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R W Teasell

Publications and source records attributed to R W Teasell.

41 records · Page 3Linked to original sources
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Spasticity measurement in stroke: a pilot study.

The ability to objectively measure spasticity, related to cerebral stroke, is important in the rehabilitation therapies since many therapeutic modalities have been developed over the years to reduce spasticity. The unproven clinical expectation is that function would be improved were spasticity to be reduced. Unfortunately, the ability to measure spasticity to conduct efficacy studies of spasticity-reducing therapies is not possible. This relates to the multi-variable nature of the spastic syndrome with the result that no clinical measurement technique has been proven to be sensitive, valid and reliable. Therefore, it is important to develop a research-oriented spasticity measurement system to meet this need. We describe the current development of such a system. Details of our pilot study of a reflex excitability technique, designed to measure certain components of cerebral spasticity, are presented. The technique combined biomechanical and electrophysiological measures to investigate a homogenous stroke sample (n = 6); it incorporated the H-reflex in soleus, during passive ankle movements, as a measure of faulty neural inhibition. This component significantly (p < .05) differentiated the stroke sample from a matched, healthy control group (n = 6). Evocation of a cutaneous reflex in soleus was a condition that was problematic and it had to be dropped from the protocol. Joint stiffness, which is thought to affect measures of spasticity during passive movement, did not contaminate the measures. Further research in this direction is required to delineate and measure other neural components of spasticity while taking into account related non-neural variables. The final objective in this line of research is to develop a valid, reliable and sensitive spasticity measurement system that could be used to judge the efficacy of physical neurorehabilitation treatments currently employed to reduce spasticity following stroke.

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A reflex technique to measure presynaptic inhibition in cerebral stroke.

The purpose of this study was to evaluate the feasibility of reflex excitability measurement techniques in the partial measurement of spasticity related to cerebral stroke. Techniques involved the testing of the soleus H-reflex at specific ankle positions during passive dorsiflexing movements with and without background plantarflexing contractions; conditions attempted to simulate the terminal stance phase of gait. Testing of 12 stroke subjects, having cerebrovascular lesions related only to occlusion of the middle cerebral artery, demonstrated significantly (p < 0.01) less inhibition of the H-reflex during passive ankle dorsiflexion compared to 12 matched, healthy controls. However, evocation of the H-reflex during a low-level, voluntary plantarflexing contraction concomitant with passive dorsiflexion, did not reflect a statistical difference between the two groups. The two conditions were thought to each represent measures of faulty presynaptic inhibition as indicators of cerebral spasticity. A Chi-square calculation of sensitivity for the passive ankle movement without background plantarflexing contraction condition, was shown to significantly differentiate (p < 0.05) between the stroke and normal groups. A positive, but weak, correlation was found for stroke subjects between this reflex measure and the Ashworth clinical measure of spasticity (r = 0.49). Although stroke subjects exhibited increased joint stiffness when the full range of passive ankle dorsiflexion movement was considered, in comparison to the matched healthy control subjects, no significant increase in passive stiffness was found at the joint position of the reflex evocation. Size of the cerebral lesion, as determined from CT or MRI scan, was not related to the spasticity measures. Therefore, in a homogeneous stroke sample, a component of cerebral spasticity i.e., faculty Ia presynaptic inhibition, has been measured during a simulated functional movement in the lower extremity and was shown to differentiate this group from a matched, healthy, control sample. Joint stiffness did not contaminate the measures.

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