Vagal modulation of nociception: A commentary on the issues of facilitation, inhibition, and silent ischemia

Abstract

D rs. Gebhart and Randich have provided a well-written theoretical review of studies that support the proposal that activation of cardiopulmonary vagal afferent fibers leads to modulation of pain. The purpose of this commentary is to raise questions about findings that have been discussed and to expand on certain issues. The role of the facilitatory effects of vagal afferent stimulation (VAS) has been addressed2S; however, issues about these effects need to be raised. The first issue concerns the possibil ity of non-vagal fibers eliciting the facilitatory response. Chase et al. ~.~2 reported that the digastric or masseteric reflex was facilitated and inhibited with electrical stimulation of the cervical vagus nerve, as cited in the focus article. However, the facilitatory response to VAS on the digastric reflex was not observed when the thoracic vagus or the cardiac branch of the vagus was stimulated. 23 This observation raises the possibility that non-vagal fibers may be ensheathed with the cervical vagus. The facilitatory response may be elicited at lower intensities by stimulating the aortic depressor nerve, which is ensheathed with the vagus nerve. 1,2,~9 Occasionally we noted that activity of spinothalamic tract (STT) cells increased during electrical stimulation of the thoracic vagus after the cervical vagus was transected. 3 This increase may have been produced by activating sympathetic afferent fibers that were ensheathed in the vagus. The second issue addresses vagal excitation of