Background: Demyelination is similar with malignancy in clinical symptoms. Magnetic resonance imaging (MRI) is an important auxiliary examination in the diagnosis of demyelinating diseases and malignancy. Since MRI and symptoms can be difficult to distinguish demyelination from malignancy, other auxiliary examinations, such as demyelinating disease-specific antibodies, play an important role in distinguishing them. Previous studies have reported demyelinating disease-specific antibodies in patients with malignancy. What's more, it is more difficult to confirm the diagnosis when the malignant tumor co-occurs with demyelinating diseases, which has never been reported in previous studies. We report the diagnosis of myelin oligodendrocyte glycoprotein antibody associated encephalomyelitis (MOG-EM) in a patient who had astrocytoma for several years.
Case Presentation: Patient's concerns and diagnoses: our case report records a 49-year-old woman with astrocytoma for more than 4 years, who recently developed the symptoms of MOG-EM, including dizziness, vomiting, and vision loss. This astrocytoma patient was diagnosed with MOG-EM according to comprehensive evidence, including MRI, visual evoked potential (VEP), serum myelin oligodendrocyte glycoprotein antibody (MOG-IgG), and therapeutic effect. Interventions and outcomes: this patient was diagnosed with astrocytoma by surgical biopsy 4 years earlier. This patient has been treated with tumor resection, postoperative radiation treatment and chemotherapy. After treatment, the patient was left with right limb weakness while other symptoms were improved. Recently, the intravenous steroid agent was used to treat this patient after being diagnosed with MOG-EM. Dizziness, vomiting, and vision loss have gone into remission. This patient did not relapse in 7 months after discharge. This patient is still being followed up at the outpatient clinic. And the patient will next be treated with azathioprine.
Conclusions: In previous studies, polyclonal antibody has been found in cancer patients, such as aquaporin-4 and MOG-IgG in astrocytoma patients. But the case of our study finds that astrocytoma can coexist with MOG-EM. Therefore, MOG-EM should not be excluded easily in astrocytoma patients when the relative antibody of encephalomyelitis is positive. What's more, it reminds us that the pathogenesis of MOG-EM might be related to astrocytoma.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9542675 | PMC |
http://dx.doi.org/10.1097/MD.0000000000031003 | DOI Listing |
J Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFMult Scler
January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Testing for myelin oligodendrocyte glycoprotein immunoglobulin G antibodies (MOG-IgG) is essential to the diagnosis of MOG antibody-associated disease (MOGAD). Due to its central role in the evaluation of suspected inflammatory demyelinating disease, the last 5 years has been marked by an abundance of research into MOG-IgG testing ranging from appropriate patient selection, to assay performance, to utility of serum titers as well as cerebrospinal fluid (CSF) testing. In this review, we synthesize current knowledge pertaining to the "who, what, where, when, why, and how" of MOG-IgG testing, with the aim of facilitating accurate MOGAD diagnosis in clinical practice.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Neuroscience and Mental Health Innovation Institute, Cardiff University, Hadyn Ellis Building, Cardiff CF24 4HQ, UK.
Deletion and duplication in the human 16p11.2 chromosomal region are closely linked to neurodevelopmental disorders, specifically autism spectrum disorder. Data from neuroimaging studies suggest white matter microstructure aberrations across these conditions.
View Article and Find Full Text PDFBiomolecules
December 2024
Neurochemical Research Unit and Bebensee Schizophrenia Research Unit, Department of Psychiatry and Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB T6G 2G3, Canada.
Schizophrenia is a complex heterogenous disorder thought to be caused by interactions between genetic and environmental factors. The theories developed to explain the etiology of schizophrenia have focused largely on the dysfunction of neurotransmitters such as dopamine, serotonin and glutamate with their receptors, although research in the past several decades has indicated strongly that other factors are also involved and that the role of neuroglial cells in psychotic disorders including schizophrenia should be given more attention. Although glia were originally thought to be present in the brain only to support neurons in a physical, metabolic and nutritional capacity, it has become apparent that these cells have a variety of important physiological roles and that abnormalities in their function may make significant contributions to the symptoms of schizophrenia.
View Article and Find Full Text PDFASN Neuro
January 2025
Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI, USA.
In light of the increasing importance for measuring myelin ratios - the ratio of axon-to-fiber (axon + myelin) diameters in myelin internodes - to understand normal physiology, disease states, repair mechanisms and myelin plasticity, there is urgent need to minimize processing and statistical artifacts in current methodologies. Many contemporary studies fall prey to a variety of artifacts, reducing study outcome robustness and slowing development of novel therapeutics. Underlying causes stem from a lack of understanding of the myelin ratio, which has persisted more than a century.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!