Felipe von Glehn1, Sven Jarius2, Rodrigo Pessoa Cavalcanti Lira3, Maria Carolina Alves Ferreira3, Fadua H Ribeiro von Glehn4, Stella Maris Costa E Castro3, Guilherme Coco Beltramini5, Felipe Pg Bergo4, Alessandro S Farias6, Carlos Otávio Brandão7, Brigitte Wildemann2, Benito P Damasceno4, Fernando Cendes4, Leonilda M B Santos6, Clarissa Lin Yasuda4. 1. Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas, Brazil Laboratory of Neuroimaging, Department of Neurology, University of Campinas, Brazil fglehn@terra.com.br leonilda@unicamp.br yasuda.clarissa@gmail.com. 2. Division of Molecular Neuroimmunology, Department of Neurology, University of Heidelberg, Germany. 3. Department of Ophthalmology, University of Campinas, Brazil. 4. Laboratory of Neuroimaging, Department of Neurology, University of Campinas, Brazil. 5. Laboratory of Neuroimaging, Department of Neurology, University of Campinas, Brazil Institute of Physics "Gleb Wataghin", University of Campinas, Brazil. 6. Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas, Brazil. 7. Neuroimmunology Unit, Department of Genetics, Evolution and Bioagents, University of Campinas, Brazil Laboratory of Neuroimaging, Department of Neurology, University of Campinas, Brazil.
Abstract
BACKGROUND: Although aquaporin-4 (AQP4) is widely expressed in the human brain cortex, lesions are rare in neuromyelitis optica (NMO) spectrum disorders (NMOSD). Recently, however, several studies have demonstrated occult structural brain atrophy in NMO. OBJECTIVE: This study aims to investigate magnetic resonance imaging (MRI) patterns of gray matter (GM) and white matter (WM) abnormalities in patients with NMOSD and to assess the visual pathway integrity during disease duration correlation of the retinal nerve fiber layer (RNFL) and pericalcarine cortex thickness. METHODS: Twenty-one patients with NMOSD and 34 matched healthy controls underwent both high-field MRI (3T) high-resolution T1-weighted and diffusion-tensor MRI. Voxel-based morphometry, cortical analyses (Freesurfer) and diffusion-tensor imaging (DTI) analyses (TBSS-FSL) were used to investigate brain abnormalities. In addition, RNFL measurement by optic-coherence tomography (OCT) was performed. RESULTS: We demonstrate that NMOSD is associated with GM and WM atrophy, encompassing more frequently the motor, sensory and visual pathways, and that the extent of GM atrophy correlates with disease duration. Furthermore, we demonstrate for the first time a correlation between RNFL and pericalcarine cortical thickness, with cortical atrophy evolving over the course of disease. CONCLUSIONS: Our findings indicate a role for retrograde and anterograde neurodegeneration in GM atrophy in NMOSD. However, the presence atrophy encompassing almost all lobes suggests that additional pathomechanisms might also be involved.
BACKGROUND: Although aquaporin-4 (AQP4) is widely expressed in the human brain cortex, lesions are rare in neuromyelitis optica (NMO) spectrum disorders (NMOSD). Recently, however, several studies have demonstrated occult structural brain atrophy in NMO. OBJECTIVE: This study aims to investigate magnetic resonance imaging (MRI) patterns of gray matter (GM) and white matter (WM) abnormalities in patients with NMOSD and to assess the visual pathway integrity during disease duration correlation of the retinal nerve fiber layer (RNFL) and pericalcarine cortex thickness. METHODS: Twenty-one patients with NMOSD and 34 matched healthy controls underwent both high-field MRI (3T) high-resolution T1-weighted and diffusion-tensor MRI. Voxel-based morphometry, cortical analyses (Freesurfer) and diffusion-tensor imaging (DTI) analyses (TBSS-FSL) were used to investigate brain abnormalities. In addition, RNFL measurement by optic-coherence tomography (OCT) was performed. RESULTS: We demonstrate that NMOSD is associated with GM and WM atrophy, encompassing more frequently the motor, sensory and visual pathways, and that the extent of GM atrophy correlates with disease duration. Furthermore, we demonstrate for the first time a correlation between RNFL and pericalcarine cortical thickness, with cortical atrophy evolving over the course of disease. CONCLUSIONS: Our findings indicate a role for retrograde and anterograde neurodegeneration in GM atrophy in NMOSD. However, the presence atrophy encompassing almost all lobes suggests that additional pathomechanisms might also be involved.
Authors: F Pache; H Zimmermann; C Finke; A Lacheta; S Papazoglou; J Kuchling; J Wuerfel; B Hamm; K Ruprecht; F Paul; A U Brandt; M Scheel Journal: Eur Radiol Date: 2016-03-24 Impact factor: 5.315
Authors: Axel Petzold; Mike P Wattjes; Fiona Costello; Jose Flores-Rivera; Clare L Fraser; Kazuo Fujihara; Jacqueline Leavitt; Romain Marignier; Friedemann Paul; Sven Schippling; Christian Sindic; Pablo Villoslada; Brian Weinshenker; Gordon T Plant Journal: Nat Rev Neurol Date: 2014-07-08 Impact factor: 42.937