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BackgroundPredictive models have revealed promising results for the individual prognosis of treatment response and relapse risk as well as for differential diagnosis in affective disorders. Yet, in order to translate personalized predictive modeling from research contexts to psychiatric clinical routine, standardized collection of information of sufficient detail and temporal resolution in day-to-day clinical care is needed. Digital collection of self-report measures by patients is a time- and cost-efficient approach to gain such data throughout treatment. ObjectiveThe objective of this study was to investigate whether patients with severe affective disorders were willing and able to participate in such efforts, whether the feasibility of such systems might vary depending on individual patient characteristics, and if digitally acquired assessments were of sufficient diagnostic validity. MethodsWe implemented a system for longitudinal digital collection of risk and symptom profiles based on repeated self-reports via tablet computers throughout inpatient treatment of affective disorders at the Department of Psychiatry at the University of Münster. Tablet-handling competency and the speed of data entry were assessed. Depression severity was additionally assessed by a clinical interviewer at baseline and before discharge. ResultsOf 364 affective disorder patients who were approached, 242 (66.5%) participated in the study; 88.8% of participants (215/242) were diagnosed with major depressive disorder, and 27 (11.2%) had bipolar disorder. During the duration of inpatient treatment, 79% of expected assessments were completed, with an average of 4 completed assessments per participant; 4 participants (4/242, 1.6%) dropped out of the study prematurely. During data entry, 89.3% of participants (216/242) did not require additional support. Needing support with tablet handling and slower data entry pace were predicted by older age, whereas depression severity at baseline did not influence these measures. Patient self-reporting of depression severity showed high agreement with standardized external assessments by a clinical interviewer. ConclusionsOur results indicate that digital collection of self-report measures is a feasible, accessible, and valid method for longitudinal data collection in psychiatric routine, which will eventually facilitate the identification of individual risk and resilience factors for affective disorders and pave the way toward personalized psychiatric care.

BACKGROUND: Obesity is highly prevalent and disabling, especially in individuals with severe mental illness including bipolar disorders (BD). The brain is a target organ for both obesity and BD. Yet, we do not understand how cortical brain alterations in BD and obesity interact. METHODS: We obtained body mass index (BMI) and MRI-derived regional cortical thickness, surface area from 1231 BD and 1601 control individuals from 13 countries within the ENIGMA-BD Working Group. We jointly modeled the statistical effects of BD and BMI on brain structure using mixed effects and tested for interaction and mediation. We also investigated the impact of medications on the BMI-related associations. RESULTS: BMI and BD additively impacted the structure of many of the same brain regions. Both BMI and BD were negatively associated with cortical thickness, but not surface area. In most regions the number of jointly used psychiatric medication classes remained associated with lower cortical thickness when controlling for BMI. In a single region, fusiform gyrus, about a third of the negative association between number of jointly used psychiatric medications and cortical thickness was mediated by association between the number of medications and higher BMI. CONCLUSIONS: We confirmed consistent associations between higher BMI and lower cortical thickness, but not surface area, across the cerebral mantle, in regions which were also associated with BD. Higher BMI in people with BD indicated more pronounced brain alterations. BMI is important for understanding the neuroanatomical changes in BD and the effects of psychiatric medications on the brain.

AIMS: Rates of obesity have reached epidemic proportions, especially among people with psychiatric disorders. While the effects of obesity on the brain are of major interest in medicine, they remain markedly under-researched in psychiatry. METHODS: We obtained body mass index (BMI) and magnetic resonance imaging-derived regional cortical thickness, surface area from 836 bipolar disorders (BD) and 1600 control individuals from 14 sites within the ENIGMA-BD Working Group. We identified regionally specific profiles of cortical thickness using K-means clustering and studied clinical characteristics associated with individual cortical profiles. RESULTS: We detected two clusters based on similarities among participants in cortical thickness. The lower thickness cluster (46.8% of the sample) showed thinner cortex, especially in the frontal and temporal lobes and was associated with diagnosis of BD, higher BMI, and older age. BD individuals in the low thickness cluster were more likely to have the diagnosis of bipolar disorder I and less likely to be treated with lithium. In contrast, clustering based on similarities in the cortical surface area was unrelated to BD or BMI and only tracked age and sex. CONCLUSIONS: We provide evidence that both BD and obesity are associated with similar alterations in cortical thickness, but not surface area. The fact that obesity increased the chance of having low cortical thickness could explain differences in cortical measures among people with BD. The thinner cortex in individuals with higher BMI, which was additive and similar to the BD-associated alterations, may suggest that treating obesity could lower the extent of cortical thinning in BD.

Individuals with bipolar disorders (BD) frequently suffer from obesity, which is often associated with neurostructural alterations. Yet, the effects of obesity on brain structure in BD are under-researched. We obtained MRI-derived brain subcortical volumes and body mass index (BMI) from 1134 BD and 1601 control individuals from 17 independent research sites within the ENIGMA-BD Working Group. We jointly modeled the effects of BD and BMI on subcortical volumes using mixed-effects modeling and tested for mediation of group differences by obesity using nonparametric bootstrapping. All models controlled for age, sex, hemisphere, total intracranial volume, and data collection site. Relative to controls, individuals with BD had significantly higher BMI, larger lateral ventricular volume, and smaller volumes of amygdala, hippocampus, pallidum, caudate, and thalamus. BMI was positively associated with ventricular and amygdala and negatively with pallidal volumes. When analyzed jointly, both BD and BMI remained associated with volumes of lateral ventricles  and amygdala. Adjusting for BMI decreased the BD vs control differences in ventricular volume. Specifically, 18.41% of the association between BD and ventricular volume was mediated by BMI (Z = 2.73, p = 0.006). BMI was associated with similar regional brain volumes as BD, including lateral ventricles, amygdala, and pallidum. Higher BMI may in part account for larger ventricles, one of the most replicated findings in BD. Comorbidity with obesity could explain why neurostructural alterations are more pronounced in some individuals with BD. Future prospective brain imaging studies should investigate whether obesity could be a modifiable risk factor for neuroprogression.

