Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral palsy (CP) results from an upper motoneuron (UMN)lesion in the developing brain. Secondary to the UMNl esion,which causes spasticity, is a pathological response by muscle - namely, contracture. However, the elements within muscle that increase passive mechanical stiffness, and therefore result in contracture, are unknown. Using hamstring muscle biopsies from pediatric patients with CP (n =33) and control (n =19) patients we investigated passive mechanical properties at the protein, cellular, tissue and architectural levels to identify the elements responsible for contracture. Titin isoform, the major load-bearing protein within muscle cells, was unaltered in CP. Correspondingly, the passive mechanics of individual muscle fibres were not altered. However, CP muscle bundles, which include fibres in their constituent ECM, were stiffer than control bundles. This corresponded to an increase in collagen content of CP muscles measured by hydroxyproline assay and observed using immunohistochemistry. In vivo sarcomere length of CP muscle measured during surgery was significantly longer than that predicted for control muscle. The combination of increased tissue stiffness and increased sarcomere length interact to increase stiffness greatly of the contracture tissue in vivo. These findings provide evidence that contracture formation is not the result of stiffening at the cellular level, but stiffening of the ECM with increased collagen and an increase of in vivo sarcomere length leading to higher passive stresses.
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PMID:Hamstring contractures in children with spastic cerebral palsy result from a stiffer extracellular matrix and increased in vivo sarcomere length. 2163 28

We studied the effect of spasticity-induced overload on tendons from the gracilis and semitendinosus muscles from cerebral palsy (CP) and healthy subjects (CT) stained with haematoxylineosin, Sirius red and Alcian blue. Vascularity was also characterized using an anti-CD34 antibody. Light microscopy analysis of haematoxylin-eosin stained sections revealed that the overall structure of tendons was maintained, characterized by parallel and slightly wavy collagen fibers in both CT and CP tendons. However, hypercellularity, cell rounding, increased vascularity and lipoid degeneration were observed in CP samples. Sirius red stained collagen fibers were more evident in CP tendons, suggesting an increased collagen content induced by spasticity. Alcian blue staining revealed an overall increase of glycosaminoglycans in CP tendons as observed in tendinopathy. Our results suggest that CP-induced spasticity may be considered as a chronic, persisting and repetitive loading of tendons, inducing ECM remodeling as adaptive response to increased functional demand. At the same time, the evidence of some tendinopathic-like markers in CP tendons suggests that the chronic nature of the CP condition could represent a pathologic condition, possibly leading to a transient weakness of the tissue making it more susceptible to damage from cumulative loading until an overt tendinopathy develops.
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PMID:Tendon structure and extracellular matrix components are affected by spasticity in cerebral palsy patients. 2388 44