MANAGEMENT OF SPASTICITY -HOW REHABILITATION MEDICINE WORKS IN SPASTICITY-
Yoshihisa Masakado (Department of Rehab. Med., Keio University, Tokyo, Japan)
In 1980, Lance defined spasticity as follows: "Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks.", which is commonly used. But the underlying pathophysiological mechanism is unknown.
Several pathophysiological changes might coexist in spasticity. In segmental motor system, various changes in spinal reflex pathways have been reported with reflex method: imbalance in reciprocal la inhibition, decrease in presynaptic inhibition, decrease in lb inhibition and recurrent inhibition, exaggerated flexor reflex.
Apart from the neural mechanism as described above, mechanical factors concerning viscoelastic and contractile properties of the muscle must not be underestimated. In the past, it has focused on the contribution of reflex mechanisms to the increased muscle stiffness. Passive muscle stiffness is determined by elasticity of the contractile elements and connective tissues. Increased muscle stiffness is also observed even in the absence of muscle activity.
I will show some our results about reflex studies and muscle stiffness in stroke patients, and discuss on how rehabilitation medicine modifies spasticity and how effective rehabilitation medicine is.
EFFECTS OF SPASTICITY ON REFLEX MODULATION DURING WALKING
Richard B. Stein and E. Paul Zehr (University of Alberta, Edmonton, Alberta, Canada)
Spasticity is commonly measured with a subject sitting quietly while the clinician moves the limb in a stereotyped way. The stiffness or resistance to movement can be assessed qualitatively or quantitatively (Prochazka et al., 1997, Movement Disorders 12:2. However, the effects of spasticity may be quite different if the subject is actively trying to make a movement. It has become clear that all the common reflexes (stretch, tension, cutaneous) are highly modulated during normal movements in an adaptive fashion and that this modulation may be compromised in spasticity. Some years ago we showed that the H-reflex (an electrical analog of the stretch reflex) is high in mid to late stance and low in the rest of the gait cycle, but that this modulation is lost in some subjects after spinal cord injury (SCI; Yang et al., 1991, Can. J. Neurol. Sci. 18: 443). The high gain of the reflexes when the foot hit the ground during early stance was associated with oscillations (clonus) that could perturb and slow gait. Stimulation of the tibial nerve evokes a flexor response during swing, but inhibition during the transition to stance. In subjects after SCI modulation of reflexes was seen, but inhibition was reduced and abnormal excitation was seen in both flexor and extensor muscles (Jones and Yang, 1994, Exp. Neurol. 128:239). Recently, we have been studying cutaneous reflexes from the dorsum of the foot (Sup. peroneal nerve) that produce a stumble-correction during gait in normal subjects (Zehr et al., J. Neurophysiol., in press. This pattern persists in part after stroke, but an abnormal inhibition is seen in ankle and knee extensors during stance that could compromise stability. Thus, as well as its classic effects on passive muscle stretch, spasticity has a variety of excitatory and inhibitory effects on reflexes during movements. Supported by Medical Research Council of Canada and Alberta Heritage Foundation for Medical Research.