First we greatly appreciate Dr. Levin for carefully reading our paper and providing very thoughtful comments. The above post-publication review expresses some interesting thoughts with regards to both the existence of a discogenic component to lower back pain, its identification in the clinical setting, and the role of surgery in its management. Although several of these concerns reflect major areas of further debate and research in the surgical community, they are also largely irrelevant to this biomechanical study which does not attempt to address them. With regards to the existence of this patient population, the simple fact that a discogenic etiology to low back pain exists in a subgroup of patients that are suffering with chronic low back pain has been clearly established (1-3). In addition, to deny this and the inclusion criteria utilized in this study is to deny the clinical reality in which we live. The identification of disc-related symptoms remains a difficult task despite advances in modern diagnostic techniques. However; it is also a task which falls in the hands of physicians in general and spine surgeons specifically on a daily basis. The presence of discogenic pain in our study was initially assessed using plain radiographs and MRI imaging. Such imaging studies remain the gold-standard at assessing the presence and degree of IVD degeneration as evidenced by the presence of validated grading scales that have been found to correlate imaging changes with the both the presence of degeneration in pathologic specimens and the presence of clinical symptoms of lower back pain. The Modic system classifies degenerative end-plate and vertebral body changes seen on MRI (4-6). The Pfirrmann system classifies the morphology of the disc as seen on axial T2-weighted MRI (7). We refer our readers to the numerous articles that have been published demonstrating the validity of these systems that have also stood the test of time and were thus utilized in our study. Pain provocation using discography was also utilized in our series as confirmation. The use of lumbar discography is both common and controversial. Without delving into the tremendous body of research that exists evaluating this test; we simply reply that there are proponents in the spine community and a better test simply does not presently exist. A recent systematic review evaluating discography as a diagnostic test for spinal pain revealed that it is a useful imaging and pain evaluation tool (8). We also have modified the standard discography technique that we utilize with the addition of injection of a small amount of bupivicaine into the painful degenerated disc, which has been shown in a recent randomized controlled trial to improve surgical results presumably by increasing its accuracy as a diagnostic tool (9).

Inclusion of a normal control group is actually more beneficial than the above reviewer acknowledges; as it provides baseline reference data on the movement patterns of the human lumbar spine using a highly accurate in vivo technique developed by Li et al (10-12). Prior to the publication of this data by our group detailed knowledge of these normal physiological movements was limited at best with measurements largely being obtained in limited planes of motion due to technology limitations. Previously documented motion on the lumbar spine using in vitro and in vivo techniques may not allow for a meaningful analysis of our data which explains the basic need for a normal control group. As a matter of fact, there are “2 control groups” in this study as the discogenic LBP patients themselves also serve as their own control group; as multiple segments of the lumbar spine were included in testing. It is obviously not reasonable to assume that segmental hypomobility would ensue at the affected levels simply secondary to symptoms of pain, as pain would presumably affect all tested levels (we didn’t ask the patients to move their L4-5 segment we had them move their entire lumbar spine) and also obviate the finding of hyper-mobility at the superior adjacent level, as was the case in our series.

The above critique also mentions that our finding of diminished motion among degenerative levels is an expected and obvious finding. This might be an oversimplification of the effects of degeneration on spinal kinematics. In a cadaveric study, Fujiwara et al. noted that segmental motion initially increased with degeneration but then decreased in extreme degeneration. Wilke et al. found that segmental stability increased in flexion-extension and lateral bending but decreased in axial rotation with increasing degenerative disc disease grades. Given what we know from previous studies together with that of our own all we believe that regarding the effects of disc degeneration on spinal motion is that it is has a complex effect with diminished motion only present at the extremes of degeneration (13-15).

With regards to the request for clinical follow-up of the included patients; inclusion of clinical follow-up is irrelevant to the conclusions reached in our study. This is a biomechanical study and is aimed at examining the segmental motion of a group of DDD patients before fusion surgeries. Extensive literature has been published with regards the diagnosis, treatment, and outcomes of painful degenerative conditions of the lumbar spine and we refer our readers to that body of literature. However; in order to quench the interest expressed above the clinical results of discogenic LBP published at our large tertiary referral academic center have been similar to those findings and published previously in many of larger clinical studies which all treating spine physicians should be well versed in. The author of this critique validates the importance of one of our hypotheses in saying that “no differences in spinal mobility have been identified between individuals with “discogenic low back pain” and individuals with degenerative disc disease without pain”; as prior to our publication this was true. If one carefully reads our conclusions they will realize that no conclusions were made with regards to indications for fusion surgery, cause, effect, or outcomes as these are clinical issues that are addressed in well-designed randomized and prospective series and not in in-vivo biomechanical studies as our own. Therefore, our results should be interpreted for what they are and not inferred as data relevant in the clinical setting in and of itself.

