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Spasticity can be painful, interfere with functional recovery and hinder rehabilitation efforts. If not managed appropriately, stroke survivors may experience a loss of range of motion at involved joints of the arms, which can result in contracture. Although it is a common in clinical practice to use range-of-motion or stretching exercises and splints to prevent or treat spasticity or contracture following stroke, there is a lack of evidence supporting their benefit. Harvey et al. (2017) included the results of 49 RCTs in a Cochrane review including participants with neurological condition, advance age, those with a history of trauma and those with underlying joint or muscle pathology. Of these, 11 trials included stroke cohorts treated for upper limb impairment. Trials evaluated the effect of stretching programs (casting, splinting, self-administered, positioning, and sustained passive stretch) on preventing contractures. Stretching programs did not significantly increase joint mobility, improve spasticity, activity limitations, or pain either after the intervention or at follow-up, when compared with usual care. Splints have been widely-used in clinical practice with the aim of the prevention of contractures and reducing spasticity; however, evidence of their effectiveness is lacking. Basaran et al. (2012) randomized 39 participants to participate in a 5-week, home-based exercise program in which patients were advised to stretch wrist and finger flexors for 10 repetitions and to try reaching and grasping an object for 10 repetitions 3x/day, in addition to conventional therapy. Patients in the 2 experimental groups wore either a volar or dorsal splint for up to 10 hours overnight throughout the study period, while patients in the control group wore no splint. At the end of the study period, there were no significant differences among groups in terms of reductions in spasticity or wrist passive range of motion.
While it is well-established that treatment with Botulinum toxin–type A (BTX-A) reduces focal spasticity in the finger, wrist and elbow, it remains uncertain whether there is also improvement in upper-limb function. In the BOTOX® Economic Spasticity Trial (BEST), 273 persons with chronic post-stroke upper and lower limb spasticity were randomized to receive a single dose of BTX-A with an optional second dose offered ≥ 12 weeks after the first, or placebo in addition to usual care. Dosing and site of injection was based on clinician judgement. In the publication of the trial that was dedicated to functional outcomes (Ward et al. 2014), there were no significant differences between groups at weeks 12, 24 or 52 with respect to the percentage of patients who achieved their principal active functional goal (33.1% vs. 28.9%, 40.9% vs. 33.3% and 45.0% vs. 52.4%, respectively), although a higher number of persons in the BT-XA groups achieved their secondary passive functional goals at 24 weeks, (60.6% vs. 38.6%, p=0.016), but not at weeks 12 or 52. BTX-A was more effective than placebo in reducing pain from baseline to week 12 (Wissel et al. 2016). Higher proportions of patients with pain in the BTX-A group achieved ≥30% and ≥50% reductions in pain. Shaw et al. (2011) randomized 333 subjects < 1 month following stroke with spasticity of the elbow (MAS>2) and/or spasticity of the shoulder, wrist or hand with reduced arm function to receive 100 or 200 U Dysport in addition to a standardized therapy program provided for 1 hour/day, 2x/week for 4 weeks) or therapy program only. Repeat injections were available to subjects in the intervention group at 3, 6 and 9 months. There was no significant difference in the percentage of patients who had achieved a successful outcome (defined by 3 different levels of improvement on the Action Research Arm Test, depending on baseline arm function) at one month following treatment: 25% of patients in the treatment group compared with 19.5% of patients in the control group (p=0.232). However, significant differences in favor of the intervention group were seen in muscle tone at 1 month; upper limb strength at 3 months; basic arm functional tasks (hand hygiene, facilitation of dressing) at 1, 3, and 12 months, and pain at 12 months. McCrory et al. (2009) reported there were no significant between group differences in Assessment of Quality of Life scale change scores, pain, mood, disability or carer burden at 20 weeks in 102 patients with moderate to severe spasticity of the arm, who received 750-1,000 U Dysport or placebo an average of 6 years following stroke.
In cases where spasticity is generalized, and it would be impractical, or contrary to patients’ wishes to inject multiple muscle groups with BTX-A, the use of oral agents may be considered as an alternative treatment. Traditional pharmacotherapies for spasticity include centrally acting depressants (baclofen and tizanidine) and muscle relaxants; (dantrolene) however; these treatments are only partially effective in treating spasticity and have the negative side effects of weakness and sedation. Treatment with oral baclofen has not been well studied in the stroke population and is used more frequently in patients recovering from spinal cord injury. Tizanidine has been well-studied in other conditions including multiple sclerosis and acquired brain injury, and has a better side effect profile than other oral agents. There is only a single open-label trial of the use of tizanidine post stroke (Gelber et al. 2001). Following 16 weeks of treatment in which 47 patients received a maximum daily dose of 36 mg (mean 20 mg), there was a decrease in mean combined total modified Ashworth Scale scores (9.3 vs. 6.5, p=0.038). There were also significant improvements in pain, quality of life, and physician assessment of disability.