1 took this finding as evidence that the parkin- sonian patients did not program the sequence as a whole. Further inspec- tion of the data yielded a surprising result: the patient group exhibited a considerable lengthening of the first intertap interval, regardless of tapping sequence. Stelmach et a1 suggested that this was evidence that parkinson- ian patients did not program the se- quence as a whole.

A subsequent experiment considered whether patients with Parkinson's dis- ease could perform more complex sequential movements.2H Patients were required to produce a sequence of taps at a fast (200 milliseconds) or slow (600 milliseconds) rate. Stress (and force) components of the se- quences were varied in simple and choice reaction-time paradigms. Both the introduction of a stressed tap and the uncertainty of its position ad- versely affected reaction time, intertap interval, and error rates. These results suggest that difficulty with sequential movements could be the result of force-control deficits. Flash2"as dem- onstrated recently that parkinsonian patients do not tend to superimpose elementary motor programs in multi- joint movements, but rather complete one movement before starting the next. The lack of ability to superim- pose elementary movement compo- nents is in line with similar observa- tions by Benecke et aljO and Shimizu et al.51

Akinesia and bradykinesia may result from force-control deficits. Stelmach and Worringhaml6 examined the pro- duction of forces during isometric

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contraction of arm muscles in patients with Parkinson's disease. Patients were required to produce forces at 25%, 50%, and 75% of the maximum force they could produce. Although patients were slow, and somewhat variable, in force production, they were as accurate as age-matched con- trols. Inspection of the forces' curves revealed that they were irregular and asymmetrical. A subsequent experi- ment considered production of these forces in more detail.32 Patients with Parkinson's disease were required to produce forces at 15%, 30%, 45%, and 60% of the maximum force they could produce. Although the patients showed accurate force production compared with age-matched controls, they took longer to reach their peak forces and exhibited very irregular time curves. This finding suggests Par- kinson's disease does not cause im- pairment in the intentional control of forces (indeed, patients intentionally compensate for their rate deficits), but in the rate of force development.

Taking a slightly different approach, Flowers33 found that aiming accuracy of ballistic movement in patients with Parkinson's disease was disrupted when visual guidance was removed. When the target could not be seen, movement speed also appeared to decrease. Judging from these results, it would seem that patients with Par- kinson's disease slow their movement to make use of visual feedback. In further support of this view, Inzelberg et aP4 found that although arm move- ments, with vision, followed a straight path in healthy subjects, they under- went multiple time-consuming correc- tions in patients with Parkinson's disease. Thus, it appears that parkin- sonian patients are highly dependent on visual feedback.

Force-control deficits may also be understood by considering how par- kinsonian movement deviates from optimum movement trajectories. A variety of indexes are available to bet- ter describe movement trajectories. Stelmach and associates32 used a mea- sure of smoothness and economy of movement15 to characterize move- ment trajectories in patients with Par-

kinson's disease. An examination of the change of sign in the second de- rivative of force gave an indication of the number of changes in the rate of force production. Whereas healthy subjects produced near-optimal forces, patients with Parkinson's dis- ease showed considerably more jerki- ness in their force production. Sheri- dan et a135 summarized the Parkinson's disease motor problem as difficulty in maintaining a computed force, difficulty in initiating a force, and a difficulty of increased variability in time and space.

Teulings and Stelmach" considered the regularity, relative to the variabil- ity, of features of parkinsonian pa- tients' handwriting movement trajecto- ries. They used signal-to-noise-ratio (SNR) analyses to indicate the effi- ciency of the control of aspects of movement trajectories. The SNR ex- presses the ratio between the amount of modulation attributable to the in- variant, programmed component (sig- nal) and the amount of modulation attributable to the impairment (noise). Thus, the SNR is high if a movement pattern is reproduced ac- curately and low if a pattern is vari- able because of motor impairment. This experiment explicitly raised the question of whether patients with Par- kinson's disease had impairments in force amplitude or force duration.

Force amplitude refers to the strength of the force and force duration to the control of force initiation and cessa- tion. It was found in patients with mi- crographia that handwriting was more impaired in terms of force amplitude than in terms of force duration. This impairment is suggested to be located at the level of motor unit recruitment. Phillips et aP6 provide a slightly dif- ferent view, that slowness of hand- writing movements in patients with Parkinson's disease may be explained partially by temporal characteristics of muscle-force changes and, to a lesser degree, by low-level force amplitude problems. They also reasoned that the impaired force amplitude may con- tribute to a deliberate compensatory behavior for movement duration.

