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Outdated Pain Theories, Part I – Damage and Degeneration

Back in the early 1600’s, a famous philosopher and mathematician named René Descartes came up with a theory to explain pain.

This theory can be summed up by the painting to the right (created by Descartes himself): a disturbance is passed along a nerve fiber until it reaches the brain. When the brain becomes conscious of the pain signal, it somehow reacts (by moving you away from the fire, for example).

Prior to this, people believed that pain was caused by spiritual or mystical forces. With Descartes new theory, pain finally had a physical explanation.

Innumerable treatments for pain are based on this model of “pain receptors” (nerve endings) detecting damage or degeneration, and sending “pain signals” to the brain. Many people continue to think this way – including a lot of healthcare professionals.

It is thought that pain can simply be “killed” by using medications to numb pain receptors. If pain persists (becoming “chronic”), some sort of degeneration or mechanical problem must exist that continues to aggravate pain receptors, and therefore must be “corrected” through surgery.

How well does this model explain pain?

More importantly, how well do these treatments work?


Medications – a cure all?

Pharmacological treatments (over the counter or prescription drugs) are usually one of the first things used in the fight against pain. But do they even work well?

In many cases, pain medications do work reasonably well for acute pain – the type of pain that typically accompanies some sort of new damage or injury. For example, NSAIDs (Nonsteroidal anti-inflammatory drugs) have been shown to be effective for muscle soreness after exercise 1, injuries (like ankle sprains) 2, and after surgery 3 (such as a knee replacement).

However, not all pain is that simple. For chronic pain, medications (such as NSAIDs, and opioids like morphine) are only slightly effective, with a lot of variation – it works like a charm in some people, and not at all in others. Research studies have shown only “small effect sizes”, averaging about 1 – 2 points of improvement on a 10 point scale. 4, 5 That’s not very impressive!

Of course, it’s been known for a while that pain medications are not magic bullets for pain. That’s why people continue to look for something in the body that’s causing the pain. Perhaps something is permanently damaged, or mechanically out of place?

Using the low back as an example, let’s take a look at the research.

Damage, Degeneration, & Surgery

When people hurt their lower back, they immediately worry that some sort of damage or degeneration has occurred in their spine. Of course, a new injury to the spine will probably cause pain. But when pain persists beyond typical healing times (3-6 months), it’s often blamed on the presence of degenerative changes like bulged (herniated) discs, degenerative disc disease, subluxation, scoliosis, osteoarthritis, pinched nerves, etc., which require surgery to correct.

However, surgery for low back pain has been shown to provide only short-term benefits, that are often no better than intensive rehabilitation, 6 or cognitive-behavior (talk) therapy. 7 For serious conditions that cause disability, surgery is effective for improving physical function 8 – but not necessarily pain. 9 Furthermore, surgery often has the side-effect of causing chronic pain. 10, 11, 12

Obviously, back surgery is extremely complicated due to the complex anatomy of the area, and the fact that things need to be cut in the process. Surgical methods may improve in the future, but it’s certainly no sure-fire solution for chronic pain. But why not? Aren’t these degenerative changes the cause of pain?

Apparently, not so much. Studies using x-rays, CT scans, and MRI’s have consistently shown that the presence of one or more of these ‘problems’ is unrelated to whether or not someone experiences chronic pain. 13, 14, 15, 16 Bulged discs almost always heal (reabsorb) on their own, 17, 18, 19, 20 and even when they don’t, pain still improves! 21

That’s right, you can have a bulged disc or degenerated spine, maybe even impinging on one of your nerves, and still not have pain. Or you could have none of these problems, and still have persistent pain! In fact, people who get MRI’s to investigate their low back pain end up no better than people who don’t. 22 It seems the details of these degenerative problems do not deserve the attention they get.

Then what’s causing the pain?

In September 2012, a study was published in the research journal Arthritis & Rheumatism that looked at the relationship between knee osteoarthritis and pain. 23 The study found people who had a little arthritis and high pain, and people with severe arthritis but low pain. They also tested their pain sensitivity through a number of different techniques.

The results demonstrated that people with high pain / low arthritis had increased pain sensitivity, while those with low pain / high arthritis has decreased pain sensitivity. The researchers concluded that the level of knee pain was due to “central sensitization”, rather than the level of osteoarthritis.

In other words, the level of pain in these people had more to do with changes in their nervous system, not changes in knee structure!

Central sensitization involves the whole nervous system – the nerves in your body, the spinal cord, and especially the brain. We’ll talk about this more in future articles.


