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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasticity is one of many consequences after stroke. It is characterized by a velocity-dependent increase in resistance during passive stretch, resulting from hyperexcitability of the stretch reflex. The underlying mechanism of the hyperexcitable stretch reflex, however, remains poorly understood. Accumulated experimental evidence has supported supraspinal origins of spasticity, likely from an imbalance between descending inhibitory and facilitatory regulation of spinal stretch reflexes secondary to cortical disinhibition after stroke. The excitability of reticulospinal (RST) and vestibulospinal tracts (VSTs) has been assessed in stroke survivors with spasticity using non-invasive indirect measures. There are strong experimental findings that support the RST hyperexcitability as a prominent underlying mechanism of post-stroke spasticity. This mechanism can at least partly account for clinical features associated with spasticity and provide insightful guidance for clinical assessment and management of spasticity. However, the possible role of VST hyperexcitability cannot be ruled out from indirect measures. In vivo measure of individual brainstem nuclei in stroke survivors with spasticity using advanced fMRI techniques in the future is probably able to provide direct evidence of pathogenesis of post-stroke spasticity.
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PMID:New insights into the pathophysiology of post-stroke spasticity. 2591 38

Walking dysfunction occurs at a very high prevalence in stroke survivors. Human walking is a phenomenon often taken for granted, but it is mediated by complicated neural control mechanisms. The automatic process includes the brainstem descending pathways (RST and VST) and the intraspinal locomotor network. It is known that leg muscles are organized into modules to serve subtasks for body support, posture and locomotion. Major kinematic mechanisms are recognized to minimize the center of gravity (COG) displacement. Stroke leads to damage to motor cortices and their descending corticospinal tracts and subsequent muscle weakness. On the other hand, brainstem descending pathways and the intraspinal motor network are disinhibited and become hyperexcitable. Recent advances suggest that they mediate post-stroke spasticity and diffuse spastic synergistic activation. As a result of such changes, existing modules are simplified and merged, thus leading to poor body support and walking performance. The wide range and hierarchy of post-stroke hemiplegic gait impairments is a reflection of mechanical consequences of muscle weakness, spasticity, abnormal synergistic activation and their interactions. Given the role of brainstem descending pathways in body support and locomotion and post-stroke spasticity, a new perspective of understanding post-stroke hemiplegic gait is proposed. Its clinical implications for management of hemiplegic gait are discussed. Two cases are presented as clinical application examples.
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PMID:Post-stroke Hemiplegic Gait: New Perspective and Insights. 3012 49