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Gentle care. Remarkable results.
2757 University Dr, A, Auburn Hills, MI 48326
New Patient Line: 248-598-4002
Why do I have chronic pain? Why does pain become chronic? Studies into Fibromyalgia syndrome show us a few reasons why a brief, acute pain can slowly or suddenly become something we’re fighting daily. Learning the current understanding behind chronic pain can help us in a few important ways:
The title of this article doesn’t suggest that the explanation for chronic pain is simple. But perhaps we can offer a simplified explanation that most people can understand.
Much of this article comes from distilling the key points out of a 2016-2017 review in the journal Neuroscience called “The neurobiology of fibromyalgia and chronic widespread pain.” (1)
There are some technical concepts here that may require further reading if this is your first time reading an article like this. In the interest of making this article short, sweet, and helpful for someone in chronic pain, the concepts are presented in an abbreviated way.
Fibromyalgia. Irritable Bowel. TMJ. Prostatitis. Pelvic Floor Pain. Complex Regional Pain Syndrome. Different doctors may be dealing with these different painful regions with these differently named pain syndromes…However, the mechanism that leads to pain in the TMJ or the pelvic floor, or even in digestive tract may be similar enough to each other to be describing the same problem, just in a different location of the body.
In each of these cases, there may be
Because doctors cannot point to a single organ, or tissue, or area of injury and connect it with the pain in a way that makes sense, then the cause of the pain is classified as unknown.
This will lead to many patients working with neurologists, rheumatologists, and other pain specialists, or with doctors that may focus on a single body region or organ, like a urologist or gastroenterologist. In doing so chronic pain patients then may end up with multiple diagnosis and come to see their separate painful parts as separate entities.
The important takeaway, however, is that the chronic pain, wherever it may be, may just be the same problem showing up in different tissues.
Therefore, what tends to calms the IBS may also calm the fibro pain and vice versa. Dealing with chronic pain as a condition unto itself and instead of different conditions in different parts may be a global approach that some chronic pain patients may find more helpful.
Most temporary pain is pain of the periphery. The periphery means from the “edges or outside,” and here we mean a region from outside the central nervous system (CNS, or brain and spinal cord).
According to peripheral pain theory, the brain is getting excited pain signals from pain sensors out in the body due to a direct irritation from some sort of major or minor trauma to the tissue. There are different paths these pain signals can take.
Striking your thumb with a hammer as you attempt to hammer in a nail is an example of a common trauma that many of us have experienced.
This is pain out in the body (the thumb) due to the compression and tearing of tissue (skin and underlying soft tissue) which sends a pain signal to the brain, that says “Careful, we’re getting damaged.”
A more complex example might be a whiplash injury after a rear impact crash. In this case, stress to neck joints from the accelerated “flattening” of the neck stimulate pain sensors in the ligaments that lock the neck into a protective spasm. Broken blood vessels around joints may flood tissue with blood flow. There may be swelling that also expands tissue and compresses pain sensors, as the body attempts to heal from the injury and uses the natural, normal inflammation cycle to do so.
Whether it’s a thumb or a neck, pain is being felt due to an injury to a “peripheral nerve” communication path that sends pain signals back to the brain, essentially telling us to “watch out” or “be careful’ as part of recovery mechanism.
A smashed thumb rarely becomes a chronic pain, but a whiplash in the neck can. So what’s the difference between these two?
Centralized pain may have started out as a compression, tearing, or injury in the periphery of the body, but the pain has taken on a life of its own, separate from the original mechanism of the injury. When pain becomes central, it’s no longer a symptom of an injury, but a condition that stands on its own. Fibromyalgia syndrome (which often starts after an injury) is one example of this kind of pain.
When pain becomes centralized, the pain itself morphs into something different in how it behaves. Hyperalgesia and allodynia are two characteristics of centralized pain. Hyperalgesia means a minor irritant causes much more pain than normally expected. For example, a minor pin prick of the skin creates spams. Allodynia occurs when normally non-irritating movement, touch, or stimulation causes pain. For example, when brushing the skin around the shoulder creates pain in a fibro patient.
In the case of Fibromyalgia studies have shown that elevated pain levels (often called augmented pain) and differences in pain processing (sensory processing) are found. Fibro patients often tend to be more sensitive in other sensory experiences, like processing sound, as well as their response to heat, cold, and electrical sensations on the skin.
All of this points to the likelihood that when chronic pain becomes its own condition, the CNS is more easily excited in certain areas while the body simultaneously loses the effectiveness of the normal pain suppression system.
The review in Neuroscience points to the possibility that chronic pain patients have greater amounts of neurotransmitters (think nervous system chemicals that stimulate nerves) that deliver pain signals. Substance P in the cerebrospinal fluid and glutamate in the brain are two examples of excitable neurotransmitters that may may increase in chronic pain and elevate pain levels.
This can happen without an increase of inflammation in the body, so this may be called the non-inflammatory pain response – different from the pain potentially influenced by the immune system.
