Associations Between Back Pain History and Lumbar
MRI Findings
Tapio Videman, MD, PhD,*† Michele C. Battie´, PhD,* Laura E. Gibbons, PhD,‡
Kenneth Maravilla, MD,‡ Hannu Manninen, MD, PhD,§ and Jaakko Kaprio, MD, PhD†储
Study Design.Retrospective monozygotic twin cohort study.
Objectives.Our goal was to investigate the associa-tions between different spinal MRI findings and current, past year, and lifetime low back pain after adjusting for occupational physical loading, smoking, genetics, and early family influences.
Summary of Background Data.The role of spinal pa-thology in back symptoms continues to be controversial.
Methods. The study participants consisted of 115 monozygotic male twin pairs 35 to 69 years of age. The qualitatively assessed MRI parameters were as follows: disc height, bulging, herniations, anular tears, osteo-phytes, spinal stenosis, and endplate changes. Signal in-tensity was measured quantitatively.
Results.After controlling for age, disc height was as-sociated with all back pain variables studied and anular tears with LBP frequency and intensity during the 12 months before imaging. Both were associated with life-time frequency of low back pain interfering with daily activities, disability, and intensity of the worst lifetime pain episode. Other MRI findings did not explain the var-ious symptom histories. Adjusting for physical loading in the past 12 months increased the associations of anular tears and “low back pain today” and 12-month low back pain parameters. After controlling for genotype and other familial influences, the within-pair differences in disc height and anular tears accounted for 6% to 12% of the total variance in the within-pair differences of low back pain variables.
Conclusion.These findings raise new questions about the underlying mechanisms of LBP. The sensitivities of the only significant MRI parameters, disc height narrow-ing and anular tears, are poor, and these findnarrow-ings alone are of limited clinical importance. [Key words: anular tears, back pain, disc degeneration, genetics, heredity, spinal disorders, twins]Spine 2003;28:582–588
“It is quite a striking fact, however, that [in] the great majority of those seeking treatment for pains in the back, . . . in spite of the most careful clinical examination, no pathologic changes can be found. . . .”14This statement by Hirsch and Schajowicz in 1952 also describes today’s situation well. Disc pathology has been thought to be the primary culprit in low back pain (LBP) symptoms.29Yet,
specific pathologic findings in the disc that might under-lie these symptoms remain uncertain. Despite this, the disc has continued to be a primary target of diagnostic procedures and therapeutic interventions of the spine.
Doubts about disc pathology as a cause of LBP have been fueled by findings of high prevalence of abnormal MRI findings among study participants without LBP.5,17,34,43Similar results were reported earlier, based
on myelographic and CT scan studies.15,44 However,
there are studies documenting an association between disc pathology and LBP.3,6,22 Jensen et al compared
study participants without and with a history of LBP; 27%versus54% had a disc protrusion and 1%versus
26% had an extrusion in magnetic resonance imaging (MRI).18In a study of back surgery candidates, anular ruptures were highly associated with patients’ back pain reproduction.28In an autopsy study, the study
partici-pants with a history of at least 1 month of disabling back pain had more pathology of symmetric disc degenera-tion, anular ruptures, endplate defects, osteophytes, and facet joint degeneration. However, the only statistically significant difference was for anular ruptures: 60% of those with anular leak in discography had such a history of back painversus21% of those without a leak.42
There are several challenges in studying the associa-tions between spine pathology and LBP. The use of sum-mary variables for disc degeneration can be a problem. If, for example, two or more disc findings reflecting both atrophic and proliferative changes were combined, pos-sible associations between structural findings and pain could be obscured. Therefore, we should use “clearly” defined structural parameters, when available, in study-ing the associations of pathology and pain, rather than summary variables.41
In addition, there are several modifiers for LBP. Phys-ical loading of pathologic structures through materials handling or postures has been shown to exacerbate symptoms.12,36This was supported by a linear
associa-tion between the severity of LBP and heaviness of work, after adjusting for spine pathology in an autopsy study.42
However, results from functional restoration rehabilita-tion programs demonstrated no changes in pain experi-From the *University of Alberta, Edmonton, Alberta, Canada,
†Finn-ish Twin Cohort Study, Department of Public Health, University of Helsinki, Helsinki, Finland, ‡University of Washington, Seattle, Wash-ington, §Kuopio University Hospital and Kuopio University, Kuopio, Finland, and the储Department of Mental Health, National Public Health Institute, Helsinki, Finland.
Supported by National Institutes of Health (U.S. grant no. AR 40857), the Ministry of Education, the Finnish Work Environment Fund, the Academy of Finland (grant no. 42044), and the Alberta Heritage Foun-dation for Medical Research, Canada.
Acknowledgment date: June 5, 2002. First revision date: August 21, 2002. Acceptance date: August 22, 2002.
