Tonic vibration reflex in spasticity, Parkinson's disease, and normal subjects

Abstract

SUMMARY The tonic vibration reflex (TVR) has been studied in the quadriceps and triceps surae muscles of 34 spastic, 15 Parkinsonism, and 10 normal subjects. The TVR of spasticity develops rapidly, reaching a plateau level within 2-4 sec of the onset of vibration. The tonic contraction was often preceded by a phasic spike which appeared to be a vibration-induced equivalent of the tendon jerk. The initial phasic spike was usually followed by a silent period, and induced clonus in some patients. No correlation was found between the shape of the TVR and the site of the lesion in the central nervous system. The TVR of normal subjects and patients with Parkinsonism developed slowly, starting some seconds after the onset of vibration, and reaching a plateau level in 20-60 sec. A phasic spike was recorded occasionally in these subjects, but the subsequent tonic contraction followed the usual time course. Muscle stretch increased the quadriceps TVR of all subjects, including those with spasticity in whom the quadriceps stretch reflex decreased with increasing stretch. It is suggested that this difference between the tonic vibration reflex and the tonic stretch reflex arises from the selective activation of spindle primary endings by vibration, while both the primary and the secondary endings are responsive to muscle stretch. The TVR could be potentiated by reinforcement in some subjects. Potentiation outlasted the reinforcing manoeuvre, and was most apparent at short muscle lengths. As muscle stretch increased, thus producing a larger TVR, the degree of potentiation decreased. It is therefore suggested that the effects of reinforcement result at least partially from the activation of the fusimotor system. Since reinforcement potentiated the TVR of patients with spinal spasticity in whom a prominent clasp-knife phenomenon could be demonstrated, it is suggested that the effects of reinforcement are mediated by a descending pathway that traverses the anterior quadrant of the spinal cord.The tonic reflex evoked by muscle vibration has been studied extensively, both in normal man

Face-Referenced Measurement of Perioral Stiffness and Speech Kinematics in Parkinson's Disease

“…It is apparent that stiffness (elevated rigidity) in PD is not limited to limb or axial muscles, nor a manifestation limited to muscles endowed with muscle spindle afferents, since perioral muscles do not contain these mechanoreceptors (Folkins & Larson, 1978;Lovell, Sutton, & Lindeman, 1977). The present findings dispel the notion derived from studies of limb function that increased stiffness is principally due to increased gamma motor drive to muscle spindles (Burke, Andrews, & Lance, 1972;Rushworth, 1964).…”

Stop using the Ashworth scale for the assessment of spasticity

“…Spasticity is often defined as a component of the upper motoneuron syndrome, characterised by a velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflexes 2. What then is the impact of spasticity?…”

Spasticity: Effects of Physical Interventions

“…As a consequence, the synaptic density of afferents upon MN's mediating spinal reflex activity is increased. Anatomical evidence for similar changes involving axo-axonic connections mediating presynaptic inhibition is lacking, but there is physiological evidence for decreased response in the form of less attenuation of the H-reflex by tendon vibration in the spastic limb (12). The claspknife reflex, best demonstrated in the quadriceps muscle, is a sudden loss of resistance to knee flexion as it proceeds slowly to one-half or more complete flexion.…”

“…Ia afferents have been investigated most thoroughly. Through an IN, homonymous Ia afferents inhibit one another, which is the basis for the tendon vibration reflex inhibition of the H-reflex (12). Some pyramidal tract neurons also end upon the Ia afferents, making an axo-axonic connection (34).…”