2009 ISSLS Prize Winner: Does Discography Cause Accelerated Progression of Degeneration Changes in the Lumbar Disc: A Ten-year Matched Cohort Study

Eugene J. Carragee, MD; Angus S. Don, FRACS; Eric L. Hurwitz, DC, PhD; Jason M. Cuellar, MD, PhD; John Carrino, MD; Richard Herzog, MD


Spine. 2009;34(21):2338-2345. 

In This Article


Disruption of the anulus using a needle puncture appears to be a reliable method to induce experimental disc degenerative findings in animals.[2,3,4] In general this has involved a large bore needle puncture in a relatively small disc, resulting in rapid and near universal disc disruption. Recent experimental work suggests that even small gauge needle punctures in large discs may trigger deleterious effects with time.[6]

Our findings from this study appear to indicate that small bore needle puncture and limited pressure injection, can clearly cause an increase in progression of degenerative findings. However, these findings are not always seen and, when seen appear to develop over a long period of time. For instance, of 91 grade I or II discs at the time of injection, 50 remained at the Grade I or II level (normal) even 10 years after the disc puncture.

Nonetheless, the comparative results are striking. In every qualitative parameter measured (herniation, endplate changes, disc grade progression and anular fissures) the discography group showed more frequent and greater degenerative findings compared to a well-matched control group. Quantitative measures of loss of disc height and loss of disc signal were also clearly greater after anular puncture and injection. The finding that new herniations were most frequently located on the side of disc puncture and that the greatest difference in herniation between groups was foramenal and far-lateral herniations suggest at least some specific local injury and sequelae.

These finding are of concern for several reasons. Discography as a diagnostic test is controversial and in view of these findings the utility of this test should be reviewed.[30] Furthermore, discography in current practice will often include injecting discs with a low probability of being symptomatic in an effort to validate other disc injections, a so-called control disc.[8,9] Although this strategy has never been confirmed to increase test validity or utility, injecting normal discs even with small gauge needles appears to increase the rate of degeneration in these discs over time. The phenomenon of accelerated adjacent segment degeneration adjacent to fusion levels may be, in part, explained by previous disc puncture if discography was used in segments adjacent to the fusion. To our knowledge the potential contribution of previous discography to adjacent segment disease has not been well considered.

Similarly, intradiscal therapeutic strategies (injecting steroids, sclerosing agents, growth factors, etc.) have been proposed as a method to treat, arrest or prevent symptomatic disc disease. Our finding would suggest that the injection procedure itself is not completely innocuous and a recalculation of these demonstrated risks versus hypothetical benefits should be considered. Finally, alternative or novel strategies for the introduction of intradiscal agents, as opposed to mechanical puncture and injection, should be considered in developing future strategies for early disc interventions.

The mechanism of action by which the baseline discography may have caused the changes seen 10 years later is unclear. Animal work has stressed both the mechanical injury to the anulus[1,4,31,32] as well as secondary biochemical and cellular processes.[6,33] The activation of cytokine pathways and production of degeneration products as previously reported might all be at work.[2,34,35] Andersson et al, however, have stressed that disc puncture is a fundamentally artificial process and which likely differs from native degeneration in some respects.[36]

There are several limitations to this study. Subjects were recruited predominantly from a pool of patients with a greater than average risk of disc degeneration (i.e., most had a history of previous cervical or lumbar disc herniation). The results here may not be generalizable to a population with high genetic resistance to the degeneration process or exceptionally low exposure to environmental factors promoting degeneration. Nonetheless, most patients in whom disc injections are contemplated are necessarily in a high-risk group.

Another limitation may be the design with only a baseline and 10 year MR evaluation. With only 2 data points, the kinetics of disc degeneration cannot be estimated. We do note, however, that even by the 7 year mark, the discography group already had more clinical evaluations with MRI for lumbar problems and had also had more lumbar surgery than the control group (five vs. one). A comprehensive clinical evaluation of these discography and control subjects is currently underway, and will be the subject of a future publication.

Despite these limitations we feel our findings are real and reproducible. Disc puncture with even a small gauge needle and limited injection pressures appears to be associated with accelerated disc degenerative processes, disc herniation, loss of disc height and signal and the development of reactive endplate changes compared to match-controls. We believe, careful consideration of risk and benefit should be used in recommending procedures involving disc puncture for diagnostic or therapeutic purposes unless clear and demonstrable utility has been established.


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