The legal regulatory status of the device(s)/drug(s) that is/are the sub-ject of this manuscript is not applicable in my country.
Federal and foundation funds were received in support of this work. No benefits in any form have been or will be received from a commer-cial party related directly or indirectly to the subject of this manuscript. Address correspondence to Tapio Videman, MD, PhD, University of Al-berta, Faculty of Rehabilitation Medicine, 3-48 Corbett Hall, Edmonton, Alberta T6G 2G4, Canada; E-mail: tapio.videman@ualberta.ca
ence with increased physical performance.35
Psycholog-ical factors have as much effect on the reporting of different back-related outcomes as physical stress does.19
The experience and reporting of LBP are dependent on the perceptions and behavior of the individual, but the validity of LBP reporting in relation to LBP experienced needs to be addressed.20,25 In addition, animal studies
have shown that individual differences in both nocicep-tive and analgesic sensitivity exist.27 Among humans,
variation in pain sensitivity has been attributed to shared environment and familial modeling.23Determinants of
pressure pain threshold in adult twins provided evidence that shared environmental influences predominate.24,26
In twin studies, the proportion of variance accounted for by genetic factors has been estimated as 50% for LBP and 21% for sciatica.4,13 These associations could be
explained through physiologic variations of disc degen-eration, neurologic mechanisms, and behavioral characteristics.1,2,27,38
Our goal was to investigate the associations between different spinal MRI findings and current, previous year, and lifetime back pain measures, while controlling for physical loading and some other available factors. Be-cause our study participants were monozygotic twin pairs, we were also able to control for the confounding effects of the combined role of genetics and early family influences. We hypothesized that inconsistencies be-tween current symptoms and current measures of pathol-ogy could be expected because the occurrence of back pain varies unpredictably during a lifetime, whereas MRI findings in the spine are cumulative and usually irrevers-ible. Therefore, the strongest association between pa-thology and LBP could be expected for lifetime pain his-tory, and the weakest for current pain status. In addition, those MRI findings, which are associated with the pa-thology of innervated disc structures, such as anular tears, ruptures, and herniations, could have a direct as-sociation with pain. However, findings in structures without innervation or nonspecific changes, such as nu-clear signal intensity and disc height narrowing, would have, if anything, a weak indirect association with pre-vious year and lifetime pain histories. We also hypothe-sized that disc height narrowing at one or two disc levels, clearly worse than that of neighboring discs, may repre-sent a real trauma leading to disc failure through which innervated scar tissue would be more likely a source of pain than discs with “pure ageing” changes.
Methods
Study Participants.The study participants were selected from the Finnish Twin Cohort, which has been described earlier in more detail.2,21
Questionnaire data from 1975 and 1981 were used to select the monozygotic twin pairs discordant in occu-pational, leisure time physical activities, driving, or smoking histories. The pairs who appeared to meet these criteria were contacted, and of those solicited, 82% participated. The study participants consisted of the 230 males from 35 to 69 years of age (mean 49.4 years).
Interview. A detailed, structured interview was conducted with each volunteer. Current back pain and the frequency and intensity of episodes in the previous 12 months and over the lifetime of the study participants were assessed separately for the lower back. The frequency of pain interfering with daily activities and a disability scale based on the degree of interfer-ence with commonly performed daily tasks, such as lifting gro-ceries, getting dressed, putting on socks, and being able to sleep at night (because of back pain, and not other causes) also were obtained for both recent and lifetime pain. Pain frequency, intensity, and disability in the previous 12 months were highly correlated (r⫽0.64 – 0.80), as were the lifetime measures (r⫽
0.49 – 0.92) (Appendix; Table A).
For each job, they were asked to discuss the tasks performed and to estimate their exposure to specific types of loading con-ditions. A consolidated 4-point scale was used to categorize study participants’ jobs further: 1⫽sedentary work and 4⫽ heavy materials handling and positional loading. Similarly to occupational history, detailed data on smoking, driving his-tory, and sport and other leisure time activities were gathered (Table 1). Details of these items have been reported earlier.2
All study participants received written information about the study procedures before participation, and all study proto-cols were reviewed and approved by the Ethical Committee of the Department of Public Health at the University of Helsinki and the Human Subjects Committee at the University of Washington.
Magnetic Resonance Imaging.The study participants spent at least 45 minutes lying supine immediately before MRI. T1, T2, and proton density-weighted images of the lumbar spines of the study participants were obtained using a 1.5-Tesla scan-ner (Magnetom, Siemens AG, Germany) with surface coil. Field of view was 260 mm and the slice thickness and interslice gap were 4 mm and 0.4 mm, respectively, for sagittal images and 3 mm and 0.3 mm, respectively, for axial slices.
