Central Hypersensitivity in Chronic Shoulder Pain

Subacromial impingement syndrome is a common cause of shoulder pain that has multiple causes (subacromial bursitis to rotator cuff tendinopathy and full-thickness rotator cuff tears).  Unfortunately, for almost half of people afflicted with this syndrome, medical treatment is not successful and they will continue to have shoulder pain 2 years later [1].  Some of these patients, in spite of apparently normal anatomy, continue to suffer from shoulder pain [2,3].  It is not known why some people have shoulder pain long past the time that healing should take.  Recent research may have an explanation for this continued shoulder pain called hypersensitivity.

Hypersensitivity, a revving up of the body’s pain detection system, is a useful tool that the body uses to alert you to an injury [4].  For example, when you cut your finger while cooking dinner, your finger becomes immediately painful because your body is warning you about the potential or actual tissue damage.  This is hypersensitivity in action; your finger is now hypersensitive to painful and non-painful stimulation like touching your throbbing finger [5-7].  After the cut on your finger has healed, this hypersensitivity eventually goes away.  However, we now think that people with chronic pain, such as having shoulder pain for longer than 6 months, are experiencing unresolved hypersensitivity [8].  People who are experiencing central hypersensitivity may continue to perceive pain even after adequate treatment for their shoulder and time to heal, which may be due to hypersensitivity not shutting off as it should in the normal situation.

What is interesting about hypersensitivity in patients with chronic shoulder pain is that the hypersensitivity is not just present at the injured shoulder but is found all over the body.  This type of hypersensitivity is called central hypersensitivity [5-7].  One way to measure central hypersensitivity is through pressure-pain thresholds, which sounds scary but really is just a scientist applying slight pressure until the subject starts to feel the tiniest amount of pain.  We measure this point of pressure and call it a pressure pain threshold.  We can test if a group with chronic shoulder pain has central hypersensitivity by measuring their pressure-pain thresholds and comparing them to the pressure-pain thresholds of a pain-free group.  If the pressure-pain thresholds are low at the injured shoulder and at other sites such as their leg or the opposite shoulder, then it provides evidence that central hypersensitivity is present [8].  In our study, we found that patients with chronic shoulder pain had lower pressure pain thresholds all over their body when compared to people with no pain [9].

Other studies have found central hypersensitivity in many other chronic conditions such as whiplash injury, fibromyalgia, low back pain, osteoarthritis and hemiplegic shoulder pain [10-11].  The next step is to find a treatment that targets central hypersensitivity and once this is accomplished, we may be able to treat chronic pain successfully.

About Tracy Paul

Tracy Maria PaulTracy obtained her B.S. in Chemistry at Emory University and she is currently a third-year medical student at Case Western Reserve University School of Medicine.  She worked under the guidance of Dr. Richard Wilson at the Department of Physical Medicine & Rehabilitation, MetroHealth Rehabilitation Institute of Ohio.  She is interested in researching the etiology and management of chronic pain syndromes.


[1] Cummins CA, Sasso LM, Nicholson D. (2009). Impingement syndrome: temporal outcomes of non-operative treatment. J Shoulder Elbow Surg, 18:172-7.

[2] Dorrestijn, O., Stevens, M., Winters, J., van der Meer, K., & Diercks, R. (2009). Conservative or surgical treatment for subacromial impingement syndrome? A systematic review J Shoulder Elbow Surg, 18 (4), 652-660 DOI: 10.1016/j.jse.2009.01.010

[3] Ketola S, Lehtinen J, Arnala I, Nissinen M, Westenius H, Sintonen H, Aronen P, Konttinen YT, Malmivaara A, & Rousi T (2009). Does arthroscopic acromioplasty provide any additional value in the treatment of shoulder impingement syndrome?: a two-year randomised controlled trial. J Bone Joint Surg Br, 91 (10), 1326-34 PMID: 19794168

[4] Greene CS. (2009). Neuroplasticity and sensitization. JADA 140: 676-8.