Conclusions

Medications and surgery seem to be helpful for pain problems that originate from new injuries, but they are limited in their effectiveness against persistent (“chronic”) pain.

While extreme cases may contribute to some pain problems, degenerative changes might be nothing more than a normal part of aging – and no more painful than the wrinkles on your skin.

It seems that the formula: pain receptors detect damage / degeneration, and send pain signals to the brain - is not quite sufficient to explain pain. This is because damage does not equal pain; not all damage leads to pain, and not all pain is caused by damage. The science of pain is only beginning to make sense. Due to some very exciting scientific progress in such fields as neuroscience and biochemistry, our understanding of pain has increased dramatically over the last few decades.

There are a lot of good reasons why people should learn this new pain science. How pain “works” will be discussed very soon in upcoming articles.

But first, there are a few more myths to bust.

Stay tuned for ‘Outdated Pain Theories, Part II’!


Key Reference:

ResearchBlogging.org23. Finan PH, Buenaver LF, Bounds SC, Hussain S, Park RJ, Haque UJ, Campbell CM, Haythornthwaite JA, Edwards RR, & Smith MT (2012). Quantitative sensory tests of central sensitization are associated with discordance between pain and radiographic severity in knee osteoarthritis. Arthritis and rheumatism PMID: 22961435

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    17 Responses to Outdated Pain Theories, Part I – Damage and Degeneration

    1. Tony Ingram says:

      References:

      1. Tokmakidis SP, Kokkinidis EA, Smilios I, Douda H. The effects of ibuprofen on delayed muscle soreness and muscular performance after eccentric exercise. J Strength Cond Res. 2003 Feb;17(1):53-9. PubMed PMID: 12580656.

      2. Ekman EF, Ruoff G, Kuehl K, Ralph L, Hormbrey P, Fiechtner J, Berger MF. The COX-2 specific inhibitor Valdecoxib versus tramadol in acute ankle sprain: a multicenter randomized, controlled trial. Am J Sports Med. 2006 Jun;34(6):945-55. Epub 2006 Feb 13. PubMed PMID: 16476920.

      3. Buvanendran A, Kroin JS, Tuman KJ, Lubenow TR, Elmofty D, Moric M, Rosenberg AG. Effects of perioperative administration of a selective cyclooxygenase 2 inhibitor on pain management and recovery of function after knee replacement: a randomized controlled trial. JAMA. 2003 Nov 12;290(18):2411-8. PubMed PMID: 14612477.

      4. Kuijpers T, van Middelkoop M, Rubinstein SM, Ostelo R, Verhagen A, Koes BW, van Tulder MW. A systematic review on the effectiveness of pharmacological interventions for chronic non-specific low-back pain. Eur Spine J. 2011 Jan;20(1):40-50. Epub 2010 Jul 31. Review. PubMed PMID: 20680369; PubMed Central PMCID: PMC3036024.

      5. Romanò CL, Romanò D, Lacerenza M. Antineuropathic and antinociceptive drugs combination in patients with chronic low back pain: a systematic review. Pain Res Treat. 2012;2012:154781. Epub 2012 Apr 26. PubMed PMID: 22619711; PubMed Central PMCID: PMC3350983.

      6. Chou R, Baisden J, Carragee EJ, Resnick DK, Shaffer WO, Loeser JD. Surgery for low back pain: a review of the evidence for an American Pain Society Clinical Practice Guideline. Spine (Phila Pa 1976). 2009 May 1;34(10):1094-109. Review. PubMed PMID: 19363455.

      7. Mirza SK, Deyo RA. Systematic review of randomized trials comparing lumbar fusion surgery to nonoperative care for treatment of chronic back pain. Spine (Phila Pa 1976). 2007 Apr 1;32(7):816-23. Review. PubMed PMID: 17414918.

      8. Carreon LY, Glassman SD, Howard J. Fusion and nonsurgical treatment for symptomatic lumbar degenerative disease: a systematic review of Oswestry Disability Index and MOS Short Form-36 outcomes. Spine J. 2008 Sep-Oct;8(5):747-55. Epub 2007 Nov 26. Review. PubMed PMID: 18037354.

      9. DeVine J, Norvell DC, Ecker E, Fourney DR, Vaccaro A, Wang J, Andersson G. Evaluating the correlation and responsiveness of patient-reported pain with function and quality-of-life outcomes after spine surgery. Spine (Phila Pa 1976). 2011 Oct 1;36(21 Suppl):S69-74. Review. PubMed PMID: 21897347.

