Distinctive alterations in the functional anatomy of the cerebral cortex in pain-sensitized osteoarthritis and fibromyalgia patients 2022 Pujol et al

Abstract
Background

Pain-sensitized osteoarthritis and fibromyalgia patients characteristically show nociceptive system augmented responsiveness as a common feature. However, sensitization can be originally related to the peripheral injury in osteoarthritis patients, whereas pain and bodily discomfort spontaneously occur in fibromyalgia with no apparent origin. We investigated the distinct functional repercussion of pain sensitization in the cerebral cortex in both conditions.

Methods
Thirty-one pain-sensitized knee osteoarthritis patients and 38 fibromyalgia patients were compared with matched control groups. And new samples of 34 sensitized knee osteoarthritis and 63 fibromyalgia patients were used to directly compare each condition. A combined measure of local functional connectivity was estimated to map functional alterations in the cerebral cortex at rest.

Results
In osteoarthritis, weaker local connectivity was identified in the insula, which is a cortical area processing important aspects of the brain response to painful stimulation. In contrast, fibromyalgia patients showed weaker connectivity in the sensorimotor cortex extensively affecting the cortical representation of the body.

Conclusions
In osteoarthritis, weaker insular cortex connectivity is compatible with reduced neural activity during metabolic recovery after repeated activation. In the fibromyalgia neurophysiological context, weaker connectivity may better express both reduced neural activity and increased excitability, particularly affecting the sensorimotor cortex in patients with spontaneous body pain. Such a combination is compatible with a central gain enhancement mechanism, where low sensory tolerance results from the over-amplification of central sensory reception to compensate a presumably weak sensory input. We propose that deficient proprioception could be a factor contributing to weak sensory input.

Open access, https://arthritis-research.biomedcentral.com/articles/10.1186/s13075-022-02942-3

 

What does "functional anatomy" mean in this context? Note, the word 'functional' is used four times in the title and the short Abstract.

Do all references to 'functional' all mean the same thing?

Does it mean what ordinary mortals mean by it? I.e. the thing being referred to actually works? Or is it being used in a deceitful mental health way?

 

I really thought medicine would have left this nonsense many centuries ago. This is genuinely lacking in object permanence. It should not be explained to experts in a science-based profession that spontaneous things don't exist in this universe, everything has a cause, or several, and not knowing those causes is not the same thing as "this happens by magic". This is the stuff of religious myths.

And yet here we still are, with AI doctors on the cusp of transforming medicine, which still holds on to pre-science myths and beliefs while playing with high-tech gadgets to look for patterns confirming their beliefs, any pattern, literally anything to support the long-standing conclusions.

This reminds me of a quote from the movie Amélie Poulain: "when the statue points at the sky, the idiot looks at the finger". Obviously localized pain relates to local factors, looking to the brain for this is just plain absurd while the brain is still mostly a black box no one comes to close to understand. Seems like medicine has simply left reason behind.

 

I don't really understand how AI works. Can it be pre-set to hang on to the idea that all patients, by default, are non-compliant with their meds? (That's just one idea of many that I wonder if it could be pre-set.)

 

It refers to brain structures that (are believed !) to do something specific, understood through anatomy, vivisection and disease and physical damage in humans - see: https://www.simplypsychology.org/brodmann-areas.html

 

No one does yet But it already does useful things so that's worth it alone.

AIs can't really be "pre-set" to do anything, they can only learn from data. The problem of flawed, or incomplete data, is the same as with humans. The benefit of AIs in the case of healthcare is for the sheer mass of data and information. Physicians are already swamped with filling forms, coding things, writing this about results and that to follow-up, many things they can't really on assistants for as it would take just as much time explaining them than doing them. The system is built with a permanent shortage of labor, somewhat on purpose because it leads to higher wages.

There is too much data and not enough ability to process them, so much that most data never get put into information systems because no one can do anything with it anyway. Information overload quickly becomes a similar problem to having too many tools and not enough desk space. At some point simply managing the space and logistics of clearing space for each use is too much of a burden. With AI it doesn't matter, record everything and work it after. Bits are cheap.

