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Neuromediator & hormonal perturbations in fibromyalgia (FM) syndrome: results of chronic stress?

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Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981),numerous investigations have confirmed that FMS is a clinical

entity. However, the aetiology of the syndrome is still not

fully elucidated. It seems, however, logical to place the

origin of the disorder in the muscle. Muscle pain, especially

at the muscle-tendon junctions, fatigue and stiffness are the

first symptoms. A malfunction of energy metabolism has been

detected in part of the muscle fibres. However, it has to be

considered that the muscle is not an isolated entity. Its

activity is controlled by segmentally arranged motor units of

the ventral horn of the spinal cord in response to

proprioceptive afferent signals arising in the muscle spindles

or in other sensory elements including nociceptors. Together

with supraspinal descending inputs, the spinal motor neurone

pool is the common final pathway for segmental and

suprasegmental inputs, making the motor system extremely

powerful for adaptive adjustments but also vulnerable if

deficits occur in either of these input levels. A second,

recently discovered abnormality seen in FMS is a lowered

serotonin level in peripheral and most likely also central

structures. The underlying mechanism seems to be defective

absorption of the precursor amino acid tryptophan from the

gut. Serotonin is involved centrally in the regulation of the

sleep pattern, and at the spinal level it acts as a ‘gain

setter’ of motoneurone excitability and suppresses signal

transmission of noxious stimuli in dorsal horn neurones.

Either of these two disturbances, muscle energy depletion or

serotonin deficiency, could by itself evoke many of the

symptoms of FMS, and their combined appearance will perpetuate

the disease. Depressed levels of somatomedin C, caused by a

deficit of stage 4 sleep-dependent release of GH, might

represent an additional factor in preventing proper

development or repair of myoskeletal structures. Malabsorption

of certain amino acids, possibly due to a genetic disorder of

gut transport mechanisms, may constitute an additional

deleterious factor. The abnormalities found in the HPA and HPT

axis may be seen as an attempt of the organism to restore

homeostasis. The stimulus eliciting this counter-regulatory

reaction may be pain or other afferent signals which normally

do not reach the central nervous system. It is doubtful

whether the unspecific activation of the HPA axis in a

non-inflammatory disease is beneficial.Rather, on the

contrary, elevated glucocortocoid levels, via their mostly

inhibitory action on various enzymes, may suppress repair of

myoskeletal structures and alter feedback circuits, as shown

paradigmatically in the regulation of thyroid hormones, with

consequences on thyroid hormone-dependent mechanisms like

parathyroid hormone secretion and calcium homeostasis.

Whereas such peripheral defecits are easily discovered, their

effects on the CNS activities, especially as feedbacl signals

on hypothalamic releasing hormone neurones and their specific

interactions, need further investigation to provide a

rationale for a specific therapy of FMS.

Neeck G, Riedel W

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