      10. Borsook D, Kussman BD, George E, Becerra LR, Burke DW. Surgically Induced Neuropathic Pain: Understanding the Perioperative Process. Ann Surg. 2012 Oct 10. [Epub ahead of print] PubMed PMID: 23059501.

      11. Chan CW, Peng P. Failed back surgery syndrome. Pain Med. 2011 Apr;12(4):577-606. doi: 10.1111/j.1526-4637.2011.01089.x. Epub 2011 Apr 4. Review. PubMed PMID: 21463472.

      12. Schnabel A, Pogatzki-Zahn E. [Predictors of chronic pain following surgery. What do we know?]. Schmerz. 2010 Sep;24(5):517-31; quiz 532-3. Review. German. PubMed PMID: 20798959.

      13. Ong A, Anderson J, Roche J. A pilot study of the prevalence of lumbar disc degeneration in elite athletes with lower back pain at the Sydney 2000 Olympic Games. Br J Sports Med. 2003 Jun;37(3):263-6. PubMed PMID: 12782554; PubMed Central PMCID: PMC1724651.

      14. Borenstein DG, O’Mara JW Jr, Boden SD, Lauerman WC, Jacobson A, Platenberg C, Schellinger D, Wiesel SW. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects : a seven-year follow-up study. J Bone Joint Surg Am. 2001 Sep;83-A(9):1306-11. PubMed PMID: 11568190.

      15. Beattie PF, Meyers SP. Magnetic resonance imaging in low back pain: general principles and clinical issues. Phys Ther. 1998 Jul;78(7):738-53. Review. PubMed PMID: 9672546.

      16. Weishaupt D, Zanetti M, Hodler J, Boos N. MR imaging of the lumbar spine: prevalence of intervertebral disk extrusion and sequestration, nerve root compression, end plate abnormalities, and osteoarthritis of the facet joints in asymptomatic volunteers. Radiology. 1998 Dec;209(3):661-6. PubMed PMID: 9844656.

      17. Autio RA, Karppinen J, Niinimäki J, Ojala R, Kurunlahti M, Haapea M, Vanharanta H, Tervonen O. Determinants of spontaneous resorption of intervertebral disc herniations. Spine (Phila Pa 1976). 2006 May 15;31(11):1247-52. PubMed PMID: 16688039.

      18. Benoist M. The natural history of lumbar disc herniation and radiculopathy. Joint Bone Spine. 2002 Mar;69(2):155-60. Review. PubMed PMID: 12027305.

      19. Orief T, Orz Y, Attia W, Almusrea K. Spontaneous resorption of sequestrated intervertebral disc herniation. World Neurosurg. 2012 Jan;77(1):146-52. Epub 2011 Nov 17. PubMed PMID: 22154147.

      20. Gezici AR, Ergün R. Spontaneous regression of a huge subligamentous extruded disc herniation: short report of an illustrative case. Acta Neurochir (Wien). 2009 Oct;151(10):1299-300. PubMed PMID: 19730776.

      21. Iwabuchi M, Murakami K, Ara F, Otani K, Kikuchi S. The predictive factors for the resorption of a lumbar disc herniation on plain MRI. Fukushima J Med Sci. 2010 Dec;56(2):91-7. PubMed PMID: 21502708.

      22. Chou R, Fu R, Carrino JA, Deyo RA. Imaging strategies for low-back pain: systematic review and meta-analysis. Lancet. 2009 Feb 7;373(9662):463-72. Review. PubMed PMID: 19200918.

      23. Finan PH, Buenaver LF, Bounds SC, Hussain S, Park RJ, Haque UJ, Campbell CM, Haythornthwaite JA, Edwards RR, Smith MT. Quantitative sensory tests of central sensitization are associated with discordance between pain and radiographic severity in knee osteoarthritis. Arthritis Rheum. 2012 Sep 7. doi: 10.1002/art.34646. [Epub ahead of print] PubMed PMID: 22961435.

    2. Tony Ingram says:

      Preemptive defense:

      For those who think “well it helped me, so I know it works” – please read: Why Science? Part I – Because We’re Usually Wrong. Also check out Parts II and III. If you still don’t agree, I understand: because myth-busting ain’t easy. If you still think you’re intuition and experience is more reliable than all the scientific evidence I cited, get over yourself!

      Peace!

