Joint dependent passive stiffness in paretic and contralateral limbs of spastic patients with hemiparetic stroke.

Torque-angle relations at the elbow and ankle joints of relaxed normal controls and patients with hemiparetic stroke were compared. Low velocity flexion/hold/extension angular perturbations were applied to the joint under examination. The resulting torque-angle profiles described a hysteresis loop with similar slopes during the extension and flexion stages but separated by a vertical torque offset. Torque-angle responses obtained in the absence of significant muscle activation, as recorded by surface electromyographic activity, were designated as passive. Elbow passive stiffness estimates were calculated from the slope of the torque-angle response during the flexion stage of the perturbation. The elbow torque-angle plots exhibited linear passive stiffness with magnitude significantly lower than the passive stiffness of the ankle in both normal subjects and spastic patients. Changing ramp velocity had no significant effect on the passive torque-angle hysteresis loop at the elbow. A comparison of the torque-angle relations between hemiparetic spastic and normal control arms showed no significant differences in passive stiffness. Furthermore, no significant differences were found between paretic and contralateral upper limbs of a given hemiparetic subject. By contrast, significant differences in the torque-angle hysteresis loop were present between the paretic and contralateral ankles in all hemiparetic patients tested. These differences were more significant during dorsiflexion, and therefore seem to be related to preferential changes in mechanical properties of plantar flexor muscles. It is hypothesised that the differences in the torque-angle hysteresis loop between elbow and angle joints are related primarily to the larger amount of connective tissue in the calf muscles, as well as to a larger total physiological cross sectional area of calf muscles compared with elbow muscles. It is further hypothesized that the preferential increases in passive stiffness at the ankle in spastic legs result from immobilisation induced changes in muscle connective tissue, which are most prominent in muscles with predominantly slow-twitch fibres (such as soleus). Connective tissue surrounding such slow twitch muscle fibres have been shown to be more sensitive to immobilisation than those in fast twitch muscle. The functional, pathophysiological, and clinical implications of our findings are reviewed.     

Pathological stretch reflexes on the "good" side of hemiparetic patients.

The reflex EMG responses from a tendon tap or an imposed, medium amplitude (30 degrees), stretch at a range of stretch velocities have been recorded from the triceps and biceps muscles of normal human subjects and in both the affected and "unaffected" arms of hemiparetic patients under relaxed conditions. In the hemiparetic arm, exaggerated tendon jerks were, as expected, observed in both muscles. The response of the biceps to elbow extension was also exaggerated compared with normal values and displayed both an additional earlier component and a much reduced velocity threshold. The triceps, in contrast, showed depressed responses to elbow flexion, with a much higher velocity threshold than normal subjects. Furthermore, on the supposedly "unaffected" side of the hemiparetic subjects, the reciprocal pattern was seen, with depression of the biceps response and a raising of its threshold, along with considerably exaggerated responses in the triceps including earlier components not seen in the normal subjects. The increased excitability of the flexor musculature on the spastic side may be paralleled by increases in activity in the segmental pathways responsible for modulation of agonist/antagonist activity in the ipsi and contralateral limb, leading to an inhibition of the ipsilateral extensors and contralateral flexors and excitatory input to the contralateral extensors. Thus the "good" side of hemiparetic patients also receives pathological changes, and studies of the mechanisms of spasticity should avoid the use of the "unaffected" side of hemiparetic subjects as a control for monitoring pathological reflexes.     

Ankle spasticity and strength in children with spastic diplegic cerebral palsy

Ankle spasticity and strength in 27 children with spastic diplegic cerebral palsy (CP) (mean age 9 years, range 3 to 18 years) and a group of 12 children without CP (comparison group) (mean age 9 years, range 5 to 18 years) were observed. To measure spasticity, a KinCom dynamometer dorsiflexed the passive ankle at five different speeds and recorded the resistive plantarflexion torques. Work values for the torque-angle data were calculated at each speed. Using this data, linear regression was used to measure spasticity. To measure strength, the dynamometer rotated the ankle from maximum dorsiflexion to maximum plantarflexion at a speed of 10 degrees/s while the child performed a maximum plantarflexion concentric contraction. The movement was reversed to record maximum dorsiflexion. Maximum torques and work by the plantarflexors and dorsiflexors were calculated. The group with CP had significantly more spasticity in the plantarflexors and significantly less strength in the plantarflexors and dorsiflexors than the group without CP. Results provide objective information quantifying ankle spasticity and strength in children with CP.     

