Department of Exercise Sciences


Abnormal sensorimotor integration in Parkinson's Disease

GN Lewis, WD Byblow

Introduction

Parkinson’s disease (Pd) patients have noted difficulties in regulating the amplitude of movements, particularly when visual information is absent and patients are reliant on kinesthetic input for sensory feedback. In laboratory testing, deficiencies in sensorimotor integration tasks are routinely detected. The precise neural mechanisms associated with deficits in kinesthesia and movement amplitude scaling in Pd are less certain, with conflicting hypotheses often published in the literature.

Methods

Transcranial magnetic stimulation (TMS) was used to investigate sensorimotor integration in the upper limb of 10 patients with Parkinson’s disease (Pd) and 10 age-matched controls.

Non-conditioned and subthreshold conditioned (2 ms interstimulus interval) responses were recorded in the flexor- and extensor carpi radialis muscles (FCR, ECR) of the more impaired (non-dominant) limb. Stimuli were delivered while the wrist joint was positioned statically at various joint angles as well as during different phases of passive movement of the wrist joint (90° amplitude, 0.2 Hz). The FCR and ECR muscles remained relaxed during all stimulation.

Results

In both groups, responses in the static condition were larger when the target muscle was in a shortened position. Responses were also facilitated in the muscle shortening phases of passive movement. In both static and dynamic conditions, the extent of modulations in response amplitude was significantly reduced in the patient group. The level of intracortical inhibition (ICI) was also significantly less in the Pd patients in static conditions. During passive movement, control subjects demonstrated a clear reduction in ICI compared to the static trials, however the level of ICI was unchanged in the Pd group in the dynamic condition.

pdcort1
MEP amplitude in the FCR (left) and ECR (right) muscles while at various static wrist joint positions.

Conclusions

The results suggest an abnormal influence of afference on corticomotor excitability in Pd. This may be related to abnormal sensory input, a defective integrative unit, or an inappropriate motor response.

pdcort2
ICI (conditioned/non-conditioned MEP amplitude) in patients and controls.

Acknowledgements

Funding for this study was provided by NZ Neurological Foundation Grant No. 0125PG

For more information on this project contact:

Winston Byblow
Email: w.byblow@auckland.ac.nz