Relative contributions of neural mechanisms versus muscle mechanics in promoting finger extension deficits following stroke

The origins of impaired finger and hand function were examined in 10 stroke survivors with chronic spastic hemiparesis, with the intent of assessing whether mechanical restraint or altered neurophysiological control mechanisms are responsible for the well-known impairment of finger extension. Simultaneous extension of all four metacarpophalangeal (MCP) joints of the impaired hand was either externally imposed using a rotary actuator or attempted voluntarily by the subject. Trials were conducted both before and after administration of a local anesthetic, blocking the median and ulnar nerves at the elbow. The anesthetic was administered to reduce the activity of the muscles flexing the MCP joints, in order to distinguish mechanical from neuronal resistance to imposed MCP rotation. We found that the nerve blockade resulted in a reduction in velocity-dependent torque (P = 0.01), thereby indicating significant joint impedance due to spasticity. Blockade also produced a posture-dependent reduction in static torque in declaratively relaxed subjects (P = 0.04), suggesting some tonic flexor activity for specific hand postures. No change in either extensor isometric (P = 0.33) or isokinetic (0.53) torque was apparent, but 3 of the 10 subjects did exhibit substantial (>10 degrees ) improvement in voluntary MCP extension following the blockade. This improvement seemed largely due to a decrease in inappropriate flexor activity during the movement, rather than an increase in extensor activity. We argue that persistent and inappropriate flexor activation plays a role in limiting voluntary finger extension, and that this activation is potentially a reflection of altered supraspinal control of key spinal pathways. In all cases, this inappropriate activation was compounded by weakness, apparent in both the extensor and flexor muscles.     

Isokinetic strength and power deficits in the hand following stroke

ObjectiveThe purpose of this study was to compare the torque production in the paretic and non-paretic hands during isokinetic tasks following stroke.MethodsWe compared torque and power production at the MCP joint of chronic stroke survivors during isometric and isokinetic tasks. We also recorded surface electromyography (EMG) activity in the forearm muscles.ResultsIsokinetic torque production at all velocities was less than that produced during isometric trials. Both torque and power produced by the paretic hand was substantially impaired. Deficits were substantially greater in extension than flexion trials. EMG data suggests that excessive co-contraction of agonist and antagonist muscles does not greatly affect isokinetic torque production at the MCP joint.ConclusionsThe fact that movement velocity produces larger deficits in torque and power production may explain why patients who have limited strength impairments still experience functional deficits.SignificanceThis study demonstrates that strength testing of stroke survivors under isometric conditions may underestimate the overall level of impairment.     

Quantitative features of the stretch response of extrinsic finger muscles in hemiparetic stroke

Despite its potential importance in hand dysfunction, spasticity in the finger muscles following stroke has not been well described. To explore this area, we assessed the role of finger flexor spasticity, along with that of passive mechanical forces, in resisting finger movement in 13 chronic stroke subjects. Subjects were tested with a device that stretched the extrinsic finger muscles through imposed rotation of the metacarpophalangeal (MCP) joints. Both maintained and constant-velocity stretches were imposed. For the constant-velocity stretches, eight of the 13 stroke subjects exhibited strong stretch reflexes, as determined by electromyography and net work. The net work of this reflex response, calculated from the integral of the torque-angle plots, increased proportionally with increasing velocity, indicating a contribution from flexor muscle spasticity. Conversely, nine of the 13 stroke subjects did not possess distinctly greater passive, mechanical resistance to MCP rotation than control subjects. While extensor spasticity was not observed, stretch of the extrinsic finger flexors also produced some reflex activity in the finger extensors concomitant with reflex excitation of the flexors. These findings suggest that resistance to muscle stretching following stoke is mediated primarily by neurological rather than biomechanical disturbances, although changes in muscle fiber length may exaggerate the resistance.     

Contributions of voluntary activation deficits to hand weakness after stroke

Background: Hemiparetic stroke survivors often exhibit profound weakness in the digits of the paretic hand, but the relative contribution of potential biomechanical and neurological impairment mechanisms is not known. Establishing sources of impairment would help in guiding treatment.

Objective: The present study sought to quantify the role of diminished capacity to voluntarily active finger flexor and extensor muscles as one possible neurological mechanism.

