Central sensitisation in chronic pain conditions: latest discoveries and their potential for precision medicine) Nijs et al.

There seems to be a lot of slipping and sliding about what "central sensitisation" really is, sometimes the term is used to refer to an empirical phenomenon (temporal summation, or lowered pain thresholds to pain outside of the injured area), sometimes to high scores self-reported measures of pain and other somatic symptoms, and these authors treat all these measures as interchangeable, and measuring some single underlying phenomenon.
"....it is critical to realize that we cannot succeed if we use DSM categories as the “gold standard.” The diagnostic system has to be based on the emerging research data, not on the current symptom-based categories. Imagine deciding that EKGs were not useful because many patients with chest pain did not have EKG changes. That is what we have been doing for decades when we reject a biomarker because it does not detect a DSM category."

https://www.nimh.nih.gov/about/directors/thomas-insel/blog/2013/transforming-diagnosis.shtml

Via this S4ME comment.
 
Chronic pain is a leading cause of disability globally and associated with enormous health-care costs.

The discrepancy between the extent of tissue damage and the magnitude of pain, disability, and associated symptoms represents a diagnostic challenge for rheumatology specialists.

The problem with the bolded bit in the above sentence is that doctors look at medical records and they assume the records are completely right and so they know the patient's medical history and they think that their investigations will determine the extent of tissue damage. But medical records are often manipulated, they contain lies, and they contain doctors' own incorrect assumptions, obfuscations and mistakes. Also I've never heard of MRIs, CT scans, X-Rays or Ultrasound scans that can show up tiny nerves that could be triggering pain. And how often are investigations done using those scans that show up blood supply? I know that blood supply can be investigated using contrast materials in some kinds of scans but such contrast isn't used every single time that such investigations are carried out.

So, with often poor and misleading scan results, blood tests, and inaccurate medical records doctors think they know everything about the patient, but in reality, patients, with symptoms that can't be accurately diagnosed because of lack of accurate information are, in effect, put on trial (but the patient doesn't know it) on the basis of faulty information. Because the patient doesn't know the charges, and isn't aware they are on trial anyway, they aren't aware what they have to defend themselves against, they don't know the evidence against them, and they don't know what sentence has been passed by the judge (oops, I mean the doctor) who has found them guilty of something that will inevitably mean the patient is denied medical help.

The quote I bolded above specifically mentions rheumatology. But other specialists go through exactly the same process of condemnation, judgement and punishment every day with every patient. Some very rare patients come out of this judgement squeaky clean, but many of us don't because all those past judgements and sentences are never mentioned to us, but are continually used against us.

If I was to say to a doctor, what do you think you know about my medical history in year X, which is relevant to my current symptoms, they would (at best) consult a summary which told them what happened in that year and what the major findings were? But having bought a copy of my own records, I discovered that the summary of what happened in year X (five words) tells doctors about 2% (at best) of what really happened because the summarisation is nonsense. On the basis of that summary of what happened in year X I have been judged and dismissed many, many times. The labels attached to my records tell doctors a load of malicious rubbish about me, but they think they know what happened and they think they are justified in dismissing every word out of my mouth.

The other point about labelling patients is that the incorrect beliefs of a doctor in one speciality will be read by other doctors in another speciality, and so the poor treatment given to the patients spreads from one discipline to another and there is no escape.
 
ME was always considered to be a disease with a large pain component especially a deep burning in the muscles, pain in the joints, painful lymph nodes and so on. Most of the pain was a consequence of overdoing things so keeping ME under control can reduce it but not always probably because often ME is never truly under control.

I have always had bad pain which is only kept lower by pain killers, never gone and often gets worse for a while.

When the emphasis became about fatigue rather than an abnormal response to exercise the sense of it being a painful disease was lost and suddenly anyone with pain was told they had fibromyalgia as well. There will be people with fibro as well as ME but the idea that they were closely tied only happened after CFS was defined.

As for central sensitization, there was a lot of talk years ago about pain gates and how they opened if someone had a lot of pain so every impulse felt worse. That is when they started using personal painkiller machines after operations and treating the pain of injuries aggressively so that the gates would stay shut and there would be less pain in the long run.

I don't know if the idea has been discredited or if it just taken for granted now but it seems to be the basis of central sensitization. It is the way the idea is used that is the problem, treating pain at not actually real but a psychological construct. A cruel idea.
 
As for central sensitization, there was a lot of talk years ago about pain gates and how they opened if someone had a lot of pain so every impulse felt worse. That is when they started using personal painkiller machines after operations and treating the pain of injuries aggressively so that the gates would stay shut and there would be less pain in the long run.

