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(Stroke. 2004;35:139.)
© 2004 American Heart Association, Inc.
Original Contributions |
University of California, Irvine, Department of Neurology, Irvine, California
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Motor deficits are the most common impairment acutely after stroke and persist in nearly half of all patients.1,2 Although much focus is on hemiparesis in this setting, injury to the motor system does not produce a homogenous clinical syndrome. Instead, weakness may be accompanied by other negative findings such as slowness and fatigue and by positive findings such as synkinesia and spasticity.
Spasticity is a state of increased tone with exaggerated reflexes resulting from upper motor neuron injury. It is a condition of many contrasts. Reduced activity in one area, the descending motor tracts, results in increased activity in another area, the skeletal muscles. Spasticity is common across neurological conditions, yet accurate measurement is difficult. It is associated with weakness, yet its maintenance is critical to function in some patients. Importantly, spasticity remains a key dividing point among major schools of physiotherapy, with some aiming to inhibit3 and others aiming to encourage4 spasticity and its accompanying motor abnormalities. The medical system expends substantial resources to reduce spasticity with methods that include botulinum toxin injection, intrathecal medication, oral pharmacological agents, and physical/occupational therapy. Yet, limited information is available on its prevalence and significance after stroke. Indeed, in a recent review, Barnes5 noted the limited availability of quality data on the prevalence of spasticity after stroke.
Some of those data are now available. Sommerfeld et al6 studied consecutive patients with a first stroke over a 10-month period. Among 95 patients assessed a mean of 5 days after stroke, 21% had spasticity and
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