Methods: Two groups of stroke survivors with “severe” (N?=?9) or “moderate” (N?=?9) hand impairment and one group of neurologically intact individuals (N?=?9) participated. Subjects were asked to create isometric flexion force and extension force, respectively, with the tip of the middle finger. The maximum voluntary force (MVF) and the maximum stimulated force (MSF) produced by an applied train of electrical current pulses (MSF) were recorded for flexion and extension. Percent voluntary activation (PVA) was computed from MVF and MSF.

Results: Significant deficits in both MVF and PVA were observed for stroke subjects compared to control subjects. For example, activation deficits were >80% for extensor digitorum communis (EDC) for the “severe” group. Maximum voluntary force and PVA deficits were greater for EDC than for flexor digitorum superficialis (FDS) for stroke subjects with severe impairment. Maximum voluntary force and PVA correlated significantly for stroke subjects but not for control subjects.

Conclusions: Although extrinsic finger muscles could be successfully recruited electrically, voluntary excitation of these muscles was substantially limited in stroke survivors. Thus, finger weakness after stroke results predominantly from the inability to fully activate the muscle voluntarily.     

Electromyogram coactivation patterns of the elbow antagonist muscles during slow isokinetic movement

Electromyograms from the flexor and extensor muscles of normal human elbows were simultaneously recorded during maximal-effort isokinetic movement at 15 degrees/s over the joint's full range of motion. The antagonist electromyogram was normalized with respect to its electromyogram when acting as agonist at maximal effort and plotted as a function of joint angle. The coactivation patterns were nearly inversely related to each muscle's moment arm variations with joint angle, suggesting that the antagonist may have generated constant opposing torque throughout the movement. Female subjects had a statistically significant higher coactivation level of the flexors and extensors compared with that of males, reflecting the increase in joint efficiency associated with daily muscular activity which is manifested by reduction in antagonist activity. The functional role of antagonist coactivation in augmenting ligament stabilizing functions, equalizing the pressure distribution over the articular surface, and regulating the joint's mechanical impedance are discussed. The source of such coactivation appears to be due to proprioceptive and joint kinesthetic afferent input in addition to possible direct common drive.     

Electromyography and mechanomyography of elbow agonists and antagonists in Parkinson disease

The purpose of this study was to assess the electromyographic (EMG) and mechanomyographic (MMG) activities of agonist and antagonist muscles in Parkinson disease patients during maximal isometric elbow contraction in flexion and extension. Ten elderly females with Parkinson disease (average age 75 years) and 10 age‐matched healthy females were tested. The torque and the EMG and MMG signals from biceps brachii and triceps brachii were recorded during sustained maximal voluntary isometric contraction of the elbow flexors and extensors. There were no intergroup differences in the EMG and MMG activities of agonist and antagonist muscles or in torque. This might be because the Parkinson subjects were tested during their medication “ON” phase, or perhaps maximal isometric contraction (MVC) induced greater active muscle stiffness that affected the MMG signal. Muscle Nerve 40: 240–248, 2009     

青年男女膝关节屈伸肌群达到峰值力矩时关节角度变化规律的等速肌力测试

背景：人体各关节灵活程度不同,但屈伸运动都是具备的,在日常活动当中,屈伸运动也是最为常见的,但关节屈伸时在何角度产生的力矩是最大的呢？ 目的：掌握膝关节屈伸时发挥最大肌力的关节角度,为运动健身、训练提供理论指导。 设计、时间及地点：对比观察,试验于2008-04/06在郑州大学体育学院实验室进行。 对象：自愿参加测试的大学生男女各30名。 方法：测试仪器使用澳大利亚产Kinitech等速肌力测试系统,按照Kinitech等速肌力测试系统手册要求对参试者膝关节进行固定并测试,3种测试速度为慢速60 (°)/s、中速120 (°)/s和快速240 (°)/s。 主要观察指标：膝关节屈伸肌群的峰值力矩、达到峰值力矩时关节角度。 结果：在速度为60 (°)/s时,男女左屈肌小于右屈肌达到峰值力矩的关节角度,且左伸肌小于右伸肌;男子右屈肌达到峰值力矩的关节角度大于左屈肌,且女子与男子相同。在速度为120(°)/s时,男子屈伸肌达到峰值力矩的关节角度差异不显著,女子右伸肌达到峰值力矩的关节角度大于左伸肌。在速度为240 (°)/s时,男子左屈肌达到峰值力矩的关节角度大于右屈肌,而左伸肌和右伸肌差异不存在显著性。女子左右屈伸肌差异也不存在显著性。 结论：自然发育下人体存在优势腿,在不同速度下达到峰值力矩的关节角度有所不同,在日常运动健身时尽可能的全面训练,使屈伸肌群得到全面发展。 关键词：等速;膝关节;峰值力矩;关节角度     

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.     

