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Neurochemistry of hyponatremic encephalopathy evaluated by MR spectroscopy
Affiliation:1. University of Health Sciences, Okmeydanı Training and Research Hospital, Division of Paediatric Metabolism, Istanbul, Turkey;2. University of Health Sciences, Okmeydanı Training and Research Hospital, Division of Pediatric Neurology, Istanbul, Turkey;3. Medipol University, Department of Medical Genetics, Istanbul, Turkey;4. Medipol University, Department of Pediatric Neurology, Istanbul, Turkey;1. Department of Pediatrics and Child Health, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan;2. Biostatistics Center, Kurume University, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan;3. NPO Rett Syndrome Support Organization, 2-37-2 Tsudaminami-machi, Hirakata, Osaka, Japan;4. Department of Pediatrics, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan;5. Department of Pediatrics, Asahikawa University, Asahikawa 078-8510, Japan;6. Japan Rett Syndrome Association, 2-29-20-101 Kamiigusa, Suginami, Tokyo 167-002, Japan;7. Sakuranbokai-Rett Syndrome, 63-2-101 Kawatsu, Iizuka, Fukuoka, Japan;8. Research Center for Children, Research Center for Rett Syndrome, St. Mary’s Hospital, Kurume, Fukuoka 830-8543, Japan;9. Department of Mental Retardation and Birth Defect Research, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi-machi, Kodaira, Tokyo 187-8502, Japan;1. Department of Neurology, Perth Children''s Hospital, Nedlands, WA, Australia;2. Department of Radiology, Perth Children''s Hospital, Nedlands, WA, Australia;3. School of Medicine , University of Western Australia, Perth, WA, Australia;4. Department of Clinical Biochemistry, Path West, Nedlands, WA 6009, Australia;5. Telethon Kids Institute, Perth Children''s Hospital, Perth, WA, Australia;1. Pediatric Neurology Unit, Department of Pediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh, India;2. Department of Pediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh, India
Abstract:MR spectroscopy in a patient with hyponatremic encephalopathy due to the syndrome of inappropriate secretion of antidiuretic hormone revealed decreased N-acetyl-aspartate, creatine plus phosphocreatine, choline-containing compounds, and myo-inositol, with normal glutamate and increased glutamine, which normalized after Na normalization. The decreased concentrations of creatine plus phosphocreatine, choline-containing compounds and myo-inositol are explained by their release as osmolytes from brain cells to adapt to hypo-osmolality induced cerebral edema. Increased glutamine, which not only acts as an osmolyte but also protects neurons under excitotoxic conditions, may suggest that a disrupted glutamate-glutamine cycle may play an important role in the pathogenesis of hyponatremic encephalopathy.
Keywords:Hyponatremia  Glutamate  Glutamine  Excitotoxicity  MR spectroscopy
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