Louise Ada

A treadmill and overground walking program improves walking in persons residing in the community after stroke: A placebo-controlled, randomized trial

OBJECTIVE To evaluate the effectiveness of a treadmill and overground walking program in reducing the disability and handicap associated with poor walking performance after stroke. DESIGN Randomized, placebo-controlled clinical trial with a 3-month follow-up. SETTING General community. PARTICIPANTS A volunteer sample of 29 ambulatory individuals (less 2 dropouts) who were living in the community after having suffered a stroke more than 6 months previously. INTERVENTIONS The experimental group participated in a 30-minute treadmill and overground walking program, 3 times a week for 4 weeks. The control group received a placebo consisting of a low-intensity, home exercise program and regular telephone contact. MAIN OUTCOME MEASURES Walking speed (over 10 m), walking capacity (distance over 6 min), and handicap (stroke-adapted 30-item version of the Sickness Impact Profile) measured by a blinded assessor. RESULTS The 4-week treadmill and overground walking program significantly increased walking speed (P=.02) and walking capacity (P<.001), but did not decrease handicap (P=.85) compared with the placebo program. These gains were largely maintained 3 months after the cessation of training (P</=.05). CONCLUSIONS The treadmill and overground walking program was effective in improving walking in persons residing in the community after stroke. This suggests that the routine provision of accessible, long-term, community-based walking programs would be beneficial in reducing disability after stroke.

Strengthening interventions increase strength and improve activity after stroke: a systematic review

QUESTION Is strength training after stroke effective (ie, does it increase strength), is it harmful (ie, does it increase spasticity), and is it worthwhile (ie, does it improve activity)? DESIGN Systematic review with meta-analysis of randomised trials. PARTICIPANTS Stroke participants were categorised as (i) acute, very weak, (ii) acute, weak, (iii) chronic, very weak, or (iv) chronic, weak. INTERVENTION Strengthening interventions were defined as interventions that involved attempts at repetitive, effortful muscle contractions and included biofeedback, electrical stimulation, muscle re-education, progressive resistance exercise, and mental practice. OUTCOME MEASURES Strength was measured as continuous measures of force or torque or ordinal measures such as manual muscle tests. Spasticity was measured using the modified Ashworth Scale, a custom made scale, or the Pendulum Test. Activity was measured directly, eg, 10-m Walk Test, or the Box and Block Test, or with scales that measured dependence such as the Barthel Index. RESULTS 21 trials were identified and 15 had data that could be included in a meta-analysis. Effect sizes were calculated as standardised mean differences since various muscles were studied and different outcome measures were used. Across all stroke participants, strengthening interventions had a small positive effect on both strength (SMD 0.33, 95% CI 0.13 to 0.54) and activity (SMD 0.32, 95% CI 0.11 to 0.53). There was very little effect on spasticity (SMD -0.13, 95% CI -0.75 to 0.50). CONCLUSION Strengthening interventions increase strength, improve activity, and do not increase spasticity. These findings suggest that strengthening programs should be part of rehabilitation after stroke.

The Tardieu Scale differentiates contracture from spasticity whereas the Ashworth Scale is confounded by it

Objective: To compare the Tardieu Scale as a clinical measure of spasticity after stroke with the Ashworth Scale. Design: Cross-sectional study. Participants: Sixteen people, living in the community three years after their stroke. Main measures: The Ashworth Scale and Tardieu Scale as well as laboratory measures of spasticity (stretch-induced electromyographic (EMG) activity) and contracture (maximum passive joint excursion) were collected from the affected elbow flexors and extensors and ankle plantarflexors and dorsiflexors by three examiners who were blinded to the results of the other measures. Results: The percentage exact agreement (PEA) between the Tardieu Scale and a laboratory measure of spasticity was 100% for both the elbow flexors and ankle plantarflexors. This was significantly (P=0.02) greater than the PEA of 63% for both muscles between the Ashworth Scale and the same laboratory measure of spasticity. For contracture, the PEA between the Tardieu Scale and a laboratory measure was 94% for both the elbow flexors and the ankle plantarflexors. Pearson correlation coefficients between the Tardieu Scale and laboratory measures of spasticity were 0.86 for the elbow flexors and 0.62 for the ankle plantarflexors and between the Tardieu Scale and laboratory measures of contracture were 0.89 for the elbow flexors and 0.84 for the ankle plantarflexors. Conclusion: In all cases that spasticity was overestimated by the Ashworth Scale, participants had a contracture. These findings suggest that the Tardieu Scale differentiates spasticity from contracture whereas the Ashworth Scale is confounded by it.

