Background and Objective: Neuromyelitis optica (NMO) shows various brain MRI abnormalities with recurrent CNS attacks, although NMO predominantly affects the spinal cord and optic nerve. The features and pathomechanisms of acute brain lesions associated with edema have not been clarified in NMO. We investigated diffusion weighted imaging (DWI) of brain MRI lesions with the enhancement patterns in patients with neuromyelitis optica spectrum disorder (NMOSD). Methods: We retrospectively collected 27 patients with NMOSD, who visited our tertiary hospital from 2004 to 2009. We analyzed clinical and MRI findings of 11 patients (M:F=3:8; mean age, 357 ?9.9 years), in whom DWI within 7 days of symptom onset was available. Anti-aquaporin-4 antibody (anti-AQP4) was measured by the cell-based assay in Oxford. Results: All 11 patients with NMOSD had brain MRI lesions characteristic of NMO and 7 of them had anti- AQP4. Seven patients revealed lesions at brainstem, internal capsule and cortex. Those were not extensive, mostly <1cm in diameter and showed high signal intensity (HSI) in both DWI and ADC maps with or without enhancement. Large extensive lesions (>3cm in diameter) involving hemisphere or corpus callosum were found in 6 patients. They showed 3 DWI patterns; (1) lesions with high signal intensity (HSI) in both DWI and apparent diffusion coefficient (ADC) map, suggestive of vasogenic edema, (2) lesions with low signal intensity (LSI) in DWI and HSI in ADC, suggestive of neuronal loss, (3) lesions with HSI in DWI and LSI in ADC, suggestive of cytotoxic edema. Lesions with vasogenic edema showed gadolinium enhancement or not and sometimes were accompanied by neuronal loss. In addition, all 6 patients with large extensive lesions were seropositive. Conclusion: The lack or presence of enhancement in lesions with vasogenic edema suggests that acute lesions in NMO (or NMOSD) may be due to dysfunction of water channel elimination or disruption of bloodbrain-barrier, related to anti-AQP4. Moreover, the acute lesion with cytotoxic edema may suggest of another mechanism of anti-AQP4 to develop necrosis likely via cytotoxicity to astrocytes in NMO.
Read More: Acute-phase MRI features of brain lesions characteristic of neuromyelitis optica