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Turning Stress into Pain: A Fibromyalgia Primer by Dr. Martinez-Lavin

  [ 11 votes ]   [ 1 Comment ]
By Cort Johnson • www.ProHealth.com • August 16, 2017


Turning Stress into Pain: A Fibromyalgia Primer by Dr. Martinez-Lavin
Editor's Note:  This is the first of three articles from Cort Johnson's 2014 review of Dr. Manuel Martinez-Lavin's research on fibromyalgia.   

Reprinted with the kind permission of Cort Johnson and Health Rising

 
A Mexico City doctor and researcher, Dr. Manuel Martinez-Lavin, has been studying and treating people with Fibromyalgia for over thirty years. In a 2009 paper, he proposed two pathways for Fibromyalgia.
 
One suggested that over-activation of the sympathetic nervous system fibers (sprouting) left nerve cell bodies called the dorsal root ganglia (DRG) in a hyper-excitable state. The last way stations for sensory input from the body before it reaches the spinal cord, Martinez-Lavin believes these nerve bodies are overloading the spinal cord with pain signals. He also proposed that increased activity of the sodium channels that transmit pain signals in the DRG could be present.
 
His proposal that infections could be driving the hyper-excitability found in the dorsal root ganglia/sodium channels is reminiscent of Van Elzakker’s theory that a hidden infection may be doing the same in the vagus nerve.
 
Over the past ten years Martinez-Lavin has been validating the role of the autonomic nervous system in Fibromyalgia in much the same way Dr. Newton has in ME/CFS. His research has revealed similar autonomic issues including a hyperactive or over-responsive stress response system that paradoxically ‘folds’ under stress. A 2014 meta-analysis of 196 papers concluded that sympathetic dominance is common in FM, ME/CFS, IBS, and interstitial cystitis.
 
Martinez-Lavin believes that ‘relentless’ sympathetic nervous system activity could explain many of the symptoms present in FM (and other disorders) including chronic pain, sleep problems, anxiety, dry mouth, gut issues, and problems standing.
 
We will get to more of Dr. Martinez-Lavin’s work later, but for now we turn to his book, “How Stress Becomes Real Pain”, which he wrote for patients and doctors explaining his view of FM and how he treats it. We’ll be highlighting sections of the book in a series of blogs. I will be adding my thoughts, as usual.
 
Chapter One – Why He Wrote the Book
 
“I had to live with the medical community’s ignorance and rejection of Fibromyalgia which unfortunately persists today.”
 
Thirty years ago Dr. Martinez-Lavin believed Fibromyalgia might be due to a “drastic breakdown” of that portion of the stress response system called the autonomic nervous system, but it was not until advanced computational algorithms were developed that were able to track heart rate variability that a window into the dysfunction was opened. In the meantime (and still today), Martinez-Lavin believes that a misunderstanding of Fibromyalgia has led to massive ill-treatment of the disorder.
 
Chapter Two: Definition, History, Frequency and Socioeconomic Impact of FM
 
FM may be misunderstood, but Martinez-Lavin notes that it’s very common (2-5% of the population) and 80% of the sufferers are women. For a disorder that, like Chronic Fatigue Syndrome (ME/CFS), gets pitiful funding from the National Institutes of Health, FM has been around for quite a while. A syndrome characterized by widespread muscular pain and hypersensitivity at certain points (“tender points”), FM was called “fibrositis” (swelling of the fibrous tissues) in the early 1900s. The inability to find evidence of inflammation in the affected muscles and points, however, left researchers floundering, and the term “psychogenic rheumatism” began to be employed by some.
 
By the 1970s the name “fibrositis” had been replaced by “fibromyalgia” – a term that simply evoked the presence of muscle pain. Research languished until a seminal paper in 1990 suggested a definition (widespread muscle pain, the presence of tender points) that brought coherence to the field.
 
That study made it clear that, just as fatigue hardly defines ME/CFS, pain does not in any way define FM. Other common symptoms include fatigue that does not improve with rest, disrupted sleeping, diffuse morning stiffness, tingling sensations, numbness and cramps in the arms and legs, headaches, IBS and anxiety or depression. All these symptoms are much more common in FM than in other rheumatological disorders (disorders of the muscles and joints).
 
Chapter Three – Pain 

“Fibromyalgia … may be defined as pain transformed into a disease.”

Pain occurs when an injury to some part of our body sends pain signals coursing through our nerves to the spinal cord, which then sends them on to the brain. Just before the pain signals get to the spinal cord, though, they’re collected in ‘way stations’ called the dorsal root ganglia (DRG) that emanate from the trunk of spinal cord. The DRG process and modulate the pain signals and send them onto the spinal cord and the brain.
 
Martinez-Lavin notes that an important amount of pain modulation also occurs inside the brain in the hypothalamus and thalamus. Both activate the autonomic nervous system (ANS) – a key player in Martinez-Lavin’s conception of chronic pain – when confronted with pain signals.
 
