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LETTER |
ParaCare, Institute for Rehabilitation and Research, University Hospital Balgrist, Forchstr 340, 8008 Zurich, Switzerland
Correspondence to:
Correspondence to:
Professor Dr V Dietz;
dietz@balgrist.unizh.ch
Keywords: spastic paresis; clinical practice
| The first 150 words of the full text of this article appear below. |
One expects that convincing research results would have an impact on clinical practice. However, whether or not a new concept becomes transferred to an application in clinical practice is dependent on the medical field and on the therapeutic consequences. The issue discussed here concerns spasticity, a common motor disorder in, for example, patients who have had a stroke or a spinal cord injury.
The traditional concept
Over many years it was widely accepted that spasticity consists of muscle hypertonia (that is, "a velocity dependent resistance of a muscle to stretch"1) caused by exaggerated reflexes, leading to the spastic movement disorder.2 This concept was based on animal experiments (for example, in the decerebrate cat3) and on the physical signs evident on clinical examination at the bedside. Consequently, the aim of any treatment was to reduce reflex activity by antispastic drugs. Possible differences in pathophysiology between the clinical signs of spasticity and the
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