A few months ago I wrote a post about the work of physician and fascia researcher, Bruno Bordoni (HERE). He’s back for the attack with a brand new study called Chest Pain in Patients with COPD: The Fascia’s Subtle Silence, published in last month’s issue of the International Journal of Chronic Obstructive Pulmonary Disease.
Having written a post on COPD not too long ago, I realized that the numbers of sufferers are not limited only to smokers or ex-smokers, but I had forgotten just how many people are affected by this disease. “The World Health Organization (WHO) estimated a current mortality rate of at least 64 million people per year, and in 2030 COPD will represent the third leading cause of mortality in the world.” No matter how you slice it, COPD is both serious and common.
FASCIA AS RELATED TO BREATHING & COPD
People with COPD not only struggle with difficulty breathing, but with pain as well. This is especially true if the patient also has other diseases such as ANXIETY/DEPRESSION, HIATAL HERNIA, DIABETES, GERD, ARTHRITIS, OSTEOPOROSIS, SYSTEMIC MYOPATHY, or costochondritis (and as you’ll see momentarily, Rib Tissue Pain is a huge component as well).
As opposed to “CENTRAL SENSITIZATION,” Bordoni and his team reveal that COPD typically starts with, “peripheral sensitization provoked by the constant stimulation of inflammatory mediators.” If you are not sure what “inflammatory mediators” are, be sure to read THIS SHORT POST.
Even thought the sensitization starts peripherally, it frequently ends centrally (see earlier link) —- “hyperalgesia and allodynia, with central sensitization caused by the persistent involvement of medullary neurons and cerebral areas, and the subsequent involvement of the psychoneuroimmune system.”
Not surprisingly, HYPERALGIA & ALLODYNIA are problems that are frequently associated with fibrotic fascia (“SCAR TISSUE“). Furthermore, the authors went on to discuss this phenomenon in terms of “LEAKY NERVE SYNDROME” (“increased permeability to cations of pain receptors, with the appearance of primary hyperalgesia“).
Chronic inflammation becomes a self-potentiating viscous cycle (“This mechanism of inflammation that makes the fascial tissue fibrotic is always bidirectional. The lungs increase the fascial stiffness by releasing pro-inflammatory substances, just as the fascial tissue releases inflammatory substances toward the lung“).
The pleura becomes thickened (“The creation of pleural adhesions and scars further reduces the lung expansion in patients with COPD“), the vagus nerve is affected as these people tend toward SYMPATHETIC DOMINANCE, chronic over-inflation of the lung causes the firing of specific kinds of pain receptors. Furthermore, “the inflammation of bronchial pathways causes the production of free radicals” causing both bronchospasm “and pathological bronchial fibrosis“.
What’s critical for you to remember here is that fibrosis (Scar Tissue) is not only the world’s leading cause of death (HERE), but always occurs as the result of inflammation (HERE, HERE, HERE, HERE, HERE, HERE, HERE, HERE, and HERE). The authors went on to say….
“Chronic and acute pain can alter the functions of the baroreceptors, just like an altered function and position of the diaphragm can negatively influence the baroreceptorial system. This creates a vicious circle, and it becomes difficult to understand the cause and the effect.
We know that the compression of the vagus nerve can alter its function and ability to transport, just like the dysfunction of a peripheral nerve, mimicking the nerve entrapment syndrome. We can suppose that an anomalous tension of the diaphragm in the area of the vagal passage could induce the compression of the nerve, negatively affecting its anti-nociceptive and anti-inflammatory ability.”
Baroreceptors are nerve endings found in the walls of blood vessels that sense pressure, allowing the body to make the proper adjustments in the muscles of the vessel walls to regulate blood pressure. Nociception is your body’s ability to sense noxious stimuli as pain or similar.
This is why folks with COPD have a tough time regulating BLOOD PRESSURE. The vagus nerve is the chief nerve of the parasympathetic side of the nervous system (the feed and breed / rest and digest side) as opposed to the sympathetic system (fight or flight). Foul vagal function and you’ll likely end up with the Sympathetic Dominance I showed you earlier.
