In Pursuit of Pathology

I have recently attended a couple of seminars that have mentioned how newer and better MRI units will begin to be used in the attempt to identify pathology in patients with musculoskeletal pain.

Now this sounds a fantastic and a worthwhile cause, especially if it enables us to identify symptomatic pathology in a patient population which can then lead towards a successful treatment (finding a successful treatment being an entirely separate issue by the way!).

I do however wonder if the findings from newer and more advanced imaging procedures will actually help us as at all. I ponder this because when we look into studies on asymptomatic patients we consistently see that many of the “bad and nasty” findings on scans are actually common to see in pain free normally functioning people. Even elite athletes!! Many findings are also not related to pain and disability! There are numerous examples in the literature in relation to this topic, but here are a few I dug up quickly:

“Professional pitchers develop degenerative changes over time in both the shoulder and elbow of their dominant (pitching) arm due to chronic repetitive stresses placed across the joints. These findings do not predict time spent on the Major League Baseball disabled list”. Wright et al (2007)

“Asymptomatic shoulder abnormalities were found in 96% of the subjects. Ultrasound showed subacromial-subdeltoid bursal thickening in 78% of the subjects, acromioclavicular joint osteoarthritis in 65%, supraspinatus tendinosis in 39%, subscapularis tendinosis in 25%, partial-thickness tear of the bursal side of the supraspinatus tendon in 22%, and posterior glenoid labral abnormality in 14%. Girish et al (2011)

“We conclude that unenhanced magnetic resonance imaging of the shoulder in asymptomatic high performance throwing athletes reveals abnormalities that may encompass a spectrum of “nonclinical” findings”. Miniaci et al (2002)

“Magnetic resonance images of asymptomatic participants revealed abnormalities in 73% of hips, with labral tears being identified in 69% of the joints”. Register et al (2012)

“MRI findings of disc protrusion, nerve root displacement or compression, disc degeneration, and high intensity zone are all associated with LBP, but individually, none of these abnormalities provides a strong indication that LBP is attributable to underlying pathology. This limits their value in refining epidemiological case definitions for LBP”. Endean et al (2011)

“High prevalence of ‘abnormal’ findings on MRI in pain-free populations (disc degeneration [91%], disc bulges [56%], disc protrusion [32%], annular tears [38%])”. McCullough et al (2012)

“The association between severe Disc Degeneration (DD) and LBP ceases to be significant when adjusted for Modic Changes and disc protrusion/hernia. These results do not support DD as a major cause of chronic LBP”. Kovacs et al (2014)

“……vertebral endplate changes are not associated with chronic LBP”. Kovacs et al (2012)

“An MRI total score (0-10) for findings was calculated for Modic type I and/or II changes, a posterior high intensity zone in the disc, dark/black nucleus pulposus signal, and ≥40 % disc height decrease. We analyzed the relationship of the MRI total score to the Oswestry Disability Index (ODI) and LBP intensity scores using multiple linear regression and adjusting for age, gender, body mass index, smoking, and anxiety/depression. The combined MRI findings were not related to the degree of disability or the intensity of LBP. These degenerative MRI findings cannot explain variation in pre-treatment disability and pain in patients with chronic LBP accepted for disc prosthesis surgery”. Berg et al (2013)

“MRI performed at 1-year follow-up in patients who had been treated for sciatica and lumbar-disk herniation did not distinguish between those with a favorable outcome and those with an unfavourable outcome. A favorable clinical outcome was defined as complete or nearly complete disappearance of symptoms at 1 year”. el Barzouhi et al (2013)

“Tendon pain remains an enigma. Many clinical features are consistent with tissue disruption (the pain is localised, persistent and specifically associated with tendon loading), whereas others are not (investigations do not always match symptoms and painless tendons can be catastrophically degenerated). As such, the question ‘what causes a tendon to be painful?’ remains unanswered”. Rio et al (2014)

“The results of this study suggest that, although some Whiplash Associated Disorders patients are more likely to suffer from long-lasting neck pain, MRI findings cannot explain the symptoms”. Matsumoto et al (2010)

“While Modic changes became more common in whiplash patients in the 10-year period after the accident, they occurred with a similar frequency in control subjects. We did not find any association between Modic changes and the nature of the car accident in which the whiplash occurred. Modic changes found in whiplash patients may be a result of the physiological ageing process rather than pathological findings relating to the whiplash injury”. Matsumoto et al (2013)

This study demonstrated that progression of degenerative changes of the cervical spine on MRI was not associated with clinical symptoms during the 10-year period after whiplash injury. Ichihara et al (2009)

“The number of levels of cervical degeneration and the severity of degeneration in the discs, facets, and uncovertebral joints are not related to the levels of pain and disability” Peterson et al (2003)

“Full-thickness focal chondral defects in the knee are more common in athletes than among the general population. More than one-half of asymptomatic athletes have a full-thickness defect. Further study is needed to define more precisely the prevalence of these lesions in this population”. Flanigan et al (2010)

Let me clarify!!!

Now I am sure some of you will accuse me of bias (aren’t we all to some degree?) but before you do that let me make a couple of points:

1. I AM NOT SAYING THAT THE ABOVE FINDINGS CANNOT BE SYMPTOMATIC. I am sure they are in some patients and I am sure there is literature available suggesting this. Out of interest the ability to be able to diagnose many of these structures as a source of pain (with clinical tests) is highly debatable. Please see some of my other posts for information relating to clinical tests for the Hip, Knee Meniscus, Patellofemoral Pain, Shoulder and the Spine.
2. What I am trying to point out is that if these types of findings can be asymptomatic in normally functioning people then:
   1. WHY SHOULD OUR PATIENTS WITH SIMILAR FINDINGS NOT BE ABLE TO BECOME PAIN FREE WITH CONSERVATIVE MANAGEMENT? The “scan findings” should have little bearing on them becoming pain free or not. Surely a trial of conservative treatment should be undertaken before proceeding to more invasive treatment options.
   2. We should be very mindful of creating or contributing to incorrect beliefs relating to findings on our patients scans. In my clinical practice I see many patients that have INCORRECT BELIEFS related to their scans based on their own thoughts, beliefs of family and friends, and/or beliefs of their health care providers! Given what we can see above we should be re-assuring patients that pain free, highly functioning people also have these findings. This in turn will greatly minimise the likelihood of development of factors such as Fear of using the injured area. Fear and Fear Avoidance, amongst other factors, are significant predictors of poor outcome and development of chronicity. Please also see this and this for further information relating to poor prognostic factors.

So I hope that in the future that there is some better way of diagnosing actual symptomatic pathology, but that needs to be balanced with comparisons of asymptomatic patients. That way we shouldn’t have any false starts.

Thanks for reading.