Endometriosis is a chronic pain disorder that affects young women, impairing their physical, mental and social well-being. Apart from personal suffering, it imposes a significant economic burden on the healthcare system. We analyzed studies reporting comorbid mental disorders in endometriosis based on the ICD/DSM criteria, discussing them in the context of available neuroimaging studies. We postulate that at least one-third of endometriosis patients suffer from mental disorders (mostly depression or anxiety) and require psychiatric or psychotherapeutic support. According to three neuroimaging studies involving patients with endometriosis, brain regions related not only to pain processing but also to emotion, cognition, self-regulation and reward likely constitute the so-called "endometriosis brain". It is not clear, however, whether the neurobiological changes seen in these patients are caused by chronic pain, mental comorbidities or endometriosis itself. Given the paucity of high-quality data on mental comorbidities and neurobiological correlates in endometriosis, further research is needed.

Pregnancy and the postpartum period are characterized by physiological alterations in cortisol and cortisone levels. In the present study, we sought to explore the risk factors for postpartum depression (PPD) and self-remitting postpartum adjustment disorder (AD) and whether cortisol/cortisone metabolism might have any bearing on them. Hair samples from 196 participants (mean age = 31.44, SD = 4.71) were collected at two time points (1-6 days after childbirth and 12 weeks postpartum) to determine the cumulative hair cortisol (HCC) and hair cortisone (HCNC) exposure in the third trimester and during the 12 weeks postpartum. Compared to the non-depressed group (ND, n = 141), more women in the AD (n = 28) and PPD (n = 27) groups had a personal or family history of depression and more stressful life events. Compared to ND and PPD, more women in the AD group had birth-related complications with their children being more often transferred to a pediatric ward. The factors associated with PPD were found to include being unmarried and having a lower household income, less support at home, more subjectively perceived stress after childbirth and lower maternal sensitivity. The natural decrease in HCC concentration from the third trimester to 12 weeks postpartum was significant only in the ND and AD groups, but not in PPD. In summary, prolonged subjectively perceived postpartum stress associated with living situations may contribute to the development of PPD while birth- and child-related complications are likely to trigger brief episodes of AD. Only in ND and AD, the pregnancy-related physiological changes in glucocorticoid levels return to the pre-pregnancy baseline after 12 weeks. Our observations point to the difference between the ND and PPD groups in glucocorticoid metabolism-related postpartum adjustment, which may be a factor in the development of PPD.

Postpartum depression (PPD) and adjustment disorder (AD) affect up to 25% of women after childbirth. However, there are no accurate screening tools for either disorder to identify at-risk mothers and enable them to benefit from early intervention. Combinations of anamnestic, clinical, and remote assessments were evaluated for an early and accurate identification of PPD and AD. Two cohorts of mothers giving birth were included in the study (N = 308 and N = 193). At baseline, participants underwent a detailed sociodemographic-anamnestic and clinical interview. Remote assessments were collected over 12 weeks comprising mood and stress levels as well as depression and attachment scores. At 12 weeks postpartum, an experienced clinician assigned the participants to three distinct groups: women with PPD, women with AD, and healthy controls (HC). Combinations of these assessments were assessed for an early an accurate detection of PPD and AD in the first cohort and, after pre-registration, validated in a prospective second cohort. Combinations of postnatal depression, attachment (for AD) and mood scores at week 3 achieved balanced accuracies of 93 and 79% for differentiation of PPD and AD from HC in the validation cohort and balanced accuracies of 87 and 91% in the first cohort. Differentiation between AD and PPD, with a balanced accuracy of 73% was possible at week 6 based on mood levels only with a balanced accuracy of 73% in the validation cohort and a balanced accuracy of 76% in the first cohort. Combinations of in clinic and remote self-assessments allow for early and accurate detection of PPD and AD as early as three weeks postpartum, enabling early intervention to the benefit of both mothers and children.

There is growing evidence that pregnancy may have a significant impact on the maternal brain, causing changes in its structure. To investigate the patterns of these changes, we compared nulliparous women (n = 40) with a group of primiparous women (n = 40) and multiparous mothers (n = 37) within 1–4 days postpartum, using voxel-based and surface-based morphometry (SBM). Compared with the nulliparous women, the young mothers showed decreases in gray matter volume in the bilateral hippocampus/amygdala, the orbitofrontal/subgenual prefrontal area, the right superior temporal gyrus and insula, and the cerebellum. These pregnancy-related changes in brain structure did not predict the quality of mother–infant attachment at either 3 or 12 weeks postpartum nor were they more pronounced among the multiparous women. SBM analyses showed significant cortical thinning especially in the frontal and parietal cortices, with the parietal cortical thinning likely potentiated by multiple pregnancies. We conclude that, compared with the brain of nulliparous women, the maternal brain shows widespread morphological changes shortly after childbirth. Also, the experience of pregnancy alone may not be the underlying cause of the adaptations for mothering. As regards the exact biological function of the changes in brain morphology, longitudinal research will be needed to draw any definitive conclusions.

The human capacity to integrate sensory signals has been investigated with respect to different sensory modalities. A common denominator of the neural network underlying the integration of sensory clues has yet to be identified. Additionally, brain imaging data from patients with autism spectrum disorder (ASD) do not cover disparities in neuronal sensory processing. In this fMRI study, we compared the underlying neural networks of both olfactory–visual and auditory–visual integration in patients with ASD and a group of matched healthy participants. The aim was to disentangle sensory‐specific networks so as to derive a potential (amodal) common source of multisensory integration (MSI) and to investigate differences in brain networks with sensory processing in individuals with ASD. In both groups, similar neural networks were found to be involved in the olfactory–visual and auditory–visual integration processes, including the primary visual cortex, the inferior parietal sulcus (IPS), and the medial and inferior frontal cortices. Amygdala activation was observed specifically during olfactory–visual integration, with superior temporal activation having been seen during auditory–visual integration. A dynamic causal modeling analysis revealed a nonlinear top‐down IPS modulation of the connection between the respective primary sensory regions in both experimental conditions and in both groups. Thus, we demonstrate that MSI has shared neural sources across olfactory–visual and audio–visual stimulation in patients and controls. The enhanced recruitment of the IPS to modulate changes between areas is relevant to sensory perception. Our results also indicate that, with respect to MSI processing, adults with ASD do not significantly differ from their healthy counterparts.