Movement sequencing provides an- other task variable to explore parkin- sonian dysfunction. Stelmach et a122 showed, as previously reported in this article, that patients with Parkinson's disease have difficulty producing alter- ations of force within a movement sequence. When patients had to pro- duce a stress tap in a sequence of finger taps, they tended to break the tapping sequence at the point of the stress tap. Regardless of where in the sequence the stress (additional force) occurred, the intertap interval after the stress tap was disproportionately lengthened. Parkinsonian patients' force pulses were also more irregular than those of healthy subjects and not well sustained.16.37.3" known se- quencing problem in patients with Parkinson's disease is the "hastening phenomenon" reported by Nagasaki and Nakamura.39 Parkinsonian patients exhibited hastening of movement when tapping at frequencies of 2.5 or 5 Hz. As the predominant frequencies in handwriting are close to 5 Hz,40 such a hastening effect could cause problems in parkinsonian patients trying to write at normal speeds. Freund4' found in patients with Par- kinson's disease that serial hand movements faster than 2 Hz are pos- sible only if they are synchronized with the tremor. This is similar to the hastening phenomenon and is suggested to lead to disturbances of handwriting.

Benecke et a130 and Goldenberg et a142 found that sequential movements in patients with Parkinson's disease are executed slower than when exe- cuted in isolation. The second move- ment part especially is slowed, and pauses between the first and second movement parts are increased. Even more difficulty is experienced when patients with Parkinson's disease at- tempt to superimpose two separate motor pr0grams.30~31 This difficulty could relate to two-joint ballistic movements (eg, movements required to draw triangles and squares of dif- ferent sizes and shapes), in which a larger number of EMG bursts are ob- served in patients with Parkinson's disease than in control subjects.43

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Electromyography demonstrates that muscle activation is not optimal in patients with Parkinson's disease.12 The issue then is whether the number of bursts (peripheral control) or size of burst (central control) is impaired. For healthy subjects, movements about a single joint are known to be made via a single biphasic or triphasic burst of EMG activity. Movements of longer alnplitude have been shown to be produced by EMG patterns of in- creasing amplitude and duration. Hal- lett and Khoshbinl1 suggest that movements in patients with Parkin- son's disease are slow and irregular because of difficulty in activating mus- cles, suc1-1 that more cycles of muscle activity are required to produce a movement. In particular, they suggest that patients with Parkinson's disease require Inore bursts of muscle activi- ties to PI-oduce faster or longer move- ments. Although this is quite a plausi- ble explanation for the observed slowness and irregularity in move- ment, it tends to suggest that impair- ment occurs at a peripheral level, such thal: the size of bursts of muscle activity cannot be appropriately scaled for a required movement.

The issue of muscle activity has also been addressed by Berardelli and associates44 and Teasdale and associ- ates.12 Berardelli et aP4 examined muscle activity in parkinsonian pa- tients' movements of differing extents (wrist movements of 15" and 60"). They found that size of agonist bursts increased in a normal fashion with extent of movement, although the bursts were not scaled to meet task demands. This finding indicates that the size of bursts in muscle activity can increase in patients with Parkin- son's disease. Teasdale et all2 exam- ined parkinsonian patients' muscle activity during production of arm movements of differing durations through an angle of 20 degrees. In addition to moving their arm at a self- determined speed, they were asked to move their arm 10% faster, 30% slower, and 60% slower. The results showed that patients with Parkinson's disease were slower than control sub- jects and that they could vary their speed as requested. The results also

demonstrated that irregularities were present as the movement speed var- ied and that more bursts of muscle activity were required to produce slower movements rather than faster movements.

Experiments by Teasdale et all2 and Berardelli et aP4 demonstrated that irregular force production is not a function of the degree of muscle acti- vation. Indeed, the mechanisms for producing longer or slower move- ments would appear to be intact, with the number of bursts of muscle activ- ity increasing normally with longer or slower movements. Instead, patients exhibit difficulty in scaling the central signals involved in muscle activation.

It may be asked whether observed slowness and irregularity of move- ments in patients is simply a function of a slower and more tonic pattern of muscle activity. This is not thought to be the case; for example, Teasdale et all2 observed more bursts of muscle activity when patients moved at speeds similar to those of age- matched controls.

