Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale
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Delayed onset muscle soreness (DOMS) involves central and peripheral pain mechanisms. Referred pain patterns following stimulation of DOMS affected tissue have not been fully described. Referred pain may provide information on how central mechanisms are involved in DOMS, as referred pain is a central mechanism. ⋯ Significantly higher referred pain frequency and enlarged pain areas were found at the muscle belly and TBJ sites following injection during DOMS compared to pre-DOMS. The results indicate that muscle belly and TBJ sites are sensitised while tendon tissue per se is unaffected by DOMS. Central sensitivity changes caused by DOMS may explain the increase in referred pain frequency and enlarged pain areas.
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The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. ⋯ This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is not equivalent and care should be taken in generalizing results between them.