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Objectives: To investigate the amplitude of low-frequency fluctuations (ALFF) alteration of whole brain in patients with subcortical ischemic vascular dementia (SIVD). Materials and Methods: Thirty patients with SIVD and 35 control subjects were included in this study. All of them underwent structural MRI and rs-fMRI scan. The structural data were processed using the voxel-based morphometry 8 toolbox (VBM8). The rs-fMRI data were processed using Statistical Parametric Mapping (SPM8) and Data Processing Assistant for Resting-State fMRI (DPARSF) software. Within-group analysis was performed with a one-sample Student's t-test to identify brain regions with ALFF value larger than the mean. Intergroup analysis was performed with a two-sample Student's t-test to identify ALFF differences of whole brain between SIVD and control subjects. Partial correlations between ALFF values and Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) scores were analyzed in the SIVD group across the parameters of age, gender, years of education, and GM volume. Results: Within-group analysis showed that the bilateral anterior cingulate cortex (ACC), posterior cingulate cortex, medial prefrontal cortex (MPFC), inferior parietal lobe (IPL), occipital lobe, and adjacent precuneus had significantly higher standardized ALFF values than the global mean ALFF value in both groups. Compared to the controls, patients with SIVD presented lower ALFF values in the bilateral precuneus and higher ALFF values in the bilateral ACC, left insula and hippocampus. Including GM volume as an extra covariate, the ALFF inter-group difference exhibited highly similar spatial patterns to those without GM volume correcting. Close negative correlations were found between the ALFF values of left insula and the MoCA and MMSE scores of SIVD patients. Conclusion: SIVD is associated with a unique spontaneous aberrant activity of rs-fMRI signals, and measurement of ALFF in the precuneus, ACC, insula, and hippocampus may aid in the detection of SIVD. [ABSTRACT FROM AUTHOR]

Binswanger's disease (BD) is a common cause of vascular dementia in elderly patients; however, few studies have investigated the medial temporal lobe (MTL) atrophy in BD, and the differences in the atrophic patterns between BD and Alzheimer's disease (AD) remain largely unknown. Such knowledge is essential for understanding the pathologic basis of dementia. In this study, we collected structural magnetic resonance imaging (MRI) data from 16 normal controls, 14 patients with AD and 14 patients with BD. The volumes of the hippocampus and amygdala, and morphologic parameters (volume, surface area, cortical thickness and mean curvature) of the entorhinal cortex (ERC) and perirhinal cortex (PRC) were calculated using an automated approach. Volume reduction of the hippocampus, amygdala and ERC, and disturbance of the PRC curvature was found in both AD and BD patients compared with the controls (p<0.05, uncorrected). There were no significant differences among all the structural measures between the AD and BD patients. Finally, partial correlation analyses revealed that cognitive decline could be attributed to ERC thinning in AD and volume reduction of PRC in BD. We conclude that AD and BD exhibit similar atrophy patterns in the medial temporal cortices and deep gray matter but have distinct pathologic bases for cognitive impairments. Although atrophy of the MTL structures is a sensitive biomarker for AD, it is not superior for discrimination between AD and BD. [ABSTRACT FROM AUTHOR]

Background: Susceptibility-weighted imaging (SWI) has been proven to be superior to T2*-weighted imaging and also other existing magnetic resonance imaging (MRI) techniques for the detection of iron content and hemorrhage in the brain. The purpose of this study was to compare SWI with T1WI, T2WI and T2*WI in detecting splenic siderotic lesions. Methodology/Principal Findings: Twenty-two patients with splenic siderotic nodule were imaged with non-contrast MRI T1WI, T2WI, T2*WI and SWI at 3.0 Tesla. Imaging data were independently analyzed by two experienced radiologists. The number of splenic siderotic nodules was counted, and the size (largest diameter) was measured. The conspicuity was calculated as the nodule to background parenchyma intensity ratio. We found that SWI detected a larger average number of splenic siderotic nodules than T1WI, T2WI, or T2*WI (all P<0.05). The average size of the nodules detected by SWI was larger than that of those detected by T1WI, T2WI or T2*WI (all P<0.05). SWI provided superior contrast and visibility for splenic siderotic nodules compared to any other sequence (all P<0.001). Conclusions: SWI may be a better detection scheme for splenic siderotic nodules than T1WI, T2WI and T2*WI. [ABSTRACT FROM AUTHOR]

Background:Previous studies have demonstrated that structural deficits and functional connectivity imbalances might underlie the pathophysiology of obsessive-compulsive disorder (OCD). The purpose of the present study was to investigate gray matter deficits and abnormal resting-state networks in patients with OCD and further investigate the association between the anatomic and functional alterations and clinical symptoms. Methods:Participants were 33 treatment-naïve OCD patients and 33 matched healthy controls. Voxel-based morphometry was used to investigate the regions with gray matter abnormalities and resting-state functional connectivity analysis was further conducted between each gray matter abnormal region and the remaining voxels in the brain. Results:Compared with healthy controls, patients with OCD showed significantly increased gray matter volume in the left caudate, left thalamus, and posterior cingulate cortex, as well as decreased gray matter volume in the bilateral medial orbitofrontal cortex, left anterior cingulate cortex, and left inferior frontal gyrus. By using the above morphologic deficits areas as seed regions, functional connectivity analysis found abnormal functional integration in the cortical-striatum-thalamic-cortical (CSTC) circuits and default mode network. Subsequent correlation analyses revealed that morphologic deficits in the left thalamus and increased functional connectivity within the CSTC circuits positively correlated with the total Y-BOCS score. Conclusion:This study provides evidence that morphologic and functional alterations are seen in CSTC circuits and default mode network in treatment-naïve OCD patients. The association between symptom severity and the CSTC circuits suggests that anatomic and functional alterations in CSTC circuits are especially important in the pathophysiology of OCD. [ABSTRACT FROM AUTHOR]

Cerebral involvement is common in patients with systemic Lupus erythematosus (SLE) and is characterized by multiple clinical presentations, including cognitive disorders, headaches, and syncope. Several neuroimaging studies have demonstrated cerebral dysfunction during different tasks among SLE patients; however, there have been few studies designed to characterize network alterations or to identify clinical markers capable of reflecting the cerebral involvement in SLE patients. This study was designed to characterize the profile of the cerebral activation area and the functional connectivity of cognitive function in SLE patients by using a task-based and a resting state functional magnetic resonance imaging (fMRI) technique, and to determine whether or not any clinical biomarkers could serve as an indicator of cerebral involvement in this disease. The well-established cognitive function test (Paced Visual Serial Adding Test [PVSAT]) was used. Thirty SLE patients without neuropsychiatric symptoms and 25 age- and gender-matched healthy controls were examined using PVSAT task-based and resting state fMRI. Outside the scanner, the performance of patients and the healthy controls was similar. In the PVSAT task-based fMRI, patients presented significantly expanded areas of activation, and the activated areas exhibited significantly higher functional connectivity strength in patients in the resting state. A positive correlation existed between individual connectivity strength and disease activity scoring. No correlation with cerebral involvement existed for serum markers, such as C3, C4, and anti-dsDNA. Thus, our findings may shed new light on the pathologic mechanism underlying neuropsychiatric SLE, and suggests that disease activity may be a potential effective biomarker reflecting cerebral involvement in SLE. [ABSTRACT FROM AUTHOR]