Qualitative evaluations of MRIs were performed indepen-dently by two radiologists. Each spinal level was evaluated separately, blinded to pain histories and exposures. Each MRI finding was rated using a scale from 0 to 3, with 0 being normal
Table 1. Means and Standard Deviations for Occupational and Other Physical Exposures
Variable
Mean (SD) Mean-weighted lifetime occupational loading
score (1–4)
2.5 (0.9) Years with physically-demanding leisure-time
activities at least twice a week
1.7 (6.3) Smoking (yrs⫻packs/day) 14.9 (17.7) Mean-weighted frequency/wk of endurance
sports and activities, age 20⫹yrs
1.2 (2.0) Mean-weighted occupational loading score (1–4),
previous 12 mos
2.0 (1.0) Mean-weighted hrs sitting/day, previous 12 mos 2.1 (2.7) Total hrs occupational driving, previous 12 mos 170 (426) Mean-weighted lifting at work (kg⫻frequency/
day), previous 12 mos
268 (729) Able to move positions at work (1–5 score),
current job
1.8 (1.0) Enjoy work (1–5 score), current job 1.6 (0.8) Neuroticism (0–10 score), 1981 assessment 3.9 (2.4) Extroversion (0–10 score), 1981 assessment 4.4 (2.7)
and 1–3 representing progressive degrees of abnormality. Some of the more severe categories were combined for analyses (Ta-ble 2). Anular tears and stenosis were also analyzed. The in-trareader reliabilities of the different MRI findings were deter-mined for both radiologists, and the assessments with highest reliabilities were used for analyses. The ICCs for the in-trareader repeatabilities of the MRI parameters used were as follows: 0.84 for disc height narrowing, 0.69 for anular tears (contiguous with the outer disc margin), 0.64 for disc bulging, and 0.71 for disc herniations. The kappa coefficients for the intrareader reliability were 0.68 for the presence of endplate irregularities, 0.45 for osteophytes, and 0.51 for spinal steno-sis. Quantitative assessment of disc signal intensity (adjusted cerebrospinal fluid) was performed as previously described (in-traclass correlation coefficient⫽0.97).2
Analyses involved the mean assessment value for the L1–S1 discs, as well as the rating for the “worst” level for each MRI outcome of interest (Appen-dix; Table B).
Data Analysis.Because we had sampled twin pairs, data were analyzed by treating each pair as a cluster using STATA’s soft-ware for survey data to obtain correctPvalues and confidence intervals. Logistic and ordinal logistic models were con-structed, with ordinal outcome variables grouped as described in the Appendix (Table C). Prevalence odds ratios and 95% confidence intervals were calculated. Age was controlled for in all models. All measures significant in univariate analyses were candidates for the multivariate models. In the Appendix (Table A), Kendall’s Tau-b correlation coefficients, partialling for age, are reported for all correlations involving a dichotomous co-variate; Spearman coefficients, partialling for age, are given for the others. The significance of each association was determined through ordinal and binary logistic modeling, as above.
This report is focused primarily on the MRI–pain associa-tion, independent of the twinship of the study participants. But we also looked at the within-twin pair differences for these monozygotic pairs, which removed any familial aggregation,
including genetic differences, in MRI pathology or in LBP re-porting. Normality assumptions for the paired differences in the original, continuous versions of the frequency, intensity, and disability measures were tenable; thus, linear regression models were constructed using the paired differences in the MRI readings, so that the pain variable differences were re-gressed on the imaging variable intrapair differences. The per-cent of the variability explained was calculated using the ad-justed R2
.
Results
Results for the mean and the worst level were generally consistent with each other.
Univariate Results
Measures of decreased disc height were associated with all back pain measures and had the only significant asso-ciations with the presence of sciatica in the worst lifetime episode (Appendix; Table D). Anular tears, disc bulging, osteophytes, endplate changes, and herniations were each associated with the number of lifetime back pain episodes, the intensity of the worst episode and the re-sulting disability, and some other pain parameters. Sig-nal intensity and spiSig-nal stenosis had no significant asso-ciations with any of the pain parameters.
Multivariable Results
Only disc height narrowing and anular tears remained significant in multivariable modeling of the pain out-comes (Table 3). Disc height narrowing was significant in all models, with odds ratios for 1 point on a 0 –3 scale ranging from 1.8 to 2.2 for measures of current and recent LBP. This means that a 1-point higher mean disc height narrowing score is associated with approximately twice the risk of a 1-point higher score on the corre-sponding pain measure. The strongest associations, four-fold to fivefour-fold risks, were with lifetime frequency, inten-sity, and disability. “Sciatic” pain of the worst lifetime back pain episode was associated with a twofold risk. Adjusting for occupational physical demands, static work postures, driving, smoking, and job satisfaction had a small effect on the models. Controlling for physical loading during the past 12 months increased the associ-ations of anular tears and LBP over the past 12 months and made the association with LBP today statistically significant. Anular tears were associated with pain in the previous 12 months and with the number of lifetime episodes, and the intensity of the worst episode, with the presence of tears corresponding to a 50 –90% increase in risk. The presence of a tear was more powerfully associ-ated with pain than a variable incorporating the length of the tear. Endplate irregularities, osteophytes, bulging, herniations, spinal stenosis, and the signal intensity of the disc did not enter into the model’s explaining any of the pain parameters.
