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Will That Disc Herniation Get Better?
May 3, 2014 by Dr Matthew D. Long
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Will That Disc Herniation Get Better?
May 3, 2014 by Dr Matthew D. Long
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Will That Disc Herniation Get Better?
May 3, 2014 by Dr Matthew D. Long
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One of the most important aspects of patient care is offering an accurate prognosis for any given condition. Whether we see our role as an expert diagnostician in the neuromusculoskeletal system, or in a more functional role as a facilitator of greater wellbeing, our patients do expect us to predict the future. Or more specifically - their future. Unfortunately, predicting a patient’s recovery from lumbar disc herniation is not always straightforward. Curiously some patients with very large herniations do well with conservative care and time (1), while others with less impressive protrusions succumb to surgery and an uncertain future. Indeed, Cribb and colleagues wrote,
"Although massive herniations are rarely left alone for well-understood reasons, this small cohort of patients reveals a more benign side to this pathology which may not always deserve its fearsome reputation.”
Takada et al (2) found that 88% of patients in their study showed a > 50% reduction in hernia size within 3 - 12 months after onset, suggesting that we need to give our patients some time to heal. Conversely, the literature also tells us that successful surgery often requires earlier intervention, so as to avoid the nasty effects of sustained chemical and physical insult upon the nerve roots (which can ultimately result in demyelination and intraneural fibrosis).
So how do we decide whether a patient will ultimately recover without surgery?
Numerous studies have looked at the prognostic indicators for disc herniation, with most suggesting that shrinkage of the nuclear mass is associated with a better outcome. Autio et al (3) looked at various factors that might give us clues as to the amount of resorption possible over time. Interestingly, they found that a greater vertical migration of the herniated nucleus either above or below the adjacent vertebral body (known as the Komori classification) was associated with a higher resorption rate, together with a patient age between 41 - 50 years. Indeed, if the herniated material migrated at least 67% above or below the adjacent vertebra then it was more likely to resolve faster. It might seem curious that larger disc herniations are more likely to shrink in size than smaller ones. However, this is probably due to the fact that larger herniations typically breach the annulus and the posterior longitudinal ligament, thereby exposing themselves to the circulation in the epidural space. The liberated proteoglycans in the escaped nucleus will initially swell as they bind water, but phagocytosis will quickly reduce this water-carrying capacity and lead to significant shrinkage. But not all such herniations resolve. Some remain defiant and maintain their size, and their propensity for causing pain, long after they should have faded into the background. So what is different about these cases?
It does appear that not all disc herniations are created equal. While most commentaries focus upon the migration of nuclear material (containing the hydrophilic protoeglycan aggrecans), we know that hernia also contain other less pliable materials. A study by Rajasekaran and colleagues in the journal SPINE (4) investigated two very different mechanisms of disc failure. The first, which they dubbed a Type I herniation, occurred due to failure of the endplate junction. A Type II herniation described the more classically understood failure of the annulus fibrosus. The significance of this distinction becomes apparent when we see that Type I failure typically contains both cartilage and bone from the endplate - materials which are far less likely to spontaneously resorb than the water-rich nucleus.
So how do we decide whether a patient will ultimately recover without surgery?
Numerous studies have looked at the prognostic indicators for disc herniation, with most suggesting that shrinkage of the nuclear mass is associated with a better outcome. Autio et al (3) looked at various factors that might give us clues as to the amount of resorption possible over time. Interestingly, they found that a greater vertical migration of the herniated nucleus either above or below the adjacent vertebral body (known as the Komori classification) was associated with a higher resorption rate, together with a patient age between 41 - 50 years. Indeed, if the herniated material migrated at least 67% above or below the adjacent vertebra then it was more likely to resolve faster. It might seem curious that larger disc herniations are more likely to shrink in size than smaller ones. However, this is probably due to the fact that larger herniations typically breach the annulus and the posterior longitudinal ligament, thereby exposing themselves to the circulation in the epidural space. The liberated proteoglycans in the escaped nucleus will initially swell as they bind water, but phagocytosis will quickly reduce this water-carrying capacity and lead to significant shrinkage. But not all such herniations resolve. Some remain defiant and maintain their size, and their propensity for causing pain, long after they should have faded into the background. So what is different about these cases?
