A copy of the written consent is available for review by the Editor-in-Chief of this journal

A copy of the written consent is available for review by the Editor-in-Chief of this journal. Rabbit Polyclonal to Cytochrome P450 7B1 Availability of data and materials Data sharing not applicable to this article as no datasets were generated. Funding We acknowledge support by Open Access Publishing Fund of Karl Landsteiner University of Health Sciences, Krems, Austria. Authors’ contributions EA, CB, NA, CN, WS contributed to the writing of manuscript. MOG antibodies. In case of a positive testing treatment with steroids and immunoglobulins seems recommendable. Keywords: MOG antibody encephalitis, Brainstem encephalitis, Case report Abbreviations: AB, antibody; ADC, apparent diffusion coefficient; ADEM, acute demyelinating encephalomyelitis; ceT1w, contrast enhanced T1 weighted; CLIPPERS, Chronic lymphocytic inflammation with Exatecan mesylate pontine perivascular enhancement responsive to steroids; CNS, cerebral nervous system; CSF, cerebrospinal fluid; DW, diffusion weighted; IVIG, intravenous immunoglobulin; LETM, longitudinal extensive transverse myelitis; LP, lumbal puncture; MOG, myelin oligodendrocyte glycoprotein; MOGAD, myelin oligodendrocyte glycoprotein antibody disease; MOG-AB, myelin oligodendrocyte glycoprotein antibody; MRI, magnetic resonance imaging; MS, multiple sclerosis; NMOSD, neuromyelitis optica spectrum disorder; OCB, oligoclonal bands; T2w, T2 weighted Highlights ? A patient presenting with brain stem encephalitis and longitudinal extensive transverse myelitis was diagnosed with MOGAD. ? All lesions resolved after therapy with cortisone and immunoglobulins. ? MOGAD should be considered a differential diagnosis for brainstem encephalitis. 1.?Background Myelin oligodendrocyte glycoprotein (MOG) antibody associated disease (MOGAD) is a differential diagnosis of growing significance for demyelinating lesions in the cerebral nervous system (CNS), and occurs in the presence of MOG antibodies (MOG-AB). Due to considerable overlap between classical demyelinating diseases such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) and acute demyelinating encephalomyelitis (ADEM) regarding clinical and radiological features the diagnosis of MOGAD can be challenging [1]. In this case report we present and discuss a young patient with a rare presentation of MOGAD with initial acute meningitis, developing extensive brain stem encephalitis with only minor correlating symptoms and good clinical recovery. 2.?Case presentation A 30-year-old male patient presented with Exatecan mesylate newly occurring headache, fever, nuchal rigidity, and fatigue, increasing over the past five days. His past medical history and family history was unremarkable. Further neurological and general examinations were unremarkable. Following a normal CT check out, cerebrospinal fluid (CSF) analysis exposed pleocytosis (188 cells/l, dominantly granulocytes), elevated protein (72.1?mg/dL), normal glucose (56.0?mg/dL) and negative oligoclonal bands (OCB). Empiric treatment with aciclovir and ceftriaxone intravenously was initiated under the suspicion of acute meningitis (Fig. 1). Exatecan mesylate After careful consideration antibiotic and antiviral treatment was continued, although general serological workup including PCR and antibody checks showed bad results for common meningitis and encephalitis pathogens. Nine days after admission, the patient showed rapid progression of weakness leading to tetraparesis, predominantly affecting lower extremities, and hypoesthesia below T8 level, also long term throat tightness and gaze-evoked nystagmus to both sides. Repeated CSF analysis was comparable to the first, showing lymphatic pleocytosis (138 cells/l), elevated protein (78.6?mg/dL) and negative OCB. Ampicillin and methylprednisolone were added to the empiric treatment. Additionally, considerable antibody (Abdominal) checks for autoimmune diseases were performed, including MOG-AB, AQP4-Abdominal NMDAR-AB, AMPAR-AB, GABA-AB, LGI1-Abdominal, CASPR2-Abdominal, DPPX-AB, onconeural-AB, anti-glycin-AB, GM1-Abdominal, GQ1b AB. Open in a separate windows Fig. 1 Course of disease. _: time point of exam or starting point of therapy, .: end of therapy, CT: computed Tomography, LP: lumbal puncture, cMRI: cerebral MRI, sMRI: spinal MRI, MOG-AB: MOG Antibody screening, IVIG: Intravenous Immunoglobulin. Initial magnetic resonance imaging (MRI) depicted T2-weighted (T2w) hyperintense transmission alterations with minor swelling in the pons and, more clearly, in both cerebellar peduncles (Fig. 2). Exatecan mesylate Diffusion weighted (DW) MRI with mapping of the apparent diffusion coefficient (ADC) indicated vasogenic edema.