Cerebellum and hippocampus abnormalities in patients with insomnia comorbid depression: a study on cerebral blood perfusion and functional connectivity.

Chronic insomnia disorder and major depressive disorder are highly-occurred mental diseases with extensive social harm. The comorbidity of these two diseases is commonly seen in clinical practice, but the mechanism remains unclear. To observe the characteristics of cerebral blood perfusion and functional connectivity in patients, so as to explore the potential pathogenesis and biological imaging markers, thereby improving the understanding of their comorbidity mechanism. 44 patients with chronic insomnia disorder comorbid major depressive disorder and 43 healthy controls were recruited in this study. The severity of insomnia and depression were assessed by questionnaire. The cerebral blood perfusion and functional connectivity values of participants were obtained to, analyze their correlation with questionnaire scores. The cerebral blood flow in cerebellum, vermis, right hippocampus, left parahippocampal gyrus of patients were reduced, which was negatively related to the severity of insomnia or depression. The connectivities of left cerebellum-right putamen and right hippocampus-left inferior frontal gyrus were increased, showing positive correlations with the severity of insomnia and depression. Decreased connectivities of left cerebellum-left fusiform gyrus, left cerebellum-left occipital lobe, right hippocampus-right paracentral lobule, right hippocampus-right precentral gyrus were partially associated with insomnia or depression. The connectivity of right hippocampus-left inferior frontal gyrus may mediate between insomnia and depression. Insomnia and depression can cause changes in cerebral blood flow and brain function. Changes in the cerebellar and hippocampal regions are the result of insomnia and depression. They reflect abnormalities in sleep and emotion regulation. That may be involved in the pathogenesis of comorbidity.

Lower maternal serum 25(OH) D in first trimester associated with higher autism risk in Chinese offspring.

OBJECTIVE: The aim of this study was to examine the association between maternal serum vitamin D status in first trimester and risk of ASD at age 3-7years in the offspring. METHODS: Using a case-control design, 68 children diagnosed with ASD and 68 sex and age matched typically-developing children were included. Archived maternal blood samples from the first trimester of pregnancy (11-13weeks gestational age) were identified for those participants. Maternal serum levels of 25 hydroxyvitamin D3 [25(OH) D], unmetabolized folic acid (FA), vitamin B12, homocysteine (HCY) and High Sensitivity C Reactive protein (CRP) were measured from those samples. We examined the associations between those factors in pregnancy and diagnosis of ASD with logistic regression using SPSS. RESULTS: Mothers in autistic group had significantly lower maternal serum levels of 25(OH) D than in typically-developing group [19.2(IQR: 15.8-22.9)ng/ml vs. 24.3(19.3-27.3)ng/ml, P<0.001], with 55.9% and 29.4% being vitamin D deficient, respectively (P<0.001). Levels of 25(OH) D increased with decreasing severity of ASD as defined by the CARS score (r=-0.302, P<0.001). Maternal first trimester serum levels of 25(OH) D in the lower 3 quartiles (quartile 1, 2, 3) (compared to the highest quartile) was associated with increased odds of ASD diagnosis in offspring [OR (95% CI) Q1: 1.36(0.84-2.58, P=0.25); Q2: 2.68(1.44-4.29, P=0.006); Q3:3.99(2.58-7.12, P<0.001)]. CONCLUSIONS: Lower first trimester maternal serum levels of 25(OH) D were associated with increased risk of developing autism in offspring. If these findings are confirmed, this may present an opportunity for prenatal intervention to reduce the risk for ASD.

Reduced white matter integrity and its correlation with clinical symptom in first-episode, treatment-naive generalized anxiety disorder.

The purpose of this study was to explore white matter microstructural alterations in the patients with generalized anxiety disorder (GAD) using diffusion tensor imaging (DTI) technique, and to assess neural associations with the symptom severity. Twenty-eight first-episode, treatment-naive GAD patients without co-morbidities and 28 matched healthy controls underwent DTI acquisition and clinical symptom assessments. Tract-based spatial statistics (TBSS) was used to analyze white matter microstructural abnormalities in patients with GAD, as well as their associations with clinical symptom scores in a voxel-wise manner. Compared to controls, patients showed decreased fractional anisotropy (FA) values in 7 clusters of white matter in bilateral uncinate fasciculus, body of corpus callosum, left middle cingulum (cingulate gyrus), bilateral anterior thalamic radiation and corona radiate, right anterior limb of internal capsule, bilateral inferior frontal-occipital fasciculus, bilateral superior and inferior longitudinal fasciculus, and increased mean diffusivity and radial diffusivity in widespread white matter regions. Reduced FA values in right uncinate fasciculus, left cingulum bundle showed significantly negative correlations with clinical symptom severity for Hamilton anxiety Rating Scale scores. Our findings suggest microstructural abnormalities in uncinate fasciculus and cingulum bundle play key roles in the underlying neural basis of GAD.

Aberrant regional neural fluctuations and functional connectivity in generalized anxiety disorder revealed by resting-state functional magnetic resonance imaging.

The purpose of this study was to investigate the neural activity and functional connectivity in generalized anxiety disorder (GAD) during resting state, and how these alterations correlate to patients' symptoms. Twenty-eight GAD patients and 28 matched healthy controls underwent resting-state functional magnetic resonance (fMRI) scans. Amplitude of low-frequency fluctuation (ALFF) and seed-based resting-state functional connectivity (RSFC) were computed to explore regional activity and functional integration, and were compared between the two groups using the voxel-based two-sample t test. Pearson's correlation analyses were performed to examine the neural relationships with demographics and clinical symptoms scores. Compared to controls, GAD patients showed functional abnormalities: higher ALFF in the bilateral dorsomedial prefrontal cortex, bilateral dorsolateral prefrontal cortex and left precuneus/posterior cingulate cortex; lower connectivity in prefrontal gyrus; lower in prefrontal-limbic and cingulate RSFC and higher prefrontal-hippocampus RSFC were correlated with clinical symptoms severity, but these associations were unable to withstand correction for multiple testing. These findings may help facilitate further understanding of the potential neural substrate of GAD.