It may also be asked whether ob- served irregularity of movement is simply a function of tremor. Tremor is not the sole cause of jerkiness in movement of patients with Parkin- son's disease. Parkinsonian tremor characteristically occurs at rest, and is minimal in some patients. Phillips et a136 examined handwriting in pa- tients with minimal tremor. Although their movements were jerky and ir- regular, the jerkiness was not periodic and did not occur at frequencies asso- ciated with tremor (ie, 5-8 Hz). These observations suggest that Parkinson's disease causes an attenuation in the central commands involved in muscle activation and that the basal ganglia have some role in the activation of muscles.

Gait and posture experiments have examined repetitive movement se- quences in detail and suggest that the observed changes are partly due to a reduction in the size of parkinsonian movement (ie, hastening, or festina- tion). Knutsson and Martensson45

have postulated that some of the ab- normalities of posture and gait may be the result of reduced preparatory postural adjustments, rigidity, and ad- aptation to impaired postural reflexes. Support for this view comes from Bazolgette et who found that pa- tients with Parkinson's disease did not make preparatory postural adjust- ments before initiating voluntary movement.

Experiments that have assessed long- latency reflexes in patients with Par- kinson's disease have found that, al- though the latency of stretch reflexes is normal in these patients, there are abnormalities in the gain of the longer-latency cornponent~.*?-~9 More- over, it has been noted that these ab- normalities are related to poorer bal- ance49j50 and gait.51 It appears that the abnormalities of posture and gait may be the result of parkinsonian rigidity and adaptation to impaired postural reflexes; however, much more re- search is needed.

Huntington's Dlsease and Basal Ganglia Function

Huntington's disease is a hereditary disorder characterized by a progres- sive atrophy of the caudate nucleus within the basal ganglia, and then of cortical structures.l It is thought to be a glutamate-dependent neurotoxic process, producing substantial reduc- tions in dopaminergic neurons.52 It results from the loss of specific sets of cholinergic neurons and neurons that synthesize gamma-aminobutyric acid. Although causal mechanisms are as yet unclear, it may be stated that mul- tiple neurotransmitter systems are affected; specifically, the disease is associated with enhanced dopaminer- gic activity and reduced cholinergic a~tivity.39~52.53

Because Huntington's disease is a pro- gressive disorder that involves other brain structures, one must be cautious in drawing inferences about basal ganglia function. In addition, both rigidity and hypotonia (enhanced and reduced muscle tone, respectively) are reported, depending on the age of the patient.s4<55 Huntington's dis-

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ease, in its early stages, provides two potential models for basal ganglia function. A consideration of chorei- form movement provides additional insight into the dopaminergic systems within the basal ganglia, and a consid- eration of the akinesia and bradykine- sia caused by Huntington's disease provides insight into the functional processes in the basal ganglia.

Huntington's disease begins with dis- turbances of mood and per~onality.5~ Although changes in mood and per- sonality are usually the first signs of the disease, disturbance of movement is the most obvious clinical feature.55 Jerkiness and lack of coordination develop, followed by choreiform movements. In addition, there are disturbances of speech, gait, and swal- 10wing.5~ Many patients die as a result of respiratory problems caused by impaired ~wallowing.5~ Eventually, the disease causes depression and pro- gressive dementia.55

A number of motor symptoms are associated with Huntington's disease:

1. Chorea-involuntary movement resulting from random, irregular, rapid contractions in any combina- tion of muscles.

2. Akinesia and bradykinesiaaiffi- culty in the initiation and execution of movement.

3. Rigidity and hypotonia-both en- hanced and reduced muscle tone (via palpation) are reported, de- pending on the age of the patient.

Whereas Parkinson's disease is associ- ated with reductions in the activity of dopaminergic neurotransmitter sys- tems, Huntington's disease is, in part, associated with enhanced activity in dopaminergic neurotransmitter sys- t e m ~ . 5 ~ Whereas Parkinson's disease responds to treatment with dopamine agonists, aspects of Huntington's dis- ease respond to treatment with dopa- mine antagonists.56 Indeed, excessive use of dopamine agonists produces choreiform movements, such as those seen in patients with Huntington's disease, and excessive use of dopa-

mine antagonists produces parkinsonian-like symptoms. These findings suggest that Huntington's disease may also serve as a model for basal ganglia function.56 In compari- son with Parkinson's disease, how- ever, there are fewer studies available. An understanding of excessive move- ment, related to the dopaminergic system as it operates in chorea, may provide an indication of basal ganglia function.

