Low back problems are a necessary evil of being human due to our anatomy and physiology. This is of great importance in many medicolegal claims in which an injury or repetitive stress exposure is alleged to have caused low back problems, thereby attempting to shift responsibility for the costs imposed by low back problems from the individual and his or her health insurance (if applicable) to the liability policyholder/employer and the liability/workers compensation insurance carrier. The high prevalence of low back problems in the general population makes differentiating between idiopathic problems and those caused by an accident or repetitive stress exposure extremely difficult. It is also complicated by the fact that the idea of a manifestation of a preexisting condition is at odds with our folk understanding of temporal proximity and causality, i.e. if two things happen near in time, we tend to assume they are causally related, with the first thing causing the second thing.
Human beings perform many cognitive tasks exceptionally well. Accurately assigning causation is not one of them. In particular, we are prone to making a priori assumptions about how things work and then confirming our assumptions (confirmation bias) post hoc (post hoc ergo propter hoc fallacy). Low back pain is a notable example: we often associate low back pain with lumbar disc pathology discovered on post-injury MRI despite the fact that we know from the medical literature large percentages of the general population have similar MRI findings but no low back pain. We make the assumption based on our assessment of human anatomy and physiology that lumbar discs work in a certain way and when they are compromised it must cause discernible effects such as low back pain. We then see evidence of compromised lumbar discs in persons who complain of low back pain following an injury or exposure and we leap to the bias-confirming post hoc conclusion that the pathology or compromised condition is causing the pain. So strong is this impulse that we ascribe causation even though we are well-aware of the medical literature demonstrating that disc pathology is an exceedingly poor proxy for low back pain. The coup de grace of this faulty reasoning is the post hoc association between disc pathology and pain: physicians will regularly conclude that a specific event or long term exposure caused a herniated disc despite the person being in a population cohort in which it is at least as likely than not that herniated disc was present before the injury or exposure. The only reasonable way one could reach this conclusion is with a pre-injury MRI showing there was not a herniated disc.
The problem with this sort of faulty reasoning is that it can lead to treatment that is extraordinarily expensive but ineffective. In a low back pain claim with post-injury evidence of a herniated disc, the treatment is often a discectomy/laminectomy with or without fusion. If the herniated disc was not causing the pain, the surgery will have been unnecessary. While the placebo effect will almost certainly result in some short term improvement, the long term outcomes are likely to be, at best, no different than they would have been with conservative therapy because the treatment will have been aimed at discal pathology that was benign. The triers of fact in the medicolegal systems will, however, require the workers compensation or liability carriers to absorb the costs of surgery, including non-medical costs that are recoverable under the different systems (such as indemnity payments in worker’s compensation or wage loss and pain and suffering in personal injury), because they are likely to believe the opinion that the herniated disc is the problem. This belief is based on the folk (mis)understanding of cause and effect.
There is an expression in statistics that has been borrowed by cognitive psychologists: regression to the mean. It simply holds that unusual states, events, or findings tend to be temporary and regress over time to the average or status quo. This is true with many non-malignant medical conditions as well. This is both profound and somewhat dispiriting because it means that most of these conditions will get better over time regardless of treatment. It is hence a fallacy to ascribe efficacy to treatment or causation based on recovery following treatment when a condition simply regresses to the mean because it would have regressed to the mean regardless of treatment.
Much attention has been paid to this phenomenon in the context of overusing antibiotics. Most people who go the doctor for upper respiratory infections wait to seek treatment until the condition has been present for some time. They then go to the doctor, ask for antibiotics, take antibiotics, and recover from the condition. These persons then assume that the antibiotics caused the improvement. The problem with the assumption is that most of these persons almost certainly had viral infections that simply got better according to the natural course of the condition. ANTIOBIOTICS DO NOT AFFECT VIRUSES AT ALL. The fact that the condition improved after starting antibiotics was due to the simple fact that the person started the antibiotics at about the time the condition would improve on its own. The antibiotics had nothing to do with the condition improving because ANTIBIOTICS ARE 100% INEFFECTIVE AGAINST VIRUSES.
