Abstract

The article challenges conventional wisdom of pain causation in fibromyalgia. It questions current explanatory views of the originating cause that rely heavily on central amplification.  It highlights identifiable causes of pain within the site of pain that deviate from generally accepted understandings of pain in fibromyalgia.  Peripheral abnormalities in intramuscular pressure and oxygen saturation are critical in understanding pain causation in fibromyalgia.   Elevated muscle pressure and low oxygen saturation are medical abnormalities found at the site of pain that refute the notion that pain sites of fibromyalgia are free of pathology.  With transformative medical evidence that can be verified such as this, objective measurement and early detection of fibromyalgia may be within reach. 

KEY POINTS

This article proposes a dramatic change in how pain causation in fibromyalgia is understood.  It introduces a paradyn shift from central amplification to the role of medical abnormalities in muscle pressure and oxygen saturation at the site of pain in understanding the pain of fibromyalgia.  Oxygen deprived muscle tissue brought on by internal muscle pressure is the primary source of pain in fibromyalgia.  This dramatic change in the understanding of pain causation opens the door to fresh perspectives on diagnosis and treatment targets. 

Prevailing theories play a shaping role in the understanding of pain in fibromyalgia.  For many clinicians, pain behaves as an indicator of underlying abnormalities at the site of pain.  In fibromyalgia, this expectation is not met.  The key mechanism espoused to explain fibromyalgia pain is central amplification.1  Abnormal augmentation of sensory input in the central nervous system  has become instrumental in defining pain sensitivity.2  Essentially,  a pain processing disorder in the brain causes neural signals to amplify  creating  pathways for healthy muscle tissue to be experienced as painful.1,3  Thus seemingly explaining why peripheral sites of pain can be free of pathology.1  Unfortunately,  perception of a pain processing disorder in the central nervous system  has taken    hold .1,2  Rigid fixation on a popularized perspective that shapes the way pain is understood and treated has real life implications and may be a barrier to progress. 

       Central amplification has led many investigators   to be sympathetic to the idea that people with fibromyalgia have symptoms without disease or damage at the site of pain.4   Treating medical complaints as symptoms unexplained by disease may be a harmful misconception.  More objectivity in defining the pain source may be a critical step to a better understanding. With the right measuring stick, overlooked abnormalities may be  identifiable at the site of pain.  Patients may no longer have to face the credibility conundrum of intense pain and essentially normal laboratory findings.5

       Recent evidence supports the presence of identifiable pathology in fibromyalgia that has escaped clinical attention.6,7   It raises suspicion that people with fibromyalgia are living with two invisible pathologies at the sites of pain that operate together to induce pain.6  The two pathologies involve elevated muscle pressure and low oxygen saturation, both peripheral abnormalities that are not externally evident.  Because of this,  people with  fibromyalgia can look reasonably healthy on the outside.   Their invisibility represents a challenge that can be unraveled by empirical measurement that is possible with modern technology.8   Measurement makes causation obvious, and once measured, they are objective parameters to support the diagnosis.

        Elevated intramuscular pressure (IMP) is a measurable characteristic of fibromyalgia that has been overlooked for decades.6    It is the fluid hydrostatic pressure generated within a muscle that is measured using a calibrated pressure monitor with a 22-gauge needle inserted at a 45 degree angle one centimeter into the midportion of the trapezius muscle.6,7  When an excessive volume of fluid builds up,  delivery of oxygen to muscle tissues is altered and if prolonged, can create deficiencies in oxygen saturation.9

       The IMP was highly elevated in two studies of trapezius muscle pressure in fibromyalgia.  The pressure abnormalities were first highlighted in 2021 and confirmed in 2024.6,7   The respective pressure readings at rest were 33.2 (mmhg) ± 5.9 and 33.5 (mmhg) ± 5.8.  By comparison,  IMPs in the controls were 12.2 (mmhg) ±3.3 in 2021 and  10.6 (mmhg) ± 3.8 in 2024. In terms of differences,  we are not dealing with small innocuous amounts. This is obvious medical evidence of abnormalities in peripheral mechanisms that has gone unnoticed for decades.  In addition,  changes in pressure were accurately predictive of changes in the perception of pain, with increased pressure consistently associated with increased pain, and decreased pressure consistently associated with reductions in pain.7   In this case,  there is a cause and the expected effect.  The IMP is factual medical evidence that  may come to play a key role in establishing a diagnosis.

       The 2021 and 2024  findings  locate the source of pain in the site of pain,  in the painful tender muscles of patients with fibromyalgia.6,7   These findings align well with the historical perception of muscle pain as a central feature of the fibromyalgia syndrome.10   They open the door to the possibility that the foundations of central amplification need to be reevaluated. 

       The pressurized internal forces of the IMP are of such a magnitude to reframe an understanding of the cause of fibromyalgia pain. The high IMP is  a pivotal barrier to blood flow, the primary mediator of deficiencies in oxygen saturation.  One of the unavoidable consequences of  pressure three times higher is vascular compression of blood vessels in the affected muscle.11   Pressure narrows  blood vessels which governs arterial blood circulation, the carrier of oxygen.12   Reduced blood flow or hypoperfusion influences the lower than normal delivery of oxygen downstream.  