[5] Petersen-Felix S, Curatolo M. (2002). Neuroplasticity – an important factor in acute and chronic pain. Swiss Med Wkly 132: 273-8.

[6] Curatolo, M., Arendt-Nielsen, L., & Petersen-Felix, S. (2006). Central Hypersensitivity in Chronic Pain: Mechanisms and Clinical Implications Phys Med Rehabil Clin North Am, 17 (2), 287-302 DOI: 10.1016/j.pmr.2005.12.010

[7] Latremoliere A, & Woolf CJ (2009). Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain, 10 (9), 895-926 PMID: 19712899

[8] Hidalgo-Lozano A, Fernández-de-las-Peñas C, Alonso-Blanco C, Ge HY, Arendt-Nielsen L, & Arroyo-Morales M (2010). Muscle trigger points and pressure pain hyperalgesia in the shoulder muscles in patients with unilateral shoulder impingement: a blinded, controlled study. Exp Brain Res, 202 (4), 915-25 PMID: 20186400

[9] Paul, T., Soo Hoo, J., Chae, J., & Wilson, R. (2012). Central Hypersensitivity in Patients With Subacromial Impingement Syndrome Arch Phys Med Rehabil, 93 (12), 2206-2209 DOI: 10.1016/j.apmr.2012.06.026

[10] Fernández-de-las-Peñas C, de la Llave-Rincón AI, Fernández-Carnero J, Cuadrado ML, Arendt-Nielsen L, & Pareja JA (2009). Bilateral widespread mechanical pain sensitivity in carpal tunnel syndrome: evidence of central processing in unilateral neuropathy. Brain, 132 (Pt 6), 1472-9 PMID: 19336461

[11] Soo Hoo J, Paul T, Chae J, & Wilson RD (2013). Central hypersensitivity in chronic hemiplegic shoulder pain. Am J Phys Med Rehabil, 92 (1) PMID: 23255268


  1. John Quintner says:

    Hi Stuart, the paper is awaiting completion by two of the four co-authors and we hope to submit it for review at the end of this month.

  2. stuart miller says:

    John, not that I’m impatient but…when might this new paper be available to review ? Just finished listening to NOI group course on Neurodynamics and the Neuromatrix (helpful) and Christine Novak and others on post nerve repair/transfer and cortical re-integration with effective rehab (helpful) but I still am amazed at the challenges in presenting the information to colleagues and patients that is non-threatening, meaningful to them and provides them with a strategy and a framework to move forwards. I look forward to yours and others insight. I’m still a little stuck on the concept of provision of adequate space for structures to glide and the lymphatic system’s role in cleaning up after an insult and how to integrate this information (which I think is helpful) with overarching frameworks of autopoeisis and the puzzle of pain.

  3. John Quintner says:

    Stuart, we are currently preparing a Focus article on the subject of nerve trunk pain (which we believe is mistakenly called “myofascial pain”). It will be an update of our earlier paper on the subject.

    Quintner JL, Cohen ML. Referred pain of peripheral neural origin: an alternative to the “Myofascial Pain” construct. Clin J Pain 1994; 10: 243-251.

  4. Cathy,
    I really appreciated your comments. Language is important – perception of the intent of the therapist/physician from this is important. Compassionate curiosity to me is critical. I fully accept that I am going to make mistakes in my conversational approach. I work with patients in which English is sometimes their 3rd or 4th language. I work with translators and interpreters who may have a different viewpoint than me. Body language and establishing some connection is helpful. Pictures are helpful. Clinically, though, I am looking for more insight from this forum. I appreciate Dr. Quintner’s viewpoints on neuro-immune response to stressors and understanding of nerve trunk pain but I was hoping he would elaborate further. I appreciate your first comments Ian but I don’t think that protective responses in the upper extremity are due to anxiety exclusively but are again part of a patterned response to threats from reflex withdrawal to more coordinated responses. I think that neuro-dynamic testing may help the patient adapt to…neuro-dynamic testing but I would appreciate others’ insight. Thanks.

