Insomnia and depression are highly comorbid symptoms in both primary insomnia (PI) and major depressive disorder (MDD). In the current study, we aimed at exploring both the homogeneous and heterogeneous brain structure alteration in PI and MDD patients. Sixty-five MDD patients and 67 matched PI patients were recruited and underwent a structural MRI scan. The subjects were sub-divided into four groups, namely MDD patients with higher or lower insomnia, and PI patients with higher or lower severe depression. A general linear model was employed to explore the changes in cortical thickness and volume as a result of depression or insomnia, and their interaction. In addition, partial correlation analysis was conducted to detect the clinical significance of the altered brain structural regions. A main effect of depression on cortical thickness was seen in the superior parietal lobe, middle cingulate cortex, and parahippocampal gyrus, while a main effect of insomnia on cortical thickness was found in the posterior cingulate cortex. Importantly, the interaction between depression and insomnia was associated with decreased gray matter volume in the right orbitofrontal cortex, i.e., patients with co-occurring depression and insomnia showed smaller brain volume in the right orbitofrontal cortex when compared to patients with lower insomnia/depression. These findings highlighted the role of the orbitofrontal cortex in the neuropathology of the comorbidity of insomnia and depression. Our findings provide new insights into the understanding of the brain mechanism underlying comorbidity of insomnia and depression.
Objective
Recent neuroimaging studies have found that brain function is abnormal in primary dysmenorrhea (PDM). The present study aimed to explore frequency-specific brain alterations and their occurrence in the PDM.
Methods
Forty-seven patients with PDM and 36 matched healthy controls were enrolled in the study and underwent resting-state functional magnetic resonance imaging. The alterations in brain function in patients with PDM were assessed using different frequency filter bands (Slow5, Slow4, Slow3, and full low frequency) and functional connectivity density (FCD) approach. The clinical significance of the altered FCD was then explored. Additionally, mediation analysis was employed to detect the altered FCD-mediated clinical relationships in PDM.
Results
Frequency-specific FCD alterations have been observed in patients with PDM, especially in the central executive, default mode, sensorimotor networks, and the hippocampus. The altered full low-frequency FCD in the hippocampus was associated with the duration of disease and pain severity scores. The altered Slow 5 FCD in the second somatosensory area (S2) was associated with the severity of pain in PDM. Furthermore, the FCD in S2 mediated the duration associated with pain symptoms in PDM.
Conclusion
The present study identified frequency-specific FCD alterations in PDM and suggested that the S2 area is a potential treatment target for PDM.
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