Precise quantification of the time course of voluntary activation capacity following Botulinum toxin injections in the biceps brachii muscles of chronic stroke survivors.

BACKGROUND: Spasticity is a key motor impairment that affects many hemispheric stroke survivors. Intramuscular botulinum toxin (BT) injections are used widely to clinically manage spasticity-related symptoms in stroke survivors by chemically denervating muscle fibers from their associated motor neurons. In this study, we sought to understand how BT affects muscle activation, motor unit composition and voluntary force generating capacity over a time period of 3 months. Our purpose was to characterize the time course of functional changes in voluntary muscle activity in stroke survivors who are undergoing BT therapy as part of their physician-prescribed clinical plan. METHOD: Our assessment of the effects of BT was based on the quantification of surface electromyogram (sEMG) recordings in the biceps brachii (BB), an upper arm muscle and of voluntary contraction force. We report here on voluntary force and sEMG responses during isometric elbow contractions across consecutive recording sessions, spread over 12 weeks in three segments, starting with a preliminary session performed just prior to the BT injection. At predetermined time points, we conducted additional clinical assessments and we also recorded from the contralateral limbs of our stroke cohort. Eight subjects were studied for approximately 86 experimental recording sessions on both stroke-affected and contralateral sides. RESULTS: We recorded an initial reduction in force and sEMG in all subjects, followed by a trajectory with a progressive return to baseline over a maximum of 12 weeks, although the minimum sEMG and minimum force were not always recorded at the same time point. Three participants were able to complete only one to two segments. Slope values of the sEMG-force relations were also found to vary across the different time segments. While sEMG-force slopes provide assessments of force generation capacity of the BT injected muscle, amplitude histograms from novel sEMG recordings during the voluntary tasks provide additional insights about differential actions of BT on the overall motor unit (MU) population over time. CONCLUSIONS: The results of our study indicate that there are potential short term as well as long term decrements in muscle control and activation properties after BT administration on the affected side of chronic stroke survivors. Muscle activation levels as recorded using sEMG, did not routinely return to baseline even at three months' post injection. The concurrent clinical measures also did not follow the same time course, nor did they provide the same resolution as our experimental measures. It follows that even 12 weeks after intramuscular BT injections muscle recovery may not be complete, and may thereby contribute to pre-existing paresis.

Altered nerve excitability properties after stroke are potentially associated with reduced neuromuscular activation.

OBJECTIVE: To determine limb differences in motor axon excitability properties in stroke survivors and their relation to maximal electromyographic (EMG) activity. METHODS: The median nerve was stimulated to record compound muscle action potentials (CMAP) from the abductor pollicis brevis (APB) in 28 stroke subjects (57.3 ± 7.5 y) and 24 controls (56.7 ± 9.3 y). RESULTS: Paretic limb axons differed significantly from non-paretic limb axons including (1) smaller superexcitability and subexcitability, (2) higher threshold during subthreshold depolarizing currents, (3) greater accommodation (S3) to hyperpolarization, and (4) a larger stimulus-response slope. There were smaller differences between the paretic and control limbs. Responses in the paretic limb were reproduced in a model by a 5.6 mV hyperpolarizing shift in the activation voltage of Ih (the current activated by hyperpolarization), together with an 11.8% decrease in nodal Na+ conductance or a 0.9 mV depolarizing shift in the Na+ activation voltage. Subjects with larger deficits in APB maximal voluntary EMG had larger limb differences in excitability properties. CONCLUSIONS: Stroke leads to altered modulation of Ih and altered Na+ channel properties that may be partially attributed to a reduction in neuromuscular activation. SIGNIFICANCE: Plastic changes occur in the axon node and internode that likely influence axon excitability.

Anomalous EMG-force relations during low-force isometric tasks in hemiparetic stroke survivors.

