Abstract
Brain involvement is commonly seen in patients with neuromyelitis optica spectrum disorder (NMOSD). However, little is known about the chronic changes of acute brain lesions on MRI over time. Here, our objective was to evaluate how acute brain MRI lesions in NMOSD changed on follow-up MRI. We reviewed the MRIs of 63 patients with NMOSD who had acute brain lesions and follow-up MRI over an interval of at least 3 months. Of the 211 acute brain lesions, 24% of lesions disappeared completely on T2-weighed images (WI) and a decrease in size ≥50% on T2-WI was observed in 58% of lesions on follow-up MRI. However, 47% of lesions revealed focal T1-hypointensity and, in particular, 18% showed focal cystic changes. Cystic changes were observed most commonly in corticospinal tract and corpus callosal lesions whereas the vast majority of lesions in the cerebellum, basal ganglia and temporal white matter resolved completely. MRI remission on T2-WI occurred in 82% of lesions, while approximately half of the lesions presented foci of T1-hypointensity, which may be considered a severe tissue injury over time. The extent of brain injury following an acute brain lesion in NMOSD may depend on the location of the lesion.
Highlights
The discovery of the anti-aquaporin-4 (AQP4) antibody advanced our understanding of neuromyelitis optica (NMO)
We evaluated chronic changes in acute brain lesions on magnetic resonance imaging (MRI) in patients with NMO spectrum disorder (NMOSD)
More than half of the brain lesions decreased in size significantly on T2/fluid-attenuated inversion recovery (FLAIR) images, and a quarter of the lesions disappeared completely on follow-up MRI
Summary
The discovery of the anti-aquaporin-4 (AQP4) antibody advanced our understanding of neuromyelitis optica (NMO). NMO is considered a disease distinct from multiple sclerosis (MS) in which antibodies against the water channel AQP4 play a critical role. Certain types of brain lesions are regarded as characteristic of NMO. These lesions involve the periependymal areas with high AQP4 expression, the corticospinal tracts, and hemispheric white matter [1,2,3,4,5,6,7,8,9,10]. The characteristic brain abnormalities on MRI play an increasingly important role in differentiating NMOSD from MS. Most previous studies of NMOSD have described only acute lesions or have not demonstrated a distinction between the acute and chronic stages, and little is known about the chronic changes in brain MRI lesions over time. The affected regions of the brain are usually edematous, showing hyperintensity on T2-
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