    3. Liz says:

      You know from FB. Question about nerve damage (like a bad deep cut or crush injury). Do the nerves heal under that 3-6 month umbrella or do they take longer? How does scar tissue formation disrupt nerve signaling? Any links to help too is much appreciated!! Thank you for writing about this.

      • Tony Ingram says:

        Great question! I’m writing another article about neuropathic pain, and will be sure to discuss this.
        The point of these ‘Outdated Theories’ articles is just to point out what’s wrong with the simplified “damage = pain signal” model – it completely ignores neuropathic pain, peripheral and central sensitization, and psychogenic pain contributions.

        What you’re asking about is likely one of the main reasons surgery is known to cause chronic pain. See reference number 10 above! Really good question, thanks Liz!

    4. Louis says:

      I’m looking forward to this. “The science of pain is only beginning to make sense”. Man, now everything seems more complicated than before. If I ended up hurting some part of my body, I will start asking myself if that part is damaged or just my brain making things up haha

      • Tony Ingram says:

        Hahaha, I’m gonna have to watch how I write! I don’t mean to make pain seem more scary. After I finish this series, (and you read it, hopefully) it should be a lot less scary.

        If you injure a part of your body, you can be pretty sure any pain you feel is coming from it, and it’s normal to feel it! I just becomes more complex when the pain is persistent, or begins with no obvious injury.

    5. Rob G says:

      Like alot of pain science – ‘its not as simple as that’ applies – there may be a circular effect at work here.

      One theory is that central sensitisation is a RESULT of persistent and widespread nociceptive inputs. This is brought about by temporal and spatial summation. Spinal cord (2nd order) neurons are rate dependant (i.e. higher input is expressed as higher frequency discharges) – resulting in temporal summation and potential for central sensitisation.. OA often affects many joints (spatial summation) and again potential for central sensitisation.

      The key question is why do some sub-chondral nociceptors fire with minimal degeneration and some do not with severe degeneration? There is ongoing research into biomarkers (biologically active chemicals – possibly inflammatory markers) which may hold the answer.

      The ‘issue’ may still be in the ’tissue’, but it may not be mechanical. The net result is a widespread increased nociceptive sensitivity to multiple types of input (temp.pressure etc). This is obviously NOT exclusive of higher centre modulation by memorys/beliefs/cognitions etc. This also impacts on the pain the individual experiences.

      • Tony Ingram says:

        Hi Rob,

        Thanks for the comment. You’re getting ahead of me! I haven’t begun to discuss nociception, central sensitization, or anything of the sort in this series of articles yet.

        I agree that the issue most often originates in the tissue, at least in the case of osteoarthritis (I’ve never heard of someone having clinical signs and symptoms of OA pain without some radio-graphic signs as well, but I may be wrong). I’ve been keeping my ear to the ground about the neuro-immune role as well – very interesting stuff.

        I’m not sure where I might have implied that anything here is simple – there’s nothing simple about the nervous system. I do write in the most simplistic way possible, as I do not assume I am speaking to academics. The lesson I want to communicate here is the fact that the amount of pain experienced is not a product of the amount of degeneration – I think we can agree on that.

        And I certainly did not imply that increased nociceptive sensitivity is exclusively modulated by high centers through memory/beliefs/cognition etc. However, I will say that there is some evidence that higher centers are involved (and differences there are predictive) in the transition of acute to chronic pain (reference).

        I’ll get more into this when I write about these topics specifically.

        Thanks for commenting!

        Tony

    6. Kevin says:

      I like where you are going with this as I have been teaching this for the last 5 years. The complexities involved with the generation and persistance of pain are complex and we are just starting to unravel what is occuring. This is due to the development of a greater understanding of the role of neuroplasticity in the how the individual percieves pain, how pain becomes chronic and how the nociceptive input results in motor alterations. I think you know better though to be purely biased as to the ‘research’ as any good researcher understands the limitations. For your post on exercises it do however think you missed the boat. There is a clear difference between motor control exercises which focus on neuromuscular skill development and just general exercises. The process of neuroplasticity which leads to alterations in motor tone and activation are best treated with movement designed to train both the body and brain simultaneously. This helps provide the necessary stimulus for change required to break the cycle of ongoing pain. It does’t work for everyone as pain and the variety of conditions people present with complicate the scenario. Getting the right muscles doing the right think at the right time and reinstating prepatory neuromuscular activation is an important part of restoring function. This forms the basis of the rehabilitative programs and the clinical use of kinesiology taping that I teach to health care practitioners.
      If you really want to blow your mind (i’m assuming you are as nerdy as I am about this stuff) we should start discussing the role of angiogenesis in pain generation as well as capilary bed densification’s role in whether someone will get an injury or not.