A huge reason why those pre-set ideas exist in healthcare is because conflicting information never gets recorded about it because no one can process it where it's useful. And because patient information is for the most part missing entirely, only the summary of the physician's perception. Physicians don't have the time to read 10 pages of patient info. AIs will, crunched and understood in less than a millisecond. It will be like suddenly having 10x as many physicians, each with many administrative and clerical assistants that know even more than they do, and basically aren't constrained by time.

AI won't replace workers, it will enable them in a similar way as one dude with a giant excavator can move many times as much mass as a thousand workers with cheap shovels. Think of how much less work is involved in sending a digital picture vs. the old chemical way. All that work saved can be put to other things, more creative, more high-level.

For sure at first there will be a lot of GIGO, but the benefit of AI is that it learns over time. Right now there's a lot of garbage data because any input goes through several layers of filtering, there is basically no raw data because it's overwhelming. The biggest benefit will be to have patient input, it will be so interesting seeing major discrepancies in what gets recorded vs reality.

 

Interesting...

At the moment (in theory, and with a big pinch of salt) doctors have a summary that tells them the 'highlights' of a patient's medical history. I know from my own summary that several important episodes from my history are missing. I have told doctors about something happening in my past and they have just rolled their eyes at me. I've had organs removed, mentioned it during a consultation, and had eyes rolled at me. One surgeon reported that one of my removed internal organs was perfectly healthy and still alive and well inside me. (That's happened twice, in relation to different organs, although the second time was a result of a filing error, not a surgeon's error.)

If AIs are trained on crap data then what they learn is also likely to be crap. And since I suspect AIs will end up being treated as perfect diagnosticians eventually (because to track down mistakes will be too expensive), patients will also likely end up with dodgy diagnoses and useless treatments.

 

Not that I'm qualified to assess this study, but I find it useful (me having FM and having a distinct lack of what the researchers in this MRI department in Barcelona call a 'cortical map of the body').

I don't chafe at the use of the word 'functional' in looking at brain networks in MRI studies such as this one. Should I and if so, why?

Comparing where in the brain the pain appears with osteoarthritis (which is actual tissue damaged pain) as opposed to where the pain of FM shows up (with its lack of discernible tissue damage) is relevant and interesting and maybe will lead somewhere.

 

I have doubts about this.

Data acquisition and derivation of difference maps is largely mechanical and even if I assume it is relatively unbiased, I remain unconvinced by the interpretation.

Spoiler: Interpretation

In fibromyalgia patients, imaging research has demonstrated baseline hypometabolism in the brain [42], despite patients complaining of spontaneous, resting pain. Therefore, lower local connectivity in our study is again consistent with reduced overall neural activity in the cortex. In fibromyalgia, however, the situation may be interestingly more intricate. Indeed, neurophysiological studies consistently show a deficient inhibition of the cerebral cortex in fibromyalgia patients [43]. A deficient inhibition from gamma-aminobutyric acid (GABA) interneurons may further contribute to local functional connectivity reduction, due to a loss in their synchronization effect [18]. Therefore, lower intra-regional sensorimotor cortex connectivity may express both reduced activity of principal neurons (fewer active neurons) and reduced activity of inhibitory interneurons (reduced synchronization).

In fibromyalgia, therefore, spontaneous pain and bodily discomfort occur without an obvious sensory input increase in individuals with low basal metabolism in a hyperexcitable sensorimotor cortex.

The interpretation appears based on assumptions about the nature of fibromyalgia as neuropathic derived from two reviews (refs 42, 43 which I cannot read due to Elseviers paywall) and makes what appears to me to be potentially an a priori assumption, that there is no afferent pain signal based on these review papers, the abstracts of which give cause to doubt their provenance.

"Neuroimaging of fibromyalgia."
https://www.sciencedirect.com/science/article/abs/pii/S1521694211000271

"Is Motor Cortical Excitability Altered in People with Chronic Pain? A Systematic Review and Meta-Analysis"
https://www.brainstimjrnl.com/article/S1935-861X(16)30050-X/fulltext

After Cochrane, I am sceptical of review papers as they can sometimes be made to say what vested interests want them to say.

This assumption does not seem proven to me and the logic seems sketchy conjecture.

Which is why I think there is a risk that a biased interpretation is being "datawashed" and passed off as good money, as it were, in a manner which reinforces the 'in your head' approach to interpreting the FM patient experience without a genuine justification from empirical science.