Modeling movement disorders-CRPS-related dystonia explained by abnormal proprioceptive reflexes

JOURNAL OF BIOMECHANICS

卷:45

Article

Mugge, Winfred¹  Munts, Alexander G.^2,3  Schouten, Alfred C.^1,4  van der Helm, Frans C. T.^1,4 

[1] Delft Univ Technol, Lab Neuromuscular Control, Dept Biomech Engn, NL-2628 CD Delft, Netherlands

[2] Leiden Univ, Med Ctr, Dept Neurol, NL-2300 RC Leiden, Netherlands

[3] Kennemer Gasthuis, Dept Neurol, NL-2000 AK Haarlem, Netherlands

[4] Univ Twente, MIRA Inst Biomed Technol & Tech Med, Lab Biomech Engn, NL-7500 AE Enschede, Netherlands

关键词: Human motion control;    Neuromuscular modeling;    Movement disorders;    Dystonia;    Golgi tendon organs;    Muscle spindles;    Force feedback;   

DOI  :  10.1016/j.jbiomech.2011.09.024

来源: Elsevier

【 摘 要 】

Humans control their movements using adaptive proprioceptive feedback from muscle afferents. The interaction between proprioceptive reflexes and biomechanical properties of the limb is essential in understanding the etiology of movement disorders. A non-linear neuromuscular model of the wrist incorporating muscle dynamics and neural control was developed to test hypotheses on fixed dystonia. Dystonia entails sustained muscle contractions resulting in abnormal postures. Lack of inhibition is often hypothesized to result in hyperreflexia (exaggerated reflexes), which may cause fixed dystonia. In this study the model-simulated behavior in case of several abnormal reflex settings was compared to the clinical features of dystonia: abnormal posture, sustained muscle contraction, increased stiffness, diminished voluntary control and activity-aggravation. The simulation results were rated to criteria based on characteristic features of dystonia. Three abnormal reflex scenarios were tested: (1) increased reflex sensitivity-increased sensitivity of both the agonistic and antagonistic reflex pathways; (2) imbalanced reflex offset-a static offset to the reflex pathways on the agonistic side only; and (3) imbalanced reflex sensitivity-increased sensitivity of only the agonistic reflex pathways. Increased reflex sensitivity did not fully account for the features of dystonia, despite distinct motor dysfunction, since no abnormal postures occurred. Although imbalanced reflex offset did result in an abnormal posture, it could not satisfy other criteria. Nevertheless, imbalanced reflex sensitivity with unstable force feedback in one of the antagonists closely resembled all features of dystonia. The developed neuromuscular model is an effective tool to test hypotheses on the underlying pathophysiology of movement disorders. (C) 2011 Elsevier Ltd. All rights reserved.

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