The same holds true for many persons with low back pain who undergo surgery to remove a herniated disc. Low back pain usually stabilizes over time after an acute exacerbation regardless of treatment. Given enough time, it is highly likely that the person would have gotten better or at least recovered to the same extent regardless of the treatment received (including no treatment). The fact that the person improved after surgery does not indicate that the surgery caused the improvement. Instead, the relation of surgery and improved low back pain is almost certainly coincidental. We regress to the mean. That the surgery occurred and improvement subsequently happened is not evidence that the surgery was effective or that the herniated disc was causing the low back pain.
How do we know this? The medical literature is replete with evidence to that end. Take for example the study, “Influence of Low Back Pain and Prognostic Value of MRI in Sciatica Patients in Relation to Back Pain.” The study was undertaken to evaluate the correlation between MRI findings and outcomes in patients with sciatica alone versus patients with sciatica and back pain. As the authors note, “it remains unclear to what extent morphological changes seen on MRI in sciatica patients are associated with back pain, rather than being a representation of irrelevant differences between individuals.” The study found “that herniated discs and nerve root compression on MRI were more prevalent among patients with predominantly sciatica compared to those who suffered from additional back pain.” Interestingly, patients with sciatica and low back pain but without a herniated disc or nerve root compression fared worse after one year than those patients with a herniated disc or nerve root compression. And “remarkably large disc herniations and extruded disc herniations were … equally distributed between the two groups,” causing the authors to conclude that “the worldwide accepted mechanical compression theory therefore seems not to offer a sufficient explanation for the cause of the disabling back and leg symptoms in sciatica.”
Other studies demonstrate similar findings that call into question our ability to assign causation of low back pain to herniated discs and nerve root compression. The well-known twin study demonstrates the difficulty in linking specific activities with low back pain. As the authors in that study report, “disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected.” As noted above, other studies have found that large portions of the general population have disc pathology on MRI, but no low back pain. Still other studies find low back pain in the absence of disc pathology on MRI. Despite this evidence, triers of fact routinely base liability decisions on medical opinions that conclude an injury or exposure caused a herniated disc based on a post-injury MRI (which is almost impossible to conclude from a rational, evidentiary perspective in the absence of a pre-injury or exposure MRI) and that the herniated disc is causing low back pain (which runs contrary to the received scientific evidence).
What does this mean for medicolegal claims? It suggests that every claim for injury- or exposure-related back pain based on post-injury MRI scans demonstrating a herniated disc should be carefully scrutinized. In addition, worker’s compensation and liability carriers should take every opportunity to educate triers of fact regarding the lack of a causal nexus between herniated discs and low back pain. Independent medical examiners should point to the relevant literature to begin convincing triers of fact that there is no evidentiary link between low back pain and herniated lumbar discs. In this regard, insurance carriers can look to how the relationship of carpal tunnel syndrome to repetitive keyboard use evolved over time. When these claims first started arising, triers of fact in worker’s compensation accepted the link based on treating physician opinions seemingly without question. This was based on the fact that claimants reported experiencing symptoms while using computer keyboards. The medical literature did not support this association. Independent medical examiners began citing to research finding the opposite: that repetitive keyboarding is not a risk factor for or a cause of carpal tunnel syndrome. In at least some jurisdictions, the triers of fact and treating physicians eventually listened and stopped finding a relationship between repetitive keyboarding and carpal tunnel syndrome.
A similar shift ought to occur in the context of herniated discs and low back pain. While this does not suggest that low back pain itself is unrelated to an injury or exposure, it would radically reduce costs because it would limit surgery for herniated discs to cases where there is discernible nerve impingement causing motor and sensory deficits rather than in cases of low back pain alone. Although human beings are not very good at accurately assessing causation, we can learn to go against our instincts if there is high quality evidence denying causation and experts willing to hammer that point home. It is time to hammer home the point that disc pathology on MRI is poorly correlated to low back pain and limit expensive surgical procedures the efficacy of which is not supported by the medical literature. The simple fact of the matter is that costs for treating a condition that cannot be reliably related to an accident or repetitive stress exposure should not be borne by a liability or worker’s compensation carrier (especially when the condition is poorly correlated with the alleged health effects).
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