One out of four patients showed involvement of the cortical grey matter (Figure 4(c)) and infratentorial lesion (Figure 4(d)), 1/4 showed enlargement of the Sylvian fissures and posterior horn of lateral ventricles (Figure 5(d)), 1/4 showed T2 hyperintensities in the cervical medulla (Figure 6(c)), without gadolinium enhancement. One out of eight patients showed only two lesions in the supratentorial brain (Figure 7(a)), symmetrical, hyperintense in T2-weighted images, located in the right and left thalamus, coexisting with infratentorial lesions in the pons and medulla oblongata (Figure 7(c)) and patchy hyperintensities of the cervical medulla. The patient with double positivity for MOG and AQP4-Abs showed two lesions of the supratentorial white matter (Figure 7(a) and (?(b)),b)), patchy T2 hyperintensities in the cervical medulla and longitudinally extensive transverse myelitis extending over D3, D4 and D5. In our group, only 1/8 patient showed significant swelling of the optic nerve on the affected side (Figure 6(a)). After the resolution of the acute phase, all patients showed a complete recovery of the visual impairment with restoring of the pre-ON visual score (median visual score: 7.8). The follow up MRI of the patient in Figure 1 (Figure 9) showed mild reduction of the extensively confluent T2-hyperintensity of the white matter of frontal and parietal lobes. Open in a separate window Figure Levatin 9. MRI follow-up at three months of the patient in Figure 1. were found seropositive for myelin oligodendrocyte glycoprotein antibodies, comparing our data with the findings described in the literature. Keywords: Anti-myelin oligodendrocyte glycoprotein, demylinating disorders, magnetic resonance imaging, neuromyelitis optica, optic neuritis, recurrent optic neuritis Introduction Myelin oligodendrocyte glycoprotein (MOG) is a protein exclusively expressed on the surface of oligodendrocytes and myelin in the central nervous system, located on the outer surface of the myelin sheath.1,2 Antibodies (Abs) against MOG were initially detected in children with demyelinating syndromes3C10 and more recently reported in a broad spectrum of central nervous system demyelinating diseases in adults: in patients with aquaporin-4 (AQP4)-Abs-negative neuromyelitis optica spectrum disorder (NMOSD),11C17 in bilateral optic neuritis (ON),18 in isolated ON,19 in recurrent ON,20 clinically isolated syndrome (CIS),17 acute disseminated encephalomyelitis (ADEM),16,17 Levatin in patients with demyelinating diseases distinct from multiple sclerosis (MS) and neuromyelitis optica (NMO),21 and in patients with clinically defined MS according to the McDonald criteria.22C27 It has been hypothesised that the presence of anti-MOG Abs in distinct diseases may limit the use of the MOG-Abs assay as a specific diagnostic biomarker. Patients with MOG-Abs-associated demyelination appear to have unique clinical, radiological features and outcomes.26 The detection of the association between MOG-Abs and demyelinating disorders in adults is recent and in the literature we can find papers describing mainly clinical features, diagnosis and prognosis of patients with this type of antibody, with brief mention of radiological appearance but, to the best of our knowledge, no one reporting groups of Italian patients presenting with ON or focused on the radiologic aspects of this disorder, so we want to retrospectively report magnetic resonance imaging (MRI) features of a group of eight patients, who came to our Ophthalmologic Emergency Department Levatin for ON and were found seropositive for MOG-Abs, comparing our data with findings described in the literature. Material and methods Eight patients, (six females and two males, age range: 26C40 years; mean age: 32.8??5.7 years) came to our Ophthalmologic Emergency Department between February Rabbit Polyclonal to OR13F1 2015CNovember 2016 complaining of ocular pain, worsened by eye movement (8/8), visual loss in one eye (5/8), visual field loss (3/5) diagnosed as ON (three of the left eye, four of the right eye and one recurrent bilateral ON, first left, afterwards right ON). All patients underwent ophthalmologic and neurological evaluation and no contrast computed tomography (CT) scan of brain and orbits on their admission, and MRI of brain, cervical spine and orbits in a time from 2C20 days after the onset of symptoms (mean days: 5.7??5.4). MRI of thoracolumbar spine was executed depending on Levatin the symptoms (1/8). CT scans were executed on Somatom Definition Flash (Siemens, Forchheim, Germany) with the following acquisition parameters: kV:120, mAs: 320, collimation: 40??0.6?mm, tube rotation: 1?s; reconstruction thickness: 3?mm; reconstruction filters: H21s smooth for soft tissues and H60 sharp for bone. All MRI examinations were executed on a 1.5 T magnet (Avanto, Siemens, Forchheim, Germany), with sequences on the brain: sagittal T1 spin echo (SE) (thickness: 5?mm), axial proton density (PD) + T2 turbo spin echo (TSE) (thickness: 5?mm), diffusion weighted imaging with b values?=?0, 500, 1000?s/mm2 (thickness: 5?mm), axial T1 SE, coronal fluid attenuated inversion recovery (FLAIR) (thickness: 5?mm), sagittal dark fluid T2 space (thickness: 1?mm, with multiplanar reformation on axial and coronal planes); on the orbits: axial T2 TSE with fat saturation (FS) (thickness: 3?mm), T2 short tau inversion recovery (STIR) space (thickness: 1?mm, with multiplanar reformation on sagittal and coronal planes); on the spine: sagittal T2 TSE (thickness: 4?mm), sagittal T1 TSE (thickness: 4?mm), sagittal T2 STIR. Gadolinium (1?ml/10?kg of gadobutrol, Gadovist, Bayer Schering Pharma) was administered to all patients intravenously, before the acquisition of: axial and coronal T1 SE FS on the orbits (thickness: 3?mm), axial T1 SE FLOW (thickness: 5?mm) and axial volumetric interpolated brain examination (VIBE) (thickness: 1?mm) on the brain, and sagittal T1 TSE.