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January 15, 2013; 80 (3 Supplement 2) Article

Pathophysiology of spasticity in stroke

David Burke, Jörg Wissel, Geoffrey A. Donnan
First published January 14, 2013, DOI: https://doi.org/10.1212/WNL.0b013e31827624a7
David Burke
From the Department of Neurology (D.B.), Royal Prince Alfred Hospital and University of Sydney, Australia; Neurorehabilitation Hospital (J.W.), Klinkiken Beelitz GmbH, Clinical Department of Neurological Rehabilitation, Beelitz-Heilstaetten, Germany; and Florey Neuroscience Institutes (G.A.D.), University of Melbourne, Carlton South, Victoria, Australia.
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Jörg Wissel
From the Department of Neurology (D.B.), Royal Prince Alfred Hospital and University of Sydney, Australia; Neurorehabilitation Hospital (J.W.), Klinkiken Beelitz GmbH, Clinical Department of Neurological Rehabilitation, Beelitz-Heilstaetten, Germany; and Florey Neuroscience Institutes (G.A.D.), University of Melbourne, Carlton South, Victoria, Australia.
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Geoffrey A. Donnan
From the Department of Neurology (D.B.), Royal Prince Alfred Hospital and University of Sydney, Australia; Neurorehabilitation Hospital (J.W.), Klinkiken Beelitz GmbH, Clinical Department of Neurological Rehabilitation, Beelitz-Heilstaetten, Germany; and Florey Neuroscience Institutes (G.A.D.), University of Melbourne, Carlton South, Victoria, Australia.
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Citation
Pathophysiology of spasticity in stroke
David Burke, Jörg Wissel, Geoffrey A. Donnan
Neurology Jan 2013, 80 (3 Supplement 2) S20-S26; DOI: 10.1212/WNL.0b013e31827624a7

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Abstract

Spasticity is defined clinically by increased muscle tone and tendon jerk hyperreflexia in patients who are at rest. However, the excitability of spinal circuits changes during movement, and this definition provides no insight into the extent to which spasticity and associated motor disturbances cause disability. Only a few spinal circuits have been shown to underlie the abnormalities of patients at rest. Movement can be restrained by pathologically enhanced muscle tone, and there is defective control of the feedback to active motoneurons through virtually all spinal reflex pathways. Spasticity does not necessarily require treatment: in fact, some patients rely on the increased muscle tone to help support otherwise weak muscle contractions for stance and locomotion. In addition, much of the increase in muscle tone arises from changes in muscle and motor units, independent of reflex mechanisms. Managing a patient with impairment after a stroke requires therapy tailored to that particular patient because the mechanisms contributing to the disability experienced by one patient may differ from those affecting another.

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  • Author disclosures are provided at the end of the article.

  • This Neurology® supplement was not peer-reviewed. Information contained in this Neurology® supplement represents the opinions of the authors. These opinions are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology®.

  • © 2013 American Academy of Neurology
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  • Article
    • Abstract
    • MOTOR DEFICITS ACCOMPANYING HEMIPLEGIA
    • PATHOPHYSIOLOGY OF THE INCREASED MUSCLE TONE OF SPASTICITY
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    • DISCLOSURE
    • ACKNOWLEDGMENT
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