Hemispheric brain injury resulting from a stroke is often accompanied by muscle weakness in contralateral limbs. In neurologically intact subjects, appropriate motoneuronal recruitment and rate modulation are utilized to optimize muscle force production. In the present study, we sought to determine whether weakness in an affected hand muscle in stroke survivors is partially attributable to alterations in the control of muscle activation. Specifically, our goal was to characterize whether the surface EMG amplitude was systematically larger as a function of (low) force in paretic hand muscles as compared to contralateral muscles in the same subject. We tested a multifunctional muscle, the first dorsal interosseous (FDI), in multiple directions about the second metacarpophalangeal joint in ten hemiparetic and six neurologically intact subjects. In six of the ten stroke subjects, the EMG-force slope was significantly greater on the affected side as compared to the contralateral side, as well as compared to neurologically intact subjects. An unexpected set of results was a nonlinear relation between recorded EMG and generated force commonly observed in the paretic FDI, even at very low-force levels. We discuss possible experimental as well as physiological factors that may contribute to an increased EMG-force slope, concluding that changes in motor unit (MU) control are the most likely reasons for the observed changes.

Disturbances of motor unit rate modulation are prevalent in muscles of spastic-paretic stroke survivors.

Stroke survivors often exhibit abnormally low motor unit firing rates during voluntary muscle activation. Our purpose was to assess the prevalence of saturation in motor unit firing rates in the spastic-paretic biceps brachii muscle of stroke survivors. To achieve this objective, we recorded the incidence and duration of impaired lower- and higher-threshold motor unit firing rate modulation in spastic-paretic, contralateral, and healthy control muscle during increases in isometric force generated by the elbow flexor muscles. Impaired firing was considered to have occurred when firing rate became constant (i.e., saturated), despite increasing force. The duration of impaired firing rate modulation in the lower-threshold unit was longer for spastic-paretic (3.9 ± 2.2 s) than for contralateral (1.4 ± 0.9 s; P < 0.001) and control (1.1 ± 1.0 s; P = 0.005) muscles. The duration of impaired firing rate modulation in the higher-threshold unit was also longer for the spastic-paretic (1.7 ± 1.6 s) than contralateral (0.3 ± 0.3 s; P = 0.007) and control (0.1 ± 0.2 s; P = 0.009) muscles. This impaired firing rate of the lower-threshold unit arose, despite an increase in the overall descending command, as shown by the recruitment of the higher-threshold unit during the time that the lower-threshold unit was saturating, and by the continuous increase in averages of the rectified EMG of the biceps brachii muscle throughout the rising phase of the contraction. These results suggest that impairments in firing rate modulation are prevalent in motor units of spastic-paretic muscle, even when the overall descending command to the muscle is increasing.

Characterizations of reflex and nonreflex changes in spastic multiple sclerosis.

BACKGROUND: Spasticity, an increased resistance of a limb to movement, is associated with functional limitations and a major source of disability in neurological disorders, including multiple sclerosis (MS) and stroke. Despite the clinical significance of spasticity in brain and spinal cord injuries, it is often not clear whether the spasticity is due to reflex or non-reflex changes. NEW METHOD: Reflex and nonreflex properties of the human knee joint were studied in eight MS patients with spasticity and ten healthy subjects. A digitally controlled joint driving device was used to apply small-amplitude, and band-limited white-noise perturbations to the knee to manifest the reflex and nonreflex properties. The subjects were asked to maintain a steady level of background muscle torque during the perturbation. A nonlinear delay differential equation model was used to characterize the reflex and intrinsic properties of the knee in terms of phasic stretch reflex gain, tonic stretch reflex gain, joint elastic stiffness, and coefficient of viscosity. RESULTS: It was found that joint coefficient of viscosity and tonic stretch reflex gain of the spastic MS patients were significantly lower than those of normal controls. On the other hand, spastic MS patients showed higher phasic stretch reflex gains than normal controls and a trend of increased joint stiffness. CONCLUSIONS: Simultaneous characterizations of changes in tonic and phasic reflexes and nonreflex changes in joint elastic stiffness and viscosity in neurological disorders may help us gain insight into mechanisms underlying spasticity and develop impairment-specific treatment.

