Affiliations: Centre for Neuromuscular and Neurological Disorders,
The University of Western Australia, Australia | School of Exercise, Biomedical and Health Sciences,
Edith Cowan University, Western Australia, Australia | Berenson-Allen Center for Noninvasive Brain
Stimulation, Beth Israel Deaconess Medical Center, Harvard Medical School,
Boston, USA | Institut Guttman de Neurorehabilitacio, Universitat
Autonoma, Barcelona, Spain
Abstract: Corticomotor excitability is reduced during rhythmic passive
movement compared to rest, but it is not known whether the mechanism is purely
segmental or includes a supraspinal pathway. To determine how interruption of
sensory projections at a supraspinal level affects corticomotor excitability
during passive movement, we measured the amplitude of motor evoked potential
(MEP) during 1 Hz cyclic index finger movements in a patient with a brainstem
and thalamus lesion that resulted in a pure sensory stroke. Measurements of MEP
amplitude and proprioception were made 14 and 64 days post-stroke. In the first
study, when subjective position sense was reduced for the index finger, MEP
amplitude was significantly increased during passive movement compared to rest
(4.6 ± 0.2 SEM mV vs. 4.0 ±
0.2 mV; p=0.0281). However in the second study, when position
sense had returned to normal, MEP amplitude was significantly reduced during
movement compared to rest (6.2 ± 0.3 mV
vs. 6.6 ± 0.1 mV; p=0.0224). These
observations provide evidence that supraspinal sensory pathways are involved in
reducing corticomotor excitability during rhythmic passive movement.