Even more odd than an increase in neurotransmitters, processes inside the neuron cells may lead to enhanced pain through a changing of gene expression that makes the cells literally more excitable! (This is too technical for our purposes here, but you may want to search “increases in transcription factor CREB”). In this case the nerve cell may become more excited because it starts programming itself to become more excited, rather than being excited by a change in the surrounding chemicals alone.
The centralized pain condition doesn’t just mean that nerves are more excited, but that the natural pain relieving system of the the body is suppressed. That’s right, we have our own internal pharmacy that makes analgesics (pain relievers) for us, that are a natural part of the pain/healing cycle. Endorphins are one kind of natural analgesics that are familiar to many people. In chronic pain patients these natural anlagesics of the CNS may not work as well due to a depression of other neurotransmitters.
Serotonin is one neurotransmitter that may decrease with chronic pain, suppressing the normal pain relief that serotonin provides. Less Serotonin in the body may be responsible for a greater perception of pain.
In a more complicated case than seratonin is the case of the body’s endogenous opioids. Endogenous means “native to” – and endogenous opioids are the opioid chemicals that the body naturally produces which help the body process pain as it heals. Endorphins are one example of endogensou opioids. In chronic pain patients, the body may over compensate by producing far more endogenous opioids than it needs.
While at first glance you might assume that this would help control pain (more opioids, more pain control), the situation is more complex. Neurotransmitters have specific places where they land in the central nervous system to produce their effects. These landing places are called receptor sites. An over-abundance of opioids may actually overwhelm the receptor sites, lowering their function.
These are two examples where the body’s natural pain suppression in the CNS is itself suppressed.
Finally, in a final but different example of chronic pain changing the central nervous system, there is the issue of gray matter loss in the brain. The image in this articles shows scans of patients with chronic back pain and Fibromyalgia with diminished density of brain tissue in certain areas of the brain. This loss of tissue alone cannot necessarily explain the pain itself, but it may be the long term consequence of chronic pain on the brain. In other words, an effect not a cause. Still loss of CNS tissue would seem to support the centralized pain theory, as it shows that something is happening at a metabolic and cellular level in the brain in people with chronic pain!
For a collection of research on the relationship between chronic pain in different regions of the body and changes in brain scans, see the end of this article.
It’s well known that immune system cells are involved in creating pain, for both acute and chronic pain. Mast cells, neutrophils, macrophages, and (killer) T-Cells are different immune system cells that create pain in human and animal tissues. One important immune system cell that may be linked to fibromyalgia pain are the inflammatory cytokines (IL-6), which can increase pain in muscles, and whose presence may be increased with the increase in fatty tissue.
Whatever the specific mechanism of pain and different kindss of immune system cell, the story is essentially the same: there comes to be an inappropriate inflammation response, where inflammation becomes a raging fire instead of a controlled burn. Over time, this disproportionate inflammation response becomes programmed into the body’s response. Why? No one is exactly sure. But with over-abundance of inflammation, there is over-abundance of inflammatory cells, and therefore greater pain.
(The ability of the CNS via the Vagus Nerve to “control and limit” this inflammatory response from the cytokines is an exciting area of study in pain treatment (2). It’s one that upper cervical chiropractors in particular have an interest in due to the influence the upper cervical procedures most likely have on the Vagus nerve and the autonomic system.)
Some minor or major trauma may have initiated the initial pain response, but now the pain has “grown beyond” the original injury to become its own issue. In many confusing cases, the site of the original injury is no longer injured in a way to explain the widespread pain. This causes many people with chronic pain and their family and physicians to wonder, if in fact, the pain is real.
In other words, pain is a warning system that shouldn’t immediately be covered up with pain killers, and instead should be allowed to inform us of where the problem might be. Pain that has a mechanical origin, for example, will have a mechanical solution. And treating symptom pain with only pharmaceuticals may only cover up the trauma instead of helping the body process it.
Likewise, when pain become chronic, widespread, and a condition unto itself, then non-pharmaceutical options to decrease inflammation and potentially “reset” pain signals in the CNS are important to consider.
The relationship between chronic pain in various regions of the body and changes in brain scans is the subject of some interesting research. The now inactive ChiroAccess website has a small collection of these reviews, which covers
(1) Sluka KA, Clauw DJ. Neurobiology of fibromyalgia and chronic widespread pain. Neuroscience. 2016;338:114–129. doi:10.1016/j.neuroscience.2016.06.006 Accessed via: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5083139/
(2) Johnston GR, Webster NR. Cytokines and the immunomodulatory function of the vagus nerve. British Journal of Anaesthesia Volume 102, Issue 4, April 2009, Pages 453-462 doi.org/10.1093/bja/aep037
Featured image Human Head in Wire by Reimund Bertrams from Pixabay
No Pain Like This Body (Neon) from a photograph by Sarah Lötscher from Pixabay , representing the art of Lani Maestro
Shematic of CNS Changes in Chronic Pain by Borsook D, Moulton EA, Schmidt KF, Becerra LR. [CC BY 2.0], via Wikimedia Commons
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