Atrophic Corpus Callosum Associated with Altered Functional Asymmetry in Major Depressive Disorder.

PURPOSE: Impairments in intra- and inter-hemispheric information transfer circuits have been reported in patients with major depressive disorder (MDD). However, the specific anomalous connection (intra- and/or inter-hemispheric) and hemisphere (left and/or right) in which this connection plays a more dominant role in the pathogenic mechanism underlying MDD are still poorly understood. PATIENTS AND METHODS: Structural magnetic resonance imaging and resting-state functional magnetic resonance imaging were performed in 33 patients with MDD and 33 healthy controls. The intra- and inter-hemispheric functional connectivity (FC) strength in the default mode network areas and volume of the callosal subregions were computed using independent samples t-tests. The partial correlations between the volumes and FCs were also computed. RESULTS: The patients with MDD had smaller volumes in the genu of the corpus callosum than the controls. The intrahemispheric FCs of the bilateral posterior cingulate gyrus, left precuneus, left medial superior frontal gyrus, left medial orbitofrontal gyrus, left angular gyrus and left middle temporal gyrus, and interhemispheric FCs of the bilateral posterior cingulate gyrus in the patients with MDD were lower than those in the controls. Moreover, the intrahemispheric FCs of the precuneus and interhemispheric FCs of middle frontal gyrus, orbital middle frontal gyrus, and anterior cingulate gyrus in the patients with MDD showed right-lateralized asymmetry, which were opposite from the asymmetry patterns observed in the controls. The functional asymmetry of the anterior cingulate gyrus was correlated with the volume of the genu of the corpus callosum and disease duration. CONCLUSION: These findings provide robust evidence that intra- and inter-hemispheric disconnections are involved in MDD, and that functional disruptions in the left hemisphere may be more relevant to the pathophysiology of MDD. Furthermore, imbalanced interhemispheric exchanges may contribute to the anatomical deficits in the corpus callosum in patients with MDD.

Asymmetry in cortical thickness and subcortical volume in treatment-naïve major depressive disorder.

BACKGROUND: Numerous cognitive and emotional functions are executed asymmetrically between the left and right hemispheres. Right hemisphere hyperactivity/left hemisphere hypoactivity often appears to be a feature in neuroimaging studies of depression. However, few studies have evaluated abnormalities in structural asymmetry in untreated patients with major depressive disorder (MDD). METHODS: In this study, 3-dimensional high-resolution structural magnetic resonance images were acquired from 35 treatment-naïve patients with MDD (mean age = 28.9 years, 22 females) and 35 normal controls. The asymmetry index in cortical thickness and subcortical volume were calculated based on an automated surface-based technique. RESULTS: Abnormalities in structural asymmetry in patients with MDD were mainly located in the cortical-striatal-pallidal-thalamic circuit, including the superior frontal cortex, rostral middle frontal cortex, caudal middle frontal cortex, nucleus accumbens, pallidum and thalamus. No significant correlation was observed between symptom severity and asymmetric measurements. CONCLUSION: These findings provide further evidence for the altered morphological interhemispheric imbalances in depression and these alterations were independent of depressive symptom severity, suggesting that cerebral asymmetry could be an appropriate indicator of morphological variations in mental disease.

Altered Structural Covariance Among the Dorsolateral Prefrontal Cortex and Amygdala in Treatment-Naïve Patients With Major Depressive Disorder.

Background: Impairments in cognitive and emotional processing are a characteristic of major depressive disorder (MDD), and the dorsolateral prefrontal cortex (DLPFC) and amygdala are involved in these processes. However, the structural covariance between these two areas in patients with MDD has not been examined. Whether anatomical patterns are further damaged or compensated in untreated multiple-episode MDD compared to those in first-episode MDD is unclear. Methods: Structural magnetic resonance imaging was performed in 35 treatment-naïve, currently depressed patients with MDD and 35 age-, sex-, and education-matched controls. The cortical thickness and subcortical volume were calculated using FreeSurfer software. Patients were divided into two subgroups based on the previous number of episodes. Results: Regional abnormalities in patients with MDD were primarily observed in the frontal-limbic circuits. The negative structural association between the left DLPFC and left amygdala and the positive structural association between the bilateral DLPFC observed in controls were absent in patients with MDD. The medial orbitofrontal cortex and posterior cingulate cortex were thicker in patients with multiple-episode MDD than in patients with first-episode MDD and were positively correlated with disorder duration. No structural alterations were correlated with symptom severity. Conclusions: These findings may provide structural evidence for deficits in functional networks in MDD and supports an underlying structural mechanism of dysfunction involving top-down or bottom-up processes. Morphological abnormalities in the medial orbitofrontal cortex and posterior cingulate cortex may be critical for the pathophysiological progression of multiple-episode MDD.

Progressive Thinning of Visual Motion Area in Lower Limb Amputees.

Accumulating evidence has indicated that amputation or deafferentation of a limb induces functional or structural reorganization in the visual areas. However, the extent of the visual areas involved after lower limb amputation remains uncertain. In this investigation, we studied 48 adult patients with unilateral lower limb amputation and 48 matched healthy controls using T1-weighted magnetic resonance imaging. Template-based regions of interest analysis was implemented to detect the changes of cortical thickness in the specific visual areas. Compared with normal controls, amputees exhibited significantly lower thickness in the V5/middle temporal (V5/MT+) visual area, as well as a trend of cortical thinning in the V3d. There was no significant difference in the other visual areas between the two groups. In addition, no significant difference of cortical thickness was found between patients with amputation at different levels. Across all amputees, correlation analyses revealed that the cortical thickness of the V5/MT+ was negatively correlated to the time since amputation. In conclusion, our findings indicate that the amputation of unilateral lower limb could induce changes in the motor-related visual cortex and provide an update on the plasticity of the human brain after limb injury.