Although disc height narrowing and anular tears were associated with many manifestations of LBP, the predic-tive power of these MRI findings is limited. For example, disc height narrowing is strongly associated with ever
Table 2. Qualitative MRI Ratings, Categorized as Used in the Analyses
MRI Finding Ratings %*
Disc height 0⫽normal—typically disc higher than the upper disc
71.6 1⫽slight—disc as high as the normal
upper disc
13.7 2⫽moderate—disc narrower than the
normal upper disc
11.9 3⫽severe—endplates almost in contact 2.8 Anular tear (axial 0⫽none present 85.0
view) 1⫽any tear 15.0
Disc bulging 0⫽none—normal contour of disc 84.9 1⫽slight (approximately⬍2.5 mm) 14.1 2⫽moderate or severe (ⱖ2.5 mm bulge) 1.0 Disc herniation 0⫽none 93.0 1⫽slight (approximately 0–5 mm) 5.4 2⫽moderate or large (⬎5 mm) 1.6 Upper vertebral 0⫽normal 73.4 endplate 1⫽slight defect (1–5 mm) 21.1 irregularities 2⫽moderate defect (⬎5–10 mm) 4.2 3⫽severe defect (⬎10 mm) 1.3 Vertebral osteophytes 0⫽none or slight (approx. 1.5⫾1 mm) 84.9 1⫽moderate (approx. 3.5⫾1 mm) 14.2 2⫽severe (approx.ⱖ4.5 mm) 0.8 * Percent of all L1–S1 discs.
having an LBP episode lasting more than 1 day, with greater than a fourfold risk for each increment in the mean severity score. To have a mean disc height score
⬎1, a study participant would need to have moderate or severe narrowing in at least one disc. Only one of the 43 study participants who never had an episode of LBP had a mean severity score⬎1, so the specificity of this cut point is good. But only 22 (12%) of the 187 study par-ticipants who had an LBP episode had a mean score⬎1, which is poor sensitivity. Using a different cut point, 72% of the study participants with at least one episode of LBP had some disc height narrowing recorded, but so did 63% of those who never had an episode.
The associations between pain in the previous 12 months and MRI findings were small when the effect of familial aggregation was removed. When the within-pair differences in this pain variable were regressed on the within-pair differences in disc height and anular tears, they explained only 7% and 6%, respectively, of the total variance in this LBP parameter. The percentage of the variance in recent and lifetime frequency and inten-sity of LBP or the resulting disability explained varied from 0% to 7% of disc height and from 4% to 6% of anular tears (Table 4).
Discussion
Anular tears were associated with most of the LBP pa-rameters studied. However, disc height was associated with all LBP parameters, including sciatica. As expected, the associations between MRI parameters and pain were clearer for the lifetime parameters than for those for pre-vious year and current LBP. All the other abnormalities in spinal MRIs, including disc herniations, were not as-sociated with any of the LBP measures studied once anu-lar tears or disc height was accounted for. Of all the potential confounders evaluated, controlling for past 12 months, physical loading increased the association mainly of anular tears and LBP today and 12-month LBP parameters. These changes in the associations could in-dicate that there exists an interaction between loading and LBP.
The intermittent and variable nature of symptoms in the short-term, a high rate of forgotten symptoms in the long-term, and other issues affecting measurement of LBP would be expected to keep the unexplained portion of variability in pain high. The associations between spi-nal pathology, LBP, and physical loading are complex and further challenged by problems in measuring histor-ical pain and loading parameters. A structured, in-depth interview may be the best option for getting data on lifetime parameters; however, gross estimates rather than precise measurements can be expected. Despite these limitations, clear associations were found between pain and the two signs of disc pathology. Among the strengths of the study are that it is based on detailed spinal MRI findings and comprehensive data on possible confounders of pain. In addition, because the study par-ticipants were monozygotic twin siblings, we were able to control for genetics and childhood influences.