The effects of Robotic-Assisted Locomotor training on spasticity and volitional control.

We studied the effects of Robotic-Assisted Locomotor (LOKOMAT) Training on spasticity and volitional control of the spastic ankle in persons with incomplete Spinal Cord Injury (SCI). LOKOMAT training was performed 3 days/week during a 1-hr period including set-up time with up to 30 minutes of training during a single session. The training was provided for 4 weeks and subjects were evaluated before and after 1, 2, and 4 weeks of training. Spasticity was charterized in terms of neuromuscular abnormalities associated with the spastic joint. A system identification technique was used to quantify the effects of LOKOMAT training on these neuromuscular abnormalities. The effect of LOKOMAT training on volitional control was determined by measuring isometric maximum voluntary contraction (MVC) of ankle extensor and flexor muscles. Our results indicated that the reflex stiffness, abnormally increases in SCI, was significantly reduced (up to 65%) following 4-weeks of LOKOMAT training. Similarly, intrinsic (muscular) stiffness, which also abnormally increases in SCI, decreased significantly (up to 60%). MVCs were increased substantially (up to 93% in extensors and 180% in flexors) following 4-week training. These findings demonstrate that LOKOMAT training is effective in reducing spasticity and improving volitional control in SCI.

Origins of spontaneous firing of motor units in the spastic-paretic biceps brachii muscle of stroke survivors.

One potential expression of altered motoneuron excitability following a hemispheric stroke is the spontaneous unit firing (SUF) of motor units at rest. The elements contributing to this altered excitability could be spinal descending pathways, spinal interneuronal networks, afferent feedback, or intrinsic motoneuron properties. Our purpose was to examine the characteristics of spontaneous discharge in spastic-paretic and contralateral muscles of hemiparetic stroke survivors, to determine which of these mechanisms might contribute. To achieve this objective, we examined the statistics of spontaneous discharge of individual motor units and we conducted a coherence analyses on spontaneously firing motor unit pairs. The presence of significant coherence between units might indicate a common driving source of excitation to multiple motoneurons from descending pathways or regional interneurons, whereas a consistent lack of coherence might favor an intrinsic cellular mechanism of hyperexcitability. Spontaneous firing of motor units (i.e., ongoing discharge in the absence of an ongoing stimulus) was observed to a greater degree in spastic-paretic muscles (following 83.2 ± 16.7% of ramp contractions) than that in contralateral muscles (following just 14.1 ± 10.5% of ramp contractions; P < 0.001) and was not observed at all in healthy control muscle. The average firing rates of the spontaneously firing units were 8.4 ± 1.8 pulses/s (pps) in spastic-paretic muscle and 9.6 ± 2.2 pps in contralateral muscle (P < 0.001). In 37 instances (n = 63 pairs), we observed spontaneous discharge of two or more motor units simultaneously in spastic-paretic muscle. Seventy percent of the dually firing motor unit pairs exhibited significant coherence (P < 0.001) in the 0- to 4-Hz bandwidth (average peak coherence: 0.14 ± 0.13; range: 0.01-0.75) and 22% of pairs exhibited significant coherence (P < 0.001) in the 15- to 30-Hz bandwidth (average peak coherence: 0.07 ± 0.06; range: 0.01-0.31). We suggest that the spontaneous firing was likely not attributable solely to enhanced intrinsic motoneuron activation, but attributable, at least in part, to a low-level excitatory synaptic input to the resting spastic-paretic motoneuron pool, possibly from regional or supraspinal centers.

Predication of reflex recovery after stroke using quantitative assessments of motor impairment at 1 month.

