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Aims The aim of this study is to investigate differences in gray matter volume and cortical complexity between Parkinson's disease with depression (PDD) patients and Parkinson's disease without depression (PDND) patients. Methods A total of 41 PDND patients, 36 PDD patients, and 38 healthy controls (HC) were recruited and analyzed by Voxel‐based morphometry (VBM) and surface‐based morphometry (SBM). Differences in gray matter volume and cortical complexity were compared using the one‐way analysis of variance (ANOVA) and correlated with the Hamilton Depression Scale‐17 (HAMD‐17) scores. Results PDD patients exhibited significant cortical atrophy in various regions, including bilateral medial parietal–occipital–temporal lobes, right dorsolateral temporal lobes, bilateral parahippocampal gyrus, and bilateral hippocampus, compared to HC and PDND groups. A negative correlation between the GMV of left precuneus and HAMD‐17 scores in the PDD group tended to be significant (r = −0.318, p = 0.059). Decreased gyrification index was observed in the bilateral insular and dorsolateral temporal cortex. However, there were no significant differences found in fractal dimension and sulcal depth. Conclusion Our research shows extensive cortical structural changes in the insular cortex, parietal–occipital–temporal lobes, and hippocampal regions in PDD. This provides a morphological perspective for understanding the pathophysiological mechanism underlying depression in Parkinson's disease. The first row of pictures shows extensive cortical volume loss in Parkinson's disease with depression patients, primarily concentrated in the parietal–occipital–temporal lobes, parahippocampal gyrus, and hippocampus. The second row of pictures shows decreased gyrification index in the insula.

Two largely distinct bodies of research have demonstrated age-related alterations and disease-specific aberrations in both local gamma oscillations and patterns of cortical thickness. However, seldom has the relationship between gamma activity and cortical thickness been investigated. Herein, we combine the spatiotemporal precision of magnetoencephalography (MEG) with high-resolution magnetic resonance imaging and surface-based morphometry to characterize the relationships between somatosensory gamma oscillations and the thickness of the cortical tissue generating the oscillations in 94 healthy adults (age range: 22–72). Specifically, a series of regressions were computed to assess the relationships between thickness of the primary somatosensory cortex (S1), S1 gamma response power, peak gamma frequency, and somatosensory gating of identical stimuli. Our results indicated that increased S1 thickness significantly predicted greater S1 gamma response power, reduced peak gamma frequency, and improved somatosensory gating. Furthermore, peak gamma frequency significantly and partially mediated the relationship between S1 thickness and the magnitude of the S1 gamma response. Finally, advancing age significantly predicted reduced S1 thickness and decreased gating of redundant somatosensory stimuli. Notably, this is the first study to directly link somatosensory gamma oscillations to local cortical thickness. Our results demonstrate a multi-faceted relationship between structure and function, and have important implications for understanding age- and disease-related deficits in basic sensory processing and higher-order inhibitory function. •Possible links between local cortical thickness and gamma-band activity are unclear.•Adults underwent structural MRI and a somatosensory gating task during MEG.•Advanced oscillatory and surface-based morphometry analysis methods were combined.•Local cortical thickness predicted gamma response power, frequency, and gating.•Peak gamma frequency mediated the relationship between thickness and response power.

To measure the changes in cerebral cortical thickness in patients with herpes zoster (HZ) and postherpetic neuralgia (PHN) by surface-based morphometry (SBM) and further estimate its correlation with clinical scores. Twenty-nine HZ patients, 30 PHN patients and 30 well-matched healthy controls (HCs) were included. Magnetic resonance imaging (MRI) data from all subjects were collected and then analyzed by SBM. The changes in cortical thickness among the HZ, PHN and HC groups were analyzed by ANOVA and correlated with clinical scores. The thickness of the bilateral primary visual cortex (V1, V2) and right primary visual cortex (V3), left somatosensory cortex (L3A), right anterior cingulate gyrus and medial prefrontal cortex (RS32) increased in PHN group, and the thickness the left insular and frontal opercular cortex (LFOP4), left motor cortex (L3B), and right superior temporal visual cortex (RSTV) were decreased in the HZ and PHN groups compared to the HC group. The thickness measurements of RS32, LFOP4, and (L3B) in HZ and PHN patients were correlated with the duration of disease. In HZ and PHN patients, the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) scores were significantly positively correlated. Changes in cortical thickness in the areas related to sensory, motor, and cognitive/emotional changes in patients with PHN affect the neuroplasticity process of the brain, which may be the reason for the transformation of HZ into PHN and provide a possible explanation for the neuropathological mechanism of pain persistence in PHN patients.

