Neurology of Fibromyalgia Syndrome - Looking at the Role of the Central Nervous System in FMS

(Unfortunately Ambiguous)

Neuroscientists refer to pain perception as nociception.  This term is derived from the endorphin nociceptin, which is the only endorphin neurotransmitter associated with pain rather than analgesia.  Nociception happens via two major sets of somatic receptors: proprioceptors and interoceptors.  Proprioceptive dysfunction is implicated in FMS.  Proprioceptors are located in sheaths surrounding muscle fibers, membranes surrounding bones, pulp of teeth, membranes surrounding internal organs, etc; proprioceptors receive pain information in any of these contexts.  Both proprioceptors and interoceptors connect to the spinal cord at appropriate segmental levels.  Pain information from the body enters the spinal cord via the dorsal horns and decussates immediately.  The spinothalamic pathway carries pain information to the thalamus where it is interpreted via the spinal cord and brainstem.  Pain information above the cervical spinal dermatomes is carried via the trigeminal nerve and the trigeminothalamic tract.

FMS is sometimes attributed to peripheral nerve or tissue damage (Goldenberg, 1999).  Peripheral damage of either soft tissue or neural tissue often results in pain supersensitivity, which is also referred to as hyperalgesia.  In this case, normally neutral stimuli may elicit severe painful experience.  But regardless of injury, FMS patients do exhibit less tolerant pain thresholds (alodynia) as well as hyperalgesic responses to innocuous stimuli.  The most peculiar and perhaps telling finding in FMS research thus far is that FMS patients show significantly elevated levels of Substance-P (SP), which is a neurotransmitter responsible for pain sensation, in the Cerebral Spinal Fluid (CSF) (Pillemer et al., 1997).  SP is active in pain sensation within afferent nociceptive fibers throughout the body.  In addition, current research seems to indicate that levels of Nerve Growth Factor (NGF) as well as Dynorphin-A are significantly higher in the CSF of FMS patients.  NGF and Dynorphin-A are both implicated in the production of SP and its expression in afferent neurons (Giovengo et al., 1999).  Infectious diseases may also play a role in the precipitation of FMS in a number of patients (Goldenberg, 1993).

FMS patients also exhibit decreased levels of regional cerebral blood flow (rCBF) in the caudate nucleus and the thalamus (Pillemer et al., 1997).  The caudate nucleus and the thalamus are involved in recognizing and interpreting painful stimuli.  If rCBF decreases in both the caudate nucleus and thalamus, then the capacity for those regions to inhibit nociceptive signals decreases as well, and painful experience is more easily elicited.

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