Abstract
Objective:
Does early treatment of spasticity with botulinum-toxin (BoNTA), in (hyper)acute stroke patients without arm-function, reduce contractures and improve function.
Design:
Randomised placebo-controlled-trial
Setting:
Specialised stroke-unit.
Participants & Intervention:
Patients with an Action Research Arm Test (ARAT) grasp-score⩽2 who developed spasticity within six-weeks of a first stroke were randomised to receive injections of: 0.9%sodium-chloride solution (placebo) or onabotulinumtoxin-A (treatment).
Outcome-Measures:
Spasticity, contractures, splint use and arm function (ARAT) were taken at baseline, 12-weeks post-injection and six-months after stroke. Additionally, spasticity and contractures were measured at weeks-two, four and six post-injection.
Results:
Ninety three patients were randomised. Mean time to intervention was 18-days (standard deviation = 9.3). Spasticity was lower in the treatment group with difference being significant between week-2 to 12 (elbow) and week-2 to 6 (wrist). Mean-difference (MD) varied between –8.5(95% CI –17 to 0) to –9.4(95% CI –14 to –5) µV.
Contracture formation was slower in the treatment group. Passive range of motion was higher in the treatment group and was significant at week-12 (elbow MD6.6 (95% CI –0.7 to –12.6)) and week-6 (wrist MD11.8 (95% CI 3.8 to 19.8)). The use of splints was lower in the treatment group odds ratio was 7.2 (95% CI 1.5 to 34.1) and 4.2 (95% CI 1.3 to 14.0) at week-12 and month-6 respectively.
Arm-function was not significantly different between the groups MD2.4 (95% CI –5.3 to 10.1) and 2.9 (95% CI –5.8 to 11.6) at week-12 and month-6 respectively.
Conclusion:
BoNTA reduced spasticity and contractures after stroke and effects lasted for approximately 12-weeks. BoNTA reduced the need for concomitant contracture treatment and did not interfere with recovery of arm function.
Introduction
Recovery of arm function in people who survive a stroke is commensurate with severity of impairment at stroke onset.1 Those people who have severe impairment of the arm at onset and who do not recover useful arm function, are likely to develop contractures.2,3 Contracture formation is exacerbated in those who have certain forms of spasticity.4–6 It can therefore be hypothesised that the lack of movement (as a result of the paralysis) in addition to the fixed positioning (associated with some forms of spasticity) accelerate the formation of contractures.6
Contractures are characterised by the combination of increased stiffness and loss of range of movement at a joint. Contractures can be established within four weeks of a stroke and 52% of stroke survivors have developed a contracture at six months.4,7,8 In some cases where motor recovery is delayed, it is possible that contractures could limit the recovery of meaningful function rather than the lack of neuro-plastic potential.
One way of slowing contracture development is through intensive mobilisation using cyclical electrical stimulation and this has been demonstrated previously in stroke patients at risk of wrist flexion contractures.9 The aim of this study was to explore if preventing the fixed positioning associated with spasticity (using additional treatment with botulinum toxin) could reduce both contractures and the rate at which contractures were formed. It was hypothesised that the reduction of spasticity and contractures would lead to a subsequent improvement in arm function. This study, therefore, also aimed to quantify changes in arm function following treatment. […]
TBI Rehabilitation 