  5. Good article. I am a complete disaster…. Getting better, but open hands coming at me makes me cringe. I am looking into an alternative treatment that seems reasonable to me. From a pain patients view, it is demeaning to have family & friends decide you are “faking” it, and Doctors who say “you look great”. Better education on “words” would be a good beginning, no matter what the treatment. I noticed the same notion when physicians sent me their difficult cases in pregnancy. Speaking at Grand Rounds (which was voted a favorite that year), and telling the physicians what I had learned regarding their body language, words, and attitudes, DID make a big difference for many women. I have felt degraded and my health unimportant, by the attitudes of Pain Specialists – MD’s and alternative. All we want is to be better, to join life again, yet we are viewed as a “challenging” patient. Maybe we are a challenge in the physicians mind, but if we were really asked about what we are feeling, (physically and mentally), I wonder if we couldn’t be helped. I think Dr. John Q thinks along the same direction, from reading his website. Wording makes a difference. Even among professionals.

  6. John Quintner says:

    Given that the lived experience of pain is always created by the brain, to talk of “centrally mediated pain” seem illogical. Can we come up with a better descriptor? My colleague Milton Cohen has been plugging for “nociplastic” as an addition to the terminologies of “nociceptive” and “neuropathic”. Over to you.

  7. I think that what is most often absent from the examination of chronic shoulder pain is a through assessment of and screening for the signs of centrally mediated pain. There are now lots of tools to help clinicians identify this group of patients such as the PainDetect questionnaire or the SLANNS to identify neuropathic pain, fine sensory testing (vibration thresholds, PPTs, thermal testing), laterality testing, not to mention thorough history-taking (not just focusing on the shoulder pain. Gwilym and colleagues 2011 study highlighted that a large proportion of patients on the waiting list for subacromial decompression surgery had evidence of centrally mediated pain. It is no surprise that they also had worse outcomes from the surgery. I also think that as suggested by Jeremy Lewis, we stop using the unhelpful (and overly mechanistic) term “subacromial impingement” and moved to the term “subacromial pain syndrome” to more accurately reflect the spectrum of disorders that it encompasses. Perhaps the change in terminology would make clinicians more open to the early and thorough screening for sensitization?

  8. stuart miller says:

    John, really appreciated your comments – I will await further insight on pathophysiology. Tracy, of the 31 affected individuals, I noted that there were ‘significantly lower PPTs’ at all locations tested (compared to the 31 controls). Would you envision that there would be significantly lowered PPTs throughout the body ? Was there a reason for choosing contralateral tibialis anterior as a distal point ? What was your device for testing pressure threshold ? Thanks.

  9. John Quintner says:

    Stuart, please read my comment to Mike on March 1. I suspect that an understanding the pathophysiology of “nerve trunk pain” would be extremely helpful to clinicians. Watch this space!

  10. stuart miller says:

    John, appreciate the comments…I do appreciate the insight of the clinical research that has been done by members of body in mind and others. I also appreciated Mike’s clinical perspective. Clinically, I see patients with chronic shoulder, wrist and hand pain, and often on testing their other side they do not have apprehension in testing nor do they seem to have lowered thresholds to stimulation. However, I would say that for some of these patients, there is central sensitization. From my understanding, the updated IASP definition of allodynia is only for low threshold mechanical stimulation (gentle stroking). The concept of central sensitivity and widespread pain seems to be isolated (in my perspective) to a particular population of patients. In terms of central sensitivity, from what I have read (and I would appreciate direction to research to provide insight) there is a challenge clinically in determining the extent to which the patient has been sensitized and how easily they can be desensitized. Again, I ask the question, only out of curiosity, how does one determine the transition from primary hyperalgesia to secondary hyperalgesia ? Ian, I really appreciated the info… John, I will re-read the paper (maybe tomorrow – thanks) – sorry for the alarm bells; I agree I can only speak from my clinical perspective and my understanding of the literature.