Ultimately the pain signals reach the cortex of the brain, which translates them into pain sensations and sends us into an immediate search for get rid of the pain. That quick prompt to get rid of the pain — to resolve whatever injury has occurred — means that acute pain is a very effective and useful tool for maintaining our health.
 
Chronic pain is different. It doesn’t lead us to resolution of illness, and the changes that occur and the stress it invokes cause it to become pathogenic. Instead of helping us to resolve a disease or problem, it causes disease. Fibromyalgia, to Dr. Martinez-Lavin, is nothing less than pain turned into disease.
 
Two Types of Chronic Pain
 
Martinez-Lavin divides chronic pain into two types: nociceptive pain and neuropathic pain.
 
Nociceptive pain occurs when an unresolved injury prompts an inflammatory response at the site of the injury. The inflammation associated with arthritis or cancer, for instance, damages the tissues, sending pain signals to the brain.
Neuropathic pain occurs when the irritable or hypexcitable nerve fibers constantly send pain messages to the brain. That hyperexcitability gets put into play, Martinez-Lavin believes, at the dorsal root ganglia.
 
Winding Up Your Pain
 
Inside the spinal cord another source of pain intensification called “wind-up” lurks. Once again, irritable and hyper-excitable nerve fibers are featured, but because they’re actually in the spinal cord the increased pain sensitization is referred to differently: it’s called “central sensitization.”
 
If you were to apply heat to your hand every couple of minutes, you should experience heat in your hand — every couple of minutes. Wind-up, which usually occurs in response to neuropathic (but not nociceptive) pain, causes the pain to linger for longer periods of time. As wind-up progresses the pain will remain even when the heat is not present. The nerves in the spinal cord can become so ‘wound-up’ or excitable they can begin to react to any stimulation — such as clothes touching the skin — as painful.
 
Central Sensitization
 
These hyper-excitable spinal cord nerves secrete a variety of pain producing substances such as substance P, glutamate and aspartate. (This is where the microglia come into play.) As this stream of pain signals waft down the calcium channels, these channels can become hyperactive as well. Meanwhile the levels of the substances that inhibit pain, such as adenosine and GABA, drop. Now you have hyper-excitable nerves sending pain signals down hyper-excitable calcium channels and nothing to turn them off.
 
How Stress Causes Pain – the Sympathetic Nervous System (SNS) Connection
 
Martinez-Lavin believes the SNS is behind all of this. During times of acute stress, the SNS secretes substances such as epinephrine that turn off the nerves that relay pain. Pain sensations are diminished during times of danger to allow you to focus on the danger, not on your body.
 
When stress becomes chronic (as occurs during chronic pain), Martinez-Lavin reports that instead of turning off the nerves that relay pain, epinephrine actually turns them on. It also causes the sympathetic nerve fibers in the dorsal ganglia to sprout or grow.
 
That sets up a positive feedback loop, with the SNS becoming more active thus causing more pain and thus more stress which causes more nerve sprouting, and so on ad infinitum. The stage has been set for an unrelenting state of pain.
 
The stage has also been set for stress to cause not just emotional upset but real physical pain. In Martinez-Lavin’s model, chronic stress turns on pain-producing nerves in the dorsal ganglia. Then it hyper-sensitizes them by sprouting or growing, thereby sending them a steady dose of epinephrine.
 
Why the dorsal root ganglia end up botching their pain modulation job up so thoroughly in some people is not clear, but Martinez-Lavin ends the chapter noting that infectious agents – which are able to find shelter from the immune system in them – are a prime suspect.

Article #2 - How Stress Becomes Pain in Fibromyalgia Part II: the Autonomic Nervous System
Article #3 - The Fibromyalgia Mimics – When Your Pain is Not Due to FM:  How Stress Becomes Real Pain #3


About the Author: ProHealth is pleased to share information from Cort Johnson.  Cort has had myalgic encephalomyelitis /chronic fatigue syndrome for over 30 years. The founder of Phoenix Rising and Health Rising, he has contributed hundreds of blogs on chronic fatigue syndrome, fibromyalgia and their allied disorders over the past 10 years. Find more of Cort's and other bloggers' work at Health Rising.




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Article Comments Post a Comment

multi causal FM
Posted by: IanH
Aug 16, 2017
We have to remember that FM is a descriptor not an illness. There will be several routes to the final set of symptoms. An explanation or hypothesis of FM which does not include the available immunological data is likely to be relevant for a subset of FM people. In addition about 40% of people with FM also satisfy the requirements of ME/CFS. So what about these people? Do we just say that they have two conditions? I doubt it. Both FM and ME share similar symptoms consistent with a pathology of modulation. We know only a fraction of the required information about how the immune systems (signalling system) works and how the sympathetic nervous systems signals are modulated. We are now at the stage where any hypothesis or theory about FM (and ME) must integrate the information we have about the roles of the immune, nervous and endocrinological systems. These are both "multi-causal" and "multisystem" illnesses.
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