      • Tony Ingram says:

        Kevin,

        I think this comment would have been more appropriate on the other article where I discuss exercise, but I suppose I’ll respond here.

        “I think you know better though to be purely biased as to the ‘research’ as any good researcher understands the limitations.”

        I’m well aware of the possibility of bias and poor experimental design in research. But the alternative – experience and intuition – has a far higher risk of bias, as I’m sure you’re aware.

        “For your post on exercises it do however think you missed the boat.”

        Really? Missed the boat? I think that’s a bit extreme, and rather insulting. I think I presented my case with a rather sound rationale and plenty of evidence – the limitations of which you can check for yourself as I list all of my primary sources with each article. I also did not cherry pick, nor did I throw the baby out with the bathwater. I remain confident that exercise is important in the overall treatment of pain.

        “There is a clear difference between motor control exercises which focus on neuromuscular skill development and just general exercises.”

        Again, I’m well aware of the purported difference, and the theoretical mechanisms that you went on to describe. But the available evidence certainly doesn’t suggest superior effects of motor control exercise over any other type. (ref, ref, ref, ref). I don’t think I’ve “missed the boat” at all. If you have any competing evidence, then feel free to share it here.

        “If you really want to blow your mind (i’m assuming you are as nerdy as I am about this stuff) we should start discussing the role of angiogenesis in pain generation as well as capilary bed densification’s role in whether someone will get an injury or not.”

        I’m a bit skeptical of this. Do you have any primary references I can read?

        Thanks for the comment. Perhaps I took it a little too seriously but honestly I found it a little insulting.

        Tony

        • Kevin says:

          My comments were not intended to be insulting, just that it is far to common for individuals to make assumptions that if it hasn’t been validated in the research it must not be true. This is the sense I gather from your comments and you sound far too intelligent to approach things with such limitations. For references on motor control rehab you can download a discussion I wrote on the subject at http://www.fprprofessional.com

          • Tony Ingram says:

            I didn’t make any such assumptions. That’s a sort of “argumentum ad ignorantiam” in a way. But I appreciate what you’re saying, and have seen it as well.

            When there is no evidence to substantiate, I don’t assume it’s wrong… but I certainly don’t get exited.

            But from my own review, and the references I posted, it looks like there IS evidence that motor control exercise is no more effective than any other form of therapeutic exercise. But I’ll check out your write up.

            Thanks for the discussion.

            • Kevin says:

              Great, let me know what you think. We develop and teach a number of courses that we teach health care professionals around the globe ranging from rehabilitative concepts, dynamic clinical movement evaluations and taping. We are always looking for new content for our webinars, ebooks and even for instructors who are good critical thinkers who can work well in a multidisciplinary way. Let me know if this interest you and if you would like to connect. drjardine@collaborans.com. Our taping website is http://www.nstaping.com

    7. James says:

      Hi Tony,

      I’ve really enjoyed reading through this whole series and it’s been incredibly informative. There are two comments I wanted to make. The first is in response to your statement that “the amount of pain experienced is not a product of the amount of degeneration”.

      The article from Arthritis and Rheumatism cited discussing central sensitization still noted a modest association between radiological findings and knee pain. Here is an article that discusses how certain factors like that radiographic views used and the definition of pain in studies might effect that association.

      http://www.biomedcentral.com/1471-2474/9/116

      The authors still concluded that knee pain does not always match up with the level of degeneration but it does raise some interesting questions regarding other physical factors that may be overlooked. They also clearly acknowledge the cognitive component of knee OA pain. Here is a quote from the article:

      “Other factors may account for knee pain which will not be evident on the knee x ray. Figure 1 clearly shows this, indicating that the pain may be the result of other bone problems, not visible on an x ray such as oedema, or non-OA conditions such as ligament injury or tendonitis. Indeed, some chronic knee pain might be more strongly linked to issues of cognitive or emotional state such as depression rather than local pathology at the knee joint. Of course, all these things can coexist at the same time, making up multiple layers of causality of knee pain”

      Another question regarding the other OA study, could the increased pain sensitivity be related to some physical factor or aspect related to the degeneration, but not necessarily correlated with the severity. I think the only way to find out would be to know what the subjects pain sensitivity was before they developed OA.

