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AJNR Awards, New Junior Editors, and more. Read the latest AJNR updates

EditorialEDITORIAL

Can You Get a Stiff Back from Lack of Spinal Stiffness?

Pierre C. Milette
American Journal of Neuroradiology June 1999, 20 (6) 960-962;
Pierre C. Milette
M.D
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Most neuroradiologists have a keen interest in spinal tumors or spinal vascular malformations, but have little curiosity for back pain, except if they happen to suffer from it. Unless back pain is associated with a definite medullopathy or radiculopathy caused by spinal stenosis or disk herniation, traditional neurologists and neurosurgeons share this lack of interest, and tend to refer afflicted patients to rheumatologists, anesthesiologists, physiatrists, and orthopedic spine surgeons. These specialists usually interact with musculoskeletal radiologists experienced in diagnostic and therapeutic spine procedures who know that most lower back pain sufferers do not show evidence of a classical radiculopathy. Those patients actually complain of radiating pain to the lower extremities that cannot be explained by nerve-root compression or irritation, which is referred from the disk itself (1). During recent years, noninterventional neuroradiologists have received an increasing number of requests to perform diskograms, facet blocks, nerve-root sleeves, or epidural injections, not to mention chemonucleolysis and vertebroplasty. These fields are both rewarding and demanding. Becoming a key player as a pain management consultant requires an open mind and some effort to understand complex biomechanical concepts.

In this issue of the AJNR, Haughton et al (page 1161) report the results of original experimentation involving 82 lumbar motion segments harvested from cadavers. These investigators have correlated the MR appearance of lumbar intervertebral disks with their stiffness. Motion segment stiffness is defined as the ratio of an applied load to the induced displacement or rotation. A loss of stiffness results in exaggerated movement of a spinal motion segment when torque is applied. In a strictly biomechanical perspective, loss of stiffness indicates spinal instability. Clinical criteria also have been proposed to define spinal instability, but these are more controversial. Trying to assess the validity of MR imaging for diagnosis of spinal instability is most relevant because the reliability of conventional lateral flexion and extension lumbar spine radiographs is quite poor. Using a classification of annular tears originating from the same institution, these investigators have found that the presence of annular tears on MR images of these specimens was significantly associated with a loss of motion segment stiffness. Moderate loss of stiffness was apparent in disks with transverse or concentric annular tears, and severe loss was documented in disks with radial annular tears.

This study is interesting in many aspects. In most cases, the diagnosis of a radial annular tear was made, not because the radial tear was directly observed, but because the involved disk revealed a high-intensity zone (HIZ) in the annulus fibrosus or a decreased central signal intensity with bulging of the annulus fibrosus. All suspected radial tears on MR images were confirmed by cryomicrotome pathologic examinations, which were reported in a complementary paper (2). This correlates very well with the findings of lumbar diskography in living individuals. In symptomatic patients, diskograms generally reveal radial annular tears in all disks with a definite loss of central signal intensity on T2-weighted images, and the majority of these tears appear responsible for contemporary symptoms. Surprisingly, these radial tears usually are quite localized. The MR images are misleading, because the loss of signal intensity usually involves the entire nucleus pulposus and inner annulus, and therefore suggests dehydration or some vague diffuse degenerative process. Most neuroradiologists who do not use diskography are reluctant to believe such disks may cause significant symptoms. It should be emphasized that radial annular tears do not represent features of the normal aging process. In this study, the age of cadavers ranged from 49 to 87 years (average age, 74 years) at time of death, and yet only 33% of the harvested motion segments demonstrated radial annular tears or advanced degeneration (defined here as a loss of more than 50% of the disk height or the association of large osteophytes). These findings are in line with those of Kieffer et al, who had performed lumbar diskograms in 106 cadavers, and had found radial annular tears in 37% of specimens from subjects over the age of 40 (3). Because they are present in only a minority of elderly disks, radial annular tears cannot be considered incidental findings of the normal aging process.

