Understanding the Mechanism of MVA Related Injuries – A Paradigm Shift for Treatment

I have seen several thousand MVA and trauma victims over the past several years.

I think that there are some general ideas and principles that would lead to drastic cost reduction, greater efficacy of treatment results, minimizing of complications, and more rapid return of patients to activities of daily living as well as to their employment, all while decreasing periods of disability.

 Here are some observations on the basis of the many cases reviewed:

• The main injury in most MVAs is the flexion-hyperextension injury. Looking at a model of the spine, there are two areas that experience stress and shear, the intervertebral discs anteriorly (during hyperflexion) and the facet joints posteriorly (in hyper extension). As the facet joints are much smaller, and a focal or pivot  point for rotation, they are much more susceptible to injury. The discs, even while sustaining damage, are more broad based, and able to absorb forces of injury to a much greater extent
•  It has been shown in multiple papers that 40% of the general population has        asymptomatic herniated discs.
• The only discs that generate pain are those that are associated with inflammation of a nerve root. This inflammation should produce an anatomical sensory and/or motor abnormality in the distribution of the affected nerve root. This condition is, in fact, less common than the aching pain and stiffness associated with disruption of facet joints.
• There are two ways in which facet joints contribute to pain. It is always puzzling to people why it may take days for pain to develop following an MVA, but in fact, if there is trauma to the facet joint from hyperextension it may take hours or days for inflammation and the attendant pain to develop. More significantly, there are fiber-like nerves that run along the vertebrae to innervate the facet joints from above and below, and these fine nerves can become stretched and disrupted causing pain from the hyperextension injury. This causes stiffness, and dull aching sensation in the neck or back.
• Facet joint pain is also distinguished by the fact that it is non-radicular – it does not follow nerve root distribution. In the cervical spine it is associated with a symptom complex that can include dizziness, tinnitus, headache, jaw and posterior shoulder pain and spasm. In the lumbar spine it is characterized by spasm of paraspinal muscles and pain radiating to the buttocks, hips, and occasionally the groin.
• Pseudoradiculopathy: In this condition due to swelling or hypertrophy of the facet joint(s), which displaces the joint anteriorly, there can be pinching of the nerve root giving a similar clinical picture to that of true radiculopathy, usually caused by a herniated disc. Additionally, there are many instances in which peripheral nerves have been injured, and without careful physical examination, the distribution of pain will be attributed to nerve root dysfunction rather than peripheral nerve injury. Since these are generally sensory nerves causing sensory abnormalities, EMG is a virtually useless test for diagnosis.
• There are too many patients being treated for radiculopathy due to the appearance of a herniated disc on MRI, and pseudoradicular symptoms. Many of them, due to unresolved pain, go on to have epidural steroid injections which do not help for very long, then on to discography, which injures the disc, and finally, if the patient is so motivated, either percutaneous or open discectomy.

• Unless there is a frank portion of the disc displacing the nerve root, surgery – discectomy with or without fusion, is unlikely to relieve the pain or increase functionality.
• There are in essence two problems here – the first is that the diagnostic testing both EMG and MRI are more than likely to lead to the conclusion that pain is discogenic and radicular in nature. We tend to trust our eyes, even when what we see conflicts with the cognitive evidence. The best evidence for the source of the pain is not with the elaborate testing, but rather with the history and physical exam.In an injury to the small nerves that innervate the facet joint(s) due to hyperextension, there is no radiological or physiological test for this condition, iunfortunately, this injury can neither be seen nor measured. How do I know that it exists? From the claimants history of posterior shoulder pain, headache, or buttock and hip pain, claims of stiffness especially upon awakening, decreased ROM of the spine for extension, and most importantly pain to the palpation of the facet joints on the physical exam. A further confirmation is the marked diminution of pain following treatment of the innervation of the facet joint with local anesthetic. This is a temporary effect, but (with RFA – radiofrequency ablation) this effects can be prolonged for many months. The second problem is that due to experience in treating the discs as the primary cause of pain, the medical community, despite the paucity of evidence for success of treatment, (in the absence of radiculopathy, or in the presence of pseudoradiculopathy) persists in the same treatments despite numerous abject failures. I have personally seen numerous cases of patients who have undergone discectomy with or without fusion and have either worse pain or the same pain that they originally had, has persisted despite surgery. This calls for a different analysis and treatment algorithm.
• Since the majority of complaints of neck and LBP are non-radicular and localised around the neck and LB, it seems that the first structure that should be approached is the more vulnerable facet joint. It is the great paradox of how we are ‘constructed’, that on MRI it will appear that a disc is herniated at the same level that a facet joint which will appear normal on MRI is responsible for the pain. Perhaps this calls for a new way of thinking, namely, that in the absence of radiculopathy , the herniated or bulging disc is only a’marker’ of the damage caused by the hyperflexion-hyperextension injury, but the actual damage and pain is associated with the facet joint. In addition, what many clinicians consider to be radiculopathy can in some cases be pseudoradiculopathy, and this deserves careful consideration, because misdiagnosis leads to unnecessary and ineffective surgery, costing hundreds of millions of dollars, disability, and suffering.
• The main point is that by treating the facet joint first in cases of non-radicular or pseudoradicular pain, there is opportunity for tremendous cost savings, better outcomes, less opioid use and enhanced patient satisfaction. In the majority of cases, I feel that the patient will realize moderate relief enabling greater mobility and increased activity as well as improved sleep patterns. This will alleviate tremendous amounts of suffering due to the marked decrease in patients undergoing  (in many cases) unnecessary surgery. If the patient has persistent pain following treatment of the facet joint, at that point, discography and possibly surgery can be considered, thus reducing the expense and poor results of surgery.
• There is no question that by persisting in the present fashion, that results will not improve and costs will continue to climb. We need to be more discriminating in how we interpret test results and their implications in driving patient care.

JSF