Inhibition of muscle sympathetic outflow following transcranial cortical stimulation.
The possible contribution of cerebral cortical activity to sympathetic outflow to the muscle vascular bed was assessed in normal human subjects. Muscle sympathetic activity was recorded from motor fascicles of the peroneal nerve in 8 subjects while transcranial magnetic stimulation was applied over the vertex, or unilaterally over the hand area of cortex. By triggering the cortical stimulus from the R-wave of the ECG and introducing delays of 0-600 ms between the trigger and the stimulus, we found that a single cortical stimulus delayed by 200-400 ms caused a pronounced inhibition of one pulse-synchronous sympathetic burst. Stimulation over the vertex was more effective than stimulation over the hand area of cortex. In addition to this inhibition of muscle sympathetic outflow, brain stimulation caused an increase in cutaneous sympathetic activity, both sudomotor (sweating) and vasoconstrictor (decrease in skin blood flow). We suggest that the cerebral cortex may normally suppress muscle sympathetic outflow and speculate that lesions that interrupt this source of inhibition (such as those caused by stroke) may result in an augmented muscle sympathetic outflow.
Macefield
V G
VG
The Prince of Wales Medical Research Institute, Randwick NSW, Australia. vg.macefield@unsw.edu.au
Taylor
J L
JL
Wallin
B G
BG
D000328:Adult; D002540:Cerebral Cortex / Q000502:physiology*; D004558:Electric Stimulation; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000294:innervation / Q000502:physiology*; D012867:Skin / Q000294:innervation; D013564:Sympathetic Nervous System / Q000502:physiology*