7 Tesla MRI of Balo's concentric sclerosis versus multiple sclerosis lesions. Issue 8 (29th June 2018)

• Record Type: Journal Article
• Authors: Behrens, Janina R.; Wanner, Julia; Kuchling, Joseph; Ostendorf, Lennard; Harms, Lutz; Ruprecht, Klemens; Niendorf, Thoralf; Jarius, Sven; Wildemann, Brigitte; Gieß, René M.; Scheel, Michael; Bellmann‐Strobl, Judith; Wuerfel, Jens; Paul, Friedemann; Sinnecker, Tim
• Is Part Of: Annals of clinical and translational neurology. Volume 5:Issue 8(2018)
• Page Start: 900
• Page End: 912
• Publication Date: 2018-06-29
• Subjects: Nervous system -- Diseases -- Periodicals; Neurology -- Periodicals; 616.8005
• DOI: 10.1002/acn3.572
• Languages: English
• ISSNs: 2328-9503

Abstract

Abstract: Background: Baló's concentric sclerosis (BCS) is a rare condition characterized by concentrically layered white matter lesions. While its pathogenesis is unknown, hypoxia‐induced tissue injury and chemotactic stimuli have been proposed as potential causes of BCS lesion formation. BCS has been suggested to be a variant of multiple sclerosis (MS). Here, we aimed to elucidate similarities and differences between BCS and MS by describing lesion morphology and localization in high‐resolution 7 Tesla (7 T) magnetic resonance imaging (MRI) scans. Methods: Ten patients with Baló‐type lesions underwent 7 T MRI, and 10 relapsing remitting MS patients served as controls. The 7 T MR imaging protocol included 3D T1 ‐weighted (T1 w) magnetization‐prepared rapid gradient echo, 2D high spatial resolution T2 *‐weighted (T2 *w) fast low‐angle shot and susceptibility‐weighted imaging. Results: Intralesional veins were visible in the center of all but one Baló‐type lesion. Four Baló‐type lesions displayed inhomogeneous intralesional T2 *w signal intensities, which are suggestive of microhemorrhages or small ectatic venules. Eight of 10 BCS patients presented with 97 additional lesions, 36 of which (37%) had a central vein. Lesions involving the cortical gray matter and the U‐fibers were not detected in BCS patients. Conclusion: Our findings support the hypothesis that BCS and MS share common pathogenetic mechanisms but patients present with different lesion phenotypes.