Practical issues in retraining walking in severely disabled patients using treadmill and harness support systems.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
L Ada
Publications and source records attributed to L Ada.
Do associated reactions in the upper limb after stroke contribute to contracture formation?
OBJECTIVE: To establish (1) whether associated reactions could contribute to contracture formation and (2) whether the presence of spasticity was essential for their expression, after stroke. SUBJECTS: Subjects were 24 hemiparetics within 13 months of a stroke, unselected for contracture or spasticity. MAIN OUTCOME MEASURES: Associated reactions were identified by the presence of muscle activity in the affected biceps brachii and quantified as the amount of affected elbow flexor torque produced during a moderate contraction of either the contralateral biceps brachii or the contralateral quadriceps muscles. Contracture was measured as loss of elbow joint range of motion and spasticity as the presence of abnormal reflex activity. RESULTS: Associated reactions were present in at least one testing condition in seven subjects. During contractions of the contralateral biceps brachii, the median amount of elbow flexor torque produced was 0.39 (interquartile range, IQR 2.5) Nm while during contractions of the contralateral quadriceps muscle it was 0.19 (IQR 1.6) Nm. Associated reactions were not associated with contracture (p = 0.39) which was present in over half of the subjects. The incidence of associated reactions was about the same as that of spasticity, but the two were not related (p = 0.61). CONCLUSIONS: Even though associated reactions were present in 29% of the subjects during moderate contraction of the contralateral muscles, they were not large, nor were they associated with contracture or spasticity, suggesting that this phenomenon is not usually a major problem for everyday function after stroke.
Adult↗
Abnormal muscle activation characteristics associated with loss of dexterity after stroke.
The aim of this study was to characterise the abnormalities of muscle activation which underlie low dexterity after stroke. A broad definition of dexterity was adopted, where loss of dexterity refers to an inability to coordinate muscle activity in the performance of a motor task (i.e. dexterity was not confined to manual dexterity). EMG of biceps brachii and triceps brachii were monitored from 16 people after stroke and 10 neurologically normal controls as they performed a tracking task requiring coordinated elbow flexion and extension. Weakness could not interfere with performance since the task was designed to require minimal strength. Stroke subjects were assigned to a low (n=10) or high (n=6) dexterity group based on their performance. Spatiotemporal aspects of biceps and triceps EMG were analysed. Low dexterity performance after stroke was characterised by excessive biceps muscle activation (P=0.002) and decreased coupling of muscle activation to target motion (P=0.002). In this study, we could rule out weakness, slowness of muscle activation, excessive co-contraction and spasticity as causes of these abnormalities. Therefore, the loss of dexterity after stroke can be seen as a specific negative impairment which can exist independently of other motor impairments and reflects a loss of skill in generating spatial and temporal muscle activation patterns which conform with environmental demands.
Aged↗
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.
Aged↗
Effect of muscle length on strength and dexterity after stroke.
OBJECTIVE: The effect of muscle length on strength and dexterity after stroke was investigated. The aim was to determine if poor function at a particular muscle length could be attributed solely to differential weakness at this joint angle or whether an additional problem of differential dexterity exists. DESIGN: This descriptive research study measured elbow flexor and extensor strength as well as dexterity at three elbow joint angles: 30 degrees , 60 degrees and 90 degrees flexion. Dexterity was measured independently of strength. SUBJECTS: Fifteen (seven female, eight male) chronic stroke patients (mean age 67 years) who could actively flex and extend their affected elbow participated. Ten neurologically normal control subjects (mean age 67 years) acted as controls. MAIN OUTCOME MEASURES: Strength was measured as peak elbow flexor and extensor torque at three angles; and dexterity was measured as coherence for slow and fast tracking also at three angles. RESULTS: Dexterity was not affected by muscle length but strength was and this finding was the same for both stroke and controls. While the magnitude of the torque-angle curves was not significantly different between stroke and controls, the shape of torque-angle curves was altered after stroke so that both the elbow flexors (p < 0.05) and extensors (p < 0.05) tested weaker in the testing position where they were shortest. CONCLUSION: Since there was no differential loss of dexterity, it appears that differential loss of strength, especially in the shortened range, may explain the clinical observation of poorer function at one muscle length than another after stroke. Specific training to strengthen the muscles in these ranges is therefore of clinical importance for rehabilitation.