We strongly agree that chronic LBP indeed remains a difficult condition for both the physician and the patient. Identifying a subset of LBP patients who will predictably respond to operative intervention is a noble challenge as is the evaluation of which operative interventions are most effective. Our study does not attempt to address this important question and we await with equal vigor further clinical pearls with regards to its treatment. Perhaps we all are up for the challenge to do so using evidence based medicine.

References

1. Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-70.

2. Mooney V. Where is the pain coming from? Spine 1987;12:754-9.

3. Nachemson AL. The lumbar spine an orthopaedic challenge. Spine 1976;1:59-71.

4. Modic MT. Degenerative disc disease: genotyping, MR imaging and phenotyping. Skeletal Radiol. 2007;36:91-3.

5. Kuisma M, Karppinen J, Haapea M, Lammentausta E, Niinim¨aki J, Tervonen O. Modic changes in vertebral endplates: a comparison of MR imaging and multislice CT. Skeletal Radiol. 2009;38:141-7.

6. Kjaer P, Korsholm L, Bendix T, Sorensen JS, Leboeuf-Yde C. Modic changes and their associations with clinical findings. Eur Spine J. 2006;15:1312-9.

7. Pfirrmann CW, Metzdorf A, Zanetti M, Hodler J, Boos N. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine (Phila Pa 1976). 2001;26:1873-8.

8. Buenaventura RM, Shah RV, Patel V, et al. Systematic review of discography as a diagnostic test for spinal pain: an update. Pain Physician 2007;10:147-64.

9. Ohtori S, Koshi T, Yamashita M, et al. Surgical vs. nonsurgical treatment of selected patients with discogenic low back pain. Spine 2011;36:347-354.

10. Wang S, Passias P, Li G, Li G, Wood K. Measurement of vertebral kinematics using noninvasive image matching method-validation and application. Spine (Phila Pa 1976). 2008;33:E355-61.

11. Xia Q, Wang S, Passias PG, Kozanek M, Li G, Grottkau BE, Wood KB, Li G. In vivo range of motion of the lumbar spinous processes. Eur Spine J. 2009;18:1355-62.

12. Li G, Wang S, Passias P, Xia Q, Li G, Wood K. Segmental in vivo vertebral motion during functional human lumbar spine activities. Eur Spine J. 2009;18:1013-21.

13. Fujiwara A, Lim TH, An HS, Tanaka N, Jeon CH, Andersson GB, Haughton VM. The effect of disc degeneration and facet joint osteoarthritis on the segmental flexibility of the lumbar spine. Spine (Phila Pa 1976). 2000;25:3036-44.

14. Tanaka N, An HS, Lim TH, Fujiwara A, Jeon CH, Haughton VM. The relationship between disc degeneration and flexibility of the lumbar spine. Spine J. 2001;1:47-56.

15. Wilke HJ, Rohlmann F, Ring C, Mark C, Kettner A. Early stages of intervertebral disc degeneration do not necessarily cause instability. Presented during SpineWeek at the meeting of EuroSpine. Geneva, Switzerland; 2008 May 30.

To the Editor:

Passias et al. have reported an interesting in vivo analysis of segmental spinal motion in individuals in which they diagnosed “discogenic low back pain” in their article entitled, "Segmental Lumbar Rotation in Patients with Discogenic Low Back Pain During Functional Weight-Bearing Activities" (2011;93:29-37). Specifically, they report on a group of ten individuals who were indicated for spine fusion surgery based on the authors’ criteria for identifying patients with discogenic back pain. I have a number of concerns related to their patient selection, study design and conclusions.

