Contributions
Abstract: P548
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Objective: Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the CNS. It is well known that imaging findings in NMOSD are distinct from multiple sclerosis (MS). Recently some atypical imaging findings and contrast enhancement patterns have been described in NMOSD patients. Depending on the limited data on leptomeningeal involvement, we investigated leptomeningeal enhancement in our NMOSD patients during their follow-up in our tertiary center.
Material and method: We evaluated for leptomeningeal contrast enhancement in post-gadolinium T1 weighted images in 46 patients with NMOSD. NMOSD was diagnosed with new diagnostic criteria of NMOSD.
Results: We identified four patients with NMOSD who have leptomeningeal contrast enhancement in post-contrast T1-weighted images. Note that all MRI scans were acquired on admission and before lumbar puncture. The mean age of the patients was twenty nine, all patients were female, two patients experienced bilateral visual loss whereas the others had myelitis concomitant with the studies magnetic resonance imaging (MRI) scans. Aquaporin-4 (AQP4) antibody was positive in three patients, however one was seronegative. None of them experienced any systemic vasculitis. MRI revealed diffuse leptomeningeal contrast enhancement on T1-weighted images. All patients had typical NMOSD parenchymal lesions with contrast enhancement. One patient had contrast enhancement in left third cranial nerve and bilateral seventh cranial nerves. They were all treatment responsive initially and they are currently all in our follow up.
Conclusion: Leptomeningeal contrast enhancement may be a neuroimaging feature of NMOSD. Leptomeningeal enhancement is probably a result of functional impairment of AQP4 water channels in the pial and subpial surfaces. Thus, these findings suggest that AQP4 channel dysfunction in NMOSD is not only located to typical parencyhmal structures and is more disseminated in the central nervous system. Our next step will be to search whether leptomeningeal enhancement might be a new biomarker indicating disease activity prospectively.
Disclosure: Serhat V. OKAR: Nothing to disclose
Abstract: P548
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Objective: Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the CNS. It is well known that imaging findings in NMOSD are distinct from multiple sclerosis (MS). Recently some atypical imaging findings and contrast enhancement patterns have been described in NMOSD patients. Depending on the limited data on leptomeningeal involvement, we investigated leptomeningeal enhancement in our NMOSD patients during their follow-up in our tertiary center.
Material and method: We evaluated for leptomeningeal contrast enhancement in post-gadolinium T1 weighted images in 46 patients with NMOSD. NMOSD was diagnosed with new diagnostic criteria of NMOSD.
Results: We identified four patients with NMOSD who have leptomeningeal contrast enhancement in post-contrast T1-weighted images. Note that all MRI scans were acquired on admission and before lumbar puncture. The mean age of the patients was twenty nine, all patients were female, two patients experienced bilateral visual loss whereas the others had myelitis concomitant with the studies magnetic resonance imaging (MRI) scans. Aquaporin-4 (AQP4) antibody was positive in three patients, however one was seronegative. None of them experienced any systemic vasculitis. MRI revealed diffuse leptomeningeal contrast enhancement on T1-weighted images. All patients had typical NMOSD parenchymal lesions with contrast enhancement. One patient had contrast enhancement in left third cranial nerve and bilateral seventh cranial nerves. They were all treatment responsive initially and they are currently all in our follow up.
Conclusion: Leptomeningeal contrast enhancement may be a neuroimaging feature of NMOSD. Leptomeningeal enhancement is probably a result of functional impairment of AQP4 water channels in the pial and subpial surfaces. Thus, these findings suggest that AQP4 channel dysfunction in NMOSD is not only located to typical parencyhmal structures and is more disseminated in the central nervous system. Our next step will be to search whether leptomeningeal enhancement might be a new biomarker indicating disease activity prospectively.
Disclosure: Serhat V. OKAR: Nothing to disclose