Dopaminergic treatment modulates sensory attenuation at the onset of the movement in Parkinson's disease: A test of a new framework for bradykinesia.

BACKGROUND: The primary motor sign of Parkinson's disease is bradykinesia. It has been surprisingly difficult to provide a clear neurobiological mechanism for this fundamental movement deficit in Parkinson's disease. It has been proposed that in healthy individuals the gating of sensory afferents prior to and during movement is an essential step in initiating movement. This down-weighting has been proposed to account for the attenuation of the somatosensory evoked potential following median nerve stimulation at the onset of and during hand movements. The objective of this study was to test whether this sensory attenuation present at movement onset in healthy controls is present in patients with Parkinson's disease. METHODS: Eighteen right-handed patients with idiopathic Parkinson's disease and 16 right-handed age-matched healthy participants were studied. Somatosensory evoked potentials were elicited after electrical stimulation of the median nerve at the wrist. Electroencephalograms were recorded over the scalp at 3 sites on according to the International 10-20 System (F3, C3, and P3). Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of movement (a self-paced abduction movement of the right thumb). RESULTS: Off medication, Parkinson's disease patients had no sensory attenuation at movement onset. On medication, sensory attenuation at movement onset was present. CONCLUSIONS: We suggest that this preliminary result is consistent with the hypothesis that, a failure in sensory attenuation contributes to the difficulties in movement initiation in Parkinson's disease.

Sensory Attenuation Assessed by Sensory Evoked Potentials in Functional Movement Disorders.

BACKGROUND: Functional (psychogenic) movement disorders (FMD) have features associated with voluntary movement (e.g. distractibility) but patients report movements to be out of their control. One explanation for this phenomenon is that sense of agency for movement is impaired. The phenomenon of reduction in the intensity of sensory experience when movement is self-generated and a reduction in sensory evoked potentials (SEPs) amplitude at the onset of self-paced movement (sensory attenuation) have been linked to sense of agency for movement. METHODS: We compared amplitude of SEPs from median nerve stimulation at rest and at the onset of a self-paced movement of the thumb in 17 patients with FMD and 17 healthy controls. RESULTS: Patients showed lack of attenuation of SEPs at the onset of movement compared to reduction in amplitude of SEPs in controls. FMD patients had significantly different ratios of movement onset to rest SEPs than did healthy controls at each electrode: 0.79 in healthy controls and 1.35 in patients at F3 (t = -4.22, p<0.001), 0.78 in healthy controls and 1.12 at patients C3 (t = -3.15, p = 0.004) and 0.77 in healthy controls and 1.05 at patients P3 (t = -2.88, p = 0.007). CONCLUSIONS: Patients with FMD have reduced sensory attenuation as measured by SEPs at onset of self-paced movement. This finding can be plausibly linked to impairment of sense of agency for movement in these patients.