It does appear that not all disc herniations are created equal. While most commentaries focus upon the migration of nuclear material (containing the hydrophilic protoeglycan aggrecans), we know that hernia also contain other less pliable materials. A study by Rajasekaran and colleagues in the journal SPINE (4) investigated two very different mechanisms of disc failure. The first, which they dubbed a Type I herniation, occurred due to failure of the endplate junction. A Type II herniation described the more classically understood failure of the annulus fibrosus. The significance of this distinction becomes apparent when we see that Type I failure typically contains both cartilage and bone from the endplate - materials which are far less likely to spontaneously resorb than the water-rich nucleus.
Figure 1. Line diagram depicts the three situations of normality (A), failure through the annulus fibrosus (B), and failure through avulsion of the endplate junction (C). From Rajasekaran et al.
But how can we determine the components of a given patient’s disc protrusion? Is there something visible on imaging studies that might help us decide whether they have a good chance of recovery? The answer seems to be yes…
A new paper by Shan et al (5) has brought to light an interesting correlation between the possibility of disc resorption and the presence of Modic changes on MRI scans. Modic changes (MCs) have long been thought to represent a degenerative alteration to the vertebral body, usually in concert with disc degeneration and possibly segmental instability (6). While they have increasingly been associated with the presence of back pain, there has not been any thought given to their possible significance as a prognostic factor for disc resorption. The early phase of this process (Type I Modic change) is visible as an increased signal intensity on T2-weighted images, implying a high water content and presumably inflammation. Over time, fatty infiltration occurs and the damaged area becomes more prominent on T1-weighted sequences.
A new paper by Shan et al (5) has brought to light an interesting correlation between the possibility of disc resorption and the presence of Modic changes on MRI scans. Modic changes (MCs) have long been thought to represent a degenerative alteration to the vertebral body, usually in concert with disc degeneration and possibly segmental instability (6). While they have increasingly been associated with the presence of back pain, there has not been any thought given to their possible significance as a prognostic factor for disc resorption. The early phase of this process (Type I Modic change) is visible as an increased signal intensity on T2-weighted images, implying a high water content and presumably inflammation. Over time, fatty infiltration occurs and the damaged area becomes more prominent on T1-weighted sequences.
Figure 2. Type I Modic changes evident in the vertebral bodies adjacent to the L4-5 intervertebral disc.
Interestingly, Shan’s study showed that,
"Herniated tissue from patients with MCs contained relatively more hyaline cartilage endplate and relatively less nucleus pulposus. Conservative treatment was less successful in patients showing MCs, possibly because their cartilage-rich herniations showed less vascular invasion and consequently less resorption.”
They also wrote that,
"Displaced hyaline cartilage can come only from the vertebral endplate and is presumably stripped from it by herniating annulus, sometimes with underlying bone attached. If this happens, it will greatly increase the permeability of the endplate and allow greater migration of biological agents from the disc to the vertebral body, and vice versa, stimulating the development of MCs. In this way, MCs may act as a “marker” for a cartilaginous disc herniation that resorbs poorly. Mechanical stripping of the cartilage endplate may explain how bacterial infections frequently enter the nucleus of a herniated disc with MCs, causing severe back pain that can be relieved by antibiotics. It may also explain the bony endplate “erosions” that are common in the lower lumbar spine and which are associated with disc degeneration and pain."
So it may well be that if your patient with symptomatic disc herniation also shows Modic changes on their MRI, they may have a poorer prognosis than those without such vertebral body changes. If this is true, then perhaps we need to look closely at such patients and think carefully about how long we pursue a trial of conservative treatment before we decide to refer them to a surgeon.
