Modic Changes in the Spine
What are modic changes?
On rare occasions, when you receive a radiology report from one of the local diagnostic facilities, the reading radiologist may indicate that your patient has a Type I Modic change. It’s important for you to understand the clinical implications of this finding. If you don’t read MRI, no worries, as I will endeavor to make it clear to you.
Modic changes were first identified in 1987, and then put into a set of classifications by Michael Modic, MD, thus the name. It refers to changes which occur in the subchondral bone marrow as a result of trauma, disease, or aging, and it is closely associated with the presence of degenerative disc disease. Type I involves inflammation and edema in the vertebral body adjacent to the disc; Type II involves replacement of the inflammation and edema with yellow fat; and Type III involves replacement of the yellow fat with bony sclerosis. The three types are considered to be related to one another as phases in the progression of a lesion. Since Type I involves inflammation and edema, it is important to understand it in relation to the personal injury cases you are handling.
Incidentally, there is a great little book you can get from Amazon by William Morgan, DC, who was just recently named president of Parker University (formerly College) in Dallas, TX. If you have a Kindle, you can get it for $2.99, and you cannot beat it for a concise explanation of the pathology, along with really clear reproductions of Modic changes on MRI and pictorial representations which do a great job of illustrating the lesion. Actually, Dr. Morgan has several really good, and cheap, books available on MRI which can be very helpful in your understanding of MRI, and all of them are worth buying.
Rear-End Accidents and Subsequent Injuries
But here’s the deal: when occupants in a motor vehicle are rear-ended, the forces which go through their body, starting at the lumbar spine and progressing all the way up to the neck, consist of two components- shear forces and axial compression forces. It’s the axial compression forces which are the concern here, as axial compression trauma, or a series of traumas, can lead to damage to the disc, the cartilaginous endplate, the bony endplate, and the cancellous bone of the vertebral body. The disc may herniate not only posterolaterally, as we have all been taught is the most common way for it to go, but it can also herniate intradiscally, and go right through the endplates, and form what we have always called a Schmorl’s node. Or it may cause a number of microfractures in the endplates which lead to a disruption of the interface between the vertebral body, the endplates, and the disc, which leads to the introduction of substances into the capillary beds of the subchondral bone which were never meant to be there. It appears that the Schmorl’s node which we have ignored all these years may not be as innocuous as once believed.
The intervertebral disc is a two part structure, consisting of the tough outer annular fibers and the nucleus in the middle. Now the textbooks teach that the disc has three parts, the two aforementioned and a third, the endplate (Bogduk N, Clinical and Radiological Anatomy of the Lumbar Spine, 5th Ed., Elsevier, 2012, p. 19-20). The endplate is a very important organ, in that it serves two functions: 1) It separates and confines the intervertebral disc, and 2) It allows the transfer of fluids, nutrients, and waste products between the capillaries of the vertebral body and the intervertebral discs. The mature disc does not have a blood supply, and the individual cartilage cells receive their nutrition and oxygen and get rid of their waste products via osmosis into the fluids which bathe them. The endplate is a porous structure which functions as a selectively permeable barrier between the cartilage cells of the disc and the capillary beds which are found in the subchondral bone. Remember, the cancellous bone of the vertebral body is filled with red bone marrow and is highly vascularized. The exchange of the nutrients, oxygen, and metabolites is facilitated by the normal motion of the joint, which sets up a pumping action which brings the good stuff in and takes the bad stuff out. Damage to the endplates really interferes with this exchange process, and the end result is the genesis of the inflammatory cascade. The damage which ensues because of the pro-inflammatory enzymes involved in the process is what we see on an MRI as a Modic change.
Type 2 and Type 3 Modic changes are, for the most part, not nearly as symptomatic as the Type I changes, so I’m not going to discuss them here. But at worst, a Type I Modic change is representative of an intradiscal herniation which has displaced the nucleus, caused a fracture or fractures of the endplate, disrupted the internal architecture of the vertebral body, and introduced inflammation and edema into the area, and at best, it’s a bone bruise. Think of this injury to the vertebral body as a bad- really bad- bone bruise. If you have ever stepped on a rock with your heel, and gotten a bone bruise on your heel, you know what I am talking about. If you ever were involved in sports, and have had a hip pointer, you also know what I am talking about. Hip pointers are bone bruises, usually with enthesopathy, on the iliac crest, and they take forever to resolve. I had them on two occasions during my wrestling career, over 30 years ago, and to this day, when I use my foam roller on my hips, I have to watch it on those spots. If you talk to the radiologists about doing a bone scan on an area with a bone bruise to differentiate it from a fracture, they will tell you that it largely useless because the damaged area stays “hot” for a long time after the injury. When determining the extent of a fracture, CT is much better.