Pathophysiological mechanisms in cerebral palsy.

To investigate some of the pathophysiological mechanisms in cerebral palsy, surface electromyograms (EMG) were recorded from pairs of flexor/extensor muscles during both voluntary and passive flexion/extension of upper and lower limbs of 20 patients. Elbow, knee, or ankle joint angles were measured simultaneously, as well as the force required to flex/extend the limbs passively at frequencies of 0.1--1.0 Hz. In addition, single motor units were recorded from the first dorsal interosseous muscles of six of the patients. Almost all patients showed resistance to passive movements (hypertonia). This hypertonia did not necessarily impair voluntary flexion/extension movements if alternating EMG activity was maintained in at least one of the pairs of flexor/extensor muscles involved in the movement. In six severly involved patients, there was a complete breakdown in the reciprocal relationship between reciprocally acting pairs of flexor/extensor motoneurones, which resulted in synchronous activation (co-contractions) of flexor/extensor muscles during both voluntary and passive movements. In these patients the hyperactive segmental reflex added to the disabling effects of co-contractions during voluntary movements. Single motor units recorded from patients with dystonic movements were recruited with variable delays (2--10 s) and usually discharged intermittently at high frequencies (60--120/s). This abnormla motor unit discharge pattern may relate to pathology of the basal ganglia.     

Interactions between imagined movement and the initiation of voluntary movement: A TMS study

ObjectiveThe purpose was to examine motor imagery-induced enhancement in corticospinal excitability during a reaction time (RT) task.MethodsNine young and healthy subjects performed an isometric finger flexion tasks in response to a visual imperative cue. In the pre-cue period, they were instructed to: (1) rest; (2) imagine flexing their fingers isometrically (ImFlex); or (3) imagine extending their fingers isometrically (ImExt). Surface EMGs from the finger flexors and extensors were monitored to ensure EMG silence before movement onset. Transcranial magnetic stimulation (TMS) was used to evaluate changes in motor-evoked potentials (MEP) in the finger flexor and extensor muscles during the response phase. TMS was delivered either with the imperative cue, or 120 ms before and after the imperative cue.ResultsRT was slower when they were imagining finger extension prior to the visual imperative cue. MEPs were significantly increased for the finger flexors during imagined finger flexion and for the finger extensors during imagined finger extension at both TMS delivery time points, reflecting movement specific enhancement in corticospinal excitability during motor imagery. When TMS was delivered 120 ms after the cue, finger flexor MEPs were further facilitated under the Rest and ImFlex conditions, but not under the ImExt condition, suggesting additive interactions between imagery-induced enhancement and early rise in corticospinal excitability during the initiation of a reaction time response.ConclusionsOur results provide neurophysiological evidence mediating dynamic interactions between imagined movement and the initiation of voluntary movement.SignificanceMotor imagery can be integrated into a rehabilitation protocol to facilitate motor recovery.     

Was Sherrington right about co-contractions?

Differences in electromyographic (EMG) activity between brief isometric maximum voluntary contractions under conditions of agonist contraction and agonist-antagonist co-contractions were assessed for elbow flexors (biceps brachii) and elbow extensors (triceps, long head). Expressing maximum EMG co-contraction activity as a ratio of agonist maximum EMG activity of the same muscle yielded EMG ratios consistently below 1.0 (mean = 0.48 for flexion and 0.76 for extension). Flexor EMG ratios did not co-vary with elbow position but extensor EMG ratios approached 1.0 or sometimes greater at shorter muscle lengths (elbow extension). Findings were in general accord with Sherrington's original proposal of 'double reciprocal innervation'. Neural circuitry designed to limit full muscle activation during co-contractions may serve to protect the joint against excessive tangential or compressive forces.     

Reflex activity and muscle tone during elbow movements in patients with spastic paresis.

