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 system lesions, this clinical problem is ascribed to a mechanism involving uninhibited neural activity. This article reviews the literature related to an alternative explanation of stiffness in such patients, an explanation involving the mechanical orientation of myosin crossbridges. The conventional view of the crossbridge is that it is detached from actin filaments during the relaxed state of muscle. Information is presented, however, from animal studies indicating that a certain proportion of crossbridges bind weakly to actin even in the relaxed state. The muscles of patients with hypertonicity may undergo an adaptation that 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.