Disturbances of Voluntary Arm Movement in Human Spasticity: The Relative Importance of Paresis and Muscle Hypertonia
Spasticity is a term often used loosely, but most workers in the field would agree that among its major features are hyper-reflexia, a velocity-dependent muscle hypertonia and some degree of paresis (Lance 1980). A feature of the first two of these symptoms, however, is that they are defined in the passive state. In clinical practice, hyper-reflexia is assessed by eliciting tendon jerk reflexes with the patient at rest and, similarly, hypertonia is tested by imposed movement of the passive limb. Recent studies have shown, however, that changes in the tendon jerk reflex do not reflect changes in more physiological reflex components elicited by limb displacement (Thilmann and Fellows 1991; Fellows et al. 1993). It is often assumed that spastic hypertonia is a factor in disturbances of voluntary movements commonly associated with spasticity. At first glance, this may seem logical: A voluntary movement which leads to stretch of a hypertonic muscle might be expected to elicit reflex activity which would oppose the attempted movement. The situation in the spinal reflex pathways is, however, more complex during voluntary activity than in the passive state, and it cannot be taken as read that a muscle which shows hypertonia during a passive stretch will behave similarly during stretch occurring as part of a voluntary movement (McLellan 1977). Indeed, although some reports have suggested that voluntary movements in spastic patients may be disrupted by exaggerated reflexes (Corcos et al. 1986), other workers have found no evidence of hyper-reflexia during spastic gait (Dietz and Berger 1983). Furthermore, both these studies concerned the ankle joint, whereas hypertonia is commonly confined to the knee and elbow joints (Burke et al. 1971; Thilmann et al. 1991). At these latter joints earlier studies have also reported conflicting findings, however (Sahrmann and Norton 1977; Mizrahi and Angel 1979). Much of this conflict may have arisen from the heterogeneous nature of the patient groups in these studies, in whom spasticity arose from a variety of causes, such as spinal trauma, tumour, multiple sclerosis and stroke. Spasticity is a syndrome and not a disease, and thus it should not be assumed that its features will be the same irrespective of the underlying cause. Accordingly, it was decided to study a group of patients in whom spasticity arose from a homogeneous cause, namely a single, unilateral ischaemic lesion in the area of the middle cerebral artery. These subjects were asked to make voluntary movements at the elbow, in order to assess the extent to which abnormal antagonist stretch reflex activity was responsible for disruption of voluntary movement. In addition, it was considered whether alternative reasons, such as muscle paresis or inappropriate co-activation of antagonist muscles, might better explain the movement deficits of these patients.
KeywordsTorque Neurol Baclofen
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