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

  [ 57 votes ]   [ Discuss This Article ] • November 3, 1994

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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