Abstract

SUMMARYObjective: To present what is known, and to project what is likely to be found regarding pain amplification by abnormal levels of neurotransmitters in fibromyalgia syndrome [FMS].Methods: The main sources of information have been the published medical literature, but some unpublished data from the laboratories of the world will aslo be highlighted. The mechanisms to be proposed have been based on current knowledge about nociception and on the roles which neurotransmitters are believed to play in abonormal pain states, such as allodynia. Considered will be excesses of nociceptive agonists and complementary deficiencies of antinociceptive mediators.Results: Widespread body pain in FMS had prompted the hypothesis that central systemic processes might be responsible. The most dramatic and consistent finding to date has been elevated levels of substance P [SP] in FMS cerebrospinal fluid [CSF]. Statistical correlations of pain measures with CSF SP or time delta CSF SP in FMS both support the hypothesis t...

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