Loss of strength contributes more to physical disability after stroke than loss of dexterity

Objective: The major contributors to physical disability after stroke are considered to be the negative impairments of loss of dexterity (defined here as loss of the ability to co-ordinate muscle activity in the performance of any motor task) and loss of strength. The aims of this study were: (1) to determine the relative contributions of strength and dexterity to function during recovery after stroke; and (2) to determine the predictive value of initial strength, dexterity and function on long-term function after stroke. Design: A longitudinal descriptive study. Setting: The inpatient and outpatient rehabilitation departments of two metropolitan hospitals. Subjects: Twenty-two patients undergoing rehabilitation after acute stroke participated. Main outcome measures: Strength and dexterity of the elbow flexors and extensors were measured, along with arm function, at 3, 5, 7, 9, 11, 15, 19, 23 and 27 weeks after stroke. Results: Standard multiple linear regression analysis demonstrated that strength and dexterity in total contributed significantly to function at all times (r2 = 0.66-0.82, p < 0.0001). Furthermore, strength always made an additional separate contribution to function (r2 0.05-0.26, p<0.05). Function at week 3 was the best clinical predictor of function at week 27 (r2 0.55, p < 0.001). Conclusions: Loss of strength is a more significant contributor than loss of dexterity to physical disability after stroke. This suggests that, where significant weakness is present, exercise designed to increase strength will be required to decrease disability.

Muscle strengthening is not effective in children and adolescents with cerebral palsy: a systematic review

QUESTION Do strengthening interventions increase strength without increasing spasticity and improve activity, and is there any carryover after cessation in children and adolescents with cerebral palsy? DESIGN Systematic review with meta-analysis of randomised trials. PARTICIPANTS Children with spastic cerebral palsy between school age and 20 years. INTERVENTION Strengthening interventions that involved repetitive, strong, or effortful muscle contractions and progressed as ability changed, such as biofeedback, electrical stimulation, and progressive resistance exercise. OUTCOME MEASURES Strength was measured as continuous measures of maximum voluntary force or torque production. Spasticity was measured as velocity-dependent resistance to passive stretch. Activity was measured as continuous measures, eg, 10-m Walk Test, or using scales eg, the Gross Motor Function Measure. RESULTS Six studies were identified and five had data that could be included in a metaanalysis. Strengthening interventions had no effect on strength (SMD 0.20, 95% CI -0.17 to 0.56), no effect on walking speed (MD 0.02 m/s, 95% CI -0.13 to 0.16), and had a small statistically-significant but not clinically-worthwhile effect on Gross Motor Function Measure (MD 2%, 95% CI 0 to 4). Only one study measured spasticity but did not report the between-group analysis. CONCLUSION In children and adolescents with cerebral palsy who are walking, the current evidence suggests that strengthening interventions are neither effective nor worthwhile.

Relation between spasticity, weakness and contracture of the elbow flexors and upper limb activity after stroke: An observational study

Purpose. Understanding the relationship between the motor impairments and their impact on physical activity will allow rehabilitation after stroke to be based on scientific principles. The aims of this study were to determine: (i) the relative contribution of weakness and spasticity to contracture, and (ii) the relative contribution of all three impairments to limitations in physical activity during the first 12 months after stroke. Method. This longitudinal observational study charted the evolution of weakness (loss of maximal force), spasticity (stretch-evoked EMG) and contracture (loss of joint range) of the elbow flexors and limitations in upper limb activity (Motor Assessment Scale) for a year after stroke in 27 subjects who had suffered a first stroke. Spasticity was measured as abnormal reflex activity, weakness was measured as loss of maximum isometric torque, contracture was measured as the difference in range of motion between the affected and intact side, and limitations in physical activity were measured on a clinical scale. Results. The major independent contributors to contracture were spasticity for the first four months after stroke (p = 0.0001 – 0.10) and weakness thereafter (p = 0.01 – 0.05). However, the major and only independent contributor to limitations in physical activity throughout the year was weakness (p = 0.0001 – 0.05). Conclusions. For the first time, from a longitudinal study, the findings show that spasticity can cause contracture after stroke, consistent with the prevailing clinical view. However, weakness is the main contributor to activity limitations.

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.

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.

Efficacy of electrical stimulation in preventing or reducing subluxation of the shoulder after stroke: A meta-analysis

After stroke, up to 81% of individuals develop shoulder subluxation, a condition frequently associated with poor upper limb function. Recently, electrical stimulation has been applied to shoulder muscles to treat shoulder subluxation. The purpose of this meta-analysis was to examine the efficacy of surface electrical stimulation for the prevention or reduction of shoulder subluxation after stroke. A meta-analysis of all eligible randomised or quasi-randomised trials of electrical stimulation for the treatment of shoulder subluxation identified by computerised and hand searches of the literature was carried out. The primary outcome measure of interest was subluxation. Seven (four early and three late) trials met the inclusion criteria. The mean PEDro score out of 10 for quality of the methods was 5.8 for the four early trials and 4.3 for the three late trials. Data were pooled when subluxation was measured in millimetres. Analysis found that, when added to conventional therapy, electrical stimulation prevented on average 6.5mm of shoulder subluxation (weighted mean difference, 95% CI 4.4 to 8.6) but only reduced it by 1.9mm (weighted mean difference, 95% CI -2.3 to 6.1) compared with conventional therapy alone. Therefore, evidence supports the use of electrical stimulation early after stroke for the prevention of, but not late after stroke for the reduction of, shoulder subluxation.

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.