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Unique fibromyalgia brain signature could eventually lead to easier diagnosis

  [ 13 votes ]   [ 4 Comments ]
By Donna Gregory Burch • www.ProHealth.com • April 15, 2017


Unique fibromyalgia brain signature could eventually lead to easier diagnosis
By Donna Gregory Burch

Last year, University of Colorado Boulder (UCB) researchers found a brain signature that identifies fibromyalgia with 93 percent accuracy. Yep, you read that right! 93 percent! Isn't that fantastic news?

UCB researchers published their study in the journal PAIN, and while it didn't receive a huge amount of press coverage, it definitely made my list of 2016's top fibromyalgia stories because of its possible implications for the fibro community. If the study's findings can be adequately duplicated, it could potentially lead to a diagnostic tool for fibromyalgia.

I recently reached out to lead researcher Marina López-Sola, PhD, to talk about what's next in her work on fibromyalgia. I learned she will be moving to Cincinnati Children's Hospital, University of Cincinnati, later this month to set up her own research lab.

"My plan there is basically to understand whether the same or similar [brain] alterations as the ones observed in adult women with fibromyalgia are already present in the adolescent brain of women with juvenile forms of fibromyalgia and other related disorders," said López-Sola, "and to continue to understand the nature of the multisensory and pain-related brain functional abnormalities in chronic pain and their implications when navigating the real world and its impact [on] one's sense of self."

I am pretty excited about López-Sola's work at UCB since the fibromyalgia community desperately needs a reliable test for diagnosis. Having such a test would go a long way toward legitimizing our condition to physicians and loved ones who for one reason or another still doubt the reality of our pain.

The UCB study looked at two measures in fibromyalgia patients: their response to a painful stimuli and their response to non-painful multisensory stimuli.
During the painful stimuli portion of the study, researchers applied 4 kilograms of pressure to the thumb fingernail of 37 fibromyalgia patients and 35 healthy controls while they were inside of an MRI.

"What we observed is that the brains of the fibromyalgia patients overall were expressing a particular brain signature that we have from [a previous study] that was specific to measure pain processing in human brains," López-Sola said. "The [fibromyalgia] patients were expressing that brain process to the same degree as controls when exposed to a much lower pressure stimulus. When they were exposed to 4 kilograms force, patients reported high pain, and indeed they were expressing this brain signature significantly more than healthy controls did. What we saw is that their claims of pain were justified by an increased amount of pain processing signal in the brain.

We are fairly sure that what is happening to the fibromyalgia patient is that they actively engage a stronger pain process in their brains than a healthy person would," she added.

The multisensory portion of the study involved exposing fibromyalgia patients and healthy controls to alternating periods of concurrent visual, auditory and tactile motor stimulation and rest. Researchers then compared brain activity during the multisensory stimulation with brain activity during rest.

"Fibromyalgia patients showed two alterations during multisensory stimulation: 1. Fibro patients showed more activity in regions of later sensory integration and regions that are known to process self-referential information, and 2. [they showed] less activity in early stages of sensory processing and other important regions for fine motor and cognitive control," López-Sola said.

Going forward, López-Sola will try to replicate her findings.

"I will first see if the brain signatures replicate in data that has already been collected by other labs ... but since they did not use exactly the same experiments in their studies or the same basic analysis approaches, it will be difficult to compare," she said. "In my future studies, I will use more similar experiments to see how much the signatures replicate under the same or very similar conditions."

One future study will focus on juvenile fibromyalgia patients to see if they express the same brain signature as adult fibromyalgia patients.

"If we can reproduce those alterations at a much younger age, that would be very informative," López-Sola said. "That would tell us this problem can start much earlier in life, and the advantage is if we can [identify] those people when they are young, the possibility to try to help them is much bigger because of the nature of the brain at a younger age. A younger brain is a brain that can learn to readapt in a much faster and more effective way."

Other future research projects may include studying fibromyalgia patients' responses to painful stimuli around the body (versus just on the thumb), exposing fibromyalgia patients to different forms of pain (i.e. pressure, thermal, etc.), and looking at how fibromyalgia patients respond to individual multisensory stimulation.

Asked if her brain signature finding might eventually lead to a diagnostic test for fibromyalgia, López-Sola said, "My opinion is that better versions of these signatures can eventually become – not now, but with time – useful tools for physicians to use [but] ... I think it will never be able to rule out the diagnosis that a physician has to do. Why? Because of a very simple reason: You'll always have a proportion of people who will not show an active expression of that marker, and yet they will still have pain. ... So, you have to be extremely careful about using those markers as a main diagnostic tool.

"We need to learn a lot more than what we have learned so far to know if we can say that the results are really promising.”

Donna Gregory Burch was diagnosed with fibromyalgia in 2014 after several years of unexplained pain, fatigue and other symptoms. She was later diagnosed with chronic Lyme disease. Donna covers news, treatments, research and practical tips for living better with fibromyalgia and Lyme on her blog, FedUpwithFatigue.com. You can also find her on Facebook and Twitter. Donna is an award-winning journalist whose work has appeared online and in newspapers and magazines throughout Virginia, Delaware and Pennsylvania. She lives in Delaware with her husband and their many fur babies. 



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Article Comments Post a Comment

To be expected but FM MUCH more than allodynia.
Posted by: IanH
Apr 15, 2017
If the work of Marshall-Gradisnik, staines et al are to be believed then you would expect increased pain sensitivity due to the altered function of TRPM3. I think their work is now fairly conclusive that TRPM3 is clearly altered in people with ME. It is not hard to extrapolate that to FM. Also this altered function TRPM# leads to elevated Substance P, know to be associated with increased with increased nociception. I believe that FM involves both allodynia and altered nociception. That is it has BOTH peripheral sources of pain (nociceptive) and central sensitivity (allodynia).

If you have a general TRPM3 disorder you will have peripheral dysfunction in soft tissue, vascular tissue, gut and brain. TRPM3 has a major role in systemic modulation. That is the cuase of symptoms in FM are not just associated with allodynia. They can't be, they must also involve non neural tissue pathology as well as mitochondrial dysfunction.
Reply Reply

 
For example
Posted by: IanH
Apr 15, 2017
This is a very interesting article:

http://www.genengnews.com/gen-news-highlights/short-circuit-in-ion-channel-amplifies-pain/81249374

 


The relationship between TRPM3 dysfunction and pain sensitivity.
Posted by: IanH
Apr 15, 2017
Understanding what is happening with TRPM3 is very important.
While the central pore of TRPM3 is a calcium channel, when it is not functioning a second sodium channel opens. It is this secondary channel opening that causes the increased pain sensitivity and raised substance P.

"“This alternative pathway is preserved following desensitization, blockade, mutagenesis, and chemical modification of the central pore and enables massive Na+ influx at negative voltages. Opening of this alternative pathway can enhance excitation of sensory neurons and thereby exacerbate TRPM3-dependent pain.”
Reply Reply

Identical
Posted by: coloradobev
Apr 28, 2017
This study is me
Reply Reply


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