Default mode network mechanisms of transcranial magnetic stimulation in depression.

Background: Repetitive transcranial magnetic stimulation (TMS) of the dorsolateral prefrontal cortex (DLPFC) is an established treatment for depression, but its underlying mechanism of action remains unknown. Abnormalities in two large-scale neuronal networks-the frontoparietal central executive network (CEN) and the medial prefrontal-medial parietal default mode network (DMN)-are consistent findings in depression and potential therapeutic targets for TMS. Here, we assessed the impact of TMS on activity in these networks and their relation to treatment response.

Causal interactions between fronto-parietal central executive and default-mode networks in humans.

Information processing during human cognitive and emotional operations is thought to involve the dynamic interplay of several large-scale neural networks, including the fronto-parietal central executive network (CEN), cingulo-opercular salience network (SN), and the medial prefrontal-medial parietal default mode networks (DMN). It has been theorized that there is a causal neural mechanism by which the CEN/SN negatively regulate the DMN. Support for this idea has come from correlational neuroimaging studies; however, direct evidence for this neural mechanism is lacking.

Hippocampal network connectivity and activation differentiates post-traumatic stress disorder from generalized anxiety disorder.

Anxiety disorders are a diverse group of clinical states. Post-traumatic stress disorder (PTSD) and generalized anxiety disorder (GAD), eg, share elevated anxiety symptoms, but differ with respect to fear-related memory dysregulation. As the hippocampus is implicated in both general anxiety and fear memory, it may be an important brain locus for mapping the similarities and differences among anxiety disorders.

Social appraisal in chronic psychosis: role of medial frontal and occipital networks.

Persons with schizophrenia often appraise other individuals as threatening or persecutory. To evaluate social appraisal in schizophrenia, we probed brain networks with a task in which subjects judged whether or not they liked face stimuli with emotional expressions. We predicted that appraising negative expressions would engage patients, more than controls, and negative faces would be related to higher levels of negative affect and produce increased activity in the medial frontal cortex, an area involved in social appraisal.

'Do I like this person?' A network analysis of midline cortex during a social preference task.

Human communication and survival depend on effective social information processing. Abundant behavioral evidence has shown that humans efficiently judge preferences for other individuals, a critical task in social interaction, yet the neural mechanism of this basic social evaluation, remains less than clear. Using a socio-emotional preference task and connectivity analyses (psycho-physiological interaction) of fMRI data, we first demonstrated that cortical midline structures (medial prefrontal and posterior cingulate cortices) and the task-positive network typically implicated in carrying out goal-directed tasks (pre-supplementary motor area, dorsal anterior cingulate and bilateral frontoparietal cortices) were both recruited when subjects made a preference judgment, relative to gender identification, to human faces.

Low-frequency BOLD fluctuations demonstrate altered thalamocortical connectivity in schizophrenia.

The thalamus plays a central and dynamic role in information transmission and processing in the brain. Multiple studies reveal increasing association between schizophrenia and dysfunction of the thalamus, in particular the medial dorsal nucleus (MDN), and its projection targets. The medial dorsal thalamic connections to the prefrontal cortex are of particular interest, and explicit in vivo evidence of this connection in healthy humans is sparse.

Medial frontal hyperactivity in reality distortion.

Background: Schizophrenia/schizoaffective disorder involves reality distortion (RD), which impairs the ability to process socioemotional information. Because this psychological capacity maps to the medial prefrontal cortex (MPFC) and schizophrenia involves abnormal MPFC function, we tested the hypothesis that treated schizophrenic/schizoaffective patients with persistent RD (RD+) would exhibit greater MPFC dysfunction than patients without significant RD (RD-). The amygdala interacts with MPFC, also carries out socioemotional processing, and has been implicated in schizophrenia; thus, we also tested the hypothesis that patients would exhibit aberrant amygdala activity.