Contributions
Abstract: EP1560
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Objective: NMO spectrum disorders [NMOSD] are putatively accepted as inflammatory autoimmune diseases of the CNS.Imaging findings in NMOSD are distinct from MS. We previously observed leptomeningeal (LM) contrast enhancement in 4 of our 46 NMOSD patients during their attack. Recently imaging findings consistent with LM blood-CSF barrier disruption and transient leakage of contrast agent into the subarachnoid space was shown in NMOSD patients during attack.AQP4 is highly expressed throughout the CNS including grey matter. Aquaporin channels are considered to have essential functions in glymphatic system. The anatomical integrity of this pathway has been supported by astrocytic end-foot with AQP 4 water channels. These findings suggest that AQP channel pathology might be more spread than restricted to typical parenchymal areas.Our aim is to evaluate further AQP4 channel dysfunction leading to LM blood-CSF barrier disruption by studying dynamic contrast-enhanced (DCE) MR perfusion and contrast enhanced (CE)-FLAIR in clinically stable NMOSD patients.
Material and method: 19 patients were diagnosed as NMOSD according to the new diagnostic criteria.All patients were in remission under treatment.We evaluated dynamic contrast-enhanced (DCE) MR perfusion and contrast enhanced (CE)-FLAIR in addition to routine brain MRI from 19 NMOSD patients with no disease activity.
Results: Median age of our patients was 44,1 years old.15 of them were female,4 of them were male.12 of patients were positive for AQP4 antibody,3 were positive for MOG antibody,one of them was positive for both.3 of them were seronegative.Mean disease duration was 6,9 years. 5 of our patients had other autoimmune diseases.All of our patients were under immunesupressive/modulatory treatment.We identified 2 patients with NMOSD who have LM contrast enhancement in post-contrast (PC) FLAIR series while PC T1W images were normal and had no evidence of disease activity .First patient was 41 years old female.She displayed both aquaporin and MOG antibodies.CE-FLAIR revealed abnormal LM and sulcal enhancement.Second patient was 53 years old female.She was seronegative for both antibodies.She also had Sjögren's.CE-FLAIR revealed abnormal LM and sulcal enhancement. Our DCE-MR permeability data from our patients is being processed.
Conclusion: We propose that AQP4 channels may contribute to the brain microcirculation in glymphatic pathway therefore related sequences of MRI can be used to prove this hypothesis.
Disclosure: Nothing to disclose
Abstract: EP1560
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Objective: NMO spectrum disorders [NMOSD] are putatively accepted as inflammatory autoimmune diseases of the CNS.Imaging findings in NMOSD are distinct from MS. We previously observed leptomeningeal (LM) contrast enhancement in 4 of our 46 NMOSD patients during their attack. Recently imaging findings consistent with LM blood-CSF barrier disruption and transient leakage of contrast agent into the subarachnoid space was shown in NMOSD patients during attack.AQP4 is highly expressed throughout the CNS including grey matter. Aquaporin channels are considered to have essential functions in glymphatic system. The anatomical integrity of this pathway has been supported by astrocytic end-foot with AQP 4 water channels. These findings suggest that AQP channel pathology might be more spread than restricted to typical parenchymal areas.Our aim is to evaluate further AQP4 channel dysfunction leading to LM blood-CSF barrier disruption by studying dynamic contrast-enhanced (DCE) MR perfusion and contrast enhanced (CE)-FLAIR in clinically stable NMOSD patients.
Material and method: 19 patients were diagnosed as NMOSD according to the new diagnostic criteria.All patients were in remission under treatment.We evaluated dynamic contrast-enhanced (DCE) MR perfusion and contrast enhanced (CE)-FLAIR in addition to routine brain MRI from 19 NMOSD patients with no disease activity.
Results: Median age of our patients was 44,1 years old.15 of them were female,4 of them were male.12 of patients were positive for AQP4 antibody,3 were positive for MOG antibody,one of them was positive for both.3 of them were seronegative.Mean disease duration was 6,9 years. 5 of our patients had other autoimmune diseases.All of our patients were under immunesupressive/modulatory treatment.We identified 2 patients with NMOSD who have LM contrast enhancement in post-contrast (PC) FLAIR series while PC T1W images were normal and had no evidence of disease activity .First patient was 41 years old female.She displayed both aquaporin and MOG antibodies.CE-FLAIR revealed abnormal LM and sulcal enhancement.Second patient was 53 years old female.She was seronegative for both antibodies.She also had Sjögren's.CE-FLAIR revealed abnormal LM and sulcal enhancement. Our DCE-MR permeability data from our patients is being processed.
Conclusion: We propose that AQP4 channels may contribute to the brain microcirculation in glymphatic pathway therefore related sequences of MRI can be used to prove this hypothesis.
Disclosure: Nothing to disclose