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Payers Tue, 31 Jan 2023 10:52:53 +0000 Joomla! - Open Source Content Management en-gb Whatever Happened to Backache?

You’d think that we’d all agree on what back pain is. Pain in the low back is almost as common as days of the week. Most everyone has had or will have back pain in the course of their lives and it is one of the most frequent reasons for seeking healthcare.1 Despite this common, everyday experience, we continue to be vexed by competing understandings of the nature of back pain.2

To be sure, our understanding of the cause of common back pain has changed over the last fifty some odd years. However, it’s questionable whether these changes mark true advances in knowledge.

A Brief History: Backache or Back Pain?


At one time, we tended to refer to back pain as backache. The term implied similarity to neck ache and headache. Today, when aches of the head and neck occur without any overt injury or illness, we tend to associate them with over-exertion, working too much, tension, and unresolved conflict, among others. We allow, in other words, for the occasions when problems or people are literally “such a headache” or “a pain in the neck.” Still other times, especially when people are prone to neck ache or headache, we tend to perceive such aches and pains as a barometer for when we need to take better care of ourselves because life has become too busy or problematic in some manner.

In the past, backache was considered similarly. The gradual appearance of low back pain, without injury or illness, was readily taken as a sign that life and/or relationships were getting out of sync: backache could be due to working too much, leading to the subsequent need for more rest and relaxation in life; or it was due to the persistent inactivity of a desk job and the habit of watching night-time TV, resulting in an unmet need for more exercise; or it could be due to the persistent unresolved conflict with, say, a boss at work and the mounting pressure that it entailed over time.

Suffering from backache (or neck ache or headache), people tended to prescribe a return to healthier ways of living – resolutions to get more rest and relaxation, work less, seek the solace of the country or outdoors, or bathe in warm springs or spa.

Today, we might understand this conceptualization of back pain with the concept of stress. We use the term stress to refer to the hectic and chaotic nature of modern life. We work too much. We are our chronically over-stimulated from information, messaging, and screens. We persistently juggle between work, children and their activities, and the management of elderly parents. Despite the apparent promise of connection through social media, urban and rural loneliness are all too common. When such imbalances persist for too long, we experience them in any number of emotional and bodily ways, some of which are headache, neck ache and backache.

We all recognize the grain of truth in this way of understanding the occurrence of low back pain, especially when it comes on gradually and without warning. We used to call this type of pain backache.

Injury/Spinal degeneration model of back pain

A competing conceptualization of backache, however, has coexisted alongside this understanding of backache as a malady of the stress ofPhoto by Justin Luebke courtesy of Unsplash modernity. It is backache as the result of a condition of the spine brought about by injury or degeneration. Allan and Waddell3 have a rich history of the first published medical papers beginning in the late 19th century hypothesizing backache as emanating from problems associated with the spine and subsequent reports of acute back pain due to railway injuries. By the first half of the 20th century, the intervertebral disc had sunsequently come to be understood as a source of backache. With the advent of CT scans in the 1970’s and MRI scans in the 1980’s, this conceptualization eclipsed all other ways of understanding backache, as so much of the spine had become visible. Having become observable, abnormalities of the spine were readily identified as the source of pain in the back. As a result, it is now commonplace to consider pain in the back as due to injury to the disc or degenerative changes to the spine. Indeed, this view of backache has so taken hold that we no longer readily use the term backache in preference for back pain.

There is, of course, a grain of truth in this way of understanding back pain too. Like any other part of the body, we can injure our low back. We are involved in motorcycle accidents, sports injuries, slips on the ice, and falls from ladders, and countless other ways we can injure ourselves. Sometimes, these accidents cause significant enough injuries that they can be seen on scans.

Indeed, beginning in the 1980’s, but really taking off in the 1990’s and early 2000’s, the use of CT and MRI scans became widespread for all instances of back pain. It seemed to open up a whole new world in our understanding of back pain. Specifically, we made the leap from initially holding that back pain is due to spinal abnormalities from injuries on some occasions to holding that back pain is due to spinal abnormalities on all (or most all) occasions.

The primacy of what we might call the injury model for understanding back pain is evident even in those instances in which there is no overt injury associated with the onset of back pain. In response to the gradual appearance of back pain, we tend to look to what we might think of as micro-injuries: “I must have slept wrong,” “I must have tweaked my back,” or “I twisted the wrong way.” Conceptualizing it as an injury, we subsequently seek medical evaluation and oftentimes want a scan to see what’s going on with the spine. Indeed, both the general population and healthcare professionals now seem to simply assume the association of common back pain with spinal abnormalities. Subsequently, it’s now commonplace to want to look first to the vertebrae, discs and ligaments when seeking an explanation of common back pain.

The term for what’s wrong in many of these instances has tended to be spinal- or disc degeneration. It’s a way to refer to the medical equivalent of what we might think of as micro-injuries. Degenerative changes to the spine are the result of slow, wear and tear.

Moreover, such degenerative changes can and have been, of course, the object of medical and surgical intervention. Physical therapists, physiatrists, interventional pain physicians, orthopedic and spine surgeons – all are experts in the evaluation and delivery of interventions aimed at degenerative conditions of the spine.

Having reached its apex in the early 2000’s, this way of conceptualizing back pain as the result of overt or subtle injury, defined by abnormality of the spinal structures, keeps back pain squarely within the realm of healthcare, rather than lifestyle. People have come to look, not to what they can do to alleviate backache, but to healthcare providers with an expertise in the evaluation and treatment of abnormalities of the vertebrae, disc and ligaments. In this way, people with back pain must become patients, it seems, because they have little control over the abnormalities of their vertebrae, discs, and ligaments once they have them. The implication is that people with back pain went from having a problem that they resolved themselves to patients with a medical condition, akin to an injury, that healthcare providers treat.

