Causes of Fibromyalgia

There is no clear cause attributable to the disease, but different theories have been used to explain its onset.

Some recent studies highlight that patients with fibromyalgia present changes in their nociceptive system (a group of nervous system structures which regulate the perception and response to pain).

This means patients suffer a widespread reduction in their threshold to the perception of painful stimuli which affects different tissues such as muscles, skin, bones, tendons and ligaments, thus resulting in widespread, spontaneous pain predominantly in central structures (the back) as well as painful responses to non-painful stimuli, mainly upon moving different parts of the body.

Patients detect different stimuli (cold, heat, or pressure) as they normally would, but the stimuli produce pain at a much lower threshold. They also experience changes in the brain, with increased activity in the areas that process pain (both emotional and sensory areas), and reduced levels of neurotransmitters (chemicals that transmit information from one neuron to the next), which act as a barrier against painful sensations. Two of the neurotransmitters associated with fibromyalgia are noradrenaline and serotonin.

Another recent discovery is that 70% of C-type nerve fibres (responsible for conducting painful stimuli from the peripheral tissues to the spinal cord) are damaged [in patients with fibromyalgia]. This is a key factor when trying to explain the pain and other sensory symptoms as well as the induction mechanisms and maintenance of the disease.

Fibromyalgia is a syndrome that arises because of peripheral and central alterations to the nociceptive system, with repercussions on the autonomic nervous system, the neuroendocrine system and collateral effects on the activity of other motor and somatosensory areas of the cerebral cortex.