The objective of this study was to characterize the time-course of changes reflex stiffness after stroke, and to use the Fugl-Meyer Assessment (FMA) at 1 month to predict the ensuing recovery patterns over 1 year. We quantified the modulation of reflex stiffness as a function of elbow joint angles at 1, 2, 3, 6, and 12 months after stroke, using a parallel cascade system identification technique. We then used the "growth mixture" and logistic regression models to characterize recovery patterns over 1 year and to predict these patterns, based on the FMA score at 1 month. We observed two major distinct recovery classes for the relationship between reflex stiffness and elbow angle. The FMA at 1 month was a significant predictor of reflex stiffness as a function of elbow angle at different time points in the first year. The logistical regression class membership may enable us to accurately predict reflex behavior during the first year, information of great potential value for planning targeted therapeutic interventions. Finally, the findings suggest that abnormal reflex function could contribute to functional motor impairment.

Natural history of neuromuscular properties after stroke: a longitudinal study.

BACKGROUND: A rigorous description of the time course of changes in neuromuscular properties after stroke may help us to understand the mechanisms underlying major motor impairments, and it will also help us track the efficacy of rehabilitation treatments. Such time course data have not been collected to date, primarily because of the lack of accurate tools for separating muscular and neural functional measures. OBJECTIVE: To characterise the time course of changes in elbow neuromuscular properties in hemiparetic stroke survivors over a 1 year period. METHODS: Using a system identification technique based on mechanical perturbations of elbow angle, we estimated intrinsic mechanical properties of muscles and stretch reflex parameters at 1, 2, 3, 6 and 12 months after stroke, at different mean elbow joint angles. RESULTS: There were substantial and progressive changes in intrinsic and reflex stiffness in paretic elbow muscles, at all five selected time points, and over a range of mean joint angles. Two temporal patterns of change in these neuromuscular properties were identified. In the first, intrinsic and reflex stiffness increased continuously after the stroke while in the second, intrinsic stiffness decreased continuously over this 12 month interval. CONCLUSIONS: These different recovery patterns may reflect the emergence of two simultaneous but potentially opposing mechanisms; brain recovery and changes in peripheral neuromuscular properties. One consequence is that global joint stiffness measures may be misleading as opposing contributions from intrinsic and reflex neuromuscular subcomponents may confound our interpretation of the mean joint stiffness estimates.

Time course of changes in neuromuscular properties following stroke.

To characterize the natural history of stroke effects on neuromuscular properties in elbow muscles, we tracked changes in elbow mechanical properties in hemiparetic stroke survivors after stroke. Using a parallel cascade system identification technique, we estimated intrinsic and reflex mechanical properties at 1, 2, 3, 6 and 12 months post stroke. At each time point, we examined neuromuscular changes during variations in mean elbow joint angle. Modulation of intrinsic and reflex properties was assessed using small amplitude pseudorandom positional perturbations at different mean elbow angles, over the entire range of motion. We identified two patterns of stroke effects on neuromuscular properties. In Group 1, intrinsic stiffness increased continuously after the stroke. In Group 2, it decreased continuously over this interval. Analogous results were recorded for reflex stiffness. These different recovery patterns may reflect the simultaneous emergence of two opposing mechanisms; i.e. brain recovery and secondary effects on neuromuscular properties. It follows that the progress of recovery may not reflect a single mechanism, and could depend on which mechanism is dominant at each time point.

Recovery of arm movement after stroke.

To characterize the time-course of change in motor impairment, we examined voluntary elbow movement in stroke survivors over a period of one year post-stroke. We quantified several kinematic features of voluntary rapid elbow extension, by measuring the movement trajectory and its derivatives. The subjects were examined five times, at 1-, 2-, 3-, 6- and 12-months post-stroke. The data analyses had two steps. First we used the "growth mixture" model to characterize the recovery patterns of these kinematic parameters. Based on the observed measurements over 1 year, we found two classes of recovery patterns for each kinematic parameter. Subjects in class 1 started with a low value for each parameter and these values increased over time, while subjects in class 2 tended to start with higher value and showed widely divergent recovery patterns. Second, we used the logistic regression analysis to predict these recovery patterns based on Fugl Mayer Scale (FMS) of upper extremity measured on the first visit (i.e. 1 month after stroke). Based on the clinical evaluation of motor function (i.e. FMS) within the first month after stroke, these findings enable us to predict the recovery of arm impaired voluntary movement in hemiparetic stroke subjects at different times during the first year, and potentially beyond.

