Objective: Studies using quantitative neuroimaging have shown subtle abnormalities in patients with idiopathic generalized epilepsy (IGE). These findings have several locations, but the midline parasagittal structures are most commonly implicated. The cingulate cortex is related and may be involved. The objective of the current investigation was to perform a comprehensive analysis of the cingulate cortex using multiple quantitative structural neuroimaging techniques.
Methods: Thirty-two patients (18 women, 30 ± 10 years) and 36 controls (18 women, 32 ± 11 years) were imaged by 3 Tesla magnetic resonance imaging (MRI). A volumetric three-dimensional (3D) sequence was acquired and used for this investigation. Regions-of-interest were selected and voxel-based morphometry (VBM) analyses compared the cingulate cortex of the two groups using Statistical Parametric Mapping (SPM8) and VBM8 software. Cortical analyses of the cingulate gyrus was performed using Freesurfer. Images were submitted to automatic processing using built-in routines and recommendations. Structural parameters were extracted for individual analyses, and comparisons between groups were restricted to the cingulate gyrus. Finally, shape analyses was performed on the anterior rostral, anterior caudal, posterior, and isthmus cingulate using spherical harmonic description (SPHARM).
Results: VBM analyses of cingulate gyrus showed areas of gray matter atrophy, mainly in the anterior cingulate gyrus (972 mm(3) ) and the isthmus (168 mm(3) ). Individual analyses of the cingulate cortex were similar between patients with IGE and controls. Surface-based comparisons revealed abnormalities located mainly in the posterior cingulate cortex (718.12 mm(2) ). Shape analyses demonstrated a predominance of anterior and posterior cingulate abnormalities.
Significance: This study suggests that patients with IGE have structural abnormalities in the cingulate gyrus mainly localized at the anterior and posterior portions. This finding is subtle and variable among patients.
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http://dx.doi.org/10.1111/epi.13205 | DOI Listing |
Curr Res Neurobiol
June 2025
Department of Anesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster, Germany.
Although the pathophysiology of pain has been investigated tremendously, there are still many open questions with regard to specific pain entities and their pain-related symptoms. To increase the translational impact of (preclinical) animal neuroimaging pain studies, the use of disease-specific pain models, as well as relevant stimulus modalities, are critical. We developed a comprehensive framework for brain network analysis combining functional magnetic resonance imaging (MRI) with graph-theory (GT) and data classification by linear discriminant analysis.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of Magnetic Resonance Imaging, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Background: To investigate the alterations in spontaneous brain activity and the similarities and differences between monocular deprivation amblyopia and binocular deprivation amblyopia.
Methods: Twenty children with binocular deprivation amblyopia, 26 children with monocular deprivation amblyopia and 20 healthy controls underwent resting-state functional magnetic resonance imaging. The evaluation of altered spontaneous brain activity was conducted using fractional amplitude of low-frequency fluctuations (fALFF).
J Psychiatry Neurosci
January 2025
From the Department of Psychiatry, Yale University School of Medicine, New Haven, Conn., USA (Chen, Luo, Ide, C.-S. Li); Yale University, New Haven, Conn., USA (H.-T. Li); the Department of Biomedical Engineering, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China (G. Li); the Beijing International Science and Technology Cooperation Base for Intelligent Physiological Measurement and Clinical Transformation, Beijing, China (G. Li); the Department of Neuroscience, Yale University School of Medicine, New Haven, Conn., USA (C.-S Li); the Interdepartment Neuroscience Program, Yale University, New Haven, Conn., USA (C.-S. Li); the Wu Tsai Institute, Yale University, New Haven, Conn., USA (C.-S. Li).
Background: Genetic variants may confer risk for depression by modulating brain structure and function; evidence has underscored the key role of the subgenual anterior cingulate cortex (sgACC) in depression. We sought to examine how the resting-state functional connectivity (rsFC) of the sgACC was associated with polygenic risk for depression in a subclinical population.
Methods: Following published protocols, we computed seed-based whole-brain sgACC rsFC and calculated polygenic risk scores (PRS) using data from healthy young adults from the Human Connectome Project.
J Affect Disord
January 2025
Medical Imaging Center, First Affiliated Hospital of Jinan University, Guangzhou 510630, China; Institute of Molecular and Functional Imaging, Jinan University, Guangzhou 510630, China. Electronic address:
Background: The neurobiological mechanisms behind the antidepressant effect of bright light therapy (BLT) are unclear. We aimed to explore the dynamic functional connectivity (dFC) changes of the cingulate cortex (CC) in subthreshold depression (StD).
Methods: The StD participants (38 BLT and 39 placebo) underwent resting-state functional magnetic resonance imaging (rs-fMRI) and mood assessment before and after eight-week BLT.
J Psychiatr Res
January 2025
Endocrinology and Nutrition Department, Parc Taulí Hospital Universitari, Institut d'Investigació i Innovació Parc Taulí I3PT, Medicine Department, Universitat Autònoma de Barcelona, 08208, Sabadell, Spain.
Individuals with Prader Willi syndrome (PWS) often exhibit behavioral difficulties characterized by deficient impulse regulation and obsessive-compulsive features resembling those observed in obsessive-compulsive disorder. The genetic configuration of PWS aligns with molecular and neurophysiological findings suggesting dysfunction in the inhibitory gamma-aminobutyric acid (GABA) interneuron system may contribute to its clinical manifestation. In the cerebral cortex, this dysfunction is expressed as desynchronization of local neural activity.
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