Background: Anhedonia is a key symptom of major depressive disorder (MDD). Anhedonia is associated with aberrant reward processing, but whether it might interfere similarly with the neural processing of aversive stimuli, such as monetary loss, remains unknown. We aimed to investigate potential associations between anhedonia and neural response during reward and loss processing in patients with MDD. Methods: We investigated blood-oxygen-level-dependent response in the orbitofrontal cortex, cingulate cortex, insula and basal ganglia during monetary reward and loss processing in 182 patients with MDD, using a card-guessing paradigm. We measured anhedonia with the Social and Physical Anhedonia Scale (SASPAS), and we tested for the main and interaction effects of SASPAS scores and the experimental condition (reward or loss) in a full factorial model. Results: We detected a negative main effect of anhedonia, as well as a significant interaction effect of anhedonia and the experimental condition, on orbitofrontal and insular neural response. Post hoc analyses revealed that the interaction was driven by a significant association between higher anhedonia scores and hypoactivation during loss processing. We observed no significant association between anhedonia and neural response during reward processing. Limitations: This study had a cross-sectional design. Conclusion: Our findings confirmed that altered neural processing in the orbitofrontal cortex and insula is a neurobiological feature of anhedonic symptomatology in people with MDD. The pronounced association between anhedonia and blunted neural response during loss processing supports a broader concept for the neurobiological basis of anhedonia. Hence, MDD with anhedonic features might be characterized by reduced neural response to external stimuli, potentially because of amotivation., Introduction Anhedonia is one of the core symptoms of major depressive disorder (MDD) in addition to low mood, according to the International Statistical Classification of Diseases and Related Health Problems, [...]

Background: Childhood maltreatment (CM) represents a potent risk factor for major depressive disorder (MDD), including poorer treatment response. Altered resting-state connectivity in the fronto-limbic system has been reported in maltreated individuals. However, previous results in smaller samples differ largely regarding localization and direction of effects. Methods: We included healthy and depressed samples [ n = 624 participants with MDD; n = 701 healthy control (HC) participants] that underwent resting-state functional MRI measurements and provided retrospective self-reports of maltreatment using the Childhood Trauma Questionnaire. A-priori defined regions of interest [ROI; amygdala, hippocampus, anterior cingulate cortex (ACC)] were used to calculate seed-to-voxel connectivities. Results: No significant associations between maltreatment and resting-state connectivity of any ROI were found across MDD and HC participants and no interaction effect with diagnosis became significant. Investigating MDD patients only yielded maltreatment-associated increased connectivity between the amygdala and dorsolateral frontal areas [ p FDR < 0.001; η 2partial = 0.050; 95%-CI (0.023–0.085)]. This effect was robust across various sensitivity analyses and was associated with concurrent and previous symptom severity. Particularly strong amygdala-frontal associations with maltreatment were observed in acutely depressed individuals [ n = 264; p FDR < 0.001; η 2partial = 0.091; 95%-CI (0.038–0.166)). Weaker evidence – not surviving correction for multiple ROI analyses – was found for altered supracallosal ACC connectivity in HC individuals associated with maltreatment. Conclusions: The majority of previous resting-state connectivity correlates of CM could not be replicated in this large-scale study. The strongest evidence was found for clinically relevant maltreatment associations with altered adult amygdala-dorsolateral frontal connectivity in depression. Future studies should explore the relevance of this pathway for a maltreated subgroup of MDD patients. [ABSTRACT FROM AUTHOR]

Background: Obesity is highly prevalent and disabling, especially in individuals with severe mental illness including bipolar disorders (BD). The brain is a target organ for both obesity and BD. Yet, we do not understand how cortical brain alterations in BD and obesity interact., Methods: We obtained body mass index (BMI) and MRI-derived regional cortical thickness, surface area from 1231 BD and 1601 control individuals from 13 countries within the ENIGMA-BD Working Group. We jointly modeled the statistical effects of BD and BMI on brain structure using mixed effects and tested for interaction and mediation. We also investigated the impact of medications on the BMI-related associations., Results: BMI and BD additively impacted the structure of many of the same brain regions. Both BMI and BD were negatively associated with cortical thickness, but not surface area. In most regions the number of jointly used psychiatric medication classes remained associated with lower cortical thickness when controlling for BMI. In a single region, fusiform gyrus, about a third of the negative association between number of jointly used psychiatric medications and cortical thickness was mediated by association between the number of medications and higher BMI., Conclusions: We confirmed consistent associations between higher BMI and lower cortical thickness, but not surface area, across the cerebral mantle, in regions which were also associated with BD. Higher BMI in people with BD indicated more pronounced brain alterations. BMI is important for understanding the neuroanatomical changes in BD and the effects of psychiatric medications on the brain.