MRI follow-up of subchondral signal abnormalities in a selected group of chronic low back pain patients

• Published in: European spine journal 2008-10, Vol.17 (10), p.1300-1308
• Main Authors: Luoma, Katariina, Vehmas, Tapio, Grönblad, Mats, Kerttula, Liisa, Kääpä, Eeva
• Format: Article
• Language: English
• Subjects: Follow-Up Studies; Humans; Low Back Pain - diagnostic imaging; Low Back Pain - etiology; Magnetic Resonance Imaging; Medicine; Medicine & Public Health; Neurosurgery; Original; Original Article; Radiography; Spinal Diseases - complications; Spinal Diseases - diagnostic imaging; Surgical Orthopedics
• ISSN: 0940-6719; 1432-0932
• DOI: 10.1007/s00586-008-0716-8

Subchondral signal abnormalities have been suggested to play an important role in chronic low back pain (LBP) syndromes. Their natural course is not well known. In this study the morphology and natural course of isolated subchondral signal abnormalities in the lumbosacral spine were analyzed with MRI. Twenty-four chronic LBP patients with a subchondral hypointensity on T1-weighted image (hyperintense on T2), indicating edema, were selected from a base population of 1,015 consecutive LBP patients to a follow-up MRI study within 18–72 months. Exclusion criteria were age >60 years, nerve root compression, a more specific back disease or a recent or major spine operation. The size and location of each subchondral signal abnormality and endplate lesion and the degree of degenerative disc changes were evaluated and compared between the baseline and follow-up studies. Most subchondral hypointensities were found at the L4/L5 or L5/S1 disc space, anteriorly and in both adjacent endplates. Almost all (53/54) hypointensities were associated with an endplate lesion. Twelve of the 54 subchondral hypointensities enlarged, six remained constant and 36 decreased or disappeared while five new ones appeared. Twenty-two (41%) hypointensities changed totally to hyperintensities or to mixed lesions. If the hypointensity increased, decreased or changed into hyperintensity, a change tended to develop in the adjacent endplate. If the hypointensity was absent or unchanged, endplate lesions did not tend to progress. In the absence of disc herniation or other specific spinal disease, subchondral hypointensities indicating edema are uncommon. They seem to have a highly variable course. There appears to be a link between endplate lesions and subchondral signal abnormalities. Further study is needed to explain the contribution of these findings to low back symptoms.