Transverse tears, however, defined as small horizontal tears at the junction of the outer annulus with the ring apophysis, usually are not associated with loss of central disk signal intensity, loss of disk height, or a bulging annulus. They are the rule rather than the exception in the older cadavers, and therefore they appear to represent a feature of the normal aging process. It is difficult to conceive they can account for a significant decrease in motion segment stiffness, as the results of this study suggest. Transverse tears were lumped with concentric tears in a group showing significant loss of stiffness in comparison to normal disks, although this loss was not as severe as the one observed in the radial tear group. The decision to proceed to such a grouping was probably dictated by sampling size requirements; unfortunately, the presentation of results does not allow one to assess the specific contribution of the transverse tear subgroup in the reduction of stiffness. I suspect that concentric tears had a much greater impact. The exact nature of concentric tears remains very controversial. The authors explain that they represent “delamination” between concentric lamellae of the annulus fibrosus, but Ahmed and Marchand, using a layer-by-layer peeling technique and microscopic examination of various cut surfaces of the annulus fibrosus, found no evidence of layer-to-layer connections or links between the concentric fibers of the annulus fibrosus (4). Until now, concentric tears have been thought to correspond to localized accumulation of mucoid material filling the potential spaces between the layers of the outer annulus. Is it really the case or do they actually represent bona fide localized annular tears that eventually can lead to the formation of a perceivable HIZ on MR images? And, if so, do radial tears simply result from the coalescence of such contiguous localized tears along a particular radius of the disk?

A study like this allows one to raise other questions which, I hope, will stimulate the authors to engage in other similar fundamental studies. In the absence of annular tears, what characterizes the normal disk's aging process? Does motion segment stiffness increase or decrease as we get older? Is nature compensating for a loss of stiffness caused by “age-related” tears (ie, transverse and concentric) by producing osteophytes limited to the anterior and lateral aspect of the adjacent vertebral bodies, because they can be found in all skeletons of individuals over 40 (5)? Interestingly, disks with severe collapse and large osteophytes were shown to have increased stiffness with respect to disks with radial tears. After a radial tear has seriously compromised stability, the progressive replacement of the residual nucleus and annulus by collagenous fibrous tissue probably represents another mechanism nature uses to restore some of the lost stiffness.

With this study, Haughton et al have clearly demonstrated that a radial annular tear causes severe loss of motion segment stiffness and, therefore, significant biomechanical spine instability. The exact relationship between instability and pain, of course, remains to be established. As the authors suggest, exaggerated motion caused by instability may result in greater stress in adjacent innervated connective tissue, and may also cause greater risk of nerve-root compression and irritation in the foramina. I might add that, when severe pain occurs, a “stiff back” caused by muscle spasm may well be another mechanism nature has found to restore spinal stability temporarily.

References

  1. ↵
    Ohnmeiss DD, Vanharanta H, Ekholm J. Degree of disc disruption and lower extremity pain. . Spine 1997;22:1600-1605
    CrossRefPubMed
  2. ↵
    Schmidt TA, An HS, Lim TH, Nowicki BH, Haughton VM. The stiffness of lumbar spinal motion segments with a high-intensity zone in the anulus fibrosus. . Spine 1998;23:2167-2173
    CrossRefPubMed
  3. ↵
    Kieffer SA, Stadlan EM, Mohandas A, Peterson HO. Discographic-anatomical correlation of developmental changes with age in the intervertebral disc. . Acta Radiol 1969;9:733-739
  4. ↵
    Marchand F, Ahmed AM. Investigation of the laminate structure of lumbar disc anulus fibrosus. . Spine 1990;15:402-410
    CrossRefPubMed
  5. ↵
    Nathan H. Osteophytes of the vertebral column. An anatomical study of their development according to age, race, and sex, with consideration as to their etiology and significance. . J Bone Joint Surg Am 1962;44:243-268
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American Journal of Neuroradiology
Vol. 20, Issue 6
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Pierre C. Milette
Can You Get a Stiff Back from Lack of Spinal Stiffness?
American Journal of Neuroradiology Jun 1999, 20 (6) 960-962;

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Can You Get a Stiff Back from Lack of Spinal Stiffness?
Pierre C. Milette
American Journal of Neuroradiology Jun 1999, 20 (6) 960-962;
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