During this period of shifting emphasis towards spinal abnormalities as the explanation of back pain, the period of the 1990’s to the 2010’s saw the use of scans, interventional procedures, and surgeries grow at exponential rates.4

2010’s: Cracks in the Injury/Spinal Degeneration Model

Looking back, we might question the logic of what happened. Just because some instances of common back pain are due to injury doesn’t mean that all instances of common back pain are the result of injury. In logic, this type of error is called affirming the consequent and it’s considered a fallacy. It is, however, exactly what happened in our understanding of pain in the back.

We were captivated by a model for understanding a particular set of a phenomenon, through which we came to see all instances of the given phenomenon.5 We sometimes think that science and knowledge comes from empirical observation, which then lead us to developing models for understanding those observations. Of course, it can happen this way, but the reverse can also be true. Sometimes, our models determine what empirical observations we make. Science and knowledge can be a reciprocal process in this regard. It’s the latter that occurred from the 1990’s to at least the early 2010’s, but even to some extent to this day. Our injury model of back pain has determined how we perceive the empirical data of back pain.

Our captivation to this model was aided, of course, by the development of high-powered abilities to perceive spinal structures – the CT and MRI machines in the 1970’s and 1980’s, respectively. With them, we could find abnormalities of the spine even when the onset of back pain occurred without any overt precipitating injury – we could still find micro-injuries, if you will, in the form of degenerative changes of the spine. Thus, the injury model of back pain could still explain back pain even when there was no demonstrable outward injury. In other words, we could see the apparent spinal correlates to those instances when we explain to ourselves that we “must have” have injured our backs with a tweak or a wrong twist, even though we hadn't previously observed such a tweak or twist when the pain had come on subtly and progressively.

Despite the power of explanatory models determining what we see, empirical data can still break through in the form of counter-factuals to the model and lead to a change in the conceptual model itself. It takes, however, time, sometimes on the order of years, and it can be aided by changes in society.6

One early instance of counter-factual data, aided by events in society, was that despite the exponential growth of scans and treatments for spinal degeneration, disability claims for back pain grew at a corresponding exponential rate.7

How could this be? If common back pain is due to injury and we have the capabilities to both accurately assess these injuries with the use of scans and treat them with, say, the use of physical therapy and spinal interventions and surgeries, people with back pain should be get better and go back to work at high rates. It’s not what happened, though. With the practice of scanning and treating spinal abnormalities, people have been becoming more disabled. It is hard to escape the possibility that, in at least some instances of common back pain, we have been assessing and treating the wrong things – things that in fact were not the cause of these instances of back pain.

Another set of empirical data that arose in the 1990’s to challenge the injury model of back pain was the discovery that spinal abnormalities are common even among people without back pain. The use of scans, when turned on people without back pain, find the very same things that are found in people with back pain, and which are used to explain back pain.8, 9 As it turns out, disc herniations and degenerative changes are common in people, with or without back pain. Jarvik, et al.,10 and Borenstein, et al.,11 subsequently followed their subjects without back pain over a period of three and seven years, respectively, to see if the presence of such degenerative changes predict later onset of back pain. The progression of degenerative changes over time had no statistical correlation with who later developed back pain.

To place the importance of these findings in perspective, we might use an analogy of the brown-haired bank robber. Suppose that a bank was being robbed one morning and the police had received a tip that the bank robber had brown hair. They surrounded the bank and out came a young man with brown hair. They promptly arrested him and placed him in the back of a squad car, confident that they had found the robber. Upon entering the bank to tell the customers and staff that they were now safe, the police came to realize that many people in the bank had brown hair. Had they found the culprit? They’d have to admit that their confidence could no longer be so certain.

Similarly, having become able to find spinal abnormalities with the occurrence of back pain, we had become confident that back was due to these spinal abnormalities. However, once we came to recognize that we find such abnormalities commonly in people without back pain, we can't and shouldn't so certain that we have found the culprit of back pain.

At the time of the publication of these findings in the 1990’s and early 2000’s, these findings were indeed puzzling, and made a splash among healthcare providers. Nonetheless, they weren’t sufficient to alter the model through which we had come to understand and perceive back pain. We continued, as we still do today, to understand back pain as the result of injury or degeneration of the spine.

I recall occasions in the 2000’s when patients reported to me, “I never knew how much pain I was in until my surgeon read me my MRI results.” Still, to this day, I have patients who report to me that their interventional pain physician or surgeon, when reading their MRI results, exclaim in wonder as to how they can even walk with a spine like they have. Rather than privileging the facts, in this case that the patient doesn’t report much pain or can readily walk, and thus interpret the scans as not representative of their pain and abilities, they privileged the findings of the scans and then told the patients that they are actually worse than they are. Such is the power of the injury model to captivate and determine our understanding of the phenomenon in front of us.

If, however, we are able to step out of the injury model for understanding back pain, we might not wonder such things. We would understand better why people don’t have a lot of pain or difficulty walking, even when finding the presence of spinal abnormalities on scans. CT and MRI scans commonly reveal such findings in people with or without back pain.

Moreover, we might come to understand that these findings have little or no relationship to pain levels or functional abilities. We might, in other words, realize that we are pointing to the wrong things when attempting to explain many instances of common back pain.

This conclusion bears out in large-scale studies that fail to find either statistical or clinically meaningful relationships between back pain and spinal degenerative changes.12, 13 It’s hard to make a case that we have found the cause of back pain when the purported cause doesn’t even correlate, or correlates poorly, with back pain. The most charitable thing we can say is that the lion’s share of what accounts for back pain isn’t captured by scans. Back pain is likely due to many different things that when put together adds up to pain in a person’s back and that what’s found on a scan is just one small factor that accounts for any given person’s back pain.

Modern lifestyle or injury and degeneration?

While we can, of course, injure our back, as we can any other location of our body, should we then infer that all back pain is due to injury? When we so commonly find spinal abnormalities upon scanning the backs of people who report an injury, it is tempting to think that spinal abnormalities are the objective correlate to the reported injury. Similarly, it is tempting to think that such spinal abnormalities are the cause of back pain when it occurs gradually, without a precipitating injury, as we can find spinal abnormalities in these cases too. Thus, it can come to seem that all back pain is the result of spinal abnormalities, whether as the result of injury or more subtle degeneration of the spine.

