Do brain changes really contribute to persistent low back pain?

If you’ve recently attended a pain conference, had a glass of wine with a pain boffin or spent time googling ‘pain’ you’ve no doubt come across the terms ‘neuroplasticity’ and ‘central sensitization’. These buzzwords are increasingly used to describe biological changes that might contribute to persistent low back pain. But do they really explain why some people get better after hurting their back while others do not?

An increasing body of work suggests the brain is involved when pain becomes persistent. Researchers have shown substantial anatomical and functional reorganisation of the human brain (‘neuroplasticity’) and increased sensitivity of neurons in the brain and spinal cord (‘central sensitisation’) [see a few examples here (1-3)]. Importantly, because these changes have the ability to maintain pain after the initial injury has resolved they are widely believed to explain, at least in part, why pain becomes persistent(4). But – if this is the case then why can’t we predict who will develop persistent back pain and who will not?

Two major limitations hamper our ability to predict outcome in low back pain. First, although it is clear that brain organisation is altered in persistent low back pain, and these changes appear to relate to symptoms, the literature mostly consists of studies that use a cross-sectional design. In other words, there are lots of studies that examine people with persistent back pain at a specific point in time. There has been very limited e.g.(5) investigation of brain changes in the transition from acute to persistent low back pain – which is precisely when some people are getting better while others are not. Second, a range of other mechanisms (such as genetics, psychosocial factors, hormones) are all likely to interact with brain changes to predict who will develop persistent low back pain and who will not. But the interaction between these different pieces of the low back pain puzzle has not been examined during the transition from acute to persistent pain.

To answer these important questions, we recently received a National Health and Medical Research Council (NHMRC) Project Grant to follow more than 260 people with acute low back pain as they either i) get better or ii) develop persistent pain. Over a period of 12 months we will examine changes in the brain, spinal cord, genetics, hormones and psychosocial factors of each individual to determine whether these factors, and their possible interaction, can predict who gets better after hurting their back and who does not.  We hope that the results of our study will have an impact on the way we understand, treat and perhaps even prevent the transition to persistent low back pain in the future.

Passionate about pain and the brain? Want to contribute to our understanding of why some people get persistent back pain while others do not? Join our team!

We are looking for two highly motivated individuals to undertake full-time PhD scholarships (fully funded for 3 years) and one exceptional post-doctoral researcher (fully funded for 4 years). You will join active research groups at University of Western Australia and Neuroscience Research Australia, benefiting from engagement with top researchers in the fields of brain plasticity and pain. You will gain skills and knowledge in transcranial magnetic stimulation to measure neuroplasticity in the human brain, neuronavigation, phlebotomy, central sensitisation and the transition from acute to chronic low back pain. For more information or to apply, please send a CV to s.schabrun@uws.edu.au.

About Siobhan Schabrun

Siobhan M SchabrunSiobhan is a NHMRC Clinical Research Fellow and 2014 Fulbright Scholar at University of Western Sydney. After blending a degree in physiotherapy with a PhD in neuroscience, she is passionate about understanding, treating and preventing persistent pain. Her research has a particular focus on that buzzword… ‘neuroplasticity’. Siobhan was the winner of the inaugural Australasian Brain Stimulation Conference joke contest – which says something about her sense of humour… You can find her published research here.

References

1.  Flor H, Braun C, Elbert T, & Birbaumer N (1997). Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neuroscience letters, 224 (1), 5-8 PMID: 9132689

2. Tsao H, Danneels LA, & Hodges PW (2011). ISSLS prize winner: Smudging the motor brain in young adults with recurrent low back pain. Spine, 36 (21), 1721-7 PMID: 21508892

3.  Tsao H, Galea MP, & Hodges PW (2008). Reorganization of the motor cortex is associated with postural control deficits in recurrent low back pain. Brain, 131 (Pt 8), 2161-71 PMID: 18669505

4.  Apkarian AV. The brain in chronic pain: clinical implications. Pain Manag. 2011;1:577-86.

5.  Baliki MN, Petre B, Torbey S, Herrmann KM, Huang L, Schnitzer TJ, Fields HL, & Apkarian AV (2012). Corticostriatal functional connectivity predicts transition to chronic back pain. Nature neuroscience, 15 (8), 1117-9 PMID: 22751038

Comments

  1. Healed in an instance.

    Talking about comforting and Quotes
    “Each galaxy, star, or person is the temporary owner of particles that have passed through the births and deaths of entities across vast reaches of time and space. The particles that make us have traveled billions of years across the universe; long after we and our planet are gone, they will be a part of other worlds.”

  2. John Quintner says:

    Marcel, I think it was Carl Jung who remarked “only the wounded physician can heal.” Does this console you?

  3. John,
    In answer to your question: the pain one feels is the same, however I am biased to say it decreases in time. I am PT and besides that “my own patient” as well. So from an experience point of view I know how it feels. That is if you believe frozen shoulder for 1.5 years fits the term “chronic” pain.
    Another question I ask myself is how would my knowledge of pain neuroscience influence ie. modulate nocicepsis, I try a different way of soeech: explain pain edu. is believed to downregulate the treath value and decrease pain in patients but what about the educator when he starts to experiemce painfull problems is there a decrease to start with or would that decrease come (if it comes) in a later fase?

  4. John Quintner says:

    Marcel, in endeavouring to answer your question on the transition of pain from acute to chronic, may I pose this question? From the viewpoint of the sufferer, does acute pain feel different to chronic pain? I suspect that the experience is much the same at various points along the time course.

