Proprioceptive impairment and postural orientation control in Parkinson's disease.

摘要

Impairment of postural control is a common consequence of Parkinson's disease (PD). Increasing evidences demonstrate that the pathophysiology of postural disorders in PD includes deficits in proprioceptive processing and integration. However, the nature of these deficits has not been thoroughly examined. We propose to establish a link between proprioceptive impairments and postural deficits in PD using two different experimental approaches manipulating proprioceptive information. In the first one, the subjects stood on a platform that tilted slowly with oscillatory angular movements in the frontal or sagittal planes. The amplitude and frequency of these movements were kept below the semicircular canal perception threshold. Subjects were asked to maintain vertical body posture with and without vision. The orientations of body segments were analyzed. In the second one, the postural control was tested using the tendon-vibration method, which is known to generate illusory movement sensations and postural reactions. Vibrations were applied to ankle muscles. The subject's whole-body motor responses were analyzed from center of pressure displacements. In the first experiment, the parkinsonian patients (PP) were unable to maintain the vertical trunk orientation without vision. Their performances with vision improved, without fully reaching the level of control subjects (CS). In the second experiment, the postural reactions of the PP were similar to those of the CS at the beginning of the perturbation and increased drastically at the end of the perturbation's period as compared to those of CS and could induce fall. These results will bring new concepts to the sensorimotor postural control, to the physiopathology of posture, equilibrium and falls in PD and to the role of basal ganglia pathways in proprioception integration. Nevertheless, in order to assess precisely the role played by sensorimotor integration deficits in postural impairments in PD, further studies establishing the links between clinical features and abnormalities are now required.