This explanation of back pain can seem so compelling until, at least, we come to find similar levels of spinal abnormalities in people without back pain. We now have about three decades of repetitive studies coming to the same finding. Most of these studies find no statistically significant relationship between back pain and spinal abnormalities. Even in the minority of studies that do show statistical significance, the relationship is poor and of questionable clinical significance. At best, spinal abnormalities play only a minor role in the cause of back pain.

This fact might shed some light on why spine surgery, despite its widespread use, has failed to produce any conclusive empirical studies showing its effectiveness. The largest and longest study to date, the SPORT trial for lumbar disc herniation, has shown no considerable difference between those who have surgery for disc herniation and those who do not.14, 15, 16

This study was originally designed as a longitudinal, clinical trial, meaning that subjects, who all had disc herniations in their low back, were randomly assigned to either receive surgery or conservative care without surgery (the clinical trial aspect of the study) and then followed to obtain data on their status over the course of 1, 2, 4, and 8 years (the longitudinal aspect). When the data was compared for the two groups, strictly defined by those who remained in their randomized groupings over the course of the study (which is how a clinical trials are run, for instance, for testing the effectiveness of a medication), outcomes were no different between those who received surgery and those who did not receive surgery, at any of the follow-up periods from 1 to 8 years.

If this clinical trial tested the effectiveness of a medication, or of a psychological treatment, no one would question the conclusion that the treatment failed to work. It was no more effective than usual care, which is to say that adding surgery to the overall treatment provided no value. Surgery for disc herniation is no more effective than not having surgery.

However, a funny thing happens when we are captured by an explanatory model of a particular phenomenon and are then met with counterfactual data. Counterfactual data are hard to believe. It’s no truer when it comes to the specific situation of a widespread treatment for spinal abnormalities like surgery. We all collectively might want to ask: how can this be that surgery for disc herniation doesn’t work? Surely, it can’t be true.

As it turns out, the study had some problems, which ironically leads to a reframing of the data towards an alignment with the explanatory model that back pain is due to spinal abnormalities. Specifically, the study suffered from a lot of crossover of randomized subjects. Crossover occurs when subjects of a clinical trial fail to stay in their randomized groupings and so don’t end up getting the treatment to which they were randomized to get. So, in the instance of the SPORT trial, some subjects randomized to get surgery subsequently decided against getting surgery after all; and some of the subjects randomized to conservative care without surgery eventually decided to get surgery anyway. The investigators did the best they could given this circumstance and compiled the data in accordance to the re-assorted groupings and compared those who received surgery against those who did not receive surgery.

Because the subjects in these newly sorted groupings were not fully randomized anymore, this lack of randomization introduces additional variables that might influence the effectiveness of the procedure, outside of the actual procedure itself. There might be something unique to the individuals who decide for or against a certain treatment that in turn influences the effectiveness of the treatment, something that might have been more evenly distributed and therefore washed out, if they had stuck to the initial randomization of who got which treatment. We know, for instance, that motivation and belief in the effectiveness or lack of effectiveness of a treatment can influence the effectiveness of a treatment. It's feasible that such motivation and belief may have played a role in the degree of crossover from one randomized treatment to another, and, as such, they may have also played a role in the degree of effectiveness that those treatments exhibited in the study. 

Nonetheless, the data derived from the re-sorting of the groupings might shed some light on the effectiveness of the procedure, even if it is not as rigorous of a study as a clinical trial. The name for this type of study that the investigator’s secondarily pursued, given the circumstances, is called an observational study. The results of an observational study are not considered as conclusive as the results of a clinical trial.

What they found was that, at the 4-year and 8-year follow-up periods, both the group that received surgery and the group that did not receive the surgery improved, but that there was a statistically significant difference in favor of the surgery. In other words, those who had received the surgery improved a little bit more than those who id not receive surgery. This small improvement amounted to about a 13% greater reduction in pain for those who received surgery, which is roughly the equivalent of a one-point greater reduction on the commonly used 0 to 10 scale. There was no difference in the rate of returning to work between those who received surgery and those who didn’t.

The most charitable interpretation of these longitudinal findings of both the randomized clinical trial aspects of the study and the observational aspects of the study are that surgery for a herniated disc might show a small reduction in pain four years and eight years down the road, when compared to not getting surgery. Again, both the surgery group and the non-surgery group showed improvements, but the surgery group improved just a little more than those who did not receive surgery.

Nonetheless, this small improvement is of questionable clinical significance – is the difference, say, of having a pain level of a 7 rather than an 8, four to eight years down the road, enough of a difference to really make a difference in the actual experiences of one’s life?

Thus, the SPORT Trial, which is the best study to date of surgery for disc herniation is far from conclusive. It points to the conclusion that surgery for disc herniation might produce a small improvement in pain level over time.

This small effect for pain reduction but not work status improvement falls in line with what we have been discussing – spinal abnormalities might play a causal role in back pain, but if they do, it is a small role, and so targeting them surgically produces only small improvement. Again, all of this is to suggest that the lion’s share of what causes common back pain lies outside of what scans can identify and what therapies targeting such abnormalities can effectively treat.


Despite decades of data pointing to a cause of common back pain as more complex than simply the presence of spinal abnormalities, a large portion of society continue to have a default understanding that back pain is due to an injury for which spinal degenerative changes are its correlate.17, 18 This default understanding involves, of course, a subsequent default implication that first-line treatments of back pain should target these degenerative changes.

We continue this default understanding because we are captured by an explanatory model that back pain is due to injury, and spinal degenerative changes are the correlate to injury. We continue to do so at the peril of persistent pain, disability and cost.

What, then, of our alternative understanding of back pain – that of back pain as backache, similar to a headache?