Reflex behavior and tension development in upper limb muscles were analyzed and comparisons made between the unaffected and spastic sides of patients with spastic hemiparesis. During sinusoidal (0.3-Hz) isometric or isotonic elbow tracking, with a control either of joint position or of torque, randomly timed displacements were induced (at one of three velocities) stretching either the activated flexor or the extensor muscles. On the spastic side, exaggerated short-latency reflexes were apparent, but in contrast, the amplitude of long-latency electromyography (EMG) responses was reduced. The latter responses were differentially modulated on the unaffected side, predominantly by the acceleration signal during control of position and more by the velocity signal during control of torque, while the mode of muscle contraction (isometric or isotonic) had little influence on this behavior. This difference in reflex modulation was lost on the spastic side. The functional consequence of this reduced EMG modulation could be difficulty in performing finely controlled arm movements. The ratio of torque to EMG activity during displacements was higher for both background and reflex-induced EMG on the spastic limb than on the unaffected side. This effect was more pronounced for the flexor than for the extensor muscles. Consequently, the development of spastic muscle hypertonia cannot be attributed to an increase in EMG activity. It is suggested that secondary to a supraspinal lesion, mechanical muscle properties change in such a way that the activated spastic muscle develops more tension when it is stretched.     

Knee extensor torque,work, and EMG during subjectively graded dynamic contractions

We examined knee extensor peak torque, work, and electromyogram (EMG) during dynamic contractions to perceived exertion levels in men and women. Thirty subjects performed three maximal effort isokinetic knee extensions (60 deg x s(-1)), followed by three contractions to each of nine separate levels of perceived exertion. Surface EMG of the vastus medialis (VM), vastus lateralis (VL), and rectus femoris (RF), and knee extensor peak torque and work were normalized to a percent of each respective value obtained during the maximal effort contractions. The results demonstrated a significant linear increase in voluntary knee extensor peak torque and work across perceived exertion levels. Knee extensor peak torque and work were less than 70%, 80%, and 90% maximal voluntary contraction (MVC) at perceived exertion levels 7, 8, and 9, respectively. A significant increase in VM, VL, and RF muscle EMG was observed across perceived exertion levels 1 through 9, with EMG increase highest for the VL. The findings demonstrate that dynamic contractions guided by perceived exertion are underproduced at relatively high perceptual intensities, and that reliance on VL activation occurs across submaximal torque levels. The overestimation of knee extensor peak torque and work at relatively high perceptual intensities may suggest the presence of a subconscious mechanism aiming to reduce high muscle and joint forces.     

Action of dantrolene sodium in spasticity with low dependence on fusimotor drive.

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.     

Effects of changing wrist positions on finger flexor hypertonia in stroke survivors

We sought to establish whether spastic hypertonia results from changes in intrinsic muscle properties or from altered stretch reflex properties. We hypothesized that finger flexor spastic hypertonia is primarily of neural origin, and that the dynamics of spastic muscle responses to stretch should therefore reflect the dynamics of muscle spindle receptor responses. In 12 stroke survivors, we recorded torque and electromyographic (EMG) responses of extrinsic finger flexors to constant-velocity rotation of the metacarpophalangeal (MCP) joints of the affected hand, over a range of initial muscle lengths. Stretch velocity was set to 6 degrees, 50 degrees, 150 degrees, or 300 degrees per second. Muscle length changes were imposed by changing wrist angle between 0 degree, 25 degrees, and 50 degrees of flexion. We found that reflex torque and EMG responses exhibited both velocity and length dependence, and there were significant interactions between velocity and length, replicating known characteristics of muscle spindle receptors. Our results support the hypothesis that finger flexor hypertonia is primarily of neural origin, and that it accurately reflects spindle receptor firing properties.     

Strength deficits in primary focal hand dystonia.

Cortical activation is reduced when patients with focal dystonia perform movements that do not induce dystonic posturing. This finding suggests that the cortical drive to muscles may in some circumstances actually be reduced not increased, as suggested by basal ganglia models of dystonia as a hyperkinetic disorder. The purpose of this study was to examine flexor and extensor strength at the wrist (a clinically affected joint) and elbow (a nonclinically affected joint) in 18 patients with primary focal hand dystonia compared to matched control subjects. We measured peak torque from maximum voluntary contractions, and agonist and antagonist muscle activation by means of surface electromyograms. Patients were significantly weaker than controls at both the elbow and wrist joints and in both flexors and extensors compared to controls. Peak elbow flexion torque was, on average, 14.4% lower in the dystonic compared to the control group, elbow extensor peak torque was 28.6% lower, wrist flexor peak torque was 17.4% lower, and wrist extensor peak torque was 20.7% lower. Strength did not differ as a function of clinical severity. Reductions in peak torque were accompanied by reduced agonist activation, although this finding only reached statistical significance at the elbow. The amount of co-contraction of antagonistic muscles was not significantly different between the two groups. These results are discussed in the context of dystonia as a disorder resulting from dysfunction of basal ganglia output.     

