Neurobiological concepts of fibromyalgia--the possible role of descending spinal tracts.

Abstract

In the spinal cord, long descending pathways are known to exist which modulate pain sensations by either inhibiting or facilitating the discharges of spinal nociceptive neurones. In this article, the hypothesis is discussed that the pain of fibromyalgia may be due to a dysfunction of these pain-modulating pathways. Theoretically, two kinds of disturbance could lead to pain, namely reduced activity in the pain-inhibiting (antinociceptive) system or increased activity in the pain-facilitating (pronociceptive) pathways. Data from animal experiments show that interruption of the dorsal descending systems leads to hyperactivity of spinal nociceptive neurones, namely increase in background activity, lowering in stimulation threshold, and increase in response magnitude to noxious stimuli. The responses of the neurones to input from nociceptors in deep tissues were more strongly inhibited by the descending pathways than were responses to input from cutaneous nociceptors. Collectively, the findings indicate that the dorsal descending systems are tonicly active and have a particularly strong inhibitory action on neurones that mediate pain from deep tissues. If these systems operate in a similar way also in patients, an impairment of their function is likely to lead to 1. spontaneous deep pain (because of an increased background activity in nociceptive neurones supplying deep tissues), 2. tenderness of deep tissues (because of a lowered mechanical threshold of the same neurones), and 3. hyperalgesia of deep tissues (because of increased neuronal responses to noxious stimuli). These changes will affect large areas of the body because the descending inhibitory systems have widespread terminations in the spinal cord. Thus, a dysfunction of the descending inhibitory pathways could mimick to a large extent the pain of fibromyalgia.