FM is considered a disease of amplified pain. How we get FM is the "mechanism" of FM as contrasted to why we get FM, or the "cause." Here's how I think we get (got!) FM:
Pre-wired genetics: I think we start off more vulnerable to getting fibro due to our genes. FM is way too common (seen in 2-5% of the population worldwide) to be considered a "random" disease. There are many studies supporting the genetic connection to FM. Whether we inherit less effective neurotransmitters like serotonin and norepinephrine, or more potent neurotransmitter-degrading enzymes, or less potent endorphins, we have a pre-wired "lower chronic pain threshold." We are more prone to getting FM.
We can develop full-blown FM without any obvious "trigger." Both men and women normally lose some ability to inhibit chronic pain signals as they get older. Normal women are even more vulnerable because their pain inhibitory system has been found to be more "defective" to begin with. Those with inherited fibro genes are less able to inhibit pain signals as she (more than he) ages and can develop amplified pain once a certain "aging threshold" is met.
What does this mean? We can develop "spontaneous" FM just by getting older if we inherited fibro genes. Usually this happens around ages 25 - 45 but it's variable.
Epigenetics: This is the study of changes in gene expression that do not involve alterations to the pre-wired genetic code but still can get passed down to the next generation. This may eventually be found to play a role in how the first person in a family develops fibro, ie the "index case" when no previous relative was diagnosed with it. Environmental factors, nutrition, exposures, chronic conditions etc may switch "on" certain genes leading to FM, and this new FM trait could be passed on to the offspring! This may explain a different way one gets "spontaneous" FM without an obvious trigger.
Triggers: This is likely the most common way a vulnerable person (inherited genes) gets actual FM. Last week's discussion reviewed causes. Here's how the cascade of events may unfold:
A genetically vulnerable person without clinical FM gets exposed to a trigger.
If trauma (ie a whiplash injury) occurs, the tissue injury leads to persistent activation of the nociceptors (specialized pain nerve endings). Infections, inflammatory and autoimmune conditions and other causes can also damage the nociceptors and cause them to be more sensitized, more irritated, and signal more pain (they become "pain generators")
These persistent pain generators bombard the sensory nerves and autonomic nerves and leave them wondering, "what is happening?" At first, these nerves try to diminish or accomodate the signals, but the pain triggers don't stop, so the nerves are forced to permanently react and they become hypersensitized.
At the spinal cord level, the fibro begins to establish itself. Pain signals become amplified and spread to different cord levels and cause the spinal nerves to rewire themselves to create even more efficient pain pathways. Our ability to inhibit pain signals at the spinal cord level becomes defective, leading to more pain getting through.
Our poor brains don't have a chance, do they? The brain gets bombarded by the continuous pain signals below, causing it to form pain memories, and to attach emotional characteristic to pain (like fear, anger, anxiety, depression) The brain gets overwhelmed and spends a lot of attention and energy monitoring the pain, leading to fatigue and fibrofog. Many biochemical changes are occurring along the way, but I want to portray the basic "fibromyalgia cascade."
The end result: Welcome to your rewired central nervous system that has designed a lean, mean, pain-producing machine!
Dr. P