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Quantitative Measurement of Poststroke Spasticity and Response to Treatment With Botulinum Toxin: A 2-Patient Case Report

E. Cousins, BSc (Hons), is a PhD student, Institute for Life Course Studies, Keele University, Keele, Staffordshire, United Kingdom.
A.B. Ward, BSc, FRCP(Ed), FRCP, is Director, North Staffordshire Rehabilitation Centre, and Professor of Rehabilitation Medicine, University Hospital of North Staffordshire, Stoke on Trent, Staffordshire, United Kingdom.
C. Roffe, MD, FRCP, is Stroke Physician, University Hospital of North Staffordshire, Stoke-on-Trent, Staffordshire, United Kingdom; Clinical Lead, Midlands Stroke Research Network; and Reader, Institute for Life Course Studies, Keele University.
L.D. Rimington, PhD, is Lecturer, Institute for Life Course Studies, Keele University.
A.D. Pandyan, PhD (BioEng), is Senior Lecturer, Institute for Life Course Studies, Keele University, Keele, Staffordshire, United Kingdom ST5 5BG.

Address all correspondence to Dr Pandyan at: a.d.pandyan{at}shar.keele.ac.uk

Background and Purpose. Spasticity (hypertonicity) is a frequent problem that can develop after stroke and can lead to a number of secondary complications, such as contractures and pain. Consequently, many rehabilitation resources are used in treating the condition and its secondary complications. At present, the clinical assessment of spasticity incorporates descriptive scales of resistance to passive movement, but the use of a neurophysiological measure of muscle activity levels has been advocated. This case report focuses on the diagnosis of spasticity through the use of a neurophysiological measure.

Case Descriptions. Two individuals who required botulinum toxin treatment for poststroke spasticity were assessed over a course of 20 weeks with both clinical (Modified Ashworth Scale) and neurophysiological (surface electromyography recording of levels of muscle activity) measures of spasticity. Additionally, arm function, arm movement, and pain were measured. The individuals’ responses to treatment with botulinum toxin and overall recovery after stroke are described.

Outcomes. There were discrepancies between the clinical and the neurophysiological measures of spasticity. The clinical measure of spasticity was not effective in consistently identifying the presence of spasticity and, therefore, also was ineffective in documenting the individuals’ responses to treatment. The neurophysiological measure was able to identify when muscle activity levels had been reduced, but a reduction in muscle activity levels did not always correspond with a reduction in Modified Ashworth Scale scores.

Discussion. The accurate identification of spasticity is important not only for assessment but also for the selection of appropriate treatments after stroke.

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