Neuromuscular abnormalities associated with spasticity of upper extremity muscles in hemiparetic stroke.

Our objective was to assess the mechanical changes associated with spasticity in elbow muscles of chronic hemiparetic stroke survivors and to compare these changes with those recorded in the ankle muscles of a similar cohort. We first characterized elbow dynamic stiffness by applying pseudorandom binary positional perturbations to the joints at different initial angles, over the entire range of motion, with subjects relaxed. We separated this stiffness into intrinsic and reflex components using a novel parallel cascade system identification technique. In addition, for controls, we studied the nonparetic limbs of stroke survivors and limbs of age-matched healthy subjects as primary and secondary controls. We found that both reflex and intrinsic stiffnesses were significantly larger in the stroke than in the nonparetic elbow muscles, and the differences increased as the elbow was extended. Reflex stiffness increased monotonically with the elbow angle in both paretic and nonparetic sides. In contrast, the modulation of intrinsic stiffness with elbow position was different in nonparetic limbs; intrinsic stiffness decreased sharply from full- to mid-flexion in both sides, then it increased continuously with the elbow extension in the paretic side. It remained invariant in the nonparetic side. Surprisingly, reflex stiffness was larger in the nonparetic than in the normal control arm, yet intrinsic stiffness was smaller in the nonparetic arm. Finally, we compare the angular dependence of paretic elbow and ankle muscles and show that the modulation of reflex stiffness with position was strikingly different.

A comparison of the effects of imposed extension and flexion movements on Parkinsonian rigidity.

OBJECTIVE: To test a hypothesis that Parkinsonian rigidity is more pronounced in imposed extension than flexion movement. METHODS: Twelve Parkinsonian subjects (both "Off" and "On" medication states) and seven control subjects participated in the protocol, in which a servomotor imposed wrist flexion and extension. Rigidity was quantitatively evaluated by the rectified torque integral with time, i.e., temporal score, and by the torque integral with joint angle, i.e., work score, for extension and flexion, respectively. RESULTS: In the "Off" state, the imposed extension induced a significantly higher resistance than did flexion. Dopaminergic medication significantly reduced the temporal score associated with imposed extension, and significantly decreased the work score of both movements. Compared with controls, the scores were higher for patients in the "On" state. CONCLUSIONS: Rigidity is more readily elicited in extension movement. The distinction is not evident in clinical practice, whereas it can be clearly revealed with the application of biomechanical analyses. SIGNIFICANCE: This distinction may prove to be a standard feature of rigidity. The procedures may be helpful in diagnosis and useful in evaluating new treatments and developing rehabilitation programs.

Comparison of neuromuscular abnormalities between upper and lower extremities in hemiparetic stroke.

We studied the neuromuscular mechanical properties of the elbow and ankle joints in chronic, hemiparetic stroke patients and healthy subjects. System identification techniques were used to characterize the mechanical abnormalities of these joints and to identify the contribution of intrinsic and reflex stiffness to these abnormalities. Modulation of intrinsic and reflex stiffness with the joint angle was studied by applying PRBS perturbations to the joint at different joint angles. The experiments were performed for both spastic (stroke) and contralateral (control) sides of stroke patients and one side of healthy (normal) subjects. We found reflex stiffness gain (GR) was significantly larger in the stroke than the control side for both elbow and ankle joints. GR was also strongly position dependent in both joints. However, the modulation of GR with position was slightly different in two joints. GR was also larger in the control than the normal joints but the differences were significant only for the ankle joint. Intrinsic stiffness gain (K) was also significantly larger in the stroke than the control joint at elbow extended positions and at ankle dorsiflexed positions. Modulation of K with the ankle angle was similar for stroke, control and normal groups. In contrast, the position dependency of the elbow was different. K was larger in the control than normal ankle whereas it was lower in the control than normal elbow. However, the differences were not significant for any joint. The findings demonstrate that both reflex and intrinsic stiffness gain increase abnormally in both upper and lower extremities. However, the major contribution of intrinsic and reflex stiffness to the abnormalities is at the end of ROM and at the middle ROM, respectively. The results also demonstrate that the neuromuscular properties of the contralateral limb are not normal suggesting that it may not be used as a suitable control at least for the ankle study.

