Parkinsonian rigidity is characterized by an increased resistance of a joint to externally imposed motion that remains uniform with changing joint angle. Two candidate mechanisms are proposed for the uniformity of rigidity, involving neural-mediated excitation of shortening muscles, i.e., shortening reaction (SR), or inhibition of stretched muscles, i.e., stretch-induced inhibition (SII). To date, no study has addressed the roles of these two phenomena in rigidity. The purpose of this study was to differentiate these two phenomena, and to quantify the potential contribution of each to wrist joint moment in 17 patients with parkinsonian rigidity, in both Off- and On-medication states. Joint position, torque, and EMGs of selected muscles were collected during externally imposed flexion and extension motions. Moments of shortened and stretched muscles were estimated using a biomechanical model. Slopes of the estimated torque-angle curve were calculated for shortened and stretched muscles, separately. A mixed model ANOVA was performed to compare the contribution between the two mechanisms. During flexion, slopes were significantly (P = 0.003) smaller for SR than for SII, whereas during extension, slopes for SII were significantly (P = 0.003) smaller. Results showed that both SR and SII contributed to rigidity. Which mechanism predominates appeared to be associated with the direction of movement. The findings provide new insights into the biomechanical underpinnings of this common symptom in Parkinson's disease.
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