  11. John Quintner says:

    Stuart, to find the answer to your question you will need to re-read our paper.
    When anyone says “I think we all know …” alarm bells start ringing for me. Arguing from authority is a well known fallacy. It prompts me to ask – how do we know these things? Do you get my drift?

  12. stuart miller says:

    John, thanks for the insight. I think we all know from the research that the longer pain persists, the less it has to do with tissue pathology and the more it has to do with cortical reorganization and ? central sensitization (‘the orchestra playing the pain aria over and over again.’ It is also known that focussing on tissue based pathology with persistent pain can be counter-productive). It is easy to sense that if patients have agonizing pain to light touch (allodynia) that there is some element of central sensitization but what I have trouble discerning is the transition from primary to secondary hyperalgesia (obviously with widespread pain and lowered thresholds it is not that difficult). If it is dermatomal or in whole nerve distribution with neurogenic inflammation (we see this all the time with digital nerve injury and gross swelling to whole median nerve distribution) it is easier to explain. The challenge when working with a patient in the acute stage in terms of providing explanations that are ‘less dangerous’ is that implying that stiffness is their challenge and there is a need to work on the stiffness to assist with their patterns of movement is an easier and often more productive explanation (I would suggest people read papers on ‘dart thrower’s arc’ with their challenging wrist cases). The extent to which the neurophysiology is explained to the patient in the acute stage (to some degree) is dependent obviously on how much time you have with them, how they are progressing and whether you need to introduce GMI and ‘get under the radar’ to quote Moseley. In terms of neuropeptide release (let’s stick with substance P and CGRP for the moment), any inflammation in the system has to be dealt with appropriately whether by explanation of the lymphatic system, decreasing the threat of the presentation or providing simple strategies for edema management. Again, I would really like to hear how people assess inflammation in the shoulder clinically. In term of the neuro-immune response to threat for body protection, other than explaining to the patient that the nociceptive system acts as a quick response and immune response as slower response in a coordinated manner, do you have a paper in mind that might help with more detailed but clear explanation that can be provided to patient ? Finally, just out of interest, why did Lyon’s paper focus mainly on substance P / NK1 receptor and not the role of glutamate / NMDA receptor ? (maybe I should re-read, it’s been awhile) ? Thanks a lot for the discussion…

  13. John Quintner says:

    Mike, what do you mean by “engagement of the brain of the patient”? Hopefully all your patients choose to engage with you at this level.
    I must disagree about your assessment of the biological predicament of these patients as not being dangerous. From their point of view it is exceedingly dangerous, which is why they may curtail the performance of certain activities involving use of the affected limb(s). I suspect “danger” signaling molecules emanate from the relevant peripheral neural tissues at their interface with surrounding tissues.
    I really cannot see how this scenario has anything to do with a loss of connection with their “sense of self”. Could you please explain as I seem to be missing the point.

    Mike Caruso Reply:

    John, sorry it’s been long since your question- have been busy with patients and other things; and needed some time to think about how to respond to your question and comments.
    The way I interact with chronic pain patients has been shaped over the years by Gordon Waddell, Nortin Hadler, Richard Deyo, Jerome Groopman, and othere…more recently Michael Sullivan (McGill).
    The danger molecule that may be of most relevant is the one in the therapist mind not the patient. Gordon Waddell writes, ‘the trouble with medial education is that students are taught the latest in pain neurobiology and then come the pharmacology lectures. What is strikingly absent in medical education is information about what the patient can do for themselves and the ways we elicit that a favorable response or suppress it. Nortin Hadler has assesses the epidemiology data and found that those that seek care for problems that are not serious injury of joint and bone are not normal. They seek care and soon find themselves within the “therapeutic envelope” which changes their life forever. Richard Deyo write about the power of the MRI image to deepen the conviction of danger. Jerome Groopman informs about cognitive traps impair or view of the patient. Michael Sullivan informs that only 10% of the variance in the perception of disability are physical findings. Life role re-integration is powerful in improving people’s lives.
    Perhaps the molecules that we should be most concerned about is testosterone and cortisol. See http://on.ted.com/Cuddy to learn about something people can do for themselves to change those molecules and their lives.
    When I see a patient for the first time I what them to leave the office ‘engaged’ in their own self-care.