Our finding of an association of anular tears with LBP is consistent with what is known about the innervation of the disc and is supported by some earlier stud-ies.28,37,42The lack of correlation between disc
hernia-tion and LBP parameters is unlikely to be the result of
Table 3. Multivariate Models for Nine Measures of LBP, Controlling for Age and Clustering by Twin Pair
Back Pain Parameter Modeled
Anular Tears (Any) OR (95% CI)
Disc Height Narrowing* OR (95% CI)
†Adjusted †Adjusted
LBP today NS‡ 2.1 (1.0, 4.4) 2.4 (1.2, 4.7) 2.3 (1.0, 5.0) Ever back pain lasting⬎1 day NS‡ 4.5 (1.9, 10.6)
Frequency LBP past 12 mos (0–3) 1.8 (1.1, 2.9) 2.0 (1.1, 3.5) 2.2 (1.4, 3.7) 2.1 (1.2, 3.7) Intensity of pain past 12 mos (0–3) 1.8 (1.2, 3.0) 2.2 (1.3, 3.9) 1.8 (1.1, 2.9) 1.8 (1.0, 3.1) Disability past 12 mos (0–2) NS‡ 1.9 (1.1, 3.0) 1.8 (1.1, 2.9) 1.9 (1.1, 3.3) Number of episodes (lifetime) (0–2) 1.9 (1.1, 3.2) 4.0 (2.3, 7.0)
Pain intensity in worst episode (0–2) 1.5 (1.1, 2.1) 5.0 (2.7, 9.1) Disability from worst episode (0–2) 1.9 (1.1, 3.3) 4.2 (2.4, 7.2) Sciatica in lifetime worst LBP episode NS‡ 2.1 (1.2, 3.8) LBP⫽low back pain; OR⫽odds ratio; CI⫽confidence interval; NS⫽not significant.
* OR for 1 point on a 0 –3 score. Mean score L1–S1.
† In addition, 4 pain measures for the past 12 months were adjusted for physical loading in the past 12 months. ‡ Did not enter the model.
Table 4. Percent of Variance in Paired Differences in Pain Accounted for by Paired Differences in Mean Disc Height and Presence of Anular Tears
Pain Contrast Disc Height Anular Tears Both Combined Frequency LBP past 12 mos 7 6 12 Intensity of pain past 12 mos 1 6 6 Disability past 12 mos 3 5 8 No. of episodes (lifetime) 0 6 6 Pain intensity in worst episode 5 4 7 Disability from worst episode 5 5 9 Percents below 3 are not statistically significant.
insufficient statistical power because 28% of study par-ticipants had at least one herniation. But because hernia-tions decrease in size or can disappear over time, our chances of finding an association may have decreased when comparing worst lifetime sciatica episode with “endpoint” spine MRI.8However, our finding is
concor-dant with some earlier studies, in which disc bulges and herniations were not associated with LBP.5,18,44In
addi-tion, recent studies have indicated that sciatic pain is not only caused by compression but also by biochemical ef-fects associated with disc ruptures.16,31,32
Disc height narrowing is commonly regarded as a nonspecific outcome of aging with little clinical impor-tance. The clear association of disc height with all stud-ied LBP parameters, even for “LBP today,” was there-fore, partly, an unexpected result, although not totally new. Frymoyeret alfound that there were differences in traction spurs and/or disc space narrowing at L4 –L5 between three groups of men with no history, moderate, or with severe back pain.11 Similarly, in longitudinal
study, radiographic disc degeneration was associated with future back pain.39,40
Nachemson has suggested that premature aging changes render the disc mechanically incompetent, cre-ating abnormal motion that subject spinal structures to undue stress and lead to pain.30In a recent study, there
was “evidence of instability” in 11% of motion segments with narrowed disc space using “functional” radiogra-phy.33Brownet alfound angiogenesis (proliferation of
blood vessels and nerve fibers) in the endplate regions and underlying vertebrae in patients with severe back pain and markedly reduced disc height, suggesting that endplates and vertebrae were the source of pain.9
How-ever, the prevalence of angiogenesis in the endplate re-gions of narrowed discs is unclear. Nerve ingrowth has been demonstrated also through anular tears and is sus-pected to be a disc-related causal factor for LBP.10,14
We had hypothesized that a disc with markedly more degeneration than its neighbor discs (an outlier) could be a true injury and would be a more likely source of pain than narrowed discs throughout the lumbar spine, sug-gesting generalized ageing. However, the associations with pain of an outlier narrowed disc and mean disc height narrowing were generally the same (data not given).
Conclusion
After considering the consistent effects of disc height and anular tears, the other spine MRI findings, such as disc herniations, osteophytes, stenosis, and endplate irregu-larities were not associated with LBP. Adjusting for ex-trinsic factors thought to worsen LBP had almost no effect on the associations. After taking the combined ef-fects of genetics and shared environment into account, disc height and tears each explained 7% and 6%, respec-tively, of the total variance in the LBP in the past year. The association of pain and pathologic anulus, an inner-vated structure, has a physiologic explanation. However,
we can only speculate that narrowed discs could be as-sociated with prior pain as a consequence of disc failure and related ingrowth of nerve fibers through endplate or anular lesions or irritation of surrounding tissues. More information on the occurrence rates of angiogenesis in discs could increase our current limited understanding about the phenomenon as a possible source for common back pain. However, our results suggest that the use of MRI assessments of anular tears and disc height alone in clinical practice would be of limited value, concordant with earlier conclusions.7,17
Key Points
● Disc height and anular tears are associated with LBP history, but their sensitivity is poor, rendering them of limited clinical value.
