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Available from: Chueh-Hung Wu, Oct 05, 2015
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    ABSTRACT: Increased resistance to stretch of muscles after stroke may be the result of centrally mediated neural factors such as spasticity or local, peripheral factors such as muscle contracture or thixotropy. The aim was to investigate evidence for an abnormal thixotropic response and compare this with two other factors-contracture and spasticity-which could potentially contribute to muscle stiffness after stroke. Thirty patients with stroke whose calf muscles were assessed clinically as stiff and 10 neurologically normal subjects were recruited. To measure thixotropy, their calf muscles were stretched through two cycles after two prestretch conditions: one in which the muscles were maintained in a shortened position and one in which they were maintained in a lengthened position. Spasticity was defined as the presence of tonic stretch reflexes in relaxed muscles. Contracture was defined as being present when maximum passive ankle dorsiflexion fell at least 2 SD below the mean value of the control subjects. Both controls and patients with stroke exhibited a thixotropic response but this was no greater in the patients than the controls. About one third of the patients displayed muscle contracture and most exhibited spasticity. Contracture made a significant contribution (p=0.006) to the clinical measure of calf muscle stiffness while spasticity made a significant contribution (p=0.004) to the laboratory measure of calf muscle stiffness. Measuring thixotropy at the level of joint movement was sufficiently sensitive to determine the thixotropic response in both neurologically normal subjects and patients impaired after stroke. The thixotropic response was not higher than normal after stroke, suggesting that whereas thixotropy may produce enough immediate resistance to impede movement in those who are very weak, it is not a substantial contributor to long term muscle stiffness. Contracture did significantly contribute to muscle stiffness, supporting the importance of prevention of contracture after stroke. Spasticity contributed to muscle stiffness only when the limb was moved quickly.
    Journal of Neurology Neurosurgery & Psychiatry 08/2000; 69(1):34-9. DOI:10.1136/jnnp.69.1.34 · 6.81 Impact Factor
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    ABSTRACT: Muscle function often becomes progressively more compromised in children with spastic cerebral palsy, leading to reduced mobility. This study aimed to examine the role that muscle connective tissue plays in this process. Severity of spasticity as determined by a range of clinical measures was assessed in 26 children (14 males 12 females; age range 4 to 17 years) with either diplegic or quadriplegic cerebral palsy (CP). Muscle biopsies from the vastus laeralis muscle were obtained for biomedical and histological analysis during orthopaedic surgery as part of the child's ongoing care. Total collagen was quantified by hydroxyproline determination. Two clinical measures of severity, Modified Ashworth Scale and Balance, were shown to have a highly significant correlation with collagen content, and Ambulatory Status, Clonus, and Selective Muscle Control all showed positive trends. Collagen I accumulated in spastic muscle's endomysium which appeared to be thickened, and fibrotic regions with sparse muscle fibres were evident in more severe cases. This suggests that collagen may be involved in increases in muscle stiffness observed in spasticity. Once developed, these changes are essentially irreversible and we suggest that future treatments should consider including prevention of muscle fibrosis.
    Developmental Medicine & Child Neurology 06/2001; 43(5):314-20. DOI:10.1111/j.1469-8749.2001.tb00211.x · 3.51 Impact Factor
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    ABSTRACT: The aim of this paper is to review briefly our understanding of the phenomenon of spasticity based in current evidence.
    Disability and Rehabilitation 01/2005; 27(1-2):2-6. DOI:10.1080/09638280400014576 · 1.99 Impact Factor