Intramuscular Pressure is Almost Three Times Higher in Fibromyalgia Patients..., 2020, Katz et al

Joan Crawford

Senior Member (Voting Rights)
Apologises if this has been posted - I searched and could not find it.

Intramuscular Pressure is Almost Three Times Higher in Fibromyalgia Patients: A Possible Mechanism for Understanding the Muscle Pain and Tenderness

https://www.jrheum.org/content/early/2020/09/10/jrheum.191068

Robert S. Katz, Frank Leavitt, Alexandra Katz Small and Ben J. Small
The Journal of Rheumatology September 2020, jrheum.191068; DOI: https://doi.org/10.3899/jrheum.191068

Abstract
Objective Widespread pain in the fibromyalgia syndrome (FMS) is conventionally viewed as arising from disordered central processing. This study examines intramuscular pressure in the trapezius as an alternative mechanism for understanding FMS pain.

Methods 108 patients who satisfied the ACR criteria for FMS and 30 patients who met the ACR criteria for another rheumatic disease comprised the study groups. Muscle pressure was measured in mmHg using a pressure gauge attached to a No. 22 needle inserted into the mid portion of the trapezius muscle. In addition, FMS patients and rheumatic disease controls had dolorimetry testing, digital palpation, and reported pain scores.

Results Muscle pressure was substantially higher in patients with FMS with a mean value of 33.48± 5.90 mmHg. Only 2 of 108 patients had muscle pressure of <23 mmHg. The mean pressure in rheumatic disease controls was 12.23±3.75 mmHg, with a range from 3-22 mmHg. FMS patients were more tender than controls based on both dolorimetry (p<0.001) and digital palpation (p<0.001). The mean pain score in patients with FMS and controls was 6.68±1.91 and 1.43±1.79 (p<0.001).

Conclusion Pressure in the trapezius muscle of patients with FMS is remarkably elevated and may be an intrinsic feature of FMS that could be monitored as part of the diagnostic evaluation. The burden of the pressure abnormality may help explain the diffuse muscle pain of FMS. Therefore, FMS as a disorder of exclusively central pain processing should be revisited. Therapeutically, the reduction of muscle pressure may change the clinical picture significantly.

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Any thoughts on this as a finding? Reliable testing method use? Easy to carry out in routine clinical practice? Value clinically?
 
The relatively high sensitivity and specificity is rather curious. I'd like this to be replicated by blind examiners before getting too excited. The FMS pain score vs muscle pressure plot suggests the association is weak, but that could be due to too much variation in the anchoring of the pain rating scores themselves.

Proposed mechanism:
The trapezius is a large muscle that runs from the upper back to the neck and shoulders14 and covers areas of the body that are considered primary pain sites in FMS15. Considering the compressing effects of extended pressure on the small capillaries in muscles, elevated pressure in the trapezius could be a mechanism for diffuse muscle pain. Abnormally high IMP is known to compress capillaries, which in turn obstructs blood flow and thereby prevents adequate oxygenation of muscle tissue, a condition well known to set off and maintain pain sensations10,16. Muscle biopsy studies have shown evidence of hypoxia and no inflammation11,16,17. It is possible that increased muscle pressure could be compressing capillaries and reducing blood flow to muscle. The burden of hyperpressure in the trapezius over time is likely to affect health more broadly and could be the mechanism for the muscle pain and fatigue that characterize FMS18,19,20.
 
Sounds interesting because the differences between groups are enormous, especially since they didn't use healthy controls but patients with other rheumatic conditions.

The FMS pain score vs muscle pressure plot suggests the association is weak
Looks like more than a weak correlation to me:
upload_2021-7-20_13-53-27.png

I'd like this to be replicated by blind examiners before getting too excited.
Agree
 
Hydrostatic pressure in relaxed muscle should be slightly below atmospheric. That suggests to me that the pressures here are indications of muscle contraction. It would not be surprising if people with a diagnosis of fibromyalgia contracted the trapezius harder when a needle was stuck in.
 
Interesting but like @Trish indicates it looks like three individuals are contributing a lot to the heavy lifting.

Also it would be interesting to have data from other comparator groups, as even if the association is robust, it would be good to have more confirmation about the possible direction of any causality.
 