  5. Jennifer Gait says:

    This is Dr Fricton’s e-mail. frict001@umn.edu

  6. Hi Jennifer, I like to email them on international accreditation but see no general email adress do you have it?

    Thanks

  7. Jennifer Gait says:

    I am looking forward to it as well. I e-mailed Dr. Fricton and asked if neuroplasticity would be included in the discussion, and he said it was the whole focus of the course. So I think it unlikely that trigger points will be put forth as a cause of chronic pain.

  8. John Quintner says:

    Jennifer, I have duly enrolled but the course does not commence until May 2014. I hope that Dr Fricton does not still support the scientifically implausible “trigger point” construct. There are some in the field of musculoskeletal medicine who view these nebulous lesions (with poor inter-observer reliability) as being “pain generators” that are responsible not only for localized pain but also for more widespread pain syndromes. This then gives them license to launch unlimited “search and destroy” operations upon innocent muscles. That there is no scientific evidence of muscle damage nor any positive outcome data for dry or wet needling do not sway them from their self-appointed task. Anyway, I will await with interest the commencement of the course.

  9. John Barbis says:

    Dear Siobhan,
    Nobel attempt that needs to be done. It appears, however, that you are making the assumption that- if LBP persists, it must be from a centrally mediated source. This assumption seems to negate the possibility that there can be persistent nociceptive generators or triggers of low back pain. I think this approach can be as misleading to clinicians as those who assume all LBP is nociceptive or mechanical in origin. In the evaluation of factors that could be influencing factors (genetics, psychosocial factors, hormones) in your study, the failure to consider nociceptive factors that could be influencing or driving the brain findings is a concern to me. I know that “gold standard” level criteria for identifying specific nociceptive generators for LBP (and other musculoskeletal problems) are controversial, but so is the interpretation (or over interpretation) of fMRI data for the brain and pain.

    i applaud your work and efforts. this work needs to be done; but I have concerns when we take a complex physical phenomena, like persistent pain, and try to present it as simple entity that can be comfortably fitted into mechanical nociceptive, neuropathic nociceptive, or centrally mediated boxes. For effective patent management we need to be more discerning. I hope your work can help us lead to that discernment rather than be used as evidence to support a pre ordained proposition. Good luck. Johnb

  10. Jennifer Gait says:

    John,

    Then you may be interested in taking the free on-line Coursera course
    Preventing Chronic Pain: A Human Systems Approach! led by Dr. James Fricton, President of the International Myopain Society previously on the board of the American Pain Society and American Academy of Orofacial Pain, and previously Pain Specialist, at the Minnesota Head and Neck Pain Clinic. In his description of the course he notes the considerable burden of ongoing suffering that chronic pain and its treatments place upon the individual, and goes on to say:

    By using a human systems approach, we can better understand how individual risk factors in the cognitive, behavioral, physical, emotional, spiritual, social, and environmental realms of our lives can interact to perpetuate chronic pain and, if improved, can prevent it.

    During this course, you will: Identify the problems of our health care system in dealing with chronic pain. Review the diagnosis, mechanisms, and etiology of musculoskeletal pain conditions. Explore specific risk factors that can contribute to chronic pain. Learn how a human systems approach can be applied through evidence-based self-management strategies to prevent chronic pain. Experience active strategies designed to enhance the protective factors that can transform our own lives, and those of our patients, to one of health and wellness.

    The course is for everyone so the material won’t be taxing, but I am looking forward to hearing about the strategies he suggests. Having had chronic pain for several years, then releasing it when I realized how I was causing it I agree that it is a trajectory. You can’t tell from day 1 of acute pain who will get chronic pain and who won’t, because its what people focus on and do once they have pain, rather than how badly they were injured or where, that determines who will go on to recover and who won’t.

    Anyway, if anyone is interested in the course, go to https://www.coursera.org/course/chronicpain

  11. June Trenholm says:

    I’ve been listening to the candidates for the Canadian Pain chair and a conference on Pain and Addictions. There is a strong suggestion that some changes may start with early life events, e.g. peri-natal experiences. Other life events including ones leading to PTSD are stong suggestions. Conditions like ADHD which is associated with increased muscle tone may also be a risk factor. You can perhaps check out the work of Javeria Ali Hashmi and Loren Martin and Marsha Campbell Yeo.
    When I read the job description for the PhD scholarships I can’t help but feel so envious of whoever qualifies for them. I’m so glad this type of work is happening and hopefully I will be around to pass the benefits along to my patients.

  12. That is a great point John, is there such a thing as transition from acute to chronic?
    Do you think that “chronicity” or length of a pain experience starts at maybe day one?

  13. Jukka Aho says:

    Hi everyone!
    I agree with John about the importance of being able to predict the possible course of back pain as early as possible. However, I do think that this is a very good subject for research and find this particularly fitting for the patients I see at my clinic. The most acute episodes of LBP in Finland rarely make it to physiotherapy before the problem has resolved itself or they are already in the sub-acute stage. To know more about the transition (or what ever name one might use for it) from acute to chronic will help us understand the aspects surrounding ones LBP episode. Through knowledge, we’ll be able to better design trials and plan treatment interventions to all groups of LBP (acute, sub-acute, chronic in all of their colours).

    Good luck to your study and I’ll be waiting for the outcomes with much interest!

  14. Lesley Singer says:

    I think this is a great idea. good luck finding the right people and I will love reading about it when it is done. we need to prevent acute pain from becoming chronic as we don`t do so well curing it.

  15. John Quintner says:

    Siobhan, I find the idea of there being a “transition” from acute to chronic pain hard to support. A more useful research question might be whether (or not) we can predict from day one the trajectory of the pain experience in the individual patient.