Spasticity in adults with cerebral palsy and multiple sclerosis measured by objective clinically applicable technique

Objective

The present study evaluated ankle stiffness in adults with and without neurological disorders and investigated the accuracy and reproducibility of a clinically applicable method using a dynamometer.

Relation between abnormal patterns of muscle activation and response to common peroneal nerve stimulation in hemiplegia

OBJECTIVE: To investigate the relation between response to common peroneal nerve stimulation, timed to the swing phase of walking, and abnormal ankle movement and muscle activation patterns. METHOD: Eighteen patients who took part had a drop foot and had had a stroke at least 6 months before the study Twelve age matched normal subjects were also studied. Response to stimulation was measured by changes in the speed and effort of walking when the stimulator was used. Speed was measured over 10 m and effort by the physiological cost index. Abnormal ankle movement and muscle activation were measured in a rig by ability to follow a tracking signal moving sinusoidally at either 1 or 2 Hz, resistance to passive movement, and EMG activity during both passive and active movements. Indices were derived to define EMG response to passive stretch, coactivation, and ability to activate muscles appropriately during active movement RESULTS: Different mechanisms underlying the drop foot were seen. Results showed that patients who had poor control of ankle movement and spasticity, demonstrated by stretch reflex and coactivation, were more likely to respond well to stimulation. Those with mechanical resistance to passive movement and with normal muscle activation responded less well. CONCLUSIONS: The results support the hypothesis that stimulation of the common peroneal nerve to elicit a contraction of the anterior tibial muscles also inhibits the antagonist calf muscles. The technique used may be useful in directing physiotherapy by indicating the underlying cause of the drop foot.     

Non–reflex and reflex mediated ankle joint stiffness in multiple sclerosis patients with spasticity

In this study, we have measured the passive, the intrinsic, and the reflexmediated mechanical response to stretch of the ankle extensors and flexors in 13 spastic multiple sclerosis patients and 10 healthy control subjects. In the ankle flexors, the patients had no reflex-mediated stiffness. The passive stiffness was increased by 138% (95% confidence interval: 26–91%) and the intrinsic stiffness by 79% (41–158%) when compared with the healthy subjects. In the ankle extensors, the reflex-mediated stiffness and the intrinsic stiffness of the patients were equal to the reflex-mediated and the intrinsic stiffness in healthy subjects. The passive stiffness was increased by 152% (41–352%). We conclude that spastic muscles in multiple sclerosis patients have an increased non-reflex stiffness (passive plus intrinsic stiffness), and that the reflex-mediated stiffness in the extensors during a sustained voluntary contraction does not differ significantly from healthy subjects. © 1993 John Wiley & Sons, Inc.     

Impaired stretch reflex and joint torque modulation during spastic gait in multiple sclerosis patients

The modulation of the short latency stretch reflex of the soleus muscle during walking was investigated in seven spastic multiple sclerosis (MS) patients and nine healthy control subjects. Ankle joint stretches were applied by a system which can rotate that ankle joint in any phase of the step cycle during treadmill walking. The torque related to the muscle fibres contracting prior to the stretch and the passive tissues around the ankle joint were measured as the non-reflex torque. At the same time the short latency stretch reflex-mediated EMG response was measured. The findings show that the stretch reflex modulation was impaired in spastic patients during walking. The stretch reflex modulation was quantified by a modulation index of on average 50% (range –5 to 100%) in the patients and 93% (78–100%) in the control subjects (P < 0.05). The passive stiffness of the ankle joint was at the same time increased in the patients (P < 0.05). It is proposed that the impaired modulation of the stretch reflex along with increased ankle joint stiffness contribute to the impaired walking ability in spastic MS patients.     

