A Longitudinal Brain Magnetic Resonance Imaging Study of Neuromyelitis Optica Spectrum Disorder

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.

Neuromyelitis optica spectrum disorder and multiple sclerosis: Differentiation by a multimodal approach

“…We did not focus on the distribution of the T2-hyperintense lesions, and thus the effects of T2-hyperintense lesions on the focal FA values was not excluded. However, recent MRI studies showed that, as opposed to MS lesions, NMO lesions in the brain were nearly absent in the basal ganglia and cortical regions (Kim et al, 2014;Kister et al, 2013;Sinnecker et al, 2012). These results may indicate that the change of thalamic microstructure in NMOSD patients is derived from the secondary condition of disease rather than from the direct interference.…”

Bilateral symmetrical basal ganglia and thalamic lesions in children: an update (2015)

“…Many autoimmune disorders in the pediatric population can affect the basal ganglia, including post-streptococcal autoimmunity [39], N-methyl-D-aspartate receptor (NMDAR) antibodies [40], neuromyelitis optica (NMO)/neuromyelitis optica spectrum disorders (NMOSD) [41], and ADEM ( Fig. 6) [42].…”

“…Central nervous system involvement beyond the optic nerves and spinal cord is still compatible with NMO [51], although in fairness, this would be an uncommon presentation. T2 hyperintense lesions may affect the basal ganglia (and are characteristically Bblurred^), hypothalamus, white matter (more frequently the frontal lobes), corpus callosum, periventricular and periaqueductal regions, [41]. Interestingly, basal ganglia lesions may resolve completely over time [41].…”

“…T2 hyperintense lesions may affect the basal ganglia (and are characteristically Bblurred^), hypothalamus, white matter (more frequently the frontal lobes), corpus callosum, periventricular and periaqueductal regions, [41]. Interestingly, basal ganglia lesions may resolve completely over time [41].…”

“…Bilaterally symmetrical involvement would be incredibly rare. In both ADEM and NMO, vasogenic edema characterizes the acute phase of the disease, as demonstrated by ADC map [41,42]. The presence of vasogenic edema at symptom onset may be helpful in distinguishing primary brain viral infections from autoimmunity [42].…”