Dr. Jaudy explains the causes of fibromyalgia.
Fibromyalgia has numerous causes; however, alterations in the normal functioning of the nervous system, specifically brain centers responsible for sensing pain, is a major factor. In this article, I will discuss some of the causes of fibromyalgia and how problems in the nervous system can lead to the myriad symptoms associated with this condition.
Fibromyalgia Syndrome (FMS) is one of the most ambiguously understood conditions that patients suffer from today. The National Institutes of Health state that the causes of fibromyalgia are unknown and that some factors involved include (1) stressful or traumatic events, (2) repetitive injuries, (3) illness, and (4) certain diseases. 1
While it is true that these are risk factors, they are not always necessarily causes. The truth is that every patient is different, and what causes fibromyalgia in one patient will not always be what causes fibromyalgia in another patient.
When we talk about causes, we are talking about causal mechanisms. In other words, what are the neurological, physiological, and chemical mechanisms that lead to the symptoms associated with fibromyalgia?
For many years, the causes of FMS have been thought to be psychological, or ‘all in the mind’ of patients. However, new research has shown that FMS is no longer poorly understood. Recent studies have suggested that the condition is characterized by cortical and subcortical augmentation of pain processing, which means alterations of pain processing in the central nervous system. 2 3
What this means is that pain processing in various brain regions is heightened, causing pain when pain should not be present or causing more pain than would be typically experienced in a majority of the population. In short, fibromyalgia is a disorder of pain processing. 3
Now let’s take a look at the four main mechanisms that occur in fibromyalgia: lack of pain inhibition, fiber sprouting, central sensitization, and autonomic nervous system dysfunction.
The Causes of Fibromyalgia: Pain Disinhibition (Lack of Pain Inhibition). Pain signals are often inhibited by various brain pain control (analgesic) centers such as the periaqueductal grey (PAG), nucleus coeruleus (locus coeruleus), nucleus raphe magnus (NRM), nucleus reticularis gigantocellularis (Rgc), and the rostral ventromedial medulla (RVM), which are located in the brain stem. These areas and others are part of a pain modulation system, which acts to decrease the incoming pain signals from various regions of the body. These areas give the brain the ability to inhibit pain far more than any pain relieving medication; in fact, these areas are often manipulated by various ‘pain killer’ drugs, such as opioids.
There is surmountable evidence that these areas are dysfunctional in patients with fibromyalgia. 4 – 14 Basically what this means is that signals that are normally not perceived as painful may be experienced as pain due to lack of signal inhibition. Also, pain signals that are normally inhibited are not inhibited. This causes the central nervous system to become highly sensitized, which is another feature of fibromyalgia called central sensitization, which we’ll discuss shortly. But before we talk about that, let’s talk about fiber sprouting.
The lack of pain inhibition either causes or results in the growth of new A fibers and C fibers. This is referred to as fiber sprouting. 15 – 20 This ‘sprouting phenomenon’ is a form of maladaptive neuroplasticity. Neuroplasticity is changes in neural circuits or pathways, either structurally or functionally.
Very simply stated, there is a lack of inhibition from the brain analgesia centers. The pain modulation centers of the brain (such as the PAG and nucleus coeruleus) have opioid receptors and these receptors inhibit pain or they lessen the perception of pain. When they cannot be inhibited, the pain is perceived more and then the pathways increase in number, because the tissue is being destroyed faster. Basically, the brain is trying to protect an area from further damage, which results in the growth of more pain fibers.
Early, I mentioned the spinothalamic tracts. Within these tracts, we find nerve fibers responsible for the conduction of pain signals. If you remember from above, the two main types of nerve fibers that conduct pain (and temperature) signals are A delta (A) fibers and C fibers. When we talk about pain signals, we’re not only talking about hits, bruises, and traumas; these types of pain signals are conducted along the A fibers. We are also talking about the constant processing, elimination, circulation, metabolism, and exchange of billions of billions of chemical processes on a second-by-second basis that allow for slow, secondary pain, which is conducted along the C fibers.
When something goes wrong and this orchestration of metabolic systems is decreased from its proper function, inflammatory chemicals such as substance-P, interleukins, catecholamine’s, etc. start irritating the C-fibers causing burning pain and migration of this pain to any region that this inflammation gets shunted to (or erupts). In this situation, the proper neurological coding system, which is the proper receptor transmission, becomes skewed, misread, misinterpreted, misfired, misled, misdirected, and misperceived, and the brain and spinal cord gradually lose control over the C fiber network (the control codes are lost).
When our neurological coding system becomes dysfunctional, this leads to what we call ‘neurological havoc’. This havoc is a neurological chaos that can result in our brain’s inability to control and inhibit our C fibers.
Now, the C-fibers are a group of fibers that have no insulation (no myelin sheath; non-myelinated) around them. As I mentioned, a myelin sheath is similar to the insulation on a wire. In contrast, A fibers are myelinated, so that the signals can be shunted directly to brain as quickly as possible. The C fibers, alternately, do not have this insulation and the signals can become more dispersed leading to a sensation of ‘generalized’ or ‘widespread’ pain that migrates around different regions of the body, which is a hallmark of fibromyalgia.