The spasticity paradox: movement disorder or disorder of resting limbs?

BACKGROUND: Spasticity is defined/assessed in resting limbs, where increased stretch reflex activity and mechanical joint resistance are evident. Treatment with antispastic agents assumes that these features contribute to the movement disorder, although it is unclear whether they persist during voluntary contraction. OBJECTIVES: To compare reflex amplitude and joint resistance in spastic and normal limbs over an equivalent range of background contraction. METHODS: Thirteen normal and eight hemiparetic subjects with mild/moderate spasticity and without significant contracture were studied. Reflex and passive joint resistance were compared at rest and during six small increments of biceps voluntary contraction, up to 15% of normal maximum. A novel approach was used to match contraction levels between groups. RESULTS: Reflex amplitude and joint mechanical resistance were linearly related to contraction in both groups. The slopes of these relations were not above normal in the spastic subjects on linear regression. Thus, reflex amplitude and joint resistance were not different between groups over a comparable range of contraction levels. Spastic subjects exhibited a smaller range of reflex modulation than normals because of decreased maximal contraction levels (weakness) and significant increases of resting contraction levels. CONCLUSIONS: Spasticity was most evident at rest because subjects could not reduce background contraction to normal. When background contractions were matched to normal levels, no evidence of exaggerated reflex activity or mechanical resistance was found. Instead, reduced capacity to modulate reflex activity dynamically over the normal range may contribute to the movement disorder. This finding does not support the routine use of antispastic agents to treat the movement disorder.     

Relief of hemiparetic spasticity by TENS is associated with improvement in reflex and voluntary motor functions.

Our previous studies showed that a single 45 min application of transcutaneous electrical nerve stimulation (TENS) prolonged soleus H and stretch reflex latencies in hemiparetic subjects. In addition, 9 daily 30 min TENS applications enhanced vibratory inhibition of the H reflex and tended to decrease hyperactive stretch reflexes. These findings suggested that longer-term TENS may be effective in reducing hemiparetic spasticity. Our present objectives were 2-fold: to determine whether longer-term repetitive TENS stimulation would lead to a reduction in clinical spasticity in hemiparetic subjects, and whether such a reduction could be associated with a decrease in stretch reflex excitability and an improvement in voluntary motor function. We compared the effects of 15 daily 60 min TENS treatments over a 3 week period, with those of placebo stimulation applied to the common peroneal nerve of the affected leg in similar groups of spastic hemiparetic subjects. Our test battery consisted of 5 measurements which assessed (1) clinical spasticity scores, (2) maximal H reflex to M response ratios, (3) vibratory inhibition of H reflex, (4) stretch reflexes, and (5) maximal voluntary isometric plantarflexion and dorsiflexion, in standing. In contrast to placebo stimulation which produced no significant effects, repeated applications of TENS over time decreased clinical spasticity (P less than 0.05), and increased vibratory inhibition of the soleus H reflex (P = 0.02) after 2 weeks. These changes occurred with a substantial improvement in voluntary dorsiflexing force up to 820%, but not plantarflexing force. They were followed by a reduction in the magnitude of stretch reflexes (P = 0.05) in the spastic ankle plantarflexor, concomitant with a decrease in the EMG co-contraction ratios after a further week of stimulation. Our results thus indicated that repeated applications of TENS can reduce clinical spasticity and improve control of reflex and motor functions in hemiparetic subjects. Furthermore, the underlying mechanisms may be due partly to an enhancement in presynaptic inhibition of the spastic plantarflexor, and partly to a possible "disinhibition" of descending voluntary commands to the paretic dorsiflexor motoneurons.     