Although there are any number of other mechanisms of pain and dysfunction with COPD, this study spent a dozen or so paragraphs talking about the various ways that it affects the FASCIA SYSTEM.
After describing the fascial system thusly (“The fascial organization that covers the contractile part of the muscle can be defined as the myofascial system. The fascia allows the muscles to act in synergy, thanks to the fact that the fascial tissues connect all the muscular districts.“), Bordoni went on to talk about how this screws up the BIOMECHANICS of the chest wall, the diaphragm, the ribs, as well as the “somatic fascial system (thoracic rib muscles)“.
“There are different muscles that operate on the ribs and that take part in the respiratory acts, whose behavior is not always easy to determine. Externally, the intercostal muscles are covered by the deep fascia originating from the deep cervical fascia, while, internally, they are covered by the endothoracic fascia. Costal (rib) position changes in patients with COPD.
The muscular respiratory disadvantage increases the risk of hospitalization. Costal muscles work harder, and weakness, fatigue and inflammation appear. The level of inflammatory cytokines found in costal muscles is linked to the seriousness of COPD. Muscles suffer from hypotrophy with an increase in the amount of fat inside contractile fibers. Costal muscles can be a source of chronic pain.”
Although I CHERRY PICKED the quotes from today’s study, leaving out mass quantities of highly technical information, the point I wish to make here is that these rib tissues, as Bordoni says, “can be a source of chronic pain“. Another point is that hypertrophy and “thickening” (it was mentioned earlier) are frequently the result of problems with the fascial system (HERE & HERE).
In the paragraph below his team talks about the importance of hydration and HYALURONIC ACID as well as the inability of the various layers of pathologically adhesed fascia to slide on each other (HERE are two 7 second videos side by side, normal fascia -vs- adhesed fascia). Oh; I almost forgot — his study reveals that fascia acts not only as an ORGAN OF PROPRIOCEPTION, but as it’s own nervous system as well (HERE).
It’s a long (also cherry-picked) quote, but it contains ENOUGH MEAT to live on for a month!
“We know that the rib cage suffers from a biomechanical limitation and that costal muscles tend to become fibrotic. We know that the fascial tissue is in close proximity to the muscles (deep fascia and epimysium) and that it can suffer from the same non-physiologic adaptation of the contractile districts (and vice versa). We know that the nociceptors that are in the fascia have a lower threshold of activation if the fascial tissue is less compliant (greater stiffness). We can suppose that the deep fascia covering externally the ribs is one of the causes of thoracic pain.
The fascia influences the function of the viscera (organ) it wraps around and vice versa. The fibrosis of the muscles, the fascia or the visceral tissues is similar to the wound-healing mechanism, which modifies the mechanical abilities, without necessarily altering their shape. The deep fascia, like the endothoracic fascia, is made up of several layers that slide over one another.
The different layers will lose the ability to slide if they lose water and hyaluronic acid (like in fibroses), creating greater stiffness and density of the tissue. This happens in the fascial tissue of many anatomic areas where there is chronic pain (back, neck) or in pathologies (diabetes, trauma and surgery and hormonal variations) and aging. The fascial tissue that loses part of its ability to slide could create adhesions to the tissues it comes into contact with, further stimulating the nociceptive fascial afferences.
The different organs of the mediastinum communicate with one another, thanks to visceral fascial relations. This scenario could be one of the reasons for the lack of motor coordination found in patients with COPD. The pain coming from the viscera, caused by the stiffness of the visceral fascia, could not only be one of the causes of perceived pain but also contribute to the patients’ lack of neuromotor coordination [since] the visceral fascial system could be considered as a proprioceptive organ.”
No matter what sort of problem you may have, it is important to treat it as though it were systemic (the topic of tomorrow’s post). If you found this post relevant or interesting, please get this information into the hands of those that need it. The easiest way to reach those you love and care about most is by liking, sharing, or following on FACEBOOK.