The disc-endplate-bone-marrow complex classification: progress in our understanding of Modic vertebral endplate changes and their clinical relevance.

BACKGROUND CONTEXT: The disc, endplate (EP), and bone marrow region of the spine form a single anatomical and functional interdependent unit; isolated degeneration of any one structure is rare. Modic changes (MC), however, are restricted to the subchondral bone alone and based on only T1 and T2 sequences of MRI. This results in poor reliability in differentiating fat from edema and hence may give a false impression of disease inactivity. PURPOSE: To study the changes in disc, endplate, and bone marrow as a whole in degeneration and propose a classification based on the activity status of this complex with the addition of STIR MRI sequences. STUDY DESIGN: Observational cohort. PATIENT SAMPLE: Patients with isolated brain, cervical, or thoracic spine injury and patients with low back pain (LBP) who underwent MRI formed the control and study groups, respectively. OUTCOME MEASURES: Demographic data, the prevalence of MC and disc-endplate-bone marrow classification (DEBC) changes, EPs undergoing reclassification based on DEBC, and comparison of the prevalence of MC, DEBC, H+modifier and DEBC with H+concordance between control and LBP group. The study determined the risk of LBP patients undergoing surgery as well as the incidence of postoperative infection based on DEBC changes. Significance was calculated by binomial test and chi-square test with the effect size of 0.3 to 0.5. Prevalence and association of outcome were calculated by Altman's odds ratio with the 95% CI and the scoring of z statistics. Logistic expression was plotted for independent variables associated with each class of both Modic and DEBC against dependent variables surgery and nonsurgery. METHODS: Lumbar segments in both groups were assessed for MC types. The DEBC classification was developed with the addition of STIR images and studying the interdependent complex as a whole: type-A: acute inflammation; type-B: chronic persistence; type-C: latent and type-D: inactive. Modifier H+ was added if there was disc herniation. The classification was compared with MC and correlated to clinical outcomes. RESULTS: A total of 3,560 EPs of 445 controls and 8,680 EPs in 1,085 patients with LBP were assessed. Four nonMC, 560 MC-II, and 22 MC-III EPs were found to have previously undetected edema in STIR (n=542) or hyperintensity in discs (n=44) needing reclassification. The formerly undescribed type-B of DEBC, representing a chronic persistent activity state was the most common (51.8%) type. The difference between the control and LBP of H+(12% vs 28.8%) and its co-occurrence with DEBC type 1.1% vs 23.3%) was significant (p<.0001). The odds ratio for the need for surgery was highest (OR=5.2) when H+ and DEBC type change co-occurred. Postoperative deep infection (as determined by CDC criteria) was 0.47% in nonDEBC, compared with 2.4% in patients with DEBC (p=.002), with maximum occurrence in type-B. CONCLUSION: Classification based on the classic MC was found to need a reclassification in 586 EPs showing the shortcomings of results of previous studies. Considering the DEBC allowed better classification and better predictability for the need for surgical intervention and incidence of postoperative infection rate than MC.

Factors that influence neurological deficit and recovery in lumbar disc prolapse-a narrative review.

Neurodeficit due to lumbar disc herniation (LDH) is a serious complication and can range from sensory hypoesthesia in a single dermatome to a debilitating condition like cauda equina syndrome (CES). Many authors have described variable clinical and radiological risk factors for neurodeficit in LDH. Similarly the prognostic factors influencing recovery have been variable across the studies. This narrative review discusses the pathogenesis, most consistent factors associated with the occurrence of neurodeficit in LDH patients and also the factors which have a prognostic role in recovery. Pathological mechanisms like venous congestion, neuronal ischaemia and multiple root impairment act either individually or in combination to result in neurodeficit in LDH patients. Among the clinical risk factors, diabetes mellitus and acute onset of symptoms have been associated with neurodeficit while pre-existing spinal canal stenosis, non-contained discs (sequestrated/migrated) are potential radiological risk factors for developing neurodeficit. When considering prognostic factors for recovery, pre-operative muscle strength is the only significant factor. Knowledge about the causative and prognostic factors in neurodeficit following LDH would help in the successful management of this condition.