With each time we develop a headache, we don’t automatically think that we must have injured our head, and subsequently seek medical evaluation and a scan to determine the specific nature of the injury that we figure we must have had. We also don’t automatically think that we must seek out therapies that target the presumed injury. Rather, we tend to naturally think of it as due to tension and stress, or working too much, or not getting enough sleep, or just the hectic pace of our modern lifestyle. We subsequently think that we need to take better care of ourselves and engage in some healthy changes to the life we live.

Maybe, it’s time to return to a similar understanding of back pain. We could start by going back to referring to back pain as backache.

More Information

For more information, see also:


1. St. Sauver, J. L, Warner, D. O., Yawn, B. P., Jacobson, D. J., McGree, M. E., Pankratz, J. J., Melton, L. J., Roger, V. L., Ebbert, J. O., & Rocca, W. A. (2013). Why do patients visit their doctors? Assessing the most prevalent conditions in a defined US population. Mayo Clinic Proceedings, 88(1), 56-67. doi: 10.1016/j.mayocp.2012.08.020

2. Hartvigsen, J., Hancock, M. J., Kongsted, A., Louw, Q., Ferreira, M. L… Lancet Low Back Pain Series Working Group. (2018). What low back pain is and why we need to pay attention. Lancet, 391(10137), 2356-2367. doi: 10.1016/S0140-6736(18)30480-X

3. Allan, D. B., & Waddell, G. (1989). An historical perspective on low back pain and disability. Acta Orthopaedica Scandinavica, 60(suppl. 234), 1-23. doi: 10.3109/7453678909153916

4. Brooks, M. I., Deyo, R. A., Mirza, S. K., Turner, J. A., Comstock, B. A., Hollingworth, W., & Sullivan S. D. (2008). Expenditures and health status among adults with back and neck problems. Journal of the American Medical Association, 299, 656-664.

5. Wittgenstein, L. (1953). Philosophical Investigations. New York: Macmillan.

6. Kuhn, T. S. (1996). The Structure of Scientific Revolutions (3rd Edition). Chicago: University of Chicago Press.

7. Deyo, R. A., Mirza, S. K., Turner, J. A., & Martin, B. I. (2009). Overtreating back pain: Time to back off? Journal of the American Board of Family Medicine, 22(1), 62-68. doi: 10.3122/jabfm.2009.01.080102

8. Boden, S. D., Davis, D. O., Dina, T. S., Patronas, N. J., & Wiesel, S. W. (1990). Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: A prospective investigation. Journal of Bone and Joint Surgery: American Volume, 72(3), 403-408.

9. Jensen, M. C., Brant-Zawadzki, M. C., Obuchowski, N., Modic, M. T., Malkasian, D., & Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. New England Journal of Medicine, 331, 69-72. doi:10.1056/NEJm199407143310201

10. Jarvik, J. G., Hollingworth, W., Heagerty, P. J., Haynor, D. R., Boyko, E. J., & Deyo, R. A. (2005) Three-year incidence of low back pain in an initially asymptomatic cohort. Spine, 30, 1541-1548.

11. Borenstein, D. G., O’Mara, J. W., Boden, S. D., Lauerman, W. C., Jacobson, A., Platenberg, C., Schellinger, D., & Wiesel, S. W. (2001). The value of magnetic-resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: A seven-year follow-up study. Journal of Bone and Joint Surgery: American Volume, 83(9), 1306-1311. doi: 10/2106/00004623-200109000-00002

12. Brinjikji, W., Luetmer, P. H., Comstock, B., Bresnehan, B. W., Chen, L. E., Deyo, R. A., Halabi, S., Turner, J. A., Alvins, A. L., James. K., Wald, J. T., Kallmes, D. F., & Jarvik, J. G. (2016). Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. American Journal of Neuroradiology, 36(4), 811-816.

13. Corniola, M. V., Stienen, M. N., Joswig, H., Smoll, N. R., Schaller, K., Hildebrandt, G., & Gautschi, O. P. (2016). Correlation of pain, functional impairment, and health-related quality of life with radiological grading scales of lumber degenerative disc disease. Acta Neurochirurgica, 158(3), 499-505.

14. Weinstein, J. N., Tosteson, T. D., Lurie, J. D., Tosteson, A. N., Hanscom, B., Sinner, J. S., Abdu, W. A., Hilibrand, A. S., Boden, S. D., & Deyo, R. A. (2006). Surgical vs. nonoperative treatment for lumbar disk herniation: The Spine Patient Outcomes Research Trial (SPORT): A randomized trial. JAMA, 296(20), 2441-2450. doi: 10.1001/jama.296.20.2441

15. Weinstein, J. N., Lurie, J. D., Tosteson, T. D., Tosteson, A. N., Blood, E., Abdu, W. A., Herkowitz, H., Hilibrand, A. S., Albert, T., & Fischgrung, J. (2008). Surgical versus non-operative treatment for lumbar disk herniation: Four-year results for the Spine Patient Outcomes Research Trial (SPORT). Spine, 33(25), 2789-2800. doi: 10.1097/BRS.0b013e318ed8f4

16. Lurie, J. D., Tosteson, T. D., Tosteson, A. N., Zhao, W., Morgan, T. S., Abdu, W. A., Herkowitz, H. & Weinstein, J. N. (2014). Surgical versus nonoperative treatment for lumbar disk herniation: Eight-year results for the spine patient outcomes research trial. Spine, 39(1), 3-16. doi: 10.1097/BRS.0000000000000088

17. Weber, C., Behbahani, M., Baardsen, R., Lehmberg, J., Meyer, B., & Shiban, E. (2107). Patients’ beliefs about diagnosis and treatment of cervical spondylosis with radiculopathy. Acta Neurochirurgica, 159(12), 2379-2384. doi: 10.1007/s00701-017-3356-0

18. Franz, E. W., Bentley, J. N., Yee, P. S., Chang, K. W., Kendall-Thomas, J., Park, P., & Yang, L. J. Patient misconceptions concerning lumbar spondylosis diagnosis and treatment. Journal of Neurosurgery, Spine, 22(5), 496-502. doi: 10.3171/2014.10.SPINE14537

Date of initital publication: 12-6-2021

Date of last modification: 1-3-2021

]]> (Murray J. McAllister, PsyD) Chronic Pain Rehabilitation Sun, 06 Dec 2020 21:30:03 +0000
Is Degenerative Disc Disease Painful?

