Open Access7 Tesla MRI of Balo's concentric sclerosis versus multiple sclerosis lesions
Author(s) -
Behrens Janina R.,
Wanner Julia,
Kuchling Joseph,
Ostendorf Lennard,
Harms Lutz,
Ruprecht Klemens,
Niendorf Thoralf,
Jarius Sven,
Wildemann Brigitte,
Gieß René M.,
Scheel Michael,
BellmannStrobl Judith,
Wuerfel Jens,
Paul Friedemann,
Sinnecker Tim
Publication year - 2018
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.572
Subject(s) - multiple sclerosis , medicine , lesion , magnetic resonance imaging , white matter , pathology , ectasia , hyperintensity , nuclear medicine , radiology , psychiatry
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 T 1 ‐weighted (T 1 w) magnetization‐prepared rapid gradient echo, 2D high spatial resolution T 2 *‐weighted (T 2 *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 T 2 *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.