The migrainous aura has different clinical phenotypes. While the various clinical differences are well-described, little is known about their neurophysiological underpinnings. To elucidate the latter, we compared white matter fiber bundles and gray matter cortical thickness between healthy controls (HC), patients with pure visual auras (MA) and patients with complex neurological auras (MA+). 3T MRI data were collected between attacks from 20 patients with MA and 15 with MA+, and compared with those from 19 HCs. We analyzed white matter fiber bundles using tract-based spatial statistics (TBSS) of diffusion tensor imaging (DTI) and cortical thickness with surface-based morphometry of structural MRI data. Tract-based spatial statistics showed no significant difference in diffusivity maps between the three subject groups. As compared to HCs, both MA and MA+ patients had significant cortical thinning in temporal, frontal, insular, postcentral, primary and associative visual areas. In the MA group, the right high-level visual-information-processing areas, including lingual gyrus, and the Rolandic operculum were thicker than in HCs, while in the MA+ group they were thinner. These findings show that migraine with aura is associated with cortical thinning in multiple cortical areas and that the clinical heterogeneity of the aura is reflected by opposite thickness changes in high-level visual-information-processing, sensorimotor and language areas.

Aggression occurs across the population ranging on a symptom continuum. Most previous studies have used magnetic resonance imaging in clinical/forensic samples, which is associated with several confounding factors. The present study examined structural brain characteristics in two healthy samples differing only in their propensity for aggressive behavior. Voxel- and surface-based morphometry (SBM) analyses were performed on 29 male martial artists and 32 age-matched male controls. Martial artists had significantly increased mean gray matter volume in two frontal (left superior frontal gyrus and bilateral anterior cingulate cortex) and one parietal (bilateral posterior cingulate gyrus and precuneus) brain clusters compared to controls (whole brain: p  < 0.001, cluster level: family-wise error (FWE)-corrected). SBM analyses revealed a trend for greater gyrification indices in martial artists compared to controls in the left lateral orbital frontal cortex and the left pars orbitalis (whole brain: p  < 0.001, cluster level: FWE-corrected). The results indicate brain structural differences between martial artists and controls in frontal and parietal brain areas critical for emotion processing/inhibition of emotions as well as empathic processes. The present study highlights the importance of studying healthy subjects with a propensity for aggressive behavior in future structural MRI research on aggression.

Parkinson's disease (PD) is a common neurodegenerative disease with progressive gait, cognition, and overall functional decline. Surface area changes are frequently seen with aging. In neurodegenerative diseases, the changes can be evident with disease progression. The current study aimed to study the regional microstructural alterations using surface-based morphometry to correlate with gait measures of the pace and rhythm domains in PD patients. We hypothesize that specific regional surface changes can be associated with PD gait impairments. Surface analysis might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker in adjacent with other imaging markers. Twenty-seven PD patients and 37 healthy controls were included. The clinical assessment included Mini-Mental State Exanimation, PD motor assessment, clinical gait testing and objective/quantitative gait assessment. For patients with PD, all motor and gait testing were performed during both OFF and ON medication states. Three tesla MRI and high-resolution 3D structural images were acquired with a MP-RAGE pulse sequence. Structural image data preprocessing was performed using the DPABISurf toolbox. Clinical characteristics between PD and control group were compared, and correlation between the surface area and behavioral data were analyzed. At left lateral temporal cortex (LTC) and right inferior parietal cortex (IPC), PD patients have significant larger surface areas when compared to controls (P<0.05) using the surface-based morphometry. The surface area changes of the left LTC and right IPC were associated with worse performance of gait assessed by Berg Balance scale and Timed Up and Go during OFF (P<0.01). The left LTC area changes significantly correlated with number of steps, velocity, stride length of the pace domain in the ON state. Our findings suggest that PD is associated with a characteristic regional pattern of larger surface area in left LTC and right IPC. These regional changes were associated with the pace domain of the gait in ON state. Overall, surface-based analyses might provide a useful tool for assessing PD for functional status and specific motor domains, such as gait in PD, and potentially could serve as an imaging marker.

The purpose of this study is to observe the changes of cortical morphological characteristics and their potential contribution to cognitive function in ALL survivors by using surface-based morphometry (SBM). Using SBM analysis, we calculated and compared group differences in cortical thickness, sulcal depth, gyrification, and fractal dimension of the cerebral cortex between 18 pediatric ALL survivors treated on chemotherapy-only protocols and off treatment within 2 years, and 18 healthy controls (HCs) with two-sample t-tests [ P  < 0.05, family-wise error (FWE) corrected]. Relationships between abnormal cortical characteristic values and cognitive function parameters were investigated with partial correlation analysis, taking age as a covariate. We found decreased cortical thickness mainly located in the prefrontal and temporal region, and increased sulcal depth in left rostral middle frontal cortex and left pars orbitalis in the ALL survivors compared to HCs. There were no statistically significant differences in the gyrification and fractal dimension between the two groups. In ALL survivors, cortical thickness and sulcal depth of above areas values revealed no significant correlation with the cognitive function parameters. In conclusion, pediatric ALL survivors show decreased cortical thickness in prefrontal and temporal regions, and increased sulcal depth in prefrontal region. These results suggest that SBM-based approach can be used to assess changes of cortical morphological characteristics in pediatric ALL survivors.