● Adjusting for physical loading in past the 12 months increased the associations of anular tears and LBP in the past 12 months.
● The associations between pain and MRI findings were reduced after controlling the effect of familial aggregation.
References
1. Annunen S, Paassilta P, Lohiniva J, et al. An allele of COL9A2 associated with intervertebral disc disease. Science 1999;285:409 –12.
2. Battie´ MC, Videman T, Gibbons LE, et al. 1995 Volvo Award in clinical sciences: determinants of lumbar disc degeneration. A study relating lifetime exposures and magnetic resonance imaging findings in identical twins. Spine 1995;20:2601–12.
3. Beattie PF, Meyers SP, Stratford P, et al. Associations between patient report of symptoms and anatomic impairment visible on lumbar magnetic reso-nance imaging. Spine 2000;25:819 –28.
4. Bengtsson B, Thorson J. Back pain: a study of twins. Acta Genet Med Ge-mellol (Roma) 1991;40:83–90.
5. Boden SD, Davis, DO, Dina TS, et al. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint Surg Am 1990;72:403– 8.
6. Boos N, Dreier D, Hilfiker E, et al. Tissue characterization of symptomatic and asymptomatic disc herniations by quantitative magnetic resonance im-aging. J Orthop Res 1997;15:141–9.
7. Borenstein DG, O’Mara JW Jr, Boden SD, et al. The value of magnetic resonance imaging of the lumbar spine to predict low-back pain in asymptomatic subjects: a seven-year follow-up study. J Bone Joint Surg Am 2001;83:1306 –11. 8. Bozzao A, Gallucci M, Masciocchi C, et al. Lumbar disk herniation: MR
imaging assessment of natural history in patients treated without surgery. Radiology 1992;185:135– 41.
9. Brown MF, Hukkanen MV, McCarthy ID, et al. Sensory and sympathetic innervation of the vertebral endplate in patients with degenerative disc dis-ease. J Bone Joint Surg Br 1997;79:147–53.
10. Freemont AJ, Peacock TE, Goupille P, et al. Nerve ingrowth into diseased intervertebral disc in chronic back pain. Lancet 1997;350:178 – 81. 11. Frymoyer JW, Newberg A, Pope MH, et al. Spine radiographs in patients
with low-back pain: an epidemiological study in men. J Bone Joint Surg Am 1984;66:1048 –55.
12. Hartvigsen J, Bakketeig LS, Leboeuf-Yde C, et al. The association between physical workload and low back pain clouded by the “healthy worker” effect: population-based cross-sectional and 5-year prospective question-naire study. Spine 2001;26:1788 –92; discussion 92–3.
13. Heikkila¨ JK, Koskenvuo M, Helio¨vaara M, et al. Genetic and environmental factors in sciatica: evidence from a nationwide panel of 9365 adult twin pairs. Ann Med 1989;21:393– 8.
14. Hirsch C, Schajowitcz F. Studies on changes in the lumbar annulus fibrosus. Acta Orthop Scand 1952;22:184 –231.
15. Hitselberger WE, Witten RM. Abnormal myelograms in asymptomatic pa-tients. J Neurosurg 1968;28:204 – 6.
16. Igarashi T, Kikuchi S, Shubayev V, et al. 2000 Volvo Award winner in basic science studies: exogenous tumor necrosis factor-alpha mimics nucleus pul-posus-induced neuropathology. Molecular, histologic, and behavioral com-parisons in rats. Spine 2000;25:2975– 80.
17. Jarvik JJ, Hollingworth W, Heagerty P, et al. The Longitudinal Assessment of Imaging and Disability of the Back (LAIDBack) Study: baseline data. Spine 2001;26:1158 – 66.
18. Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med 1994;331:69 –73.
19. Johansson JA, Rubenowitz S. Risk indicators in the psychosocial and phys-ical work environment for work-related neck, shoulder and low back symp-toms: a study among blue- and white-collar workers in eight companies. Scand J Rehabil Med 1994;26:131– 42.
20. Kagan AR, Levi L. Health and environment—psychosocial stimuli: a review. Soc Sci Med 1974;8:225– 41.
21. Kaprio J, Koskenvuo M, Artimo M, et al. The Finnish twin registry: baseline characteristics. Kansanterveystiteen julkaisuja 1979;47:1–74.
22. Komori H, Shinomiya K, Nakai O, et al. The natural history of herniated nucleus pulposus with radiculopathy. Spine 1996;21:225–9.
23. Lester N, Lefebvre JC, Keefe FJ. Pain in young adults: I. Relationship to gender and family pain history. Clin J Pain 1994;10:282–9.