    John Quintner Reply:

    Thanks Mike. With respect, you don’t seem to have addressed my question or I might be missing the point.

  14. John Quintner says:

    Stuart, there are a few clues from the history and physical examination. The history may point to allodynia (mechanical and/or thermal) in the shoulder region and, by gently tapping over the shoulder region, the examiner can reproduce the pain (by summation). Not validated but certainly useful in my experience.

  15. ian stevens says:

    Richomond Stace covers this well .
    I think the best hope in many situations is the basic recognition clinically of persisting hyperesensitivty . Perhaps Gwilym’s research tied in with Irene Tracy at Oxford may convince orthopaedics of the validity of t he concept ? I remember years ago trying to convince Orthopaedic colleagues that many problems were more ‘neuropathic’ in nature …Patients went onto get SAD and capsular procedures and often the results were not very good . The area is complex- many peoples ‘defensive postures’ in the upper limb were much more related to peristing anxiety and other issues than anything else . Of course this isnt picked up by the MRI scanner …

  16. stuart miller says:

    John, really appreciate the Kellgren reference – nice to have the old diagnostic imaging framework (I may have missed your point). I could reference numerous studies in which healthy normals present with significant change on Xray (frank herniations, gross narrowing) with no symptoms. Again, add inflammation to the mix or forward head posture and protective positions and it changes the picture. As well, I might suggest reading something more current such as Kenneth Flowers or Paul Lastayo’s research (or others) on low load prolonged stretching (why is it effective ? – maybe cause it gives the patient some control over their progress but possibly due to tissue restrictions (capsular, myofascial etc.) that will only change under low prolonged load). Obviously, improving the pattern of movement is key. Clinically, it was very helpful for your input Mike, really appreciated it. Obviously, thorough evaluation is essential. Robert Elvey is a great reference point but what I was hoping from you, John, was a bit of clinical insight re how you did clinical testing (Spurling’s +/- modifications, neurodynamic testing etc that allowed you to be definitive that the shoulder pain was from cervical neural origin (obviously the reign of pain lies mainly in the brain and… I don’t treat pictures that often). It’s unfortunate that the meta-analyses on the effectiveness of neurodynamics come up empty but there it is…obviously the graded progression bit when challenging patients is important. Since I am off topic, again I would like to come back to how do you, John, or Tracey differentiate primary vs secondary hyperalgesia ? Thanks !

  17. John Quintner says:

    Mike, nerve stretching went out of fashion in the late part of the 19th century.

    Stuart, Kellgren is worth reading. His experiments were carried out in the late 1930s.

    Mike Caruso Reply:

    Maybe we are not stretching nerves. Just maybe we are stretching fascia. Would like to recommend Fascia:The tensional network of the human body. R Schleip 2012).
    Anyway it works if instructions are clear.
    BTW just saw my 7 hypersensitive shoulder in 6 months. This time it was both shoulder and 1 year of PT. PT actually progress the patient into a frozen shoulder followed by manipulation under anesthesia. “No one knows what is wrong” she said. “I’ve seen 4 orthopedists and a neurologist”.
    She is lacking 35 deg of external rotation both shoulders.
    I have one visit with her so I’m going to show her how she can restore external rotation for herself.

