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Summary
The clinical assessment of spasticity in stroke patients generally includes descriptive scales, such as the Modified Ashworth Scale (MAS) and the Global Pain Scale (GPS), however these may not be sufficiently sensitive to accurately detect improvements, especially at upper limb level; electromyography (EMG) may be the answer to this clinical requirement.
The aim of this study was to quantify the effects of botulinum toxin type A (BTX) in treating upper extremity spasticity in stroke patients, using clinical evaluation (MAS and GPS) and EMG.
Ten patients were assessed before, 30 days and 180 days after BTX injection using clinical evaluations and EMG. At 30 days all clinical measures improved significantly. Whereas MAS scores, after recording an improvement at the first evaluation session, were worse at the second assessment, GPS scores improved over time, both at the first and at the second evaluation session. A reduction of EMG activity was found 30 days after injections, in particular at baseline and during passive flexion movement. Our results demonstrated that measurement of EMG activity may be an effective means of detecting functional improvements and of monitoring the effects of treatment in post-stroke patients.
KEY WORDS: botulinum toxin, electromyography, spasticity, stroke, upper limb
Introduction
Stroke, a major cause of disability involving the upper and lower limbs (1), results in the development of upper motor neuron syndrome (UMNS). This syndrome is commonly associated with spasticity and muscle overactivity, which can lead to abnormal limb posturing, interfering with active and passive function. The origin of the limb deformity in patients with UMNS lies in the concept of unbalanced agonist and antagonist muscle forces acting across joints. Botulinum toxin type A (BTX) is a pharmacological treatment that modifies muscle force and, hence, can treat muscle imbalance. Intramuscular BTX has been demonstrated to be a safe and effective treatment for reducing disability in patients with severe upper limb spasticity, such as those with stroke (2,3). BTX binds to the presynaptic membranes of cholinergic motor neurons and, once internalised, cleaves components of the cell's exocytotic machinery, preventing the discharge of acetylcholine-containing vesicles and hence neurotransmission at the neuromuscular junction (4-6). Consequently, injection of BTX into selected muscles produces dose-dependent chemical denervation resulting in reduced muscular activity lasting about 12-16 weeks (7,8).
BTX...