Counting down to May 12, National Fibromyalgia Day. What is the current state of research and knowledge about fibromyalgia?

May 12 is National Fibromyalgia Awareness Day, as sponsored by the National Fibromyalgia Association. The NFA is a non-profit founded in 1997 by people with fibromyalgia who were concerned with the lag in education and attention to the needs of people with fibromyalgia (affecting from 2-5% of U.S. population, during working years, more female than male).

Over the next 12 days, I'm going to post about my experience with fibromyalgia, and about resources, research and changes in our understanding of fibromyalgia.
While this video is long, it is the best resource I have found about the science behind new understandings of fibromyalgia. Chief of Pain Management at Stanford, Dr. Sean Mackey, explains recent discoveries in research into pain, new ideas about central nervous system disease, and how they are related to fibromyalgia. The theory is that there is a disorder or disregulation in the Central Nervous System (CNS) that alters the perception and experience of pain. While the video is long, it's also extremely clear, thorough, and compassionate. It extends and connects what I have been learning over the years. If you know someone with fibromyalgia, you should watch this.


I've made some notes from the video.

Fibromyalgia (FM) is widespread pain, and hyper-sensitivity to pain. It is bow believed to have a wide variety of causes: some hereditary component with specific genetic mutations that may pre-dispose us, probably affecting a specific enzyme; environmental factors such as physical trauma, virus, emotional trauma, anything that can cause"an insult to the person" and seems to kick off the response and feedback cycle that alters the body, specifically the Central Nervous System (CNS) and transmitters called glutamate and Substance P.

What is pain? According to the International Association for the Study of Pain (IASP), pain is not just a stimulus-response mechanism; it is an experience.

Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Pain works by excitation and inhibition. If you have either too much of one or too little of the other, you have pain. If you have too much information coming into the brain, it leads to the experience of pain. Some fMRI imaging seems to back up this idea.

"Each person owns their own pain"
Nociception=the chemical signals that occur when we have injury or trauma. But a group of people who receive the same stimuli will not report the same pain scores. There is a component that is not measured by the stimulus itself.

There are some medications that treat the pain "insult" or causes, but this still leaves lots of people suffering from pain. Pain is now being understood as a disease in and of its own right that causes changes to the nervous system, that stay there after the original injury or insult is gone and the tissue has healed.

Stimulus-- burn, injury--affects nociceptors (pain receptor cells) which act as transducers by converting one form of energy such as heat or pressure, into another form of energy-- action potential--that then transmits a signal along nerve pathways.

There is fast pain and slow pain. The A-delta fibers are fast-conducting and provoke a withdrawal response. The C-delta fibers send a signal more slowly, and are what last longer and hurt more, as a way of getting us to pay attention and take care of the pain.

Nerve signals reach the thalamus which acts a relay station and sends the pain signals to two major areas of the brain. The outer area of the brain is where we perceive the sensory aspects of the pain: intensity, duration, etc. The other section of the brain is the limbic forebrain, part of our reptile brain, where we experience the emotional part of pain, the experience of pain. We are actually more wired for this emotional aspect of pain.

The system that sends inhibitory signals back down from the brain seems to be what gets screwed up in fibromyalgia. Same part of the brain that processes negative emotions resonates with the experience of pain. Negative emotions are linked to discomfort physiologically, and scientist are documenting actual visible changes in the brain among people with FM.

Neuroplasticity is the concept that the brain continues to change and adapt. Research using fMRI is exploring the enhanced sensitivy to pain in the brain, or pain amplification, that seems to be characterize fibromyalgia. Unlike other diseases such as rheumatoid arthritis or carpal tunnel syndrome, with FM, it is not tissue damage or inflamation that causes the pain, but rather an abnormal processing of pain signals. This is why taking aspirin or other pain medications don't help relieve the pain for FM.

SLEEP: he talks about the sleep connection: "Alpha-wave intrusion," which interferes with the deep sleep cycle, is something I have. Again, research is documenting the correlation of sleep cycles and pain responses.

MOOD DISORDERS: actually occur at a lower rate among people with FM.

Oooh! oooh! he talks about the hippocampus!! you have to treat both the pain and the depression, in people where both FM and depression are present, for there to be improvement in each. Education and awareness, validation, lead to significant improvement.

FM needs to be diagnosed and treated with a holistic, integrated approach, using tools from a wide variety of systems and traditions. There exists now a mucher wider array of medications that can help than there were only 10 years ago.

I was originally given a low dose of elavil (a tri-cyclic antidepressant) which helped with the sleep and pain, but left me stupid and unable to work. I have tried Celexa, but the side effects were also unacceptable. Now I take Cymbalta, and the side effects are manageable. The medication gets me to a functional level with my pain; the pain does not disappear, but it is tolerable.

I do not take any opioids, although others I know do, because the docs are wary of the baggage and there are real, negative side-effects as well. Long term use of opioids can themselves over-stimulate the CNS and cause more pain instead of less.

Some anti-seizure meds have newly been approved from FM, but I haven't tried them either.

"Patient education" (ie: taking us seriously and helping us understand what is going on with our bodies and how to manage our symptoms) is key in providing relief.
Mild (MILD) aerobic exercise, helps, but it is important to not overdo it. Fibromyalgia patients do not get the "runners' high" from endorphins that healthy people get. We feel crappy after exercise. Or, rather, we feel crappier. But gentle stretching, breathing, and mild aerobic exercise do have overall positive effects if properly paced.

He talks about the other direction of pain signals: "Descending Noxious Inhibitory Control" (DNIC) means that when you cause pain in one part of the body, (stomp on the foot) you feel less pain in another (your shoulder). Or at least this is the case with healthier people. but FM people just feel more pain, in both parts. So they think there is something out of whack with the inhibitory (descending) signals, from the brain and spinal cord, back out.

Cognitive behavior therapy (CBT) can help, with practice and guidance from skilled practitioners because it helps with awareness and changing habits.

McKay and and his colleague J. Younger study the therapeutic use of low doses of naltrexone (LDN), an opioid blocker, for FM. In a low dose it has an impact on microglial cells (clean-up cells that can get overactive in autoimmune disease states). Naltrexone shuts down narcotic receptors, and is used to treat alcohol and opioid addiction at a dose of 50 mgs. But at a lower dose, it blocks a specific receptors on the microglia, preventing the release of cytokines. So in a pilot study, at a dose of 4.5 mgs/day (10 times less than the regular dose), 7/10 of patients in the pilot trial vastly improved pain states and symptom relief. If it works, it will be very affordable. A larger trial is now underway. Note: the fact that this is a generic drug (meaning it will be cheap) means there is almost no drug company funding for research on it, unless it comes from non-profits or donors.

Apparently, LDN can have a therapeutic affect in a wide number of diseases, but its use is still awaiting FDA approval for many of those.

Mark J. Pellegrino, MD, summarizes much of this same information about pain amplification, but with less detail about the overall picture, in this report "Fibromyalgia: Ultimately a Disease of Amplified Pain".