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We refer to the interesting study by Lee et al concerning quantification of velocity dependent properties of the elbow flexors in patients with spasticity and rigidity.1 Their main finding was a velocity dependent increase in reactive torque in both groups, although this was only related to muscle length in subjects with spasticity.
However, the authors’ conclusion that their observations reflect stretch reflex hyperexcitability underlying spasticity is difficult to understand, as is their assumption that the contribution of passive mechanical change, if any, should be minor and uniform during stretch. The investigators used online monitoring of muscle activity in biceps and triceps to ensure that the limb was relaxed before and during the test. The effect of a voluntary contraction or an “unrelaxed limb” on baseline torques derived from slow stretches (fig 3, p 623) clearly demonstrates the distortion of the torque angle curves that would have been evident if a reflex contraction of the biceps muscle had resulted from the faster stretches.
Thilmann et al have examined biceps stretch reflex responses in patients with spasticity secondary to stroke.2 Stretches of similar magnitude to those used by Lee et al invoked bursts of biceps activity with shorter latencies and longer duration than those in age matched controls. Lee et al have avoided inducing activity in the biceps muscle during elbow extension.1 Therefore their findings are consistent with passive muscle elements, not stretch reflex responses, being responsible for the observed velocity dependent increase in reactive torque. This phenomenon has been reported previously in the calf muscles of normal subjects3 and of individuals with spasticity following spinal cord injury.4
The data reported by Lee et al have demonstrated a velocity dependent stretch related behaviour of the elbow flexor muscles which is viscoelastic. The velocity dependent increase in reactive torque in both spastic and rigid muscles was significantly greater than in normal muscles, with the relation between reactive torque and limb position (muscle length) in spasticity differing from rigidity or normal tone. The most likely source of this velocity and length dependent resistance is alteration of the contractile component of the muscle, although connective tissue and non-contractile proteins within the sarcomeric cytoskeletons also contribute to passive muscle tension. An increase in the number of weakly attached actin–myosin crossbridges in relaxed muscle, and/or a slower than normal detachment rate during passive stretch, may contribute to hypertonia, especially in chronic cases.5 As crossbridge detachment occurs at a steady rate during stretch, such mechanical adaptations could account for some of the velocity dependent resistance observed in this study.
The importance of distinguishing between reflex and non-reflex sources of resistance to stretch lies in the need to target treatment interventions appropriately. An overemphasis on the contribution of stretch reflex excitability to motor disability in patients with spasticity may lead to an inappropriate treatment focus.
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