Changes of Reflex, Non-reflex and Torque Generation Properties of Spastic Ankle Plantar Flexors Induced by Intelligent Stretching.

Spasticity, contracture, and muscle weakness are major sources of disability in stroke. Changes of torque-generating capacity as well as reflex and non-reflex properties of ankle plantar flexors induced by strenuous stretching in chronic hemiplegia were investigated. Twelve subjects with a unilateral stroke and 10 healthy controls underwent 30 minutes of strenuous intelligent stretching treatment. Reflex and non-reflex components of spastic hypertonia and force-generating capacity of ankle plantar flexors were investigated. Dorsiflexion (DF) range of motion (ROM) was increased (p=0.002) and passive stiffness and passive resistant torque of the spastic muscles were decreased (p=0.004 and 0.007, respectively), while reflex hyper-excitability diminished slightly but with no statistical significance. The maximal voluntary contraction (MVC) torque of the spastic ankle plantar flexors was increased after the forceful stretching treatment (p=0.041). In contrast, the stretching treatment of the healthy plantar flexors did not change any of the variables measured before and after stretching. The stroke subjects who gained more DF ROM or larger decrement of stiffness achieved greater increment of the peak torque generation after the stretching (r=0.597 with p=0.040 and r=-0.746 with p=0.005, respectively). These results suggest that the strenuous dynamic stretching could improve the force-generating capacity of spastic muscles as well as reduce the passive stiffness and increase ROM.

Evolution of reflexive and muscular mechanical properties in stroke-induced spasticity.

We studied the natural history of reflexive and mechanical properties in hemiparetic spastic stroke subjects. System identification techniques were used to characterize the mechanical abnormalities of the elbow joint and to identify the contribution of intrinsic and reflex stiffness to these abnormalities over one year post-injury. Modulation of intrinsic and reflex stiffness of the elbow joint was studied by applying PRBS perturbations to the elbow at different joint angles at five intervals following stroke. We found that both reflex and intrinsic stiffness were larger in the stroke than in the control arms. They were also strongly position dependent; they both increased with increasing elbow extension but reflex stiffness declined at full extension in some subjects. This position dependency was consistent during stroke recovery. Both intrinsic and reflex abnormally increased over time after stroke. These findings help better understanding of the origins of mechanical abnormalities associated with spasticity and document the time course of these abnormalities during stroke recovery.

Reflex reciprocal facilitation of antagonist muscles in spinal cord injury.

STUDY DESIGN: Electromyographic study in complete and incomplete spinal cord injury (SCI). OBJECTIVE: To examine the changes in the pattern of reciprocal inhibition between agonist and antagonist muscles in SCI. SETTINGS: Sensory Motor Performance Program, Rehabilitation Institute of Chicago, IL, USA. METHODS: Tendon taps were delivered manually with an instrumented hammer to the tendons of the tibialis anterior and soleus muscle in positions of full-ankle dorsiflexion and plantarflexion in eight subjects with complete SCI and eight subjects with incomplete SCI. Electromyographic activity (EMG) was recorded from ankle dorsiflexor and plantarflexor muscles. Tapping force was also recorded by a force sensor mounted to the tendon hammer, indicating the stimulus onset. Measures of reflex EMG magnitude and reflex latency were obtained for both agonist and antagonist muscles. The ratio of antagonist to agonist EMG was computed based on normalized EMG. RESULTS: Substantial reflex responses occurred in both the stretched muscle and in its antagonist. The reflex in antagonist, which we term 'reciprocal facilitation (RF)', was most evident in subjects with incomplete SCI. The magnitude of RF was consistently greater than reflex responses in agonist muscles under all test conditions. The latency of the RF was comparable to that of monosynaptic reflex response. CONCLUSIONS: Following SCI, reciprocal organization of segmental reflexes at the ankle is often partially or completely suppressed, allowing reflex activation in antagonist muscles to be manifested. Possible mechanisms underlying these changes in neural organization are discussed. SPONSORSHIP: This study was supported by Spinal Cord Research Foundation, the Paralyzed Veterans of America.

