Responses to a comment on 'Autonomic cardiovascular control and responses to experimental pain stimulation in fibromyalgia syndrome'

摘要

We agree with Dr. Helder Cavalcante that the expression "deficits in ascending pain inhibition arising from the cardiovascular system, which possibly contribute to the hyperalgesia" [1 ] may be somewhat misleading in the present context. We did not mean to challenge established knowledge about pain modulation pathways. Using the expression "ascending pain inhibition" we aimed to emphasize that the source of the assumed anti-nociceptive effect is located in the periphery (i.e. baroreceptors) and that this input is transmitted through afferences to the nucleus of the tractus solitarius (NTS). Electrical stimulation of the NTS, as well as experimental activation of the carotid baroreceptors trigger marked anti-nociception [2]. From this, one may conclude that the baroreceptors constitute the starting point of an ascending pathway by which blood pressure fluctuations modulate nociceptive processing. The NTS projects to autonomic control centres of the brain stem, modulating output to vagal motor neurons and spinal sympathetic neurons [3], which are involved in cardiovascular regulation. In addition, a number of structures of the network of nociception receive direct or indirect input from the NTS. These include the periaqueductal gray, anterior insula, anterior cingulated cortex, hypothalamus, thalamus, amygdala and prefrontal cortex [4-8]. Through modulation of the activity of these structures baroreceptor afferents can alter nociceptive processing and subjective pain experience. Also, the activity of descending pain modulatory systems may be modified, for instance through connections between the NTS and the periaqueductal gray or prefrontal centres.