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Category: General

Published on Monday, 11 August 2008 14:19

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Pathogenesis

The precise pathology of fibromyalgia remains unknown at present. However, current research indicates increasing evidence for the following mechanisms:

Pain amplification^9-12
Research clearly indicates the presence of peripheral and central sensitisation of the nervous system in fibromyalgia patients. Patients demonstrate classic signs of hyperalgesia and allodynia in response to thermal, noxious and touch stimuli. Measurements of neurotransmitter levels in the cerebrospinal fluid (CSF) have found a threefold increase in substance P together with a fourfold increase in nerve growth factor.

These increases, together with continuous peripheral pain stimulation augmenting the levels of glutamate, activate the N-methyl-D-aspartate (NMDA) receptors leading to central sensitisation. The influence of the descending inhibition pathway from the brain is severely diminished by decreased levels of serotonin and noradrenaline, further augmenting the state of pain amplification.

Sleep abnormalities^13,14
An intrusion of alpha waves into stage 4 delta sleep has been demonstrated using electroencephalograms(EEG's). This intrusion is believed to be responsible for the non-refreshing sleep symptoms and low levels of insulin growth factor-1.

A total of 80% of growth hormone is released during stage 4 delta sleep and a persistent lack of growth hormone can lead to an accumulation of biochemical and mechanical faults in the muscles and tissues of the body.

Hormone disruption^13,15
Multiple hormonal disturbances have been observed in fibromyalgia. Studies show a disruption in the hypothalamus-pituitary-adrenal axis with elevated levels of corticotropin releasing hormone (CRH) and adrenal cortical-stimulating hormone in conjunction with low 24-hour urinary cortisol levels.

Elevated levels of CRH lead to increased levels of somatostatin, which operates to reduce levels of thyroid hormone, growth hormone and oestrogen as well as increasing levels of prolactin. All of these imbalances have been observed to some extent in fibromyalgia patients.

Muscle pathology¹⁶
Muscle biopsy studies have revealed the presence of "moth eaten", ragged red fibres, type 2 fibre atrophy and decreased levels of ATP and phosphocreatine, indicating mitochondrial abnormalities and insufficient blood supply to the muscles. There is no sign of degeneration, regeneration or inflammation.

Despite these observations being in unison with other chronic neuromuscular conditions and not specific to fibromyalgia, they do indicate that the muscles are involved in the overall pathogenesis. The disturbed regulation of the microcirculation and a change in the muscle metabolism might sensitise the intramuscular nociceptors.

Also, the mitochondrial abnormalities may indicate a low oxidative capacity and therefore a reduced ability for endurance work. However, the pain cannot be sufficiently explained if a state of central sensitisation does not exist.

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