Neuromuscular reflexes contribute to knee stiffness during valgus loading.

We have previously shown that abduction angular perturbations applied to the knee consistently elicit reflex responses in knee joint musculature. Although a stabilizing role for such reflexes is widely proposed, there are as of yet no studies quantifying the contribution of these reflex responses to joint stiffness. In this study, we estimate the mechanical contributions of muscle contractions elicited by mechanical excitation of periarticular tissue receptors to medial-lateral knee joint stiffness. We hypothesize that these reflex muscle contractions will significantly increase knee joint stiffness in the adduction/abduction direction and enhance the overall stability of the knee. To assess medial-lateral joint stiffness, we applied an abducting positional deflection to the fully extended knee using a servomotor and recorded the torque response using a six degree-of-freedom load-cell. EMG activity was also recorded in both relaxed and preactivated quadriceps and hamstrings muscles with surface electrodes. A simple, linear, second-order, delayed model was used to describe the knee joint dynamics in the medial/lateral direction. Our data indicate that excitation of reflexes from periarticular tissue afferents results in a significant increase of the joint's adduction-abduction stiffness. Similar to muscle stretch reflex action, which is modulated with background activation, these reflexes also show dependence on muscle activation. The potential significance of this reflex stiffness during functional tasks was also discussed. We conclude that reflex activation of knee muscles is sufficient to enhance joint stabilization in the adduction/abduction direction, where knee medial-lateral loading arises frequently during many activities.

Adaptive assistance for guided force training in chronic stroke.

This work describes a novel form of robotic therapy for the upper extremity in chronic stroke. Based on previous results, we hypothesized that a training task that encourages subjects to consciously guide endpoint forces generated by the hemiparetic arm will result in significant gains in functional ability of the arm, superior to more conventional methods of therapy. In addition, since stroke survivors present with varying degrees of arm movement ability, we developed an adaptive algorithm that tailors the amount of assistance provided in completing the guided force training task. The algorithm adapts a coefficient for velocity-dependent assistance based on measured movement speed, on a trial-to-trial basis. The training algorithm has been implemented with a simple linear robotic device called the ARM Guide. One participant completed a two month training program with the adaptive algorithm, resulting in significant improvements in the performance of functional tasks.

Abnormal intrinsic and reflex stiffness related to impaired voluntary movement.

We studied the relationship between mechanical abnormalities associated with spasticity and impairments in voluntary movements of the spastic joint in chronic, hemiparetic stroke subjects. System identification techniques were used to characterize the mechanical abnormalities of the elbow joint and to identify the contribution of intrinsic and reflex stiffness to these abnormalities. Repeated voluntary movements of the elbow from full flexion to extension at maximum speed were also conducted. These movements were quantified by measuring their kinematics parameters. The correlation coefficient was measured to determine the relationship between abnormal modulation of intrinsic and reflex stiffness as function of joint position with the kinematics parameters. We found that both intrinsic and reflex stiffness were significantly larger in stroke than control sides and were strongly position dependent, increasing with elbow extension. Abnormal modulation of intrinsic and reflex stiffness with position (slope) was correlated with an increase in duration of movement (DM), and a decrease in peak-velocity (Pv), peak-acceleration (Pa) and maximum voluntary contraction (MVC). Weakness, quantified as a decrease in MVC, was also correlated with the reduction in Pv, Pa and active range of motion (AROM). These findings demonstrate that abnormal modulation of both intrinsic and reflex stiffness with position are related to antagonist muscle weakness that may cause stroke patients to move slower and take longer to complete reaching tasks.