Self-Referential Processing, Rumination, and Cortical Midline Structures in Major Depression

International audienceMajor depression is associated with a bias toward negative emotional processing and increased self-focus, i.e., the process by which one engages in self-referential processing. The increased self-focus in depression is suggested to be of a persistent, repetitive and self-critical nature, and is conceptualized as ruminative brooding. The role of the medial prefrontal cortex in self-referential processing has been previously emphasized in acute major depression. There is increasing evidence that self-referential processing as well as the cortical midline structures play a major role in the development, course, and treatment response of major depressive disorder. However, the links between self-referential processing, rumination, and the cortical midline structures in depression are still poorly understood. Here, we reviewed brain imaging studies in depressed patients and healthy subjects that have examined these links. Self-referential processing in major depression seems associated with abnormally increased activity of the anterior cortical midline structures. Abnormal interactions between the lateralized task-positive network, and the midline cortical structures of the default mode network, as well as the emotional response network , may underlie the pervasiveness of ruminative brooding. Furthermore, targeting this maladaptive form of rumination and its underlying neural correlates may be key for effective treatment

Associations of neural processing of reward with posttraumatic stress disorder and secondary psychotic symptoms in trauma-affected refugees

Background: Psychological traumatic experiences can lead to posttraumatic stress disorder (PTSD). Secondary psychotic symptoms are not common but may occur. Objectives: Since psychotic symptoms of schizophrenia have been related to aberrant reward processing in the striatum, using the same paradigm we investigate whether the same finding extends to psychotic and anhedonic symptoms in PTSD. Methods: A total of 70 male refugees: 18 PTSD patients with no secondary psychotic symptoms (PTSD-NSP), 21 PTSD patients with secondary psychotic symptoms (PTSD-SP), and 31 healthy controls (RHC) were interviewed and scanned with functional magnetic resonance imaging (fMRI) during a monetary incentive delay task. Using region of interest analysis of the prefrontal cortex and ventral striatum, we investigated reward-related activity. Results: Compared to RHC, participants with PTSD had decreased neural activity during monetary reward. Also, participants with PTSD-SP exhibited decreased activity in the associative striatum relative to participants with PTSD-NSP during processing of motivational reward anticipation which correlated with severity of psychotic symptoms. However, the difference between the two PTSD groups disappeared when PTSD severity and trauma exposure were accounted for. Conclusions: Anhedonia and secondary psychotic symptoms in PTSD are characterized by dysfunctional reward consumption and anticipation processing, respectively. The latter may reflect a mechanism by which abnormal reward signals in the basal ganglia facilitates psychotic symptoms across psychiatric conditions

Event-related electroencephalographic responses in children at familial high risk for schizophrenia or bipolar disorder: a single-site EEG sub-study of the Danish High Risk and Resilience Study-VIA 11

Aim: Studying children of parents with schizophrenia or bipolar disorder, i.e. who are at familial high-risk of developing similar disorders, offers the possibility to identify abnormalities preceding the emergence of mental health disorders during adolescence. This paper reports the rationale and methodology of a single-site electroencephalography-study of the register-based Danish High Risk and Resilience Study–VIA 11. Focusing on event-related electroencephalographic read-outs that have previously been proposed as endophenotypes for schizophrenia, we set out to retrieve these endophenotypes in children at familial high-risk. Method: Event-related cortical responses to repetitive auditory stimuli or visuospatial flanker stimuli will be recorded with 128-channel electroencephalography in eleven-year-old children with one or two parents diagnosed with schizophrenia spectrum psychosis (n>40) or bipolar disorder (n>40) and control children without familial high-risk (n>40). We will test for between-group differences in auditory processing, focusing on the auditory steady-state response and mismatch negativity. We will also assess between-group differences in visually evoked cortical activity implicated in the resolution of a visuomotor response conflict such as P3b potential and lateralized readiness potential. We will further examine whether the individual expression of these electroencephalographic read-outs scale with clinical characteristics. Conclusions: The study will clarify whether the electroencephalographic-derived endophenotypes are only expressed in children of parents with schizophrenia or will also be present in children of parents with bipolar disorder. The multiple electrophysiological-based read-outs of brain reactivity will enable additional exploratory analyses. Together, the study will contribute to current attempts to validate and identify electroencephalographic-based endophenotypes of vulnerability for mental health disorders