    John Quintner Reply:

    Mike, my current thinking is far removed from yours. I suggest that the interface between peripheral nerves and their surrounding tissues (e.g. fasciae, muscles) is physiologically complex. We may be trying to engage with an evolutionarily-conserved system of neuro-immune defense that is responsive to a variety of stressors perceived to be in the local environment of the peripheral nerves. This is my current hypothesis of the underlying mechanism “nerve trunk” pain (as described by Asbury and Fields in the 1980s). We are trying to flesh this out at the moment. Does it make sense to you?

    Mike Caruso Reply:

    That does make sense. I do not dispute the complexity…this is not a mechanical problem. My thinking is that it is SO complex that the remedy can best be carried out only by engagement of the brain of the patient. The patient needs to understand that the problem is not dangerous and within their control (Moseley/Butler).
    I give patients images to look at. I substitute wall chart of fascia from Anatomy Trains for the MRI (Tom Myers).
    I explain movement in the shoulder as needing external rotation first (Robert Donatelli).
    I guide them in exercise and allow them to set the pace.
    I take pictures of them doing the exerciseS and email it to them so when then get home they can reconnect with the sense of self they had when we were together (Mosley/Butler).
    Are we really that much different in our thinking?

  18. stuart miller says:

    Interesting discussion. John, really appreciated your points – could you or Tracy Paul provide a concise definition on how to differentiate primary vs secondary hyperalgesia ? – how far do the receptive fields have to expand before the transition between more peripheral generation to more central generation is made ? I would agree that lowered thresholds in the leg or opposite shoulder (just to mechanical inputs ?) would make the definition somewhat easier but just looking for clarity. I would really appreciate the insight… as well, it sometimes seems that protective patterns of movement (with ? decreased local stabilizer activation both in Cspine and shoulder) is the reason for the referred pain (chicken and egg – nice to be able to do consistent testing ) . Mike, do you go commercial in providing the low load prolonged stretching for external rotation or do you have another preferred method ? Finally, the concept of facilitated neurogenic inflammation with resultant loss of ER could be considered (much easier with lymphatic drainage when more proximal- ? no lymphatics in CNS…). How does one objectively measure swelling in the shoulder ? (easier distally). Thanks !

    Mike Caruso Reply:

    Hi Stuart
    I have used the JAS shoulder device but it’s not often needed. I have a patient lie supine with elbow at about 45 -60 deg abduction with about 2 inches under the elbow. Externally rotate to just a very mild stretch and block there. Pause 5 min. then assess if pain is: a) the same b) worse c) better. If same, keep it there 5 min longer. If worse, start over with an easier stretch. If better, go slightly further and block. Repeat sequence 3 to 6 times 2 to 3 times a day.
    Most overdo this and need to be coached that “less” is “better”.
    May take weeks to get to cool things down so they are not so sensitive. Learning “pacing” is very difficult for many at this stage… difficult to break the “push through pain” pattern.

    GIve it a try. All the best.

  19. Dear Tracy, John and Mike.

    What a sad demonstration of the truth both Mike and John speak.

    Is it not possible the simple answer to the cause of this is contained within Johns words “Referred pain” yes I am aware this is not quite what John said.

    With all of the world wide studies and practical demonstration of unsuccessful treatments is it not possible ALL Pain is referred from the Mind following Childhood Emotional Traumas still unresolved.

    My Specialism when ALL other treatments have placed long term suffering patient in this position and if I can so often resolve Pain and other mysterious symptoms via telephone or Skype; there must be some substance in my statements.

    Yes I know it is story telling – based on the secure understanding “ALL illness is as unique to a person as their finger print – therefore all treatments story telling? Especially if the outcome is always as this posting and comments describe.

    Keep up the good work we will get there some day.

    Best wishes

    Peter Smith Talking Cures

  20. John Quintner says:

    Dear Tracy It is tragic that so many sufferers of persistent shoulder pain have undergone medical treatment directed at tissues in the shoulder joint complex when the source of their problem happened to be elsewhere. Referred pain of presumed cervical neural origin was not considered in the differential diagnosis of their shoulder pain! The various physical examination techniques pioneered by Robert Elvey (physiotherapist extraordinaire) are very helpful when used in this context. Unnecessary shoulder surgery adds to the burden of many of these patients!
    Mike, I agree we have to go back to basics but to me this implies first distinguishing between primary and secondary hyperalgesia before planning and implementing a treatment regime.

