MOVEMENT DYSFUNCTION FOLLOWING CENTRAL-NERVOUS-SYSTEM LESIONS - A PROBLEM OF NEUROLOGIC OR MUSCULAR IMPAIRMENT

In most of the scientific literature that discusses the common problem of resistance to passive movement in patients with central nervous sy stem lesions, this clinical problem is ascribed to a mechanism involvi ng uninhibited neural activity. This article reviews the literature re lated to an alternative explanation of stiffness in such patients, an explanation involving the mechanical orientation of myosin crossbridge s. The conventional view of the crossbridge is that it is detached fro m actin filaments during the relaxed state of muscle. Information is p resented, however, from animal studies indicating that a certain propo rtion of crossbridges bind weakly to actin even in the relaxed state. The muscles of patients with hypertonicity may undergo an adaptation t hat involves formation of a higher proportion of binding crossbridges. This results in abnormal stiffness in the muscle and impairs movement , Such crossbridge stiffness may be particularly elevated immediately after a previous contraction.