Fibromyalgia (FM) falls into the spectrum of what might be termed
‘stress-associated syndromes’ by virtue of frequent onset
after acute or chronic stressors and apparent exacerbation of
symptoms during periods of physical or emotional stress.
Patients with FM exhibit disturbances of the major
stress-response systems, the HPA axis and the sympathetic
nervous system. Integrated basal cortisol levels measured by
24-hour urine-free cortisol are low. FM patients display a
unique pattern of HPA axis perturbation characterized by
exaggerated ACTH response to exogenous CRH or to endogenousactivators of CRH such as insulin-induced hypoglycaemia.
The cortisol response to increased ACTH in these stress paradigms
is blunted, as is the the cortisol response to exercise.
Functional analysis suggests that FM patients may also
exhibit disturbed autonomic system activity. For example,
plasma NPY, a peptide co-localized with norepinephrine in the
sympathetic nervous system, is low in patients with FM.
Abnormalities of related neuronal systems, particularly
decreased serotonergic activity, may contribute to the
observed neuroendocrine perturbations in FM. Finally, other
neuroendocrine systems, including the growth hormone axis,
are also abnormal in FM patients. Many clinical features of
FM and related disorders, such as widespread pain and
fatigue, could be related to the observed neuroendocrine
perturbations. This hypothesis is supported by the
observation that many useful treatments for FM affect the
function of these central nervous system centres.
Further clarification of the role of neuroendocrine abnormalities in
patients with FM, and the relationship of these disturbances
with particular symptoms, may lead to improved therapeutic