Correlation doesn’t imply causation. It’s a commonly expressed caution in the health sciences. What it means is that two things can tend to go together without necessarily causing each other.

The classic example that statistic professors like to give is that air conditioner use is significantly correlated with street crime. Does the use of air conditioners cause street crime? No, of course, not and yet they do tend to go together. It’s actually only because they both tend to occur in the summer. When it’s hot outside, it’s true that people tend to use their air conditioners and it’s also true that people tend to loiter outside in the city, getting into trouble more often than in the cold winter months when people tend to stay indoors. With the example, we can see that just because things tend to go together they don’t also always cause each other.

What about things that hardly go together or things that don’t go together at all? Could we say that low levels of correlation or an altogether lack of correlation imply causation? On the face of it, it seems absurd to think that lack of correlation or even minimal correlation might imply causation. Who would think that A causes B when A and B have no relationship to one another or only a minimal association with one another? That inference, however, is exactly what we assume when we think that degenerative disc disease causes chronic back or neck pain.

The logic of correlational studies of degenerative disc disease and chronic spine pain

Degenerative disc disease is a common explanation for chronic back or neck pain. Degenerative disc disease is a general phrase that refers to a number of conditions or changes of the spine, such as loss of disc height, disc bulges, annular tears, disc herniations, endplate changes, neuroforaminal and spinal canal stenosis, among others. Healthcare providers typically identify their occurrence with either X-ray, CT or MRI scans. When these tests identify degenerative disc disease in the spine of someone experiencing chronic back or neck pain, many healthcare providers and their patients consider that the degenerative disc disease is the cause of the chronic pain. In other words, they believe that the degenerative disc disease is painful.

Healthcare providers and their patients commonly justify particular types of treatment with the notion that degenerative disc disease is causing chronic back or neck pain. Spine surgery and interventional pain procedures, in particular, but also certain types of physical therapy, all attempt to reduce pain by modifying specific types of degenerative changes of the spine. Again, the underlying justifying belief is that such degenerative changes of the spine are painful.

How valid is this justification? In other words, how true is it that degenerative disc disease causes chronic back or neck pain?

The question is actually tricky to answer, especially if we want to show that it is in fact true. Theoretically, the best way to answer it would be to run a true experiment, where we induce various degenerative changes to the spine in a number of people and see whether they have pain in the back or neck (wherever the degenerative change was induced). However, we don’t know how to make degenerative changes to the spine, at least not exactly as they occur naturally. Additionally, even if we did know how, there would be all sorts of ethical problems in producing degenerative disc disease in human subjects. For instance, we don’t know how to reverse it and so we’d be inducing permanent damage to people. Because of these challenges, we don’t tend to perform true experiments when looking at the relationship between degenerative disc disease and chronic neck and back pain.

Instead, we generally rely on a different form of research in the scientific study of chronic pain – correlational research. In correlational research, we measure certain variables, such as the occurrence of degenerative disc disease and back or neck pain, and see whether they tend to go together. If two things, such as degenerative disc disease and pain, are highly correlated (i.e., they tend to go together almost always), we can at least say that one may cause the other. As we discussed in the introduction of this piece, though, we cannot say with confidence that there is a causal relationship when two things are highly correlated. There may be other factors that cause the two to occur together all the time (i.e., think of the air conditioner use and street crime example). Nonetheless, it is helpful to see whether they correlate together and what the strength of the correlation is. The reason is that if they don’t correlate at all or if the correlation is very weak, then we can say with confidence that they don’t cause each other.

To understand, we need to look at the following reasoning: when one thing causes another thing, they must occur together in some demonstrable way; if, however, when one thing occurs, another thing may or may not occur, they have no relationship to each other and so we cannot say that there is a causal relationship. A causal relationship presupposes a correlational relationship. Now, as we have said before, a correlational relationship is not enough to demonstrate a causal relationship, but to have a causal relationship, there at least has to be a correlational relationship. We have to at least be in the right ballpark, as it were. Without a correlational relationship, though, we can say with much greater confidence that we are not even in the right (i.e., causal) ballpark. In other words, if we find no correlation, we can safely assert that there is no causal relationship.

A similar, albeit slightly different logic holds with weak correlations – the situation in which two things go together in some minimal ways. With such correlations, we can say that there may be a causal relationship between the variables, just as we said with strong correlations, but we can’t know for sure because correlation doesn’t imply causation. Now, with weak correlations, however, we can go a step further. We can assume that even if there was a causal relationship between the two variables, we know that there has to be more to the picture than simply the two weakly correlated variables. In other words, there has to be additional causal variables coming into play, because if there weren’t the correlation would have to be strong. The weak correlation, even in cases where we might assume a causal relationship, shows that the variable is only part of the cause – and only a small part at that.

It would be helpful to take an example. Let’s suppose that we did a study of the relationship between the presence of eating utensils and cookware in the kitchen on the one hand and how much food people ate on the other hand. In a sample of 1,000 people, we measured a) the extent to which they had eating utensils and cookware in the kitchen and b) how much they ate on average over the course of a month. Let’s further suppose we found a weak, statistically significant, relationship between our two variables of interest. It’s a fantastical example, of course, but we might see how it could be true: the presence of eating utensils and cookware could play some small role in how much you ate on average – if you don’t have a way to prepare and eat food, it could affect how much you eat. However, we can also immediately see that there’s more to the picture in terms of what goes into the fact of how much food people eat. The extent to which you have ways to prepare and eat food are not the only variables that can lead to eating a little or a lot. People can eat raw foods; they can eat with their hands; they can buy prepared foods in the grocery store, delis, and fast food restaurants; they can go out to eat in sit-down restaurants; and so on. Personal characteristics of the people can also play a role: how hungry they are or how much stress they are under or how busy they are can also affect how much people eat – even in people who don’t have adequate means to prepare food. In all these ways, we can see that a weak, statistically significant, correlational relationship cannot explain the whole nature of the relationship between two variables, even when we assume that they are in some ways causally related.

