The aim of this study was to evaluate morphological and functional abnormalities by cerebral imaging in a series of systemic lupus erythematosus (SLE) patients with and without overt central nervous system (CNS) manifestations, and to detect possible relationships with clinical parameters and a large panel of autoantibodies, including those reactive against neurotypic and gliotypic antigens. 68 patients with SLE were investigated in a cross-sectional study which included clinical evaluation of symptoms, cerebral magnetic resonance imaging (MRI) and brain single photon emission tomography (SPECT) analysis, electroencephalography (EEG), and serological tests for antibodies directed against nuclear, cytoplasmic neuronal and glial cell-related antigens. The results of this study showed: (1) a significant positive association of (a) anti-glial fibrillary acidic protein (GFAP) serum antibodies with neuropsychiatric (NP) manifestations and (b) anti-serin proteinase 3 (anti-PR3/c-ANCA) serum antibodies with pathological cerebral SPECT; (2) the presence of significantly higher values of (a) SLICC organ damage index in patients with abnormal MRI and (b) SLAM activity index in patients with abnormal SPECT; and (3) the association of (a) abnormal MRI with nonactive NP manifestations and (b) combined abnormality of brain SPECT and MRI with the occurrence of overall overt NP manifestations and with those of the organic/major type. Neuropsychiatric manifestations, namely those of the organic/major type, appeared to be significantly associated to the presence of a serum antibody against GFAP, a gliotypic antigen. There was also evidence of an association between SPECT abnormality and the presence of anti-PR3 (c-ANCA). Furthermore, brain imaging by MRI and SPECT applied to SLE patients appears to express CNS involvement significantly related to specific categories of NP manifestations. The abnormalities detected by the two tests seem to be preferentially associated with different activity phases of the NP disorder or of the lupus disease.
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http://dx.doi.org/10.1191/096120300678828695 | DOI Listing |
Nat Med
January 2025
Huntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease with the age at which characteristic symptoms manifest strongly influenced by inherited HTT CAG length. Somatic CAG expansion occurs throughout life and understanding the impact of somatic expansion on neurodegeneration is key to developing therapeutic targets. In 57 HD gene expanded (HDGE) individuals, ~23 years before their predicted clinical motor diagnosis, no significant decline in clinical, cognitive or neuropsychiatric function was observed over 4.
View Article and Find Full Text PDFNeurocase
January 2025
Department of Radiology, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.
Catatonia may manifest as an independent entity or as a feature of a neuropsychiatric or medical illness. While electroconvulsive therapy (ECT) is the gold standard treatment for catatonia, it is typically administered if the patient's symptoms fail to respond to benzodiazepines. We describe the case of a 22-year-old male with Budd Chiari induced cirrhosis and no prior psychiatric history, who presented with symptoms of psychosis and hepatic encephalopathy, was treated in the ICU for multi-factorial delirium, developed symptoms of catatonia that failed to respond to lorazepam, ultimately requiring ECT with a favorable response.
View Article and Find Full Text PDFDement Neuropsychol
January 2025
Universidade Estadual de Campinas, Faculdade de Ciências Médicas, Departamento de Psiquiatria, Campinas SP, Brazil.
Unlabelled: Neuropsychiatric symptoms (NPS) such as depression, anxiety, and apathy are present in mild cognitive impairment (MCI) and are risk factors for cognitive decline. However, the relationship between NPS and specific cognitive domains is less clear.
Objective: This study aimed to assess whether there is a correlation between NPS and specific cognitive domains.
J Psychiatr Res
January 2025
Department of Psychological Sciences, University of Connecticut, 406 Babbidge Road, Unit 1020, Storrs, CT, USA.
Background: Schizophrenia (SZ) is a psychiatric disorder that often involves reduced social functioning. Frontal alpha asymmetry (FAA) is a neurophysiological marker extracted from electroencephalogram (EEG) data that is likely related to motivational and emotional tendencies, such as reduced motivation across various psychiatric disorders, including SZ. Therefore, it may offer a neurophysiological marker for social functioning.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
January 2025
Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada; Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada. Electronic address:
Schizophrenia is a complex neuropsychiatric disorder featuring enhanced brain oxidative stress and deficient reelin protein. GFAP.HMOX1 mice that overexpress heme oxygenase-1 (HO-1) in astrocytes manifest a schizophrenia-like neurochemical, neuropathological and behavioral phenotype including brain oxidative stress and reelin downregulation.
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