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Purpose: To explore the intrinsic alteration of cerebral 18F-FDG metabolism in acute/subacute seropositive autoimmune encephalitis (AE) and to propose a universal classification model based on 18F-FDG metabolic patterns to predict AE.
Methods: Cerebral 18F-FDG PET images of 42 acute/subacute seropositive AE patients and 45 healthy controls (HCs) were compared using voxelwise and region of interest (ROI)-based schemes. The mean standardized uptake value ratios (SUVRs) of 59 subregions according to a modified Automated Anatomical Labeling (AAL) atlas were compared using a t-test. Subjects were randomly divided into a training set (70%) and a testing set (30%). Logistic regression models were built based on the SUVRs and the models were evaluated by determining their predictive value in the training and testing sets.
Results: The 18F-FDG uptake pattern in the AE group was characterized by increased SUVRs in the brainstem, cerebellum, basal ganglia, and temporal lobe, and decreased SUVRs in the occipital, and frontal regions with voxelwise analysis (false discovery rate [FDR] p<0.05). Utilizing ROI-based analysis, we identified 15 subareas that exhibited statistically significant changes in SUVRs among AE patients compared to HC (FDR p<0.05). Further, a logistic regression model incorporating SUVRs from the calcarine cortex, putamen, supramarginal gyrus, cerebelum_10, and hippocampus successfully enhanced the positive predictive value from 0.76 to 0.86 when compared to visual assessments. This model also demonstrated potent predictive ability, with AUC values of 0.94 and 0.91 observed for the training and testing sets, respectively.
Conclusions: During the acute/subacute stages of seropositive AE, alterations in SUVRs appear to be concentrated within physiologically significant regions, ultimately defining the general cerebral metabolic pattern. By incorporating these key regions into a new classification model, we have improved the overall diagnostic efficiency of AE.
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http://dx.doi.org/10.1016/j.neurad.2023.05.001 | DOI Listing |
J Cereb Blood Flow Metab
September 2025
Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.
Preclinical PET studies offer the opportunity to elucidate molecular mechanisms underlying early neurodevelopment with minimal invasiveness. We demonstrated the feasibility of fetal brain PET in four pregnant rats ( = 42 fetuses). [F]FDG uptake in rat fetuses was readily visualized by PET imaging.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
September 2025
Department of Psychiatry and Psychotherapy, Medical University of Vienna, Vienna, Austria.
Functional PET (fPET) identifies stimulation-specific changes of physiological processes, individual molecular connectivity and group-level molecular covariance. Since there is currently no consistent analysis approach available for these techniques, we present a toolbox for unified fPET assessment. The toolbox supports analysis of data obtained with a variety of radiotracers, scanners, experimental protocols, cognitive tasks and species.
View Article and Find Full Text PDFRev Esp Med Nucl Imagen Mol (Engl Ed)
September 2025
Servicio de Medicina Nuclear, Hospital Clínico Universitario de Valladolid, Valladolid, Spain.
Nucl Med Biol
September 2025
Department of Nuclear Medicine, Hannover Medical School, Germany. Electronic address:
Purpose: The liver-brain axis regulates metabolic homeostasis, with glucose metabolism playing a key role. Liver dysfunction, such as fibrosis, may impact brain metabolism and consequently, brain function. Positron emission tomography (PET) imaging provides a non-invasive approach to study glucose metabolism in both organs.
View Article and Find Full Text PDFFront Neurol
August 2025
Department of Pediatric Neuroscience, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy.
Background: Pediatric Huntington's disease (PHD), a rare and severe form of juvenile-onset Huntington's disease (JOHD), is associated with highly expanded CAG repeats in the gene and a rapidly progressive neurodegenerative course. Recent studies have suggested that glucose metabolism may be impaired in PHD due to reduced expression of glucose transporters in the brain, resembling aspects of GLUT1 Deficiency Syndrome (GLUT1DS).
Methods: We investigated glucose metabolism in two pediatric patients with genetically confirmed PHD (CAG repeats: 76 and 79) referred to our tertiary care center.