“Our present study advances a new view of FMS pain that places the pain generator and the site of pain in the same peripheral location—the painful tender muscles. Specifically, this study challenges the prevailing theory of pain in FMS.” Katz et. Al.

Studies suggest that the pressure has been building in the cerebral spinal fluid (intracranial hypertension) in both fibromyalgia (FM) and chronic fatigue syndrome (ME/CFS). That could result in all sorts of symptoms.

a new direction for fibromyalgia?

This study shined a light in a different direction.

But what about the muscles? Many muscle studies have been done over time yet when it comes to explaining FM they are hardly mentioned. Instead its the central sensitization paradigm that holds sway.

The painful, tight and/or constricted muscles were a defining characteristic of the disease. The term fibromyalgia came from the Latin word “fibro” (fibrosis tissue), and the Greek terms for “myo” (muscle) and “algia” (pain).

My muscles, at least, feel like they’re about to pop, they’re so tight at times. It turns out that it’s possible to measure intramuscular pressure, and that’s what this study is about.

An up-ender of perceived knowledge, Katz helped overturn the old fibromyalgia definition, reported that about 75% of people diagnosed with FM do not actually have it, and stated FM is not usually associated with a physically traumatic event.

Katz also validated fibro-fog in FM, and showed that the cognitive problems in FM thankfully do not transition into Alzheimer’s, and showed in an 11-year study that FM tends to stick around for the long term.

Now Katz is upending something again. Katz has been pretty firmly embedded in the school of FM which attributes most of its manifestations to the central nervous system. In “Intramuscular Pressure is Almost Three Times Higher in Fibromyalgia Patients: A Possible Mechanism for Understanding the Muscle Pain and Tenderness“, he challenges whether the central sensitization hypothesis can explain everything.

That’s an important question because, as Katz points out, the first-line drugs (pregabalin, duloxetine, and milnacipran) used for pain in FM (the only ones most doctors know about) attempt to reduce pain by altering central nervous system activity. Given that no one is particularly pleased with the treatment options available for FM, maybe it’s time for another slant.

The authors assessed intramuscular pressure (IMP) in FM researchers’ favorite muscle – the trapezius muscle – a big triangular muscle extending over the back and the shoulders. Thus far, trapezius muscle studies have found evidence of  problems with neuromuscular control, hyperactivation, decreased collagen levels, increased levels of pyruvate and lactate (anaerobic energy metabolism), altered EMG readings, mitochondrial dysfunction and altered conduction velocity. 

Intramuscular pressure was assessed using something called a Stryker pressure gauge attached to a needle through which saline was injected to a depth of about 2 cm. Muscle pressure was recorded in mmHg. Muscle tenderness was also assessed.

The study was a big one – consisting of over 100 people with FM and 30 healthy controls.


High muscle pressure could be squeezing the capillaries – reducing blood flows to the muscles.

The researchers must have had an idea that they would find muscles under high pressure in FM, but I wonder if they were surprised at what they found. Stating that muscle pressure was “extremely elevated” in the FM patients, they reported that it was three times higher… The intramuscular pressures were so different in the FM patients, the authors suggested they might be a diagnostic biomarker.

Ninety-eight percent of FMS cases had a muscle pressure ≥ 23 mmHg. ( A normal resting value appears to be somewhere about 8 mmHg.)  Adding weight to their already impressive findings, they found that pain and tenderness was positively associated with pressure; i.e. the more pressure the muscles were under, the more pain the FM patients were in.

Muscle pressure did not vary according to age – no matter what your age, if you have FM, it looks like you have high muscle pressure.

High (Very High) Muscle Pressure

So what does high pressure do to a muscle? The authors reported that it can compress the capillaries – the smallest blood vessels – possibly obstructing blood flows to the muscles – reducing the delivery of oxygen to them – causing the muscles to rely more on anaerobic energy metabolism, resulting in fatigue and pain.

Then they referred to a 2007 hypothesis, “The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation“, which was may have been well ahead of its time. It proposed that the muscle pain in FM was due to vasoconstricted (narrowed) blood vessels that were producing low oxygen levels in the muscles.

Causal pathway FM

Proposed causal pathway from 2007.

Even back in 2007, plenty of evidence suggested muscle and blood vessel problems causing diminished blood flows and aerobic energy production problems were present in FM. The authors even proposed that autoantibodies were interfering with the ability of the blood vessels to dilate. Similar hypotheses are now being explored in ME/CFS and postural orthostatic tachycardia syndrome (POTS). The authors hypothesized that central sensitization was a reaction to a chronic ischemic state in the body.

They also suggested that hyperbaric oxygen therapy – which now has a couple of positive studies under its belt – could be helpful. They also noted that magnesium – a supplement commonly used in FM and chronic fatigue syndrome (ME/CFS) – can help to dilate the blood vessels by supporting nitric oxide (NO) release. (NO is produced by the blood vessels to dilate them.) They also suggested that the intravenous Myers’ Cocktail might help as well.

Except for one placebo-controlled study which did not find Myer’s cocktail more effective than placebo in FM, that was the extent of Katz’s contribution to FM.  A 2018 review of FM muscle findings, however, noted that many older studies did find abnormalities indicative of hypoxia or low oxygen levels. As the central sensitization hypothesis became ascendant, though, muscle studies became less frequent.

A recent blog highlighted how an “amyloid cabal” – much to the field’s detriment – blocked research into other possibilities in Alzheimer’s for decades. The authors noted that central sensitization is happening in FM but rued the overt focus on it. It has not led to effective treatments for most patients.

Now we have a large study showing a rather prominent anomaly – greatly increased muscle pressure – which is not easily explained by central sensitization at all. The authors, unfortunately, did not attempt to explain why muscle pressure was so high in FM patients. (The FM muscle studies tend to be big on finding abnormalities but not so big on explaining them.)  While the authors proposed that focusing on increased muscle pressure might open up new therapeutic treatments, they also did not say what they might be.

Still, this rather startling finding should put more emphasis on what’s happening in the muscles and the body.  As an added bonus, it opened up the possibility of the first biological diagnostic test for FM.

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