As we will see in the following review of the correlational research on degenerative disc disease and chronic back or neck pain, degenerative changes of the spine fit into one of these two categories: they either have no relationship at all with chronic back or neck pain, or they are only weakly related to chronic back or neck pain. As such, we can conclude with confidence one of two things, depending on the type of degenerative disc disease we are discussing. First, in the case where research repetitively shows no correlational relationship between certain types of degenerative disc disease and chronic back or neck pain, these particular types of degenerative changes do not cause pain, despite the common belief that they do. Second, in the case where research repetitively shows a weak, statistically significant, correlational relationship between certain types of degenerative disc disease and chronic back or neck pain, these particular types of degenerative disc disease may play some role in producing pain, but we know that it is only a minimal role, even if we assume that the correlation reflects a causal relationship. In other words, the weak correlation between certain types of degenerative disc disease and pain shows that the lion’s share of what’s causing the pain is something else entirely. This statement too stands in stark contrast to the common belief that degenerative disc disease is the predominant cause of chronic back or neck pain.

Let’s, then, review the correlational research on the relationship between the different types of degenerative disc disease and chronic back or neck pain.

Correlation (or lack thereof) between pain and degenerative disc disease

In a review of early studies, van Tulder, at al., (1997) found weak significant associations between back pain and disc space narrowing, Image by Tsunami Green Courtesy of Unsplashosteophytes, and sclerosis, with odds ratios in the range of 1.2-3.3. Other degenerative changes, such as spondylosis, spondyolisthesis, and kyphosis had no relationship to back pain.

In their review of the literature on the natural history and clinical significance of disc herniation, Grande, Maus, and Carrino (2012) conclude that there is no relationship between any characteristics of disc herniation, including size or severity, and subsequent symptoms of patients.

Mitra, Cassar-Pullicino and McCall (2004) found no relationship between evidence of an annular tear in the disc and pain.

Jarvinen, et al., (2015) found no significant correlation between Modic 1 or Modic 2 changes and low back pain.

de Schepper, et al., (2010) studied the relationship between osteophytes, disc space narrowing, and low back pain. They found that disc space narrowing, especially, at more than one level, was most significantly related to low back pain, but only weakly, with an odds ratio of 2.4.

In a more statistically oriented review, Chou, et al, (2011), systematically searched the literature and combined studies to determine the odds ratio for having lumbar degenerative changes and chronic low back pain. They found a significant, yet weak, association between the two. The range for the odds ratio was between 1.8-2.8.

Livshits, et al., (2011) found a significant relationship between all degenerative changes of the spine and pain with an odds ratio of 3.2.

In a study published after the Chou, et al. findings, Nemoto, et al., (2012) found a significant correlation between vertebral osteophytes and low back pain, but the odds ratio was a little greater at 3. In contrast to the de Schepper, et al, study cited above, they found no correlation between disc space narrowing and back pain.

All these data are what likely led Bogduk (2012), one of the founding fathers of interventional pain management, to conclude, “Degenerative changes [of the spine] lack any significant correlation with spinal pain.”

These findings are also similar to the relationship between degenerative disc disease and pain related disability. Quack, et al., (2007) found either no relationship or only weak correlations between lumbar degenerative changes and mobility. Sirvanci, et al., (2008), found no significant relationship between lumbar spinal stenosis and perceived disability, as measured by the Oswestry Disability Index. Lohman, et al., (2006) found no relationship between spinal stenosis and pain or scores on the Oswestry Disability Index. Remes, et al., (2005) in a cohort of patients who underwent fusion for spondylolisthesis twenty years ago, found no relationship between lumbar degenerative changes and the same measure of disability. Similarly, looking at a number of biological and lifestyle factors, Wilkens, et al., (2013) found that degenerative changes as found on imaging failed to correlate with perceived disability one year later as measured by the Roland-Morris Disability Questionnaire.


This review of the literature shows that the various types of degenerative disc disease either have no relationship to pain and disability or only a weak correlation to pain and disability. What this means is that degenerative disc disease is likely not painful. At best, it plays a minimal role in the cause of chronic back or neck pain. The true cause of chronic back or neck pain must be something else entirely.

For more information on degenerative disc disease, please see the previous blog post and the Institute for Chronic Pain content pages on Degenerative Disc Disease and Whatever Happened to Backache?


Bogduk, N. (2012). Degenerative joint disease of the spine. Radiology Clinics of North America, 50(4), 613-628. doi: 10.1016/j.rcl.2012.04.012

Chou, D., Semartzis, D., Bellabarba, C., Patel, A., Luk, K., Kisser, J. M., & Skelly, A. C. (2011). Degenerative magnetic resonance imaging changes in patients with chronic low back pain: A systematic review. Spine, 36, S43-S53. doi: 10.1097/BRS.0b013e31822ef700

Del Grande, F., Maus, T. P., & Carrino, J. A. (2012). Imaging the intervetebral disk: Age-related changes, herniation, and radicular pain. Radiology Clinics of North America, 50(4), 629-649. doi: 10.1016/j.rcl.2012.04.012

de Schepper, E., Damen, J., van Meurs, J. B., Ginai, A. Z., Popham, M., Hofman, A., Koes, B. W., & Bierma-Zeinstra, S. M. (2010). The association between lumbar disc degeneration and low back pain: The influence of age, gender, and individual radiographic features. Spine, 25(5), 531-536. doi: 10.1097/BRS.0b013e3181aa5b33

Jarvinen, J., Karppinen, J., Niinimaki, J., Haapea, M., Gronblad, M., Luoma, K., & Rinne, E. (2015). Associations between changes in lumbar Modic changes and low back symptoms over a two year period. BMC Musculoskeletal Disorder, 16, 98. doi: 10.1186/s12891-015-0540-3

Livshits, G., Popham, M., Malkin I., Sambrook, P. M., MacGregor, A. J., Spector, T., & Williams, F. M. (2011). Lumbar disc degeneration and genetic risk factors are the main risk factors for low back pain in women: The UK twin spine study. Annals of Rheumatic Disease, 70(10), 1740-1745. doi: 10.1136/ard.2010.137186

Lohman, C. M., Tallroth, K., Kettunen, J. A., & Lindgren, K. (2006). Comparison of radiologic signs and clinic symptoms of spinal stenosis. Spine, 31(16), 1834-1840.