On a T1 weighted MR image, edema (water) appears dark, while on a T2 weight MR image, it appears bright. Really simple. And because a radiologist will read the study before it ever gets to you, he/she will rule out lesions such as metastasis, hemangioma, or infection as the cause of the lesion.
Modic Type I lesions are not static lesions- they usually convert to Modic 0 (normal) or Modic Type 2, or they expand in magnitude. In general, these changes will take anywhere from six to eighteen months to occur. So if you are wondering why your patient isn’t responding to conservative treatment, stop wondering. But as Type I progresses to Type 2, they tend to become less painful. In one study, 73% of patients with degenerative disc disease (DDD) with Modic Type I changes had lower back pain, compared with only 11% of the DDD patients with Type II changes (Toyone T, Takahashi K, Kitahara H, et al. Vertebral Bone Marrow Changes in Degenerative Lumbar Disc Disease: An MRI study of 74 Patients with Low Back Pain. J Bone Joint Surg Br 1994;76:757-64). The same study revealed that there apparently is a relationship between the presence of a Modic Type I change and segmental hypermobility (defined as sagittal translation of 3 mm or more on dynamic flexion-extension films). 70% of the Type I patients, but only 16% of the Type II patients, were found to have segmental hypermobility, so the authors concluded that patients with chronic low back pain and Type I Modic changes had more frequent instability requiring fusion surgery than those with the Type II changes. Another study showed remarkable results when fusion of the unstable segments was performed: seventeen patients with chronic low back pain and Modic Type I changes underwent instrumented posterolateral fusion, and six months later, all of the Type I changes had converted, with 76.5% changing to Type II, and 23.5% back to normal, and clinical improvement was seen in all patients (Vital JM, Gille O, Pointillart V, et al. Course of Modic I Six Months after Lumbar Posterior Osteosynthesis. Spine 2003;28:715-21).
Say you have a patient who is complaining of acute low back pain following a car crash, and the orthopedic tests for identifying sciatic tension are either equivocal or negative. By equivocal, I mean that both straight leg raises are positive for pain, but the pain occurs at greater than 45 degrees (like 50 degrees on the right, 70 degrees on the left). Your motion palpation of the sacroiliac joints reveals bilateral fixation, and the sacroiliac and iliolumbar ligaments are “en fuego” (that’s “on fire” for all of you non-Spanish speakers!) There may or may not be some vague neurological signs (like an ankle clonus). But after two or three weeks of very conservative treatment, there is no improvement, you order an MRI, and what do you know? There’s a Modic Type I change at L4 and L5, but no evidence of any disc herniation. Based on the patient’s case history, you know that the low back pain started as a result of the MVC, and because it’s Modic Type I, you know that it’s new. And every time you have manipulated the patient, particularly if it involves the twisting of side posture, you have aggravated the area. My advice? Treat it like a rib injury and immobilize it with a brace. Use soft tissue work for the muscular and tendinous lesions, and use ice to control the pain.
Nutritionals for connective tissue support and control of inflammation are extremely important. I went to a Charlie Annunziata seminar last November in Phoenix at which I learned about the anti-inflammatory and scar tissue reduction properties of doTerra Essential Oils, and I highly recommend them after what they have done for the adhesive capsulitis in my hips. Make the patient realize that this is going to hurt for a while. Exercises? Man, I don’t know if I like that idea, especially at first. Anything that produces axial compression and increases intrathecal pressure should probably be avoided. That would eliminate just about any exercise you could think of, at least until the inflammation resolves. A follow-up MRI of the area six months after the initial MRI would be helpful to determine the progression of the lesion into other Modic types. And when the range of motion has increased to the point at which good motion information can be obtained, then do a standing lumbar motion study and determine if there is any instability. The above study only mentioned using translation for the evaluation of lumbar instability, but remember, the AMA Guides describe a method for evaluating angular motion for instability as well.
Bottom line point? We were always taught that Schmorl’s nodes were asymptomatic and merely an incidental finding. But I went to school before MRI was invented, and the knowledge base has expanded greatly over the years, particularly over the last ten years. So when these lesions are present, one should assume that they are clinically relevant, or at least have the potential to be, if they can be correlated to the patient’s complaints.