Fibromyalgia is a syndrome of widespread chronic pain associated with sleep disorders, depressed mood, cognitive impairment and fatigue. Its etiology and pharmacopathology are poorly understood but it is thought to result from a dysfunction of central pain processing mechanisms leading to generalized pain sensitization.
Pain perception is the result of a bidirectional process of ascending and descending pathways. Nociceptive input from peripheral afferent neurons is sent via the dorsal horn of the spinal cord to the higher brain centers involved in pain perception.
Some descending inhibitory projections to the spinal cord attenuate the nociceptive effects. Numerous neurotransmitters including serotonin, dopamine, noradrenaline and substance P are involved in these processes.
In other neuronal pathways in the brain, the same neurotransmitters are involved in mood control, sleep regulation and cognitive function providing a neurochemical substrate for the wide range of symptoms seen in fibromyalgia.
• Attenuation [reduction] of neuronal hyperactivity through ligands acting at the alpha2-delta subunits of voltage-dependent calcium channels [calcium channels in cell membranes, normally closed, allow entry of calcium into the cell when activated].
• And increased inhibitory activity of the descending pathways by inhibition of serotonin and noradrenaline reuptake…
…are two mechanisms that are currently exploited by new medication for the treatment of Fibromyalgia.
Source: Human Psychopharmacology, May 28, 2009;24(S1):S11-S17. PMID: 19479906, by Stahl SM. Department of Psychiatry, University of California, San Diego, California, USA.