It is interesting. I think the authors should be commended for thinking beyond a hand-wavy central sensitisation theory.

The relationship between pain and muscle pressure isn't really the key thing here - as @Snow Leopard said, there's potential for a lot of fuzziness in pain reporting. That said, I don't know why the authors didn't make a chart of the individual pressure results. That's the key finding and the dramatic differences would have made for a good chart.
this paper said:
In 98% of FMS cases, a pressure reading of 23 mmHg or above was recorded. A resting value in the area of 8 mmHg is considered normal based on an older study but using a different technique .....
The distribution of values in the two groups had almost no overlap. Intramuscular pressures in the FMS group ranged from 8 to 58 mmHg, with only two values less than 23 mmHg. Pressures in the controls ranged from 3 to 22 mmHg.

That suggests to me that the pressures here are indications of muscle contraction. It would not be surprising if people with a diagnosis of fibromyalgia contracted the trapezius harder when a needle was stuck in.
Good point, and one that the authors don't address. So, I guess the idea is that the people with fibromyalgia tensed their muscles more, because of the lower threshold to pain in the shoulder? However, the differences in muscle pressure (with virtually no overlap between the FM and control groups) seem pretty marked. If it was just a muscle contraction difference, wouldn't at least some of the controls have tensed in a similar way?

The authors suggest higher muscle pressure causing constriction of capillaries and inadequate oxygenation.
What could increase the pressure in muscles if not contraction or inflammation?
Is there be another way to test muscle pressure that wouldn't potentially cause a flinch? Some sort of ultrasound?
What measurable impacts on muscles would we expect to see if there is chronic low level hypoxia?
 
Is there be another way to test muscle pressure that wouldn't potentially cause a flinch?
What measurable impacts on muscles would we expect to see if there is chronic low level hypoxia?
Partly answering my own questions:
https://nyulangone.org/conditions/compartment-syndrome-in-adults/diagnosis
about compartment syndrome said:
Exercise increases blood flow to muscles, expanding blood vessels and increasing pressure inside muscle compartments. The pressure may eventually restrict blood flow altogether, damaging the muscles and nerves.

Symptoms of chronic compartment syndrome, such as pain, tightness, cramping, and sometimes numbness, occur during exercise but usually go away when the activity is stopped.
Compartment Pressure Testing
A compartment pressure test measures the amount of pressure within the muscle compartment. To perform this test, a doctor first injects a small amount of anesthesia into the affected muscles to numb them. He or she inserts a handheld device attached to a needle into the muscle compartment to measure the amount of pressure inside the compartment.

Doctors at NYU Langone may also use a special type of MRI to detect elevated pressure. MRI uses a magnetic field and radio waves to create computerized, three-dimensional images of structures inside the body.
So, you could anaesthetise the muscle and then do the invasive test. Or an MRI might detect the pressure.
 
@Hutan,
It would take a few thousand words to fully explain the problem here. But in simple terms human tissues are solids. Hydrostatic pressures are properties of liquids. If you try to ascribe hydrostatic pressures to solids you have to be very very careful and know exactly what you are doing. Whole careers have been wasted measuring 'hydrostatic pressures' in tissues, particularly hyaline cartilage.

To illustrate, it has been said that the hydrostatic pressure in cartilage is three atmospheres - that is why the tissue is so firm, despite being mostly just a fishnet of collagen. But if you cut it no water comes out. The response is that this is because of counteracting oncotic pressure. But it doesn't actually make sense. There is no 'hydrostatic pressure' as normally defined.

So if you are going to measure pressure in muscle you have tome very sure you know what that means.

There is no way that pressure in a relaxed muscle is going to obstruct capillaries. Muscles function under persistent tension which creates high. compressive (not hydrostatic) forces on blood vessels normally and blood flows fine. Muscle gets into trouble when compressive forces on vessels compete with arteriolar pressures. You can apply a hydrostatic analysis in the case of acute ischaemic compartment syndrome when a muscle swells to the limit of its sheath and effectively becomes a closed fluid compartment, but not otherwise.

In the 1970s and 1980s eminent research groups thought they were studying hydrostatic pressures like this and had big grants and published lots of papers - until they finally realised that they weren't measuring what they thought. I would bet this reinventing the same wheel.
 
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