Abstract
WCN 2013 No: 1101 Topic: 7 — Neuromuscular disorders Isolated acute bilateral ophthalmoplegia as a form of anti-GQ1b syndrome a case report and differential diagnostic considerations A. Toth, G. Aradi, I. Vastagh, K. Pozsegovits, L. Rencz, D. Bereczki, Z. Aranyi. Department of Neurology, Semmelweis University, Faculty of Medicine, Budapest, Hungary; Department of Neurology, Dr. Kenessey Albert Hospital, Balassagyarmat, Hungary Background: Isolated acute bilateral ophthalmoplegia is an uncommon occurrence, but it may cause differential diagnostic problems. It may be a manifestation of the Miller Fisher syndrome spectrum, which has been recently referred to as anti-GQ1b syndrome. Objective: To present a case with acute bilateral ophthalmoplegia associated with anti-GQ1b antibody positivity, but without other typical signs of Miller Fisher syndrome (MFS). Differential diagnostic aspects are highlighted. Patient: A 57-year-old female patient presented with an acute onset of diplopia, progressing to bilateral ophthalmoplegia within days. These symptoms were preceded by flu-like symptoms. Deep tendon reflexes were diminished, otherwise her neurological status was unremarkable, the typical triad of MFSwas not observed. MRI of the brain was normal. Cerebrospinal fluid examination revealed increased protein content with normal cell count. Electrophysiological assessment showed normal sensory nerve action potentials, whereas low amplitude or absent sensory nerve action potentials are characteristic findings in MFS. Serological testing confirmed anti-GQ1b class IgG antibody positivity, supporting the diagnosis of MFS spectrum. The patient fully recovered within 3 months, without any specific treatment, showing the benign nature of the condition. Discussion: Acute ophthalmoparesis may be a restricted form antiGQ1b syndrome. In addition to classical MFS, further variants include Bickerstaff's brainstem encephalitis, pharyngeal-cervical-brachial paresis, and acute ataxic sensory neuropathy. Although acute ophthalmoparesis as a manifestation of anti-GQ1b syndrome is a benign condition, it may cause differential diagnostic problems with potentially more serious conditions needing prompt treatment, such as Wernicke's encephalopathy, ocularmyasthenia, botulism, paraneoplastic brainstemencephalitis, or brainstem stroke. doi:10.1016/j.jns.2013.07.1569 Abstract — WCN 2013 No: 1413 Topic: 7 — Neuromuscular disorders “Reporting biomarker” development: Update in als patients treated with G-CSF -mobilized hematopoietic stem cells WCN 2013 No: 1413 Topic: 7 — Neuromuscular disorders “Reporting biomarker” development: Update in als patients treated with G-CSF -mobilized hematopoietic stem cells A.V. Khomenko, D. Baldaranov, J. Grassinger, S.W. Johannesen, I. Kobor, J. Roesl, K. Kollewe, S. Petri, R. Dengler, M. Deppe, A. Ludolph, J. Kassubek, G. Schuierer, T. Bruun, W. Schulte-Mattler, U. Bogdahn. Department of Neurology, University of Regensburg, Regensburg, Germany; Department of Haematology and Internal Oncology, University Hospital Regensburg, Regensburg, Germany; Clinic for Neurology, Medizinische Hochschule Hannover, Hannover, Germany; Department of Neurology, University of Muenster, Muenster, Germany; Neurological University Clinic, University Ulm, Ulm, Germany; Department of Neuroradiology, University of Regensburg,
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