Maus, T. (2010). Imaging the back pain patient. Archives of Physical Medicine and Rehabilitation, 21(4), 725-766. doi: 10.1016/j.pmr.2010.07.004

Mitra, D., Cassar-Pullicino, V. N., & McCall, I. W. (2004). Longitudinal study of high intensity zones on MR of lumbar intervetebral discs. Clinical Radiology, 59(11), 1002-1008.

Nemoto, O., Kitada, A., Naitou, S., Tsuda, Y., Matsukawa, K., & Ukegawa, Y. (2012). A longitudinal study for incidence of low back pain and radiological changes of lumbar spine in asymptomatic Japanese military young adults. European Spine Journal, 22, 453-458. doi: 10.1007/s00586-012-2488-4

Quack, C., Schenk, P., Laeubil, T., Spillmann, S., Hodler, J., Michel, B. A., & Klipstein, A. (2007). Do MRI findings correlate with mobility tests? An explorative analysis of the test validity with regard to structure. European Spine Journal, 16(6), 803-812.

Remes, V. M., Lamberg, T. S., Tervahartiala, P. O., Helenius, I. J., Osterman, K., Schlenzka, D., Yrjonen, T., Seitsalo, S., & Poussa, M. S. (2005). No correlation patient outcome and MRI findings 21 years after posterior or posterolateral fusion for isthmic spondylolisthesis in children and adolescents. European Spine Journal, 14(9), 833-842.

Sirvanci, M., Bhatia, M., Ganiyusufoglu, K. A., Duran, C., Tezer, M., Ozturk, C., Aydogan, M., & Hamzaoglu, A. (2008). Degenerative lumbar spinal stenosis: Correlation with Oswestry Disability Index and MR imaging. European Spine Journal, 17(5), 679-685. doi: 10.1007/s00586-008-0646-5

van Tulder, M. W., Assendelft, W. J., Koes, B. W., & Bouter, L. M. (1997). Spinal radiographic findings and nonspecific low back pain: A systematic review of observational studies. Spine, 22(4), 427-434.

Wilkens, P., Scheel, I. B., Grundes, O., Hellum, C., & Storheim, K. (2013). Prognostic factors of prolonged disability in patients with chronic low back pain and lumbar degeneration in primary care: A cohort study. Spine, 38(1), 65-74. doi: 10.1097/BRS.0b013e318263bb7b

Author: Murray J. McAllister, PsyD

Date of publication: 5-31-2015

Date of last modification: 3-27-2021

]]> (Murray J. McAllister, PsyD) Degenerative Disc Disease Sun, 30 Mar 2014 20:49:01 +0000
Back Pain

What is chronic back pain?

Back pain affects most everyone at some point. At any given time, 25% of the population will have had low back pain in the previous three months. It is one of the most common reasons for medical visits.1, 2 Fortunately, the vast majority of cases of new back pain will resolve within a few weeks to months.3 

Some people have back pain that does not go away. Back pain is considered chronic when it lasts longer than six months. Chronic low back pain affects about 10% of the population.4 It is one of the most common reasons for disability. Additionally, among all health conditions, back pain is one of the highest costs to the healthcare system.5, 6 

Despite these alarming statistics, it is important to recognize that most people with chronic back pain live well and do not seek healthcare for it on a regular basis. Roughly, three quarters of people with chronic back pain fit this description.7 They are neither distressed nor impaired enough to seek care for it. Or, they recognize that medical options for chronic back pain are limited and not very effective. So, they self-manage their chronic back pain. Either way, it is possible to self-manage chronic back pain and live well enough to have no need to seek care for it. In fact, the majority of people with chronic back pain are not seeking care for it.

Common causes of back pain are varied. Broadly speaking, the many common causes of back pain can be divided into three categories: muscular, orthopedic, and nervous. Muscle strain and tears can cause back pain. Degenerative changes of the spine are commonly thought to cause pain. Changes in the nervous system, commonly referred to as central sensitization, can also cause pain. Less common causes of back pain are spinal fractures, infection and cancer.

It is often difficult to know the cause of back pain in an individual case. There are no examinations or tests that can definitively prove a cause of pain for any of the three most common categories of causes mentioned above.

Take, for example, orthopedic causes of back pain. CT or MRI scans are commonly used to identify degenerative changes of the spine as possible causes of back pain. When found, it is easy to assume that these findings provide a definitive diagnosis of the cause. However, most healthcare providers know that the research does not support this assumption.

To understand this point, it is helpful to know something about how science goes about finding a cause of pain in general. In order to find a cause of pain, scientific inquiry tries to find something that is unique to those who have pain and which subsequently differentiates those who have pain from those who do not have pain. Findings of degenerative changes of the spine on MRI or CT scans are not unique to patients with back pain in this way. Numerous studies consistently show that people without back pain have degenerative changes of the spine at just as high a rate or higher than people with back pain.8, 9, 10 There currently is no way of knowing what differentiates degenerative changes of the spine that are painful from those that are not painful. Another possibility is that there is no difference and the findings of degenerative changes of the spine on MRI or CT scans are simply irrelevant. There is currently no test that can tell for certain.

