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Neurohormonal perturbations in fibromyalgia (FM)

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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

strategies. {MCMStrSt}

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