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Brain, Vol. 118, No. 5, 1339-1351, 1995
© 1995 Guarantors of Brain


research-article

Effects of stimulus rate on regional cerebral blood flow after median nerve stimulation

Vicente Ibáñez1, Marie-Pierre Deiber1, Norihiro Sadato1, Camilo Toro1, Joyce Grissom1, Roger P. Woods2, John C. Mazziotta2 and Mark Hallett1

1Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health Bethesda, Maryland 2Departments of Radiology and Neurology, University of California at Los Angeles School of Medicine Los Angeles, California, USA

Correspondence to: Mark Hallett, Building 10, Room 5N226, NINDS, NIH, Bethesda, MD 20892-1428, USA

The primary motor cortex and supplementary motor area (SMA) are purportedly involved in the generation of the P22 and N30 components of somatosensory evoked potentials (SEPs) evoked by electrical stimulation of the median nerve at the wrist. We used regional cerebral blood flow (rCBF) measurements and PET in 10 normal subjects to study the cerebral areas activated by median nerve electrical stimulation. PET scans were performed with the subjects at rest and during stimulation of the right median nerve at frequencies of up to 20 Hz. Stimulation evoked a single focus of activation in the primary somatosensory area (SI). An increase of rCBF in this area was linearly correlated with stimulus frequencies of up to 4 Hz and then reached a plateau.

The SMA was not significantly activated by stimulation at any of the frequencies tested. In contrast to the SI, the SMA showed no trend toward a correlation between the rCBF changes and the stimulus repetition rate. In order to achieve maximal resolution in the sensorimotor cortex, regions of interest were placed in individual co-registered MRI—PET images on both sides of the central sulcus. There was no significant increase of rCBF in the crown of the precentral gyrus. These results suggest that a contribution of the primary motor cortex and the SMA to the generation of the P22 and N30 components of SEPs is unlikely. Consequently, functional clinical interpretations derived from P22 or N30 abnormalities must be reconside

somatosensory evoked potentials; PET; movement disorders; primary somatosensory area

Received December 29, 1994. Revised March 23, 1995. Accepted May 8, 1995.


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