      The second comment is also more of a question about how would you view tendinopathy which is in a sense reversible degeneration?

      I’m really looking forward to your future posts on this topic. Great work!

      James

      • Tony Ingram says:

        Hey James,

        Thanks for the kind words! Good points and questions. About the study you posted, I think we have to be careful what we mean when we say “cause”. I think we can say that damage is a “sufficient” cause of pain, but not a “necessary” cause. I feel people often confuse the two, but clarity can be helpful when picking apart the details.

        The study I referenced may have only found a modest association because they used quantitative sensory testing to measure “central sensitization”, but I’m sure there’s more to central sensitization than can be measured that way. Seems to me sensory testing would focus on the peripheral sensitization (although the lines blur).

        I definitely agree that there may be other physical factors, and I hope my article didn’t imply that damage is irrelevant. Osteoarthritis is clearly multifactoral, and damage should always be taken into account. I’m just stressing the damage:pain discordance here, and the fact that “fixing” damage isn’t a perfect solution. But of course, knee replacements are sometimes necessary, and they help a lot of people!

        It’s difficult to write in a middle ground, balanced way when you are trying to stress a certain point. But I think it’s an important point to make – stop using “degenerative” and “mechanical” terminology with chronic pain patients, it’s not completely accurate and it may cause fear and misunderstanding. I’m going to drive this point home in my next article.

        Anyway, good points, very important things to consider in this discussion! Thanks for the comment!

        About the tendinopathy – I am actually a little torn about how I feel. I agree it seems as if to be ‘reversible’ degeneration… but I’m positive there are strong neuropathic and central sensitization components as well. I’m in the process of reviewing some literature to clarify my thoughts, and plan to write about it soon. It’s one topic I haven’t really delved into on this site. I usually talk about injuries and chronic pain, where tendinopathy seems to fit in the middle… sort of!

        Again, thanks!

        Tony

    8. Liz says:

      Tony, I find your writing on this area very interesting. Two years ago I had two senior basketballers who collided in mid air landing on my neck and knocking me out. My head, followed by the rest of me, hit the bitumen surface very heavily. I have a small frame and am 55 years of age. Since then I have had constant pain in my neck. C4 and C5 on the right side, the impact point, now has herniated disc bulges and there is end plate damage on these vertebrae. There was a 1.5 mm displacement of C4 on C5.

      I have constant pain when my neck is in a static position. If necessary to hold it still for driving or computer work my neck “locks”, muscle spasms develop and headaches varying from mild to debilitating.

      The workers’ compensation insurer has employed a specialist who says the pain I feel is purely psychological and the degeneration is purely age related. My parents are both in their 80’s. Neither of them have osteoarthritis. I had none prior to the accident.

      I now have a strong tremor in my right hand and in my right leg and have balance issues.

      Do you know of any papers or articles I can refer my occupational physician or lawyer to to support the fact that the pain is very real and that the evidence is not age-related but injury related. Even my rheumotologist says it is unusual for this minor injury to be causing the pain I am experiencing.

      Regards,

      Liz

      • Tony Ingram says:

        Hi Liz,

        I’m really sorry to hear about your issue with pain! I’m going to comment, but I should say first that I am not a physician, and even if I was, I cannot give medical advice over the internet – so this is just my opinion:

        While it’s true that degeneration may be due to “aging”, it could also have been due to injury – it’s impossible to know without imaging studies of your neck prior to the injury. It’s interesting that the pain is during static positions. One would think that movement would cause pain in this case, as facet joint movement would affect the end plates, and compression would affect the bulges. When you received the results of the imaging studies, was there any mention of the bulges impinging nerves? Of course, I can only speculate… I don’t know enough detail. I really doubt the pain is “psychological”… (what does that even mean?), and the tremor and balance issues may indicate neurological involvement. If I were you, I’d seek a second opinion, or referral to a chronic pain clinic or even a neurologist.

        As for references, I have many on this article, and I plan to write a few more articles soon that will have more references on such things as “psychogenic” pain (ref). The fact is, even if your pain was “psychological” (and I really think it’s terrible that they are saying this – as I’m sure there is an impression of downplaying your pain), it’s still real. All pain is real. If you’re experiencing it, it’s real, no matter what the origin.

        This may be too detailed a discussion to have on a comment thread like this, so if you’d like to continue, don’t hesitate to e-mail me. I sincerely hope you can find some people who know more about modern pain science so they can give you the assistance you need.

        Stay positive!

        Tony

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