       The same vasoconstrictive forces contribute to circulation and oxygenation disturbances affecting the microvascular environment that delivers oxygen to muscle tissue.9, 12   As a consequence, there is not enough oxygen in the blood streams to meet muscle tissue requirements, a condition known as hypoxia.12 Simply stated, the supply of oxygen to the muscles of people with fibromyalgia is insufficient.13   Deficiencies in oxygen saturation are well known activators of muscle pain.14, 15  

         This theoretical perspective marks a departure from conventional wisdom.  Peripheral medical factors that can be verified are arguably sufficient to determine pain causation independent of central amplification.

          Suspicion of an oxygen supply-muscle pain connection at the microvascular level is not new.  In pioneering work, Lund & Bengtsson16  found low tissue oxygenation in the muscles of patients with fibromyalgia. In important work 3 years later, Henriksson 17 considered a combination of muscle tension and muscle hypoxia to be the likely cause of pain in fibromyalgia.  Since then, the evolution of the oxygen saturation deficiency-pain connection has slowly developed.  In a 2007 study, pain causation was linked to oxygen deficiencies brought on by muscle hypoperfusion.9  In a 2012 study,  pain causation was linked to low tissue oxygenation.13   

       A number of other assumptions in the muscle pressure-oxygen saturation theory are research supported.  The pattern of blood flow in fibromyalgia has been actively investigated.9   There is good agreement that microcirculation is deficient.13   There is also good agreement that vasoconstriction is common.9     

       An oxygen saturation deficiency is generally not recognized clinically as central to understanding pain in fibromyalgia.  However, based on the ground work laid by the oxygen deficiency research, restoration of tissue oxygen has become a target of therapeutic study. Five research studies on the  therapeutic  value of  improved oxygenation to ameliorate  pain in fibromyalgia shared similar methodology and were found to make a difference across geographically different patient populations.18-22    In a common approach, hyperbaric oxygen therapy (HBOT) was employed as the therapeutic intervention.  The five studies confirmed that breathing 100% oxygen in a chamber of elevated atmospheric pressure stimulated a significant benefit affecting pain reduction and an improved quality of life.18-22  Tools relying on  near-infrared spectroscopy (NIRS)  are available to measure muscle oxygen saturation (SmO2) in the capillaries.23

       Reframing has substantial ramifications for clinical care. It unlocks new treatment options that target peripheral mechanisms.  Current medications for fibromyalgia such as pregabalin and duloxetine act on central mechanisms and  may not be the best option.7  For example, there are at least three potential options for restoration of oxygen at the microcirculation level in fibromyalgia,  all culminating in a vasodilatory effect.  Two are pharmacologic options. Vasodilator medications dilate blood vessels causing more blood to flow.24  This in turn increases the supply of oxygen. On the other hand, muscle relaxants provide pain relief by dissipating the compressing  forces on the microvascular structure.  They also produce a positive vasodilatory effect that increases the oxygen supply.25   A shift to nourishments containing antioxidants may also be considered as they act as vasodilators and reestablish more normal blood flow.26  Drinks such as pomegranate juice  are a rich source of antioxidants and may be beneficial.27  

       The overarching propose of the muscle pressure-oxygen saturation theory is to introduce dramatically new terrain that transforms fibromyalgia into a medical condition with  an identifiable cause of pain at the site of pain. In this paradyn shift, the pain of fibromyalgia is understood as a response to abnormalities in muscle pressure and oxygen saturation at the site of pain and  not a response triggered by central amplification.  This perspective places overlooked peripheral factors working together at the center of pain causation in fibromyalgia.   The pivotal roles of elevated intramuscular pressure and low oxygen saturation, are not externally evident to either patients or physicians.  However,  once visible through verifiable measurement,  they can become useful tools for diagnostic detection and improved outcomes.  The paradyn shift should be helpful in identifying new treatment targets and for many will legitimize the pain of fibromyalgia.

       At the present time,  there are no accepted laboratory or imaging exams for confirming fibromyalgia.28 Muscle pressure and oxygen saturation can add novel dimensions to the criteria for fibromyalgia  that are objectively measurable and not subject to the biases of self report.   Perhaps, in the future, testing for elevated muscle pressure and hypoxia will be considered a worthy part of the medical protocol for fibromyalgia.   

         Finally, the usefulness of central amplification in understanding fibromyalgia is also limited by its inability to explain the complexities of the fibromyalgia symptom profile.  On the other hand, the muscle pressure-oxygen saturation theory has the ability to pair many of the other symptoms of the fibromyalgia profile with a cause.  Many symptoms in the profile can be medically explained by the body’s response to an insufficiency of oxygen.  Low oxygenation triggers an array of symptoms that mirror many of those found in fibromyalgia.12  The symptoms include fatigue, headache, confusion, restlessness, muscle pain, weakness, stiffness and cramps.10, 29  Muscle pain and cramping can interfere with sleep.29  In addition, low oxygen saturation can lead to a buildup in lactic acid.30 Symptoms of lactic acid include nausea,  stomach pain, vomiting, exhaustion, and body aches, matching symptoms found in fibromyalgia.   With further research exploration of the muscle pressure-oxygen saturation theory, the perception of fibromyalgia as just a collection of correlated symptoms may change.

RELATED ARTICLE:

Fibromyalgia’’s  future is a biomarker

Http://sites.google.com/view/fmsbiomarker

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KEY WORDS                                                                              Fibromyalgia;  central amplification;  pain;  intramuscular pressure; oxygen saturation

RELATED ARTICLE

Fibromyalgia’s future is a biomarker

https://sites.google.com/view/fmsbiomarker