Aged↗
Slowness to develop force contributes to weakness after stroke.
OBJECTIVE: To examine weakness after stroke, in terms of both level and rate of torque generation. DESIGN: Descriptive. T tests for dependent and independent samples and Pearson's product moment correlation coefficients were performed. SETTING: A rehabilitation unit. PARTICIPANTS: Ten stroke subjects, aged 56 to 81 years, undergoing rehabilitation. Ten neurologically normal subjects aged 55 to 78 years were the controls. OUTCOME MEASURES: Peak isometric elbow flexor and extensor torque and time to 90% peak elbow flexor and extensor torque at 6 weeks and at 25 weeks after stroke. RESULTS: At 6 weeks after stroke, subjects were only half as strong and took two to three times longer to produce torque compared to controls (p < or = .05). By 25 weeks after stroke, significant improvements in peak torque (p < or = .02) and time to 90% peak flexor torque (p < or = .05) were seen so that values were within normal limits. CONCLUSION: Decreased rate of torque development compounds the problem of reduced peak torque, which may have significant implications for stroke patients, especially in situations where muscles are very weak or where force needs to be generated quickly.
Aged↗
Does spasticity contribute to walking dysfunction after stroke?
OBJECTIVES: Clinically, it is assumed that spasticity of the calf muscles interferes with walking after stroke. The aim was to examine this assumption by evaluating the contribution of spasticity in the gastrocnemius muscle to walking dysfunction in an ambulant stroke population several months after stroke. METHODS: Fourteen stroke patients who were able to walk independently and 15 neurologically normal control subjects were recruited. Both resting and action stretch reflexes of the gastrocnemius muscle were investigated under conditions that simulated walking. Resting tonic stretch reflexes were measured to assess spasticity whereas action tonic stretch reflexes were measured to assess the possible contribution of spasticity to gait dysfunction. RESULTS: Two thirds of the stroke patients exhibited resting tonic stretch reflexes which indicate spasticity, whereas none of the control subjects did. However, the stroke patients exhibited action tonic stretch reflexes that were of similar magnitude to the control subjects, suggesting that their reflex activity during walking was not different from that of control subjects. Furthermore, there was no evidence that the action stretch reflex in the stroke patients contributed a higher resistance to stretch than the control subjects. CONCLUSIONS: Whereas most of the stroke patients exhibited spasticity when measured both clinically and physiologically, they did not exhibit an increase in resistance to dorsiflexion due to exaggerated action tonic stretch reflexes. It is concluded that it is unlikely that spasticity causes problems in walking after stroke in ambulant patients. Therefore, it seems inappropriate to routinely reduce or inhibit the reflex response to improve functional movement in stroke rehabilitation. Factors other than spasticity should be considered when analysing walking after stroke, so that appropriate treatment is provided to patients.
Aged↗
Stroke rehabilitation: are highly structured units more conducive to physical activity than less structured units?
OBJECTIVE: To determine if the physical design and organizational structure of rehabilitation units is related to the amount of patients' motor activity. DESIGN: An observational study was conducted; time samples of the motor activity of patients following stroke were taken between 7AM and 7PM both on weekdays and weekends. SETTING: Two rehabilitation units associated with general hospitals with different physical design and organizational structure. One unit was spread over a large area and had a highly organized daily structure; the other was small and informally organized. SUBJECTS: Inpatients with hemiplegia as a result of stroke who gave consent to participate. MAIN OUTCOME MEASURE: The nature and frequency of 14 motor activities were compared between units. RESULTS: No significant difference was found in any of the observed motor activities between the units when using independent groups t tests (p = 0.1-0.8). Subjects in both units spent more than 70% of their day in activities largely unrelated to physical outcome (eg, conversing with visitors or doing nothing observable) and less than 20% of the day in activities that could potentially contribute to their recovery (eg, in therapy or exercising independently). CONCLUSIONS: Rehabilitation units are not functioning as learning environments. The challenge is to identify and implement measures that will change this finding.