The time-course of bilateral changes in the reflex excitability of relaxed triceps surae muscle in human hemiparetic spasticity

Summary Short, rapid dorsiflexion of the normal human ankle induces a single, synchronised reflex EMG response in the initially relaxed triceps surae muscle (TS). In subjects in whom hemiparesis is present as a result of a unilateral ischaemic cerebral lesion, a reflex EMG response can be elicited on either side with timing identical to that of the normal response. The magnitude of the response in hemiparetic subjects, however, differs from the normal on both the side contralateral and that ipsilateral to the causative lesion. Furthermore, the magnitude of this response varies over the time-course of spasticity. Contralaterally to the lesion, a gradual increase in the magnitude of the response to imposed displacement occurs. One year after stroke, the response has reached a level significantly larger than normal. Changes in the magnitude of the contralateral Achilles tendon jerk reflex EMG are apparent earlier than changes in the response to imposed displacement, with exaggerated tendon jerks already being apparent between 1 and 3 months after stroke. On the side ipsilateral to the lesion, a profound depression of the response to imposed displacement is visible as early as a month after stroke. This depression diminishes over the 1st year, but the response has not even then returned to normal values. These changes are not reflected in the ipsilateral tendon jerk response, which remains normal throughout this period. It is thus concluded that at least two processes are at work in determining the reflex excitability of the TS in hemiparetic humans: firstly, a unilateral increase in excitability at a low spinal level on the side contralateral to the lesions, appearing in the 1st month after stroke and producing the exaggerated tendon jerk response on this side; secondly, a bilateral depression mediated unlike the tendon jerk response, over a predominantly polysynaptic pathway and affecting the response to imposed displacement. This depression appears in the 1st month after stroke and gradually becomes less marked over the following year. On the contralateral side, owing to the increase in excitability at a lower level, this does not appear as a reduction in the magnitude of the response to imposed displacement, but rather is evident in the slower time-course of the development of hyperexcitability in this response, relative to that of the tendon jerk reflex.     

Effect of static stretch training on neural and mechanical properties of the human plantar-flexor muscles

To determine the contributions of neural and mechanical mechanisms to the limits in the range of motion (ROM) about a joint, we studied the effects of 30 sessions of static stretch training on the characteristics of the plantar-flexor muscles in 12 subjects. Changes in the maximal ankle dorsiflexion and the torque produced during passive stretching at various ankle angles, as well as maximal voluntary contraction (MVC) and electrically induced contractions, were recorded after 10, 20, and 30 sessions, and 1 month after the end of the training program. Reflex activities were tested by recording the Hoffmann reflex (H reflex) and tendon reflex (T reflex) in the soleus muscle. Training caused a 30.8% (P < 0.01) increase in the maximal ankle dorsiflexion. This improved flexibility was associated (r(2) = 0.88; P < 0.001) with a decrease in muscle passive stiffness and, after the first 10 sessions only, with a small increase in passive torque at maximal dorsiflexion. Furthermore, both the H- and T-reflex amplitudes were reduced after training, especially the latter (-36% vs. -14%; P < 0.05). The MVC torque and the maximal rate of torque development were not affected by training. Although the changes in flexibility and passive stiffness were partially maintained 1 month after the end of the training program, reflex activities had already returned to control levels. It is concluded that the increased flexibility results mainly from reduced passive stiffness of the muscle-tendon unit and tonic reflex activity. The underlying neural and mechanical adaptation mechanisms, however, showed different time courses.     

Voluntary muscle strength in hemiparesis: distribution of weakness at the elbow.

Maximal voluntary strength (torque) of the flexors and extensors of the elbow was measured in 56 normal subjects and 18 hemiparetic subjects. In normal subjects the ratio of extension to flexion strength averaged 55% and did not differ significantly between sides or sexes. The ratio of maximal extensor to flexor strength on the clinically unaffected side of hemiparetic subjects was the same as that for the normal subjects but it was significantly increased on the affected side. This increase indicates that the elbow flexors were relatively more weakened than the extensors on the hemiparetic side, a conclusion contrary to conventional clinical teaching. The increase in the ratio was not the result of co-contraction of either muscle group. A possible physiological basis for the observed distribution of weakness is suggested.     