24. MacGregor AJ, Griffiths GO, Baker J, et al. Determinants of pressure pain threshold in adult twins: evidence that shared environmental influences pre-dominate. Pain 1997;73:253–7.
25. Miettinen O. Low-back pain in occupational medicine: examining evidence-based guidelines. Montreal, 2001.
26. Mikkelsson M, Kaprio J, Salminen JJ, et al. Widespread pain among 11-year-old Finnish twin pairs. Arthritis Rheum 2001;44:481–5.
27. Mogil JS. The genetic mediation of individual differences in sensitivity to pain and its inhibition. Proc Natl Acad Sci USA 1999;96:7744 –51. 28. Moneta GB, Videman T, Kaivanto K, et al. Reported pain during lumbar
discography as a function of anular ruptures and disc degeneration: a re-analysis of 833 discograms. Spine 1994;19:1968 –74.
29. Mooney V, Brown M, Modic M. Clinical perspectives. In: Frymoyer J, Gor-don S, eds. New Perspectives on Low Back Pain. Chicago, IL: AAOS, 1989. 30. Nachemson A. The future of low back pain research. In: Frymoyer JW, Gordon ST, eds. New Perspectives on Low Back Pain. Chicago, IL: AAOS, 1989.
31. Olmarker K, Nordborg C, Larsson K, et al. Ultrastructural changes in spinal nerve roots induced by autologous nucleus pulposus. Spine 1996;21:411– 4. 32. Olmarker K, Rydevik B, Nordborg C. Autologous nucleus pulposus induces neurophysiologic and histologic changes in porcine cauda equina nerve roots. Spine 1993;18:1425–32.
33. Pitka¨nen M, Manninen H. Sidebending versus flexion-extension radiographs in lumbar spinal instability. Clin Radiol 1994;49:109 –14.
34. Powell MC, Wilson M, Szypryt P, et al. Prevalence of lumbar disc degener-ation observed by magnetic resonance in symptomless women. Lancet 1986; 2:1366 –7.
35. Rainville J, Ahern DK, Phalen L, et al. The association of pain with physical activities in chronic low back pain. Spine 1992;17:1060 – 4.
36. Riihima¨ki H. Low-back pain, its origin and risk indicators. Scand J Work Environ Health 1991;17:81–90.
37. Saifuddin A, Braithwaite I, White J, et al. The value of lumbar spine magnetic resonance imaging in the demonstration of anular tears. Spine 1998;23: 453–7.
38. Sambrook PN, MacGregor AJ, Spector TD. Genetic influences on cervical and lumbar disc degeneration: a magnetic resonance imaging study in twins. Arthritis Rheum 1999;42:366 –72.
39. Symmons DP, van Hemert AM, Vandenbroucke JP, et al. A longitudinal study of back pain and radiological changes in the lumbar spines of middle aged women: I. Clinical findings. Ann Rheum Dis 1991;50:158 – 61. 40. Symmons DP, van Hemert AM, Vandenbroucke JP, et al. A longitudinal
study of back pain and radiological changes in the lumbar spines of middle aged women: II. Radiographic findings. Ann Rheum Dis 1991;50:162– 6. 41. Videman T, Gibbons LE, Battie´ MC, et al. The relative roles of intragenic
polymorphisms of the vitamin D receptor gene in lumbar spine degeneration and bone density. Spine 2001;26:7–12.
42. Videman T, Nurminen M, Troup JD. 1990 Volvo Award in clinical sciences. Lumbar spinal pathology in cadaveric material in relation to history of back pain, occupation, and physical loading. Spine 1990;15:728 – 40.
43. Weinreb JC, Wolbarsht LB, Cohen JM, et al. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptom-atic nonpregnant women. Radiology 1989;170:125– 8.
44. Wiesel SW, Tsourmas N, Feffer HL, et al. A study of computer-assisted tomography: I. The incidence of positive CAT scans in an asymptomatic group of patients. Spine 1984;9:549 –51.
Appendix
Table A. Correlations Between the Pain Measures, Controlling for Age
Pain Measure LBP Today Frequency 12 mos Intensity 12 mos Disability 12 mos Back Pain 1 day Lifetime, No. Intensity, Worst Disability, Worst Sciatica, Worst Any LBP today 1.00 0.42 0.25 0.26 0.07* 0.16 0.20 0.14 0.11* Frequency LBP previous 12 mos 1.00 0.80 0.64 0.12* 0.22 0.23 0.19 0.18 Intensity of pain previous 12 mos 1.00 0.78 0.19 0.29 0.26 0.23 0.20 Disability previous 12 mos 1.00 0.26 0.31 0.31 0.29 0.19 Ever had back pain lasting more than a day 1.00 0.49 0.49 0.48 0.33
No. of episodes (lifetime) 1.00 0.87 0.86 0.31
Pain intensity in worst episode 1.00 0.92 0.29
Disability from worst episode 1.00 0.30
Sciatica (present in lifetime worst LBP episode)
