TY - JOUR
T1 - Differentiation between the contributions of shortening reaction and stretch-induced inhibition to rigidity in Parkinson's disease
AU - Xia, Ruiping
AU - Powell, Douglas
AU - Rymer, W. Zev
AU - Hanson, Nicholas
AU - Fang, Xiang
AU - Threlkeld, A. Joseph
N1 - Funding Information:
Acknowledgments This study was supported in part by the National Institutes of Health under grant R15-HD061022, in part under grant Nebraska Tobacco Settlement Biomedical Research Development Fund, and in part under Faculty Development Fund of School of Pharmacy and Health Professions, Creighton University, USA. Authors wish to thank all the subjects for their participation in the study.
Copyright:
Copyright 2011 Elsevier B.V., All rights reserved.
PY - 2011/4
Y1 - 2011/4
N2 - 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.
AB - 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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U2 - 10.1007/s00221-011-2594-2
DO - 10.1007/s00221-011-2594-2
M3 - Article
C2 - 21347660
AN - SCOPUS:79955015650
VL - 209
SP - 609
EP - 618
JO - Experimental Brain Research
JF - Experimental Brain Research
SN - 0014-4819
IS - 4
ER -