Flexor reflexes in chronic spinal cord injury triggered by imposed ankle rotation

Hypersensitivity of the flexor reflexes to input from force-sensitive muscle afferents may contribute to the prevalence and severity of muscle spasms in patients with spinal cord injuries. In the present study, we triggered flexor reflexes with constant-velocity ankle movements into end-range dorsiflexion and plantarflexion positions in 8 individuals with spinal cord injuries. We found that all 8 subjects had coordinated increases in flexion torque at the hip and ankle following externally imposed plantarflexion movements at the ankle. In addition, end-range dorsiflexion movements also triggered flexor reflexes in 3 subjects, although greater loads were required to trigger such reflexes using dorsiflexion movements (compared to plantarflexion movements). These three-joint reflex torque patterns triggered by ankle movement were broadly comparable to flexion withdrawal responses elicited by electrocutaneous stimuli applied to a toe, although the amplitude of the torque response was generally lower. We conclude that excitation of muscle and joint-related afferents induced by end-range movements may be responsible for exaggerated flexion reflex responses in spinal cord injury.     

Stepping before standing: hip muscle function in stepping and standing balance after stroke

OBJECTIVE: To compare the pattern of pelvic girdle muscle activation in normal subjects and hemiparetic patients while stepping and maintaining standing balance. DESIGN: Group comparison. METHOD: Seventeen patients who had regained the ability to walk after a single hemiparetic stroke were studied together with 16 normal controls. Median interval between stroke and testing was 17 months. Amplitude and onset latency of surface EMG activity in hip abductors and adductors were recorded in response to sideways pushes in either direction while standing. Similar recordings were made in the same subjects during gait initiation and a single stride. RESULTS: In the standing balance task, normal subjects resisted a sideways push to the left with the left gluteus medius (74 ms) and with the right adductor (111 ms), and vice versa. In hemiparetic patients, the amplitude of activity was reduced in the hemiparetic muscles, the onset latencies of which were delayed (gluteus medius 96 ms, adductor 144 ms). Contralateral, non-paretic, adductor activity was increased after a push towards the hemiparetic side of patients with stroke and the latency was normal (110 ms). During self initiated sideways weight shifts at gait initiation, hemiplegic muscle activation was impaired. By contrast, the pattern and peak amplitude of hip muscle activation in stepping was normal in both hemiparetic and non-hemiparetic muscles of the subjects with stroke. CONCLUSIONS: In ambulant patients with stroke, a normal pattern of activation of hemiparetic muscles is seen in stepping whereas the response of these muscles to a perturbation while standing remains grossly impaired and is compensated by increased activity of the contralateral muscles. This suggests that hemiparetic patients should be able to step before regaining standing balance.     

Deficits in the coordination of agonist and antagonist muscles in stroke patients: implications for normal motor control

Movement impairments about a single joint in stroke patients may be related to deficits in the central regulation of stretch reflex (SR) thresholds of agonist and antagonist muscles. One boundary of the SR threshold range for elbow flexor and extensor muscles was measured in hemiparetic subjects by analysing electromyographic activity during stretching of relaxed muscles at seven different velocities. For each velocity, dynamic SR thresholds were measured as angles at which electromyographic activity appeared. These data were used to determine the sensitivity of the threshold to velocity and the static SR thresholds for flexors and extensors. In contrast to relaxed muscles in healthy subjects, static flexor and extensor thresholds lay within the physiological range in 11/12 and 4/12 subjects, respectively. This implies that, in the range between the static SR threshold and one of the physiological joint limits, relaxation of the muscle was impossible. Subjects then made slow movements against different loads to determine their ranges of active movement. Maximal flexor and extensor torques were lower in hemiparetic subjects throughout the angular range. In some subjects, ranges were found in which no active torque could be produced in either extensor or both muscle groups. These ranges were related to the boundary values of SR thresholds found during passive muscle stretch. The range in which reciprocally organized agonist and antagonist muscle activity could be generated was limited in all but one subject. When attempting to produce torque from positions outside their measured range of movement, excessive muscle coactivation occurred, typically producing no or paradoxical motion in the opposite direction. Results suggest a relationship between spasticity measured at rest and the movement deficit in stroke by demonstrating a link between motor deficits and control deficits in the central regulation of individual SR thresholds.     