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
Something to think about...
Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
References:
1. Cribb, G. L., Jaffray, D. C., & Cassar-Pullicino, V. N. (2007). Observations on the natural history of massive lumbar disc herniation. The Journal of Bone and Joint Surgery British Volume, 89(6), 782–784. doi:10.1302/0301-620X.89B6.18712
2. Takada, E., Takahashi, M., & Shimada, K. (2001). Natural history of lumbar disc hernia with radicular leg pain: Spontaneous MRI changes of the herniated mass and correlation with clinical outcome. Journal of Orthopaedic Surgery (Hong Kong), 9(1), 1–7.
3. Autio, R. A., Karppinen, J., Niinimäki, J., Ojala, R., Kurunlahti, M., Haapea, M., et al. (2006). Determinants of spontaneous resorption of intervertebral disc herniations. Spine, 31(11), 1247–1252. doi:10.1097/01.brs.0000217681.83524.4a
4. Rajasekaran, S., Bajaj, N., Tubaki, V., Kanna, R. M., & Shetty, A. P. (2013). ISSLS Prize Winner: The Anatomy of Failure in Lumbar Disc Herniation: An In Vivo, Multimodal, Prospective Study of 181 Subjects. Spine, 38(17), 1491–1500. doi:10.1097/BRS.0b013e31829a6fa6
5. Shan, Z., Fan, S., Xie, Q., Suyou, L., Liu, J., Wang, C., & Zhao, F. (2014). Spontaneous Resorption of Lumbar Disc Herniation Is Less Likely When Modic Changes Are Present. Spine, 39(9), 736–744. doi:10.1097/BRS.0000000000000259
6. Rahme, R., & Moussa, R. (2008). The Modic Vertebral Endplate and Marrow Changes: Pathologic Significance and Relation to Low Back Pain and Segmental Instability of the Lumbar Spine. AJNR American Journal of Neuroradiology, 29(5), 838–842. doi:10.3174/ajnr.A0925
1. Cribb, G. L., Jaffray, D. C., & Cassar-Pullicino, V. N. (2007). Observations on the natural history of massive lumbar disc herniation. The Journal of Bone and Joint Surgery British Volume, 89(6), 782–784. doi:10.1302/0301-620X.89B6.18712
2. Takada, E., Takahashi, M., & Shimada, K. (2001). Natural history of lumbar disc hernia with radicular leg pain: Spontaneous MRI changes of the herniated mass and correlation with clinical outcome. Journal of Orthopaedic Surgery (Hong Kong), 9(1), 1–7.
3. Autio, R. A., Karppinen, J., Niinimäki, J., Ojala, R., Kurunlahti, M., Haapea, M., et al. (2006). Determinants of spontaneous resorption of intervertebral disc herniations. Spine, 31(11), 1247–1252. doi:10.1097/01.brs.0000217681.83524.4a
4. Rajasekaran, S., Bajaj, N., Tubaki, V., Kanna, R. M., & Shetty, A. P. (2013). ISSLS Prize Winner: The Anatomy of Failure in Lumbar Disc Herniation: An In Vivo, Multimodal, Prospective Study of 181 Subjects. Spine, 38(17), 1491–1500. doi:10.1097/BRS.0b013e31829a6fa6
5. Shan, Z., Fan, S., Xie, Q., Suyou, L., Liu, J., Wang, C., & Zhao, F. (2014). Spontaneous Resorption of Lumbar Disc Herniation Is Less Likely When Modic Changes Are Present. Spine, 39(9), 736–744. doi:10.1097/BRS.0000000000000259
6. Rahme, R., & Moussa, R. (2008). The Modic Vertebral Endplate and Marrow Changes: Pathologic Significance and Relation to Low Back Pain and Segmental Instability of the Lumbar Spine. AJNR American Journal of Neuroradiology, 29(5), 838–842. doi:10.3174/ajnr.A0925