To detect the abnormal cortical thickness and disrupted brain resting-state functional connectivity (RSFC) in patients with systemic lupus erythematosus (SLE) without neuropsychiatric symptoms (non-NPSLE). Using T1-weighted 3D brain structural data, we first determined the regions with abnormal cortical thickness in a cohort of 33 adult female non-NPSLE patients. By taking brain regions with significantly reduced cortical thickness as the seeds, we calculated their RSFC based on the resting-fMRI data and detected the relationship between the RSFC and cortical thickness in the non-NPSLE patients. Compared to the controls, the non-NPSLE patients showed significantly cortical thinning in the left fusiform gyrus (FUS.L), left lingual gyrus (LING.L), right lingual gyrus (LING.R) and left superior frontal cortex (SFC.L). As for the RSFC, statistical analyses indicated that the abnormal cortical thickness in LING.L is associated with increased RSFC in the left posterior cingulate cortex (PCC.L), and cortical thinning in SFC.L associated with decreased RSFC in left cerebellum 6 (CRBL 6.L) in non-NPSLE patients. In addition, in non-NPSLE patients, the decreased cortical thickness in LING.L was correlated to the increased RSFC in PCC.L, and decreased cortical thickness in SFC.L was correlated to the decreased RSFC in CRBL 6.L. Our findings suggest that the cortical abnormalities may affect brain intrinsic connectivity in non-NPSLE patients.

Previously, studies have demonstrated cortical impairments in those who complete or attempt suicide. Subcortical nuclei have less often been implicated in the suicidal vulnerability. In the present study, we investigated, with a specific design in a large population, variations in the volume of subcortical structures in patients with mood disorders who have attempted suicide. We recruited 253 participants: 73 suicide attempters with a past history of both mood disorders and suicidal act, 89 patient controls with a past history of mood disorders but no history of suicidal act, and 91 healthy controls. We collected 1.5 T magnetic resonance imaging data from the caudate, pallidum, putamen, nucleus accumbens, hippocampus, amygdala, ventral diencephalon, and thalamus. Surface-based morphometry (Freesurfer) analysis was used to comprehensively evaluate gray matter volumes. In comparison to controls, suicide attempters showed no difference in subcortical volumes when controlled for intracranial volume. However, within attempters negative correlations between the left ( r  = −0.35, p  = 0.002), and right ( r  = −0.41, p  < 0.0005) nucleus accumbens volumes and the lethality of the last suicidal act were found. Our study found no differences in the volume of eight subcortical nuclei between suicide attempters and controls, suggesting a lack of association between these regions and suicidal behavior in general. However, individual variations in nucleus accumbens structure and functioning may modulate the lethality of suicidal acts during a suicidal crisis. The known role of nucleus accumbens in action selection toward goals determined by the prefrontal cortex, decision-making or mental pain processing are hypothesized to be potential explanations.

Longitudinal MRI studies are of increasing importance to document the time course of neurodegenerative diseases as well as neuroprotective effects of a drug candidate in clinical trials. However, manual longitudinal image assessments are time consuming and conventional assessment routines often deliver unsatisfying study outcomes. Here, we propose a profound analysis pipeline that consists of the following coordinated steps: 1) an automated and highly precise image processing stream including voxel and surface based morphometry using latest highly detailed brain atlases such as the HCP MMP 1.0 atlas with 360 cortical ROIs; 2) a profound statistical assessment using a multiplicative model of annual percent change (APC); and 3) a multiple testing correction adopted from genome-wide association studies that is optimally suited for longitudinal neuroimaging studies. We tested this analysis pipeline with 25 Alzheimer’s disease patients against 25 age-matched cognitively normal subjects with a baseline and a 1-year follow-up conventional MRI scan from the ADNI-3 study. Even in this small cohort, we were able to report 22 significant measurements after multiple testing correction from SBM (including cortical volume, area and thickness) complementing only three statistically significant volume changes (left/right hippocampus and left amygdala) found by VBM. A one-year decrease in brain morphometry coincided with an increasing clinical disability and cognitive decline in patients measured by MMSE, CDR GLOBAL, FAQ TOTAL and NPI TOTAL scores. This work shows that highly precise image assessments, APC computation and an adequate multiple testing correction can produce a significant study outcome even for small study sizes. With this, automated MRI processing is now available and reliable for routine use and clinical trials.