When the control codes are lost, you lose the key to unlocking your relentless migrating pain and as a result, several other systems lose track of what’s happening in other regions. This becomes a cascade of neurological disorders as systems crumble causing other systems to crumble as well.
The pain associated with fibromyalgia is controlled and processed by various structures in the brain and brainstem, such as those I mentioned above (nucleus coeruleus, periaqueductal grey, pontine-paramedial reticular formation, substantia gelatinosa, and other pain control (analgesic) centers). Loss of proper coding systems between these structures leads to endless increase and migration of pain syndromes, all over the body regions, systems, organs, glands, muscles, joints, ligaments, skin, etc. This is why many fibromyalgia sufferers also experience symptoms associated with irritable bowel syndrome, arthritis, chronic fatigue, and so on.
Both the growth of new pain fibers and the disinhibition of pain signals cause or result in central sensitization.
There is ample evidence showing central sensitization in fibromyalgia and other chronic pain syndromes. 10 21 – 46 The bombardment of pain signals from C fiber sprouting and disinhibition results in central sensitization. This means that the neurons in the central nervous system become hypersensitized. Once the central nervous system becomes hypersensitized, this can result in a low tolerance to any stimuli. This is why many fibromyalgia sufferers experience painful sensitivity to multiple types of stimuli such as smells, light, noises, foods, and more.
Central sensitization also provides a connection to many of the other conditions that fibromyalgia sufferers experience, such as irritable bowel syndrome, food sensitivities, painful menstruation, chronic fatigue syndrome, and more. However, this is not the only explanation for these other conditions and symptoms. We have to understand that the areas that modulate pain are located in the brain stem, where the autonomic nervous system is housed.
Fibromyalgia, Autonomics, Integration and the Brain Stem
The brain stem plays a major role in conduction of information between the brain and the body. In fact, all information relayed from the body to the cerebrum and cerebellum must traverse the brain stem. Additionally, the brain stem is responsible for integrative functions (coordinating functions) including pain sensitivity control, cardiovascular system control, respiratory control, alertness, awareness, digestion, blood pressure, consciousness, and many other functions.
Now, if we consider the functions of the brain stem and the symptoms associated with fibromyalgia, we notice distinct similarities. The most obvious correlations are between the prominent symptoms of FMS (widespread pain or abnormal pain processing) and the brain stem’s function of pain sensitivity control. When we look further into the symptoms experienced by FMS sufferers (sleep disturbances, irritable bowel, headaches, cognitive and memory problems, etc.) we begin to notice the relationship between the many other functions of the brain stem (i.e. integration of autonomic functions such as digestion, blood pressure, consciousness, alertness, etc.).
There are extremely complex neurological control centers within the brain and brain stem. These control centers regulate, integrate, and orchestrate numerous autonomic functions, including pain sensations, digestion, breathing, blood pressure, and many others. In order for these control centers to communicate with one another and the rest of the body, they use various neurological coding systems. These coding systems allow for the proper functioning of all brain and body systems and when they become altered, we develop symptoms, disorders, and diseases due to the dysfunctions.
The hallmark of the multitude of symptoms associated with fibromyalgia is dysfunction in these complex control centers and the neurological coding systems that they use to regulate, control, process, and categorize information. What happens is that we develop a totally different dysfunctional coding system. This results in an inability of these cells to restore, control, normalize, and return to the origin and the basis of their proper neurological function.
When we lose our proper neurological function, we lose our integration. A loss of integration can result in countless symptoms, disorders, and diseases including fibromyalgia, chronic fatigue, irritable bowel, hypertension (high blood pressure), irregular respiration, declination of cognitive abilities and memory, and many, many others. These symptoms are signs of dysautonomia, or dysfunction of the autonomic nervous system.
Now, the question is: Do we find signs of dysautonomia in fibromyalgia patients? The answer is yes. 15 19 47 – 64 In fact, we need to look no further then central sensitization and alterations in the normal functioning of the pain sensitivity control to state that fibromyalgia is a subtype of dysautonomia. After all, pain sensitivity control is a function of the autonomic nervous system and this is dysfunctional in fibromyalgia patients.
What happens is that when areas of the brain begin to dysfunction, other areas must ‘take over’. You can think of this in the following metaphor: If someone doesn’t show up for work, the other workers have to ‘pick up the slack’. In the brain, when regions become overworked, such as we find in fibromyalgia, other regions have to pick up the slack. This leads to a cascade of failure, which also explains why so many sufferers of fibromyalgia also experience other symptoms and disorders, such as irritable bowel syndrome and chronic fatigue syndrome.
So, my question is: Are the causes of fibromyalgia unknown? While we cannot say what causes fibromyalgia in all people, as the causes are likely different in different people, we can say what causes the symptoms: dysautonomia, central sensitization, fiber sprouting, and disinhibition of analgesia centers in the brain.
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