As such, in the individual case, it is difficult to know what is causing pain, even if an MRI or CT scan shows degenerative changes of the spine. Are these changes relevant to the patient’s pain when we know that people without back pain are likely to have the same findings? Healthcare providers don’t ultimately know.

Is there a cure for chronic back pain?

In the absence of a known cause, healthcare providers and their patients often proceed through various therapies and procedures on a trial-and-error basis. There are many common treatments for chronic back pain:

  • Anti-inflammatory medications
  • Muscle relaxant medications
  • Antidepressant medications (used for pain)
  • Anticonvulsant medications (used for pain)
  • Opioid, or narcotic, medications
  • Chiropractic care
  • Physical therapy
  • Cognitive behavioral therapy
  • Epidural steroid injections
  • Rhizotomy
  • Back surgeries – laminectomies, disctectomies, and fusions
  • Implantable pain control devices – spinal cord stimulators and intrathecal drug delivery devices (aka, “pain pumps”)
  • Chronic pain rehabilitation programs

Many of these therapies and procedures have been shown in research to be effective in reducing pain and increasing functioning. However, in this regard, effective does not mean curative. Unfortunately, there are no known cures for chronic back pain.

Therapies & procedures for chronic back pain

In 2007, the American College of Physicians and the American Pain Society developed clinical practice guidelines for chronic back pain.11 They determined that providers should first recommend self-management for patients with back pain. Moreover, they recommended that healthcare providers educate patients on how to self-manage back pain. They do not recommend the use of immediate CT or MRI scans for back pain unless there is evidence of severe neurological problems or evidence of other severe conditions like cancer or infection. If back pain continues and becomes chronic, they recommend the use of medications and chronic pain rehabilitation therapies.

In terms of medications, they note that even the most effective medications only moderately reduce pain. They recommend the use of acetaminophen and non-steroidal anti-inflammatory medications first. If these fail to reduce pain, they recommend using tricyclic antidepressant medications. They note that these three classes of medications have the most and highest quality evidence supporting their effectiveness. They also note that the poor quality of evidence for the use of opioid and anticonvulsant medications.12 

In terms of chronic pain rehabilitation therapies, they recommend the use of exercise, cognitive behavioral therapy, and chronic pain rehabilitation programs (which put the two previous types of therapies together in a coordinated fashion).

The clinical practice guidelines recommend MRI or CT scans and possible referral for surgical evaluation only if patients meet two criteria: a) when patients fail to progress from the above-mentioned treatments and b) they show evidence of neurological problems, such as referred pain.

It is important to recognize that the order of these recommendations reflect the likelihood of their being effective. That is to say, based on the available research evidence, the first recommendation is the one that is most likely to be helpful, the second recommendation is the second most likely to be helpful, the third is the third most likely to be helpful, and so on.

It is also important to recognize how often these guidelines do not get followed in actual practice.13 While many patients have acetaminophen and non-steroidal anti-inflammatory medications recommended to them, most patients do not get tricyclic antidepressant medications, exercise, cognitive behavioral therapy, or chronic pain rehabilitation programs recommended to them. When they do, it is only after they have undergone MRI or CT scans and have tried multiple interventional and surgical procedures, all of which have either poor quality research supporting their effectiveness or are known to be less effective.


1. Deyo, R. A., Mirza, S. K., & Martin, B. I. (2006). Back pain prevalence and visit rates: Estimates from U. S. national surveys, 2002. Spine, 31, 2724-277.

2. Hart, L. G., Deyo, R. A., & Cherkin, D. C. (1995). Physician office visits for low back pain: Frequency, clinical evaluation, and treatment patterns from a U. S. national survey. Spine, 20, 11-19.

3. Andersson, G. B. (1999). The epidemiologic features of chronic low back pain. Lancet, 354, 581-585.

4. Freburger, J. K., Holmes, G. M., Agans, R. P., Jackman, A. M., Darter, J. D., Wallace, A. S., Castel, L. D., Kalsbeeck, W. D., & Carey, T. S. (2009). The rising prevalence of chronic low back pain. Archives of Internal Medicine, 169, 251-258.

5. Agency for Healthcare Research and Quality. (2009). Total expenses and percent distribution for selected conditions by type of service: United States, 2009. Washington DC: Government Printing Office. 

6. Center for Disease Control. (2009). Prevalence and most common causes of disability among adults – United States, 2005. Washington DC: Government Printing Office. Retrieved from

7. Cote, P., Cassidy, J. D., & Carroll, L. (2001). The treatment of neck and low back pain: Who seeks care? Who goes where? Medical Care, 39, 956-967.

8. Jensen, M. C., Brant-Zawadzki, M. N., Obuchowski, N., Modic, M. T., Malkasian, D., Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without back pain. New England Journal of Medicine, 331, 69-73.

9. Powell, M. C., Szypryt, P., Wilson, M., Symonds, E. M., & Worthington, B. S. (1986). Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women. The Lancet, 328, 1366-1367.

10. Takatalo, J., Karppinen, J., Niinimaki, J., Taimela, S., Nayha, S., Jarvelin, M. R., Kyllonen, E., Tervonen, O. (2009). Prevalence of degenerative imaging findings in lumbar magnetic imaging among young adults. Spine, 34, 1716-1721.

11. Chou, R., Aseem, A., Snow, V., Casey, D., Cross, T., Shekelle, P., & Owens, D. K. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147, 478-491.

12. Chou, R., & Huffman, L. H. (2007). Medications for acute and chronic low back pain: A review of the evidence for an American Pain Society/American College of Physicians clinical practice guideline. Annals of Internal Medicine, 147, 505-514.

13. Carey, T. S., Freburger, J. K., Holmes, G. M., Castel, L., Darter, J., Agans, R., Kalsbeek, W., & Jackman, A. (2009). A long way to go: Practice patterns and evidence in chronic low back care. Spine, 34, 718-724.

Date of publication: April 27, 2012

Date of last modification: October 23, 2015

]]> (Murray J. McAllister, PsyD) Common Conditions Fri, 27 Apr 2012 13:36:07 +0000