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Cortical thickness and subcortical structure volume abnormalities in patients with major depression with and without anxious symptoms.

ABSTRACT: Anxious depression is one of the common subtypes of major depressive disorder (MDD). Clinically, patients with anxious depression exhibit more severe depressive symptoms than patients with nonanxious depression. The aim of the present study was to explore the common and differing cortical and subcortical structural changes between patients with anxious and nonanxious depression.Patients were placed into one of three groups: the anxious depression group (MDD patients with high levels of anxiety symptoms, n = 23), the nonanxious depression group (n = 22), and healthy controls (n = 43) that were matched for age, sex, and education level. All participants underwent T1-weighted MRI. The Freesurfer, which uses a set of automated sequences to analyze the abnormal changes of cortical thickness, cortical and subcortical structures, was used to process the T1 images.Compared to controls, MDD patients showed thinner cortical thickness in the left inferior temporal, the right superior temporal, and the right parsorbitalis, and a smaller volume of the left hippocampus. Compared to nonanxious depression, anxious depressive patients showed a cortical thinning of the left superior frontal and right superior temporal, as well as the right lingual, and significantly increased subcortical volume of the bilateral caudate nuclei. Correlation analysis showed that the volumes of the bilateral caudate nuclei were directly proportional to the anxiety/somatization factor score.These findings suggest that smaller hippocampal volume and atrophic prefrontal and temporal cortices might be a common pattern of cortical and subcortical alterations in patients with depression and/or anxiety. However, the change in the caudate nucleus volume may be indicative of anxious depression and may potentially be used to distinguish anxious from nonanxious depression.

SUBMITTER: Zhao K

PROVIDER: S-EPMC5561315 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:Introduction22q11.2 deletion syndrome (22q11DS) represents one of the largest known genetic risk factors for psychosis, yet the neurobiological mechanisms underlying symptom development are not well understood. Here we conducted a cross-sectional study of 22q11DS to decompose cortical volume into its constituent parts, cortical thickness (CT) and surface area (SA), which are believed to have distinct neurodevelopmental origins.MethodsHigh-resolution T1-weighted scans were collected on 65 participants (31 22q11DS, 34 demographically comparable typically developing controls, 10-25 years old). Measures of cortical volume, CT, and SA were extracted from regions of interest using the FreeSurfer image analysis suite. Group differences and age-related trajectories in these structures, as well as their association with psychotic symptomatology, were assessed.ResultsRelative to controls, 22q11DS participants showed bilateral volumetric reductions in the inferior temporal cortex, fusiform gyrus, anterior cingulate, superior parietal cortex, and cuneus, which were driven by decreased SA in these regions. 22q11DS participants also had increased volumes, driven by increased CT, in bilateral insula regions. 22q11DS youth had increased CT in frontal regions, particularly middle frontal and medial orbitofrontal cortices. A pattern of age-associated cortical thinning was observed in typically developing controls in brain regions associated with visual and sensory information-processing (i.e., left pericalcarine cortex and fusiform gyrus, right lingual and postcentral cortices). However, this relationship was disrupted in 22q11DS participants. Finally, correlational analyses revealed that increased CT in right medial orbitofrontal cortex was associated with increased positive symptom severity in 22q11DS.ConclusionDifferential disruptions of CT and SA in distinct cortical regions in 22q11DS may indicate abnormalities in distinct developmental neural processes. Further, neuroanatomic abnormalities in medial frontal brain structures disproportionately affected in idiopathic schizophrenia were associated with psychotic symptom severity in 22q11DS youth, suggesting that disrupted biological processes in these cortical regions may underlie development of psychotic symptoms, both in 22q11DS and in the broader population.

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Cortical thickness and subcortical structure volume abnormalities in patients with major depression with and without anxious symptoms.

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