Normal and impaired regulation of muscle stiffness in gait: A new hypothesis about muscle hypertonia

The activation of leg muscles was analyzed in respect to ankle joint movement and the changes in tension produced by the triceps surae muscle during slow gait in spastic adults and children with cerebral palsy. In normal subjects the increase in tension of the triceps surae in the stance phase of gait is mainly due to an increase in gastrocnemius and sole EMG. In spastic patients the abnormally high tension development in triceps surae is due more to passive muscle stretch, for the reciprocally organized leg muscle EMG is reduced. It is concluded that the leg extensor muscles in spastic patients exhibit a pseudostretch-reflex behavior due to their mechanical properties, and that this is mainly responsible for muscle hypertonia. The coactivation of the leg muscles seen in children with cerebral palsy, which also is seen in the stepping of the newborn, suggests impaired maturation of the neuronal locomotor pattern.     

Contribution of thixotropy, spasticity, and contracture to ankle stiffness after stroke

OBJECTIVES: Increased resistance to stretch of muscles after stroke may be the result of centrally mediated neural factors such as spasticity or local, peripheral factors such as muscle contracture or thixotropy. The aim was to investigate evidence for an abnormal thixotropic response and compare this with two other factors-contracture and spasticity-which could potentially contribute to muscle stiffness after stroke. METHODS: Thirty patients with stroke whose calf muscles were assessed clinically as stiff and 10 neurologically normal subjects were recruited. To measure thixotropy, their calf muscles were stretched through two cycles after two prestretch conditions: one in which the muscles were maintained in a shortened position and one in which they were maintained in a lengthened position. Spasticity was defined as the presence of tonic stretch reflexes in relaxed muscles. Contracture was defined as being present when maximum passive ankle dorsiflexion fell at least 2 SD below the mean value of the control subjects. RESULTS: Both controls and patients with stroke exhibited a thixotropic response but this was no greater in the patients than the controls. About one third of the patients displayed muscle contracture and most exhibited spasticity. Contracture made a significant contribution (p=0.006) to the clinical measure of calf muscle stiffness while spasticity made a significant contribution (p=0.004) to the laboratory measure of calf muscle stiffness. CONCLUSIONS: Measuring thixotropy at the level of joint movement was sufficiently sensitive to determine the thixotropic response in both neurologically normal subjects and patients impaired after stroke. The thixotropic response was not higher than normal after stroke, suggesting that whereas thixotropy may produce enough immediate resistance to impede movement in those who are very weak, it is not a substantial contributor to long term muscle stiffness. Contracture did significantly contribute to muscle stiffness, supporting the importance of prevention of contracture after stroke. Spasticity contributed to muscle stiffness only when the limb was moved quickly.     