  21. Mike Caruso says:

    Dear Tracy
    I appreciate your prospective. We certainly need to expand our thinking beyond the tissues if we are going help improve the lives of many with chronic pain.
    My interest and frustration is raised when I see statements like “medical treatment is not successful” and “in spite of apparently normal anatomy”. The question comes to mind “what medical treatment?” “what does the movement look like”? Normal or abnormal anatomy is often not as important as the quality of movement. Did the hypersensitivity come from the medical interventions?
    This comes to mind because I’ve seen 6 patients in the last 6 months that failed medical care and work hardening only to find they did not have full external rotation. They were very hypersensitive by this time.
    At this stage of complexity in may take 3+ months to restore full rotation (using 3 30-minute low level stretches daily) as well as directing them in stretching all the soft-tissue restrictions at the shoulder girdle neck and t-spine they developed, likely due misguided assurance that is we fine to lift those boxes overhead with a impaired movement. Here in the USA we use opioids as lot to make things really complicated.
    Sometimes the right answer is to go back to the basics of movement quality with an important twist- explain the problem in a way that seems less dangerous (movement impairment and fascia restrictions are less scary than the MRI images) and give the problem for them to do in manageable steps (couch not treat). Ditching the opioids really helps too!

    Thanks for your post and best of luck in your work.

  22. John Quintner says:

    Dear Peter
    Having listened to you lecture (via the link obtained from your website) I feel confident in saying that innovative thinking is unlikely to come from your direction. You say that Fibromyalgia is simple to understand, but it does not come across in anything that has been said or written by you to date. What comes across is your resolute determination to disparage those of us who are attempting to expand the knowledge base.

  23. Dear Tracy
    For the past Thirty Years as a therapist the only treatments I have ever applied to a person are to those who are long term medical failures and it is the same today.

    Still today there is no biological scientifically proven knowledge available anywhere in the world to substantiate Medical Science ability to stamp its authority or possession of anything of value.

    The world is full of people who are only medical failures and the stupidity of Rene Descartes in the separation of the mind and body is at the very heart of the failure of Modern Medicine to be of any true value in understanding the cause of any illness and then demonstrate a cure.

    Tiredness fatigue and multiple tender spots appear to amongst the very worst, with Fibromyalgia perhaps at the very top and any person who studies this simple to understand set of symptoms and has papers seemingly accepted by the world published medical profession is so seriously deluded in any comments within their parers related to their long studied illness modality relating to the now published facts being scientifically proven; as to not even be worth the effort of laughing at.

    What is so desperately required is new an innovative thinking relating to all disorders of the Mind and Body and with current closed minded thinking it is never going to come from the Scientific Medical Profession.

    best wishes

    Peter Smith Talking Cures

  24. John Quintner says:

    Dear Tracy
    Of all of the possible explanations for the persistence of shoulder pain, this one is certainly going to occupy last place on the grounds of its total lack of biological plausibility. “Talking Cures” has been peddling this sort of nonsense (and I am being kind) for well over 12 months! Take it with a grain of salt (at most).

  25. Dear Tracy
    Do you not as I feel it so strange and sad despite the very best efforts of many Medical Scientists and Researchers so little is known about this extremely simple to understand disorder – pain – and the failure to recover with almost any form of Natural or treatment interventions.

    Post Pain Sensitivity is because the Pain was never in the area the patient presented even five minutes after the incident/accident. It is how ever stored safely – if one can say it in such a manner – within the mind as a treatment resistant process which forever interferes with the body’s chemistry now permanently causing the said sensitivity.

    Best wishes

    Peter Smith Talking Cures