Choreiform movement exhibits re- flexive, ballistic, and tonic patterns of muscle activity and is difficult to char- acterize electromyographically. In- deed, Hallett13 reported that patients may show any pattern of muscle activ- ity at any time. Marsden and associ- ates14 investigated choreiform move- ment in patients with Huntington's disease. They observed continuous change in activity from one muscle to another, and within individual mus- cles from one pattern of activity to another. Muscle activation in chorea ranges from very brief bursts of activ- ity (eg, 50-200 milliseconds) to pro- longed contractions (eg, 2 seconds).57 Muscle activity is not correctly se- quenced, because cocontractions oc- cur that interfere with voluntary movement.5'

Kinematic analysis also reveals that choreiform movement lacks a clear pattern. Myers and Falek58 used an accelerometer to assess resting hand tremor in patients with Huntington's disease and in control subjects. Whereas the control subjects had a dominant tremor frequency, the pa- tients with Huntington's disease showed intermittent bursts of tremor at no consistent frequency.

Alunesia has been reported in Hun- tington's disease.59360 The symptom of akinesia has been found to be a better predictor of functioning than severity of chorea.59161 Reaction time tends to be longer in patients with Huntington's disease.59.6' As in Parkinson's disease, however, findings of prolonged reac- tion time in patients with Huntington's disease are less reliable than those of prolonged movement tirne.59sG2 This may be because involuntary chorei-

form movement affects the initiation of voluntaly movement. For example, Lasker et a163 found that patients have difficulty suppressing eye saccades in a simple reaction-time task. On the other hand, as in the case of Parkinson's dis- ease, it would appear that patients with Huntington's disease tend to use on- line control during movement execu- tion, rather than preparing them in advance.

Bradykinesia in patients with Hunting- ton's disease has been examined by Hefter et a159 and Thompson et Hefter et a159 examined muscle activ- ity during ballistic movement in the fingers of patients with Huntington's disease. The normal agonist-antagonist pattern was maintained in these pa- tients, suggesting that the ability to select proper muscle groups was un- impaired. However, patients required longer to attain peak force. Hefter et a1 reported a linear relationship be- tween contraction time and contrac- tion amplitude in their patients (ie, movement of greater amplitude re- quired longer contraction time).

Thompson et a164 examined muscle activity during simple and complex movements in the wrists of patients with Huntington's disease. Movement was characterized by slow, prolonged contractions. Central deficits in the activation of movement were indi- cated, as patients had additional diffi- culty performing more complex si- multaneous or sequential movements (eg, squeezing the hand and flexing the elbow).

The use of reaction-time, EMG, and kinematic analyses are not so preva- lent in patients with Huntington's dis- ease. Thus, it is unclear as to how enhanced basal ganglia activity relates to functional movement control. The data that are available suggest that, as in Parkinson's disease, movement control is profoundly impaired. These impairments appear to be partially related for the temporal and spatial aspects of force control.

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Conclusion

Although insight into basal ganglia function originally came from clinical settings, more recent insights have come from experimental motor sci- ence. Deficits in proper muscle acti- vation observed in patients with Parkinson's disease and Huntington's disease support the suggestion that the basal ganglia have a general role in the normal activation of muscle. The available data on these patient populations, however, have not con- sistently tlemonstrated movement exe- cution impairments beyond those of bradykinesia. In some studies, selec- tive difficulties have been noted; in other studies, no such selectivity has been found. The data d o suggest, however, that basal ganglia impair- ment does influence the initiation and regulatior~ of force. This should pro- vide a setring for further research.

The spatial and temporal organization of a movement involves precise con- trol over the forces applied and their durations. Deficits in either parameter can lead to faulty movement execu- tion. The recent work by Teulings and Stelmachl' is promising, as it attempts to separate the force-control compo- nents. These studies suggest that, on a relative basis, force amplitude is more impaired than force duration.

The study of movement disorders, when coupled with current issues in normal motor control research, can provide converging evidence about the roles brain structures play in the control of movement. Further re- search, however, must be directed at understanding multisegmented move- ments in which the intersegments' dynamics break down in impaired populations. Movement disorders re- search may engender new paths of research and new approaches to phys- ical therapy interventions, while chal- lenging contemporary theoretical frameworks. It is hoped that this brief review illustrates some of the current issues in basal ganglia research and promotes an interdisciplinary frame- work advocating an isomorphism be- tween neurophysiological and

cognitive-psychological accounts of motor control.

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1991; 71:60-67.PHYS THER. George E Stelmach and James G PhillipsGanglia

Limb Movement and the Basal−−Movement Disorders

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