Antonio Nardone1, Marco Schieppati. 1. Division of Physical Therapy and Rehabilitation, Posture and Movement Laboratory, Fondazione Salvatore Maugeri, Scientific Institute of Veruno, Novara, Italy.
Abstract
OBJECTIVE: Foot dorsiflexion evokes a short- (SLR) and a medium-latency EMG response (MLR) in the soleus of standing subjects. SLR is mediated by spindle group Ia, while group II fibres contribute to MLR through an oligosynaptic circuit. We studied the effects of Achilles' tendon vibration on both responses in spastic patients to disclose any abnormal excitability of these pathways. METHODS: SLR and MLR were evoked in 11 hemiparetics and 11 normals. The vibration-induced changes in both responses were correlated to the Ashworth score of the affected leg. RESULTS: There were no differences between normals and patients in the size of control SLR or MLR. Vibration decreased SLR to 70% in normal subjects, but increased it to 110% in patients, in both affected and unaffected leg. Vibration did not affect MLR in normals, but increased it to 165% on the affected and 120% on the unaffected side of patients. Ashworth score was solely correlated with the degree of vibration-induced increase of MLR. CONCLUSIONS: While the lack of inhibitory effect of vibration on SLR confirms a reduced inhibitibility of the monosynaptic reflex, the increased MLR indicates a disinhibition of group II pathway in patients, connected to the loss of descending control on group II interneurones. Spastic hypertonia depends on release of group II rather than group Ia reflex pathways. SIGNIFICANCE: These findings give a neurophysiological support for the pharmacological treatment of spastic hypertonia and suggest a method for the assessment of its effects.
OBJECTIVE: Foot dorsiflexion evokes a short- (SLR) and a medium-latency EMG response (MLR) in the soleus of standing subjects. SLR is mediated by spindle group Ia, while group II fibres contribute to MLR through an oligosynaptic circuit. We studied the effects of Achilles' tendon vibration on both responses in spasticpatients to disclose any abnormal excitability of these pathways. METHODS: SLR and MLR were evoked in 11 hemiparetics and 11 normals. The vibration-induced changes in both responses were correlated to the Ashworth score of the affected leg. RESULTS: There were no differences between normals and patients in the size of control SLR or MLR. Vibration decreased SLR to 70% in normal subjects, but increased it to 110% in patients, in both affected and unaffected leg. Vibration did not affect MLR in normals, but increased it to 165% on the affected and 120% on the unaffected side of patients. Ashworth score was solely correlated with the degree of vibration-induced increase of MLR. CONCLUSIONS: While the lack of inhibitory effect of vibration on SLR confirms a reduced inhibitibility of the monosynaptic reflex, the increased MLR indicates a disinhibition of group II pathway in patients, connected to the loss of descending control on group II interneurones. Spastic hypertonia depends on release of group II rather than group Ia reflex pathways. SIGNIFICANCE: These findings give a neurophysiological support for the pharmacological treatment of spastic hypertonia and suggest a method for the assessment of its effects.
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