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January 14, 2013

Pathophysiology of spasticity in stroke

January 15, 2013 issue
80 (3_supplement_2) S20-S26


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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Information & Authors


Published In

Volume 80Number 3_supplement_2January 15, 2013
Pages: S20-S26

Publication History

Published online: January 14, 2013
Published in print: January 15, 2013


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Affiliations & Disclosures

David Burke, MD, DSc
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.
Jörg Wissel, MD, FRCP
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.
Geoffrey A. Donnan, MD
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.


Correspondence to Dr. Burke: [email protected]
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®.


Dr. Burke serves as editor-in-chief for Clinical Neurophysiology and as an editorial board member of The Journal of Clinical Neuroscience. He serves and has served in the past as chief investigator for research funded by NHMRC Project Grants, and has also received funding from the Sydney Foundation for Medical Research, the Philip Bushell Foundation, and the Brain Foundation. Dr. Wissel served on scientific advisory boards for and received speaker honoraria, funding for travel, and research support from Allergan, Inc., Merz Pharmaceuticals, Medtronic, and Ipsen Pharma. Dr. Donnan served on scientific advisory boards for and received speaker honoraria and funding for travel from Allergan, Boehringer Ingelheim, Bayer, and Sanofi. He also served as a journal editor/associate editor/editorial board member of Lancet Neurology, Stroke, Cerebrovascular Diseases, and the International Journal of Stroke.

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