Aged↗
Spasticity and muscle contracture following stroke.
It has become increasingly recognized that the major functional deficits following brain damage are largely due to "negative' features such as weakness and loss of dexterity rather than spasticity. A variety of studies suggest that spasticity is a distinct problem and separate from the loss of dexterity, but that it may be implicated in the formation of muscle contracture and even in the recovery of strength. In order to address these issues, we examined the relationship between spasticity, contracture, strength and dexterity in the affected upper limb following stroke. Spasticity was measured both as increased tonic stretch reflexes and increased resistance to passive stretch (hypertonia). Twenty-four patients were recruited non-selectively from three rehabilitation units within 13 months of their stroke. Few patients exhibited increased tonic reflexes but half were found to have muscle contracture, the earliest at 2 months following stroke. Hypertonia was associated with contracture but not with reflex hyperexcitability. Increased tonic stretch reflexes were observed only in a subgroup of those with contracture and where present could usually be elicited only at the end of muscle range. This findings suggests that instead of spasticity causing contracture, contracture may actually potentiate spasticity in some patients. However, the majority of patients with contracture did not have increased tonic stretch reflexes. In addition, we found no relationship between spasticity and either weakness or loss of dexterity. Therefore, while hypertonia remains an important problem following cerebral lesions, it would appear that the amount of attention directed to reflex hyperexcitability associated with spasticity is out of proportion with its effects. Consequently, hypertonia needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.
Adult↗
Reflex hyperexcitability and muscle contracture in relation to spastic hypertonia.
Mechanisms of spasticity and possible therapeutic interventions continue to dominate research into motor disorders following cerebral lesions. However, the accumulated evidence suggests that this focus on spasticity may be out of step with its effects. In contrast, hypertonia remains an important problem. Further investigation into its link with muscle contracture is required and it needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.
Brain Damage, Chronic↗
Hemodialysis grafts: color Doppler flow imaging correlated with digital subtraction angiography and functional status.
Twenty-two patients with hemodialysis grafts were prospectively evaluated with color Doppler flow imaging and digital subtraction angiography (DSA). Eighteen patients had normal functional parameters during hemodialysis, and four had increased venous pressure during hemodialysis. Color Doppler flow imaging allowed identification of nine macroaneurysms related to wall degeneration, two cases of spontaneous fistula formation between the graft and peripheral veins, and 20 stenoses. Use of color Doppler flow imaging led to overestimation of the degree of stenosis at the venous anastomosis when compared with use of angiography. Three cases of subclavian venous stenosis were identified only at angiography. Color Doppler flow imaging appears accurate in the detection of stenoses and seems sufficient for follow-up of normally functioning grafts. However, because of its low sensitivity for identification of proximal stenoses and the necessity of obtaining an angiogram to plan surgical or percutaneous correction, DSA remains the technique of choice.
Angiography, Digital Subtraction↗
Tonic stretch reflexes in older able-bodied people.
It is a general assumption that, in able-bodied persons, tonic stretch reflex (TSR) activity is not elicited during stretching of relaxed muscles and that the presence of TSR activity following brain damage is, therefore, indicative of spasticity. However, a variety of studies have reported age-related changes in reflex activity, raising the question of whether this assumption is justified in older subjects. The aim of this study was to determine if TSRs were activated in the relaxed elbow flexors of able-bodied people in an age-group at risk of stroke. Electromyographic (EMG) activity was recorded in 30 able-bodied subjects aged 46 to 78 years when their relaxed elbow flexors were subjected to ramp and sinusoidal stretches of different amplitudes and velocities. It was found that these subjects did not exhibit TSR activity under these conditions. Therefore, the practice of measuring TSR activity as a means of quantifying spasticity in stroke patients appears justified.
Aged↗