OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.