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) is a nonprogressive central nervous system lesion clinically characterized by impairment of voluntary movement related to spasticity, time of activation, and strength of skeletal muscle. Altered muscular control may act on tendon structure and influence extracellular matrix homeostasis, in particular, collagen. The effect of spasticity on collagen turnover in CP patients' tendons has not been described previously. We studied collagen turnover related genes in the gracilis and semitendinosus tendons of diplegic (n = 6) and quadriplegic (n = 15) patients, compared to normal subjects (n = 7). In particular, using real time RT-PCR, we analyzed the mRNA levels of the major extracellular matrix (ECM) components collagen type I (COL-I, alpha 2 chain COL1A2), the matrix metalloproteinase-1 (MMP-1) and the tissue inhibitor of MMP (TIMP-1), the enzyme responsible for collagen maturation lysyl hydroxylase 2b (LH2b), of the matricellular protein involved ECM remodelling (secreted protein acidic and rich in cysteine, SPARC), and the transforming growth factor-beta1 (TGF-beta1), a multipotent cytokine involved in collagen turnover. Our results show that gene expression profiles are quite different in CP samples compared to normal ones. In fact, spasticity induces relevant modifications of tendons at the molecular level, which modify their phenotypes to respond to the higher mechanical loading and increased functional demands. Interestingly, hypertonic quadriplegic subjects displayed the highest mRNA levels of COL1A2, LH2b, TGF-beta1, and SPARC, suggesting that their tendons undergo higher mechanical loading stimulation.
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PMID:Expression profiling of genes involved in collagen turnover in tendons from cerebral palsy patients. 1944 61

Collagenase has revolutionized the treatment of Dupuytren's disease. It acts by lysing collagen in Dupuytren's cords. It can also act on collagen in tendons, leading to tendon rupture. In this letter, we highlight caution where bowstringed flexor tendons were masquerading as Dupuytren's cords in a patient with upper limb spasticity. The initial plan was to inject the cords with collagenase; however, we proceeded with an open approach. If we had proceeded with our initial plan to inject the palpable cords with collagenase, tendon rupture would have been the likely outcome. We advise that administrators of collagenase proceed with caution in patients with upper limb neurological disorders, bearing in mind that bow-stringed flexor tendons can mimic Dupuytren's cords.
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PMID:Collagenase Use and a Trap for the Unwary in Patients With Upper Limb Spasticity. 3191 54