Friday, September 28, 2018 1:00 PM–2:30 PM abstracts: a new look at imaging: 203. Analysis of chronic low back pain with magnetic resonance imaging T2 mapping of lumbar intervertebral disc

Abstract

BACKGROUND CONTEXT Intervertebral disc degeneration (IVDD) is considered to be the principal tissue as a source of low back pain (LBP). There are many reports concerning discogenic LBP from the aspect of pathology, diagnosis, and treatment, however the mechanism and treatment still remain to be unclear. Magnetic resonance imaging (MRI) is an important modality for diagnosis of degenerative intervertebral disc (IVD). Signal variation of the discs on T2-weighted images reflects age and degeneration and allows for the determination of disc degeneration. Specifically, since signal strength in the MRI is related to water and proteoglycan content, changes in MRI signal strength in the nucleus pulposus can indicate IVDD. IVDD has been classified by T2-weighted images using the system described by Pfirrmann et al., but since this classification is based on visual evaluation, the quantification of degeneration using this strategy is unclear. In recent years, there have been several reported attempts using MRI T2 mapping and MRI T1p mapping to quantify lumbar disc degeneration. MRI T2 mapping utilizes the T2 relaxation time for quantification of moisture contents and the collagen sequence breakdown. In our previous work, we used MRI T2 mapping to quantify the extent of IVDD and reported a correlation with Pfirrmann classifications. Recently, there are a few reports regarding the quantitative evaluation of discogenic LBP with MRI T2 mapping and MRI T1p mapping, but the number is small. PURPOSE In this study, we used MRI T2 mapping to quantify IVDD and investigate possible correlations between these quantified values and the low back pain visual analog scale (VAS) scores and Japanese Orthopaedic Association Back Pain Evaluation Questionnaire (JOABPEQ) scores. STUDY DESIGN/SETTING Cross sectional study. PATIENT SAMPLE Twenty-eight (15 males, 13 females; mean age, 48.9±9.6 years; range, 22–60 years) patients whose visual analog scale scores were >30mm for CLBP were included. Further, 25 asymptomatic control participants matched with the CLBP group subjects for gender and age (13 males, 12 females; mean age, 43.8±14.5 years; range, 23–60 years) who had no low back pain, constituted the control group. OUTCOME MEASURES VAS scores and JOABPEQ scores (low back pain and lumbar function). METHODS We screened the subjects whose disc degeneration at L4-5 level was Pfirrmann grade III–V, but another discs were Pfirrmanngrade I–II. For measurement, disc was divided into five equal areas, designating the front fifth of the anterior annulus fibrosus (AF), the middle fifth of the nucleus pulposus (NP), and the last fifth of the posterior AF, referring to past report. The mean values in the region of interest (ROI) were measured. T2 values were measured with MedCalc (version 10.2.0.0, MedCalc Software, Mariakerke, Belgium). We compared T2 values of the CLBP group to the control group. We also investigated possible correlations between these quantified values at the L4-5 level (a total of 28 lumbar discs) and the VAS scores and JOABPEQ scores (low back pain and lumbar function) in the CLBP group. Differences among groups were compared using the Mann–Whitney U test. The relationship between T2 values of IVD and CLBP were analyzed by the Spearman's rank-correlation coefficient. A P value of less than .05 was considered statistically significant. RESULTS T2 values for the control and CLBP groups were 70.2±14.4ms and 63.4±20.1ms, respectively, for the anterior AF, 80.8±31.3ms and 71.7±16.7ms, respectively, for NP, 70.3±15.8ms and 54.4±9.7ms, respectively, for the posterior AF. T2 values for IVD tended to be lower in the CLBP group than in the control group, and these values were significantly different (p CONCLUSIONS Conventionally, IVDD has been characterized by MRI findings according to the classifications reported by Pfirrmann. However, there are problems with this technique, such as difficulty with assessments of early degeneration and the AF as well as poor reproducibility and objectivity because the classifications are visually performed. In the present study, we used MRI T2 mapping to quantitatively investigate a possible correlation between the degree of IVDD and CLBP. The results indicated a correlation between posterior AF degeneration and CLBP. Sinuvertebral nerves, which originate from spinal nerve roots, are distributed around the posterior AF region; therefore, this area is rich innervated. IVD with myelomeres are controlled through sinuvertebral nerves and those without myelomeres are controlled through paravertebral sympathetic nerves. We think that these changes which so rich afferent fibers around the posterior AF grow into disc provide an explanation for the induction of discogenic LBP in patients with IVDD. In addition, sensory nerve ending had differences of the sensitivity against noxious stimuli. The mechanical threshold of front part in IVD were 241g (164–279g), in contrast that of back side part (longitudinal ligament) were 80.3g (20.9–164g) . We speculated about a possibility that CLBP did not show correlations with T2 value of anterior AF or that of NP, but with that of posterior AF, because of low sensitivity against noxious stimuli at front part in IVD. Invasive discography has been conventionally used to examine discogenic LBP. This technique, which can cause pain due to the injection of contrast fluid between intervertebral discs, has a high false-positive rate; therefore, it has been reported to be not entirely suitable as an index for identifying the source of pain. Moreover, discography has been reported to cause progression of intervertebral disc degeneration. MRI T2 mapping is a noninvasive quantitative evaluation method that offers high reproducibility in contrast to discography. The results of the present study suggest that MRI T2 mapping could be used instead of invasive discography as a quantitative method for diagnosing discogenic pain.