Foot control in incomplete SCI: distinction between paresis and dexterity

OBJECTIVE: To complement the clinical assessment of motor impairment after incomplete spinal cord injury (iSCI) by introducing a test that reliably distinguishes between muscle weakness (paresis) and impairment of dexterity in a simple foot motor task. METHODS: Auditory-paced ankle dorsi- and plantarflexion, in a supine position, was studied in 30 controls (to establish control values and to test reliability) and in 16 iSCI patients (test validation). The subjects were instructed to initiate dorsi- and plantarflexion as accurately in timing and with the largest range of motion (ROM) possible. For each frequency, accuracy of timing, ROM, peak velocity of dorsi- and plantarflexion and a time quotient for changing from dorsi- to plantarflexion and vice versa were determined. In iSCI subjects, these parameters were related to clinical measures of paresis, spasticity and proprioception. RESULTS: The test parameters showed good to very good reliability. The iSCI subjects were able to follow the target frequency with high accuracy, while ROM and peak velocity for dorsi- and plantarflexion were significantly reduced. Furthermore, there was a strong correlation between ROM/peak velocities and motor scores within the iSCI patients. DISCUSSION: Repetitive foot dorsi- and plantarflexion enables a distinction to be made between muscle weakness and reduced dexterity as the underlying cause of affected foot control. This distinction between and quantification of these two movement components complements the existing clinical examination, and in follow-up works, the recovery of these components may provide further insight into the mechanisms underlying motor function improvement after iSCI.     

Characteristics of parkinsonian and ataxic gaits: a study using surface electromyograms, angular displacements and floor reaction forces

To clarify the characteristics of parkinsonian and ataxic gaits, we analyzed electromyograms (EMGs) of the thigh and leg muscles, angular displacements of the hip and leg joints, and floor reaction forces during free walking for each gait phase in 16 patients with Parkinson's disease (PD) and 14 ataxic patients with cerebellar degenerations. We studied 17 healthy elderly subjects whose walking speed was similar to that of patients with moderate disease. Free walking by PD patients was characterized by low maximum activity of the gastrocnemius/soleus (GC) and tibialis anterior (TA) muscles. Ataxic patients showed high activity of GC and TA during the period when these muscles were not active in normal walking. The ratio of changes of EMG of the distal muscles to changes in angular displacement of the ankle (DeltaEMG/Deltaangle) was reduced in GC of PD patients in ankle dorsiflexion, whereas it was high in GC and TA of ataxic patients in ankle dorsiflexion and plantarflexion, respectively. Changes in DeltaEMG/Deltaangle coincided with those in proprioceptive reflexes reported previously. Our results showed that measurement of EMG for each phase revealed disease-specific factors, and that of DeltaEMG/Deltaangle might be a conventional clue for estimation of reflexes for these gait disorders.     

Proprioceptive regulation of voluntary ankle movements, demonstrated using muscle vibration, is impaired by Parkinson''s disease

OBJECTIVE: To test the hypothesis that the proprioceptive regulation of voluntary movement is disturbed by Parkinson's disease, the effects of experimental stimulation of proprioceptors, using muscle vibration, on the trajectories of voluntary dorsiflexion movements of the ankle joint were compared between parkinsonian and control subjects. METHODS: Twenty one patients with Parkinson's disease, on routine medication (levodopa in all but one), and an equal number of age matched, neurologically intact controls, were trained initially to make reproducible ankle dorsiflexion movements (20 degrees amplitude with a velocity of 9.7 degrees /s) following a visual "go" cue while movement trajectories were recorded goniometrically. During 50% of the experimental trials, vibration (105 Hz; 0.7 mm peak to peak) was applied to the Achilles tendon during the ankle movement to stimulate antagonist muscle spindles; vibrated and non-vibrated trials were interspersed randomly. Subjects' performance was assessed by measuring end point position-that is, the ankle angle attained 2 seconds after the visual "go" cue, from averaged (20 trials) trajectories. RESULTS: Statistical analysis of the end point amplitudes of movement showed that, whereas the amplitudes of non-vibrated movements did not differ significantly between patients with Parkinson's disease and controls, antagonist muscle vibration produced a highly significant reduction in the amplitudes of ankle dorsiflexion movements in both the patient and control groups. However, the extent of vibration induced undershooting produced in the patients with Parkinson's disease was significantly less than that in the controls; the mean vibrated/non-vibrated ratios were 0.86 and 0.54 for, respectively, the patient and control groups. CONCLUSIONS: The present finding of a reduction of vibration induced ankle movement errors in parkinsonian patients resembles qualitatively previous observations of wrist movements, and suggests that Parkinson's disease may produce a general impairment of proprioceptive guidance.