I do not believe that the criteria in which the authors utilized to identify individuals with “discogenic low back” reliably identifies this select sub-population of individuals with low back pain. The authors diagnosed discogenic low back pain at L4-S1 based on a presenting chief complaint of “mechanical back pain, which was defined as worsening symptoms with weight-bearing for prolonged periods of time, exacerbation of pain while sitting and bending forward, and absence of radicular symptoms”. This symptom complex is extremely common in many individuals with both acute and chronic non-radicular low back pain and does not accurately identify any particular sub-group of individuals with LBP. They further state that “radiographic confirmation of discogenic low back pain was determined by the treating surgeon and a neuroradiologist”. I do not believe that any imaging study can “confirm” a diagnosis of pain. Images may identify pathology which could be contributing to a painful condition. Finally, they report that all of the individuals had a discography performed which demonstrated “concordant pain”. The accuracy of provocative discography to truly identify the pain generator which is both the source of an individual’s pain and to predict the likelihood of success of operative intervention is widely debated. Carragee et al. report that provocative discography did not demonstrate any predictive value in identifying intradiscal lesions as the primary source of back pain (1). Cohen et al. performed an exhaustive Medline review and report that discography has not been demonstrated to improve surgical outcomes (2). Carragee et al. also report that structural abnormalities demonstrated on both MR scanning and discography had a “weak association with back pain episodes and no association with disability or future medical care” (3). Williams et al. performed pre-operative discography on discs adjacent to the proposed fusion level and found no correlation between the provocative discogram findings and surgical outcomes (4). Carragee et al. was unable to identify a difference in the results of provocative discography in comparing a group of individuals with persistent low back pain not requiring any treatment from a group with “ chronic low back pain illness” (5).

The authors selected a control group of individuals with normal spines and demonstrated differences in segmental spinal motion between their study population and anatomically normal spines. This result is expected as we know that degenerated joints at other sites in the body tend to lose mobility. In their discussion of the results, the authors state that “this finding suggests that, with severe degenerative disc disease requiring surgery, segmental hypo-mobility ensues”. It is unclear if they are suggesting that the hypo-mobility contributes to the pain or if it is a response to the pain. The selection of a control group with normal spines instead of individuals with asymptomatic degenerative disc disease at similar levels limits any correlations or conclusions which can be drawn in reference to altered segmental mobility, symptoms and the necessity for surgery.

Finally, although the authors report on a group of patients “with severe degenerative disc disease requiring surgery”, they do not report any clinical follow-up. The lack of an outcome analysis in this group of patients significantly limits any conclusion or clinical applicability to the findings of altered segmental rotation. The most appropriate conclusion that can be drawn from their analysis is that individuals with degenerative disc disease have altered spinal mobility. No differences in spinal mobility have been identified between individuals with “discogenic low back pain” and individuals with degenerative disc disease without pain. In addition, no conclusions can be identified as to authors’ indications for fusion surgery or to the cause, effect, indications for surgery or surgical outcomes in patients with altered segmental lumbar rotation.

Chronic LBP remains an extremely frustrating condition for both the physician and the patient. Being able to reliably identify a single pain generator and a procedure which can resolve the symptomatology will benefit a large number of patients. I do not believe that this present investigation has helped us identify a subset of LBP patients who will predictably respond to operative intervention.

References

1. Carragee EJ, Lincoln T, Parmar VS, Alamin T. A gold standard evaluation of the “discogenic pain” diagnosis as determined by provocative discography. Spine (Phila Pa 1976). 2006;31:2115-23.

2. Cohen SP, Larkin TM, Barna SA, Palmer WE, Hecht AC, Stojanovic MP. Lumbar discography: A comprehensive review of outcome studies, diagnostic accuracy, and principles. Reg Anesth Pain Med. 2005;30:163-83.

3. Carragee EJ, Alamin TF, Miller JL, Carragee JM. Discographic, MRI and psychosocial determinants of low back pain disability and remission: a prospective study in subjects with benign persistent back pain. Spine J. 2005;5:24-35.

4. Willems PC, Elmans L, Anderson PG, van der Schaaf DB, de Kleuver M. Provocative discography and lumbar fusion: is preoperative assessment of adjacent discs useful? Spine (Phila Pa 1976). 2007;32:1094-9.

5. Carragee EJ, Alamin TF, Miller J, Grafe M. Provocative discography in volunteer subjects with mild persistent low back pain. Spine J. 2001;2:25-34.