Effects of velocity on maximal torque production in poststroke hemiparesis

Impaired torque production is a major physical impairment following stroke, and has been studied extensively in isometric conditions. However, functional use of a limb requires torque production during movement, and the effects of velocity on maximal torque production may be abnormally enhanced in the paretic limb. The purpose of this study was to quantify the effects of movement velocity on maximal torque production during isokinetic, concentric flexion and extension of the elbow in poststroke subjects. Three speeds were tested (30, 75, 120 deg/s) over a 100-deg range of motion. To control for strength variations between subjects and limbs, isokinetic torques were normalized by peak isometric torque. As flexion velocity increased, paretic limb torque decreased at a greater rate than in the unaffected limb. During extension, paretic limb torque was much lower than torque in the unaffected limb at all speeds. In both flexion and extension, the disparity between limbs in the constant-velocity torque-angle curves became more pronounced as velocity increased. Torque decreased 44% +/- 7% in flexion and 63% +/- 9% in extension as velocity increased from 30 to 120 deg/s, whereas the corresponding decreases in the unaffected limb were only 9% +/- 5% in flexion and 16% +/- 4% in extension. No electromyographic (EMG) abnormalities were observed during flexion. During extension, EMG data provided evidence for abnormally increased antagonist coactivation in brachioradialis and markedly reduced activation in triceps as potential contributors to the decreased extension torques. The finding that movement velocity produces large deficits in maximal torque might explain why functional use of the paretic limb is often impaired even though isometric strength appears adequate.     

Botulinum toxin injection improved voluntary motor control in selected patients with post-stroke spasticity

The effect of botulinum toxin type A injection on voluntary grip control was examined in a 53-year-old female, who sustained a hemorrhagic right middle cerebral artery stroke 3 years previously, which resulted in finger flexor spasticity and residual weak finger/wrist extension. The patient received 50 units of botulinum toxin type A injection each to the motor points (2 sites/muscle) of the left flexor digitorum superficialis and flexor digitorum profundus, respectively. Botulinum toxin injection led to weakness and tone reduction in the spastic finger flexors, but improved grip release time in grip initiation/release reaction time tasks. Improved release time was accompanied by shortened extensor electromyography activity, and improved release time likely correlated with blocked co-contraction of finger flexors during voluntary finger extension. This case report demonstrated that botulinum toxin injection improved voluntary motor control of the hand in a chronic stroke patient with residual finger extension.     

Bimanual force control strategies in chronic stroke: Finger extension versus power grip

Stroke leads to motor asymmetries in the flexor and extensor muscles of the hand. Typically, the strength deficits in the extensors are greater than the flexors. The impact of differential motor abilities of these muscle groups on the execution of bimanual force control tasks in individuals with stroke is unknown. The primary purpose of this study was to determine the influence of task constraints on visually guided bimanual force control in chronic stroke. Stroke survivors and age-matched individuals performed bimanual isometric contractions for 20s to match target submaximal force levels. Online visual feedback of the total force (sum of the forces produced by both hands) was provided. The task constraints were manipulated by (a) finger extension, and (b) finger flexion (power grip). Force asymmetry was indexed by the proportion of force contributed by the paretic hand to the total force. The stroke group demonstrated task-specific asymmetry in bimanual force control. Specifically, the paretic hand contributed less force than the non-paretic hand in finger extension whereas this relationship was reversed in power grip. Importantly, regardless of the nature of the task, reduction in motor impairments was associated with increased symmetry and coordination in bimanual tasks. Further, bimanual submaximal grip force control revealed asymmetry and coordination deficits that are not identified by investigating bimanual maximal force production alone. The motor control strategy adopted to optimize performance on bimanual tasks revealed the altered force production of the paretic hand due to the combined effect of extensor weakness and enhanced flexor bias following stroke. Bimanual asymmetries in stroke survivors highlight the need for identifying and treating the task-specific impairments for maximizing motor recovery post stroke.