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J Neurol Neurosurg Psychiatry 1998;64:628-635 doi:10.1136/jnnp.64.5.628
  • Paper

Does spasticity contribute to walking dysfunction after stroke?

  1. Louise Ada,
  2. Wantana Vattanasilp,
  3. Nicholas J O’Dwyer,
  4. Jack Crosbie
  1. School of Physiotherapy, Faculty of Health Sciences, The University of Sydney, PO Box 170, Lidcombe NSW 2141, Australia
  1. Dr Louise Ada, School of Physiotherapy, Faculty of Health Sciences, The University of Sydney, PO Box 170, Lidcombe NSW 2141, Australia. Telephone 00612 6466544; fax 00612 6466278; email L.Ada{at}cchs.su.edu.au
  • Received 21 January 1997
  • Revised 12 November 1997
  • Accepted 19 November 1997

Abstract

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.

Footnotes

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