I haven't got a research reference for this but when teasing a sibling who was hooked up to their own painkiller pump they told me that staff explained that patients tended to use a lower amount of pain medication overall when they were allowed to dose themselves. They just timed it differently.

I'm not sure I buy this flood gates opening business. By that logic if I'm already in pain, and the more pain I'm in, the more new painful stimuli will hurt.

However, much as a papercut can sting, if you give me a papercut when I have a migraine I guarantee I won't notice it.
 
Could someone please tell me if central sensitisation is a proven phenomenon or is it just an idea?


Transient central sensitisation, measured as secondary hyperalgesia can be induced through capsaicin (or other TRPV1 receptor agonists) injections, and using local ansesthesia, they claim the sensitisation must be central in nature (spinal).

Models that focus on other methods of sensitisation almost all use animal models and might not be generalisable to humans.

A key point to all of these models however is this sensitisation lasts on the order of seconds to hours, and all require peripheral input as a trigger in the first place.

To demonstrate central sensitisation associated with human disease, would require demonstration of:
These include pain mediated by low threshold Aβ fibers (determined by nerve block or electrical stimulation), a spread of pain sensitivity to areas with no demonstrable pathology, aftersensations, enhances temporal summation, and the maintenance of pain by low frequency stimuli that normally do not evoke any ongoing pain. To assess how central sensitization may present in patients, we need a detailed phenotyping of different patient cohorts to capture exactly what changes in sensitivity occur, where and when [93; 188; 86; 9; 11; 197; 55]. Ideally this should be combined with objective measures of central activity, such as fMRI, so that clear diagnostic criteria for determining the presence of central sensitization in patients can be established. The utility of diagnostic criteria for the presence of central sensitization would not only be insight into the pathophysiological mechanisms responsible for producing pain, but more so in defining potential treatment strategies. If a particular patient’s pain is primarily the result of abnormal activity in nociceptors, as in patients with primary erythromelalgia [74], the optimal therapy required is likely to be different from a patient whose tactile allodynia and secondary hyperalgesia are entirely maintained by central sensitization due to changes in synaptic efficacy in the spinal cord.
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268359/)

Note how this is descriptive - because there is a lack of direct evidence for central sensitisation being associated with real human disease/illness.

Note the "a spread of pain sensitivity to areas with no demonstrable pathology" part. Many medical practitioners and some researchers seem to want to believe this as a matter of faith, rather than as a result of exhaustive investigation.

With regard to Fibromyalgia (same paper as above quote)
Recently they have found using local anesthetic injections though, that peripheral input from muscle appears to be important in maintaining central sensitization in FM patients [217]. This would mean that fibromyalgia may have both peripheral and central contributions, whose extent may vary from patient to patient.

All of this begs the question, is it a misnomer to call it "central sensitisation" when peripheral stimulation is required to maintain it?

This is a speculative opinion, but I'd argue that some degree of spinal sensitisation is actually a normal part of nociceptive function.
 
All of this begs the question, is it a misnomer to call it "central sensitisation" when peripheral stimulation is required to maintain it?
Yes! And then isomehow this very limited phenomenon is then used to as evidence to support loose and free psychological ideas of pain catastrophising. I hate the misprepresentation and the fake neurobabble even more than the idea itself.
 
No direct evidence of aberrant muscle/tendon inputs in muscle biopsies in the maintenance of fibro pain. It is assumed that normal stimuli result in activating (via central mechanisms) and maintaining a huge input of pain signals.

But there is abnormally high Substance P levels in the spinal cord of fibro patinets. Substance P is a powerful generator of pain signals and has retrograde action (sensitization).

The first synapse of the sensory fibers of the periphery is in the spinal cord.

Hence, the spinal cord is part of the CNS, the central in the concept central sensitization.

From the c-delta synapese in the spinal cord, the pain signals go to the thalamus and other structure in the brain. There is evidence in several imaging techniques of increased activity during pain stimulation in fibro patients in the pain processing regions of the brain.

Pain is indeed interpreted by cortical structures. There isn't any refuting that.

Absent future evidence, central sensitization tries to form a picture of what must/might occur.
 
No direct evidence of aberrant muscle/tendon inputs in muscle biopsies in the maintenance of fibro pain. It is assumed that normal stimuli result in activating (via central mechanisms) and maintaining a huge input of pain signals.

Except that it often doesn't. Many fibro patients have normal pain threshold responses to various forms of stimulation.

Also notably, NK1 receptor antagonists have failed to demonstrate efficacy in clinical trials for any pain condition.
 
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