1.00 LBP⫽low back pain.
Table B. Means and Standard Deviations of the L1–S1 Average and the Worst Score in L1–S1 for the
MRI Parameters
MRI Parameter Average L1–S1
Worst Level T1 signal intensity
(cerebral–spinal fluid adjusted)*
1.05 (0.11) 0.90 (0.15) Disc height (0–3 score) 0.5 (0.5) 1.3 (1.0) Any anular tears contiguous with
the margin†
0.15 (0.17) 0.53 (0.58) Anular tears contiguous with the
margin (mm)
0.7 (0.9) 2.6 (2.9) Stenosis (mm) 0.3 (0.8) 1.2 (2.9) Herniations (0–2 score) 0.1 (0.2) 0.4 (0.6) Disc bulging (0–2 score) 0.2 (0.2) 0.5 (0.6) Endplate irregularities (0–3 score) 0.3 (0.3) 1.0 (0.9) Osteophytes (0–2 score) 0.3 (0.4) 1.1 (1.1) * Scores reversed in analyses, so a higher score is worse.
† 15% of discs had a tear, and 53% of subjects had at least one tear.
Table C. Occurrence of Pain
Pain Measure %
Any LBP today 20.4
Frequency of LPB past 12 mos
None 33.9
1 to 3 times/yr 30.4
Several times/yr to monthly 17.0 Weekly or more frequent 18.7 Intensity of worst pain in past 12 mos (0–100)
None 33.9
1–35 29.1
36–100 37.0
Disability from worst pain in past 12 mos (0–2 score)
None 35.2
0.1–1 34.3
1.1–2 30.4
Ever had LBP lasting more than a day 81.3 No. of episodes (lifetime)
None 42.5
1 or 2 31.9
3–100 25.2
Intensity of pain in worst episode
None 42.9
24–80 31.9
85–100 25.2
Disability from worst episode (0–3 scale)
None 43.4
0.3 to 2 30.1
2.3 to 3 26.5
Sciatica (present in lifetime worst episode) 32.9 LBP⫽low back pain.
Table D. Odds Ratios and 95% Confidence Intervals for Significant Univariate (Age-Adjusted) Associations Between Pain and MRI Readings
Pain Assessment MRI Reading OR (95% CI) Any LBP today Disc narrowing (0–3), mean 2.4 (1.2, 4.7)
Bulging (0–2), worst 2.0 (1.1, 3.5) Ever had back pain Disc narrowing (0–3), mean 4.5 (1.9, 10.6)
lasting more than Bulging (0–2), worst 1.8 (1.1, 3.1) a day Osteophytes (0–3), mean 3.3 (1.2, 9.3) Frequency LBP past Disc narrowing (0–3), mean 2.4 (1.4, 4.0) 12 mos (0–3 scale) Anular tears (any) 1.9 (1.2, 3.1) Endplate changes (0–3), worst 1.5 (1.1, 2.1) Intensity of pain past Disc narrowing (0–3), mean 1.9 (1.2, 3.2) 12 mos (0–3 scale) Anular tears (any) 1.9 (1.2, 3.1) Disability past 12 mos
(0–2 scale)
Disc narrowing (0–3), mean 1.7 (1.1, 2.9) No. of episodes Disc narrowing (0–3), mean 4.3 (2.5, 7.5) (lifetime) Anular tears (any) 2.3 (1.3, 3.7) (0–2 scale) Bulging (0–2), worst 2.4 (1.6, 3.7) Osteophytes (0–3), mean 2.3 (1.2, 4.2) Endplate changes (0–3), worst 1.3 (1.0, 1.7) Herniations (0–2), worst 1.7 (1.3, 2.4) Pain intensity in Disc narrowing (0–3), mean 5.6 (3.0, 10.2)
worst episode Anular tears (any) 2.2 (1.3, 3.7) (0–2 scale) Bulging (0–2), worst 2.5 (1.6, 4.1) Osteophytes (0–3), mean 2.4 (1.3, 4.7) Endplate changes (0–3), worst 1.4 (1.1, 1.9) Herniations (0–2), worst 1.7 (1.1, 2.5) Disability from worst Disc narrowing (0–3), mean 4.4 (2.6, 7.6) episode (0–2 scale) Anular tears (any) 2.2 (1.3, 3.6) Bulging (0–2), worst 2.2 (1.4, 3.5) Osteophytes (0–3), mean 2.4 (1.3, 4.5) Endplate changes (0–3), worst 1.6 (1.2, 2.0) Herniations (0–2), worst 1.7 (1.1, 2.5) Sciatica (present in
lifetime worst episode)
Disc narrowing (0–3), mean 2.1 (1.2, 3.8)
LBP⫽low back pain; MRI⫽magnetic resonance imaging; OR⫽odds ratio; CI⫽confidence interval.
