Background Over the recent years there has been a growing debate regarding the extent and nature of the overlap in neuropathology between schizophrenia (SZ) and autism spectrum disorder (ASD). Dynamic functional network connectivity (dFNC) is a recent analysis method that explores temporal patterns of functional connectivity (FC). We compared resting-state dFNC in SZ, ASD and healthy controls (HC), characterized the associations between temporal patterns and symptoms, and performed a three-way classification analysis based on dFNC indices. Methods Resting-state fMRI was collected from 100 young adults: 33 SZ, 33 ASD, 34 HC. Independent component analysis (ICA) was performed, followed by dFNC analysis (window = 33 s, step = 1TR, k-means clustering). Temporal patterns were compared between groups, correlated with symptoms, and classified via cross-validated three-way discriminant analysis. Results Both clinical groups displayed an increased fraction of time (FT) spent in a state of weak, intra-network connectivity [ p < .001] and decreased FT in a highly-connected state [ p < .001]. SZ further showed decreased number of transitions between states [p < .001], decreased FT in a widely-connected state [p < .001], increased dwell time (DT) in the weakly-connected state [p < .001], and decreased DT in the highly-connected state [ p = .001]. Social behavior scores correlated with DT in the widely-connected state in SZ [ r = 0.416, p = .043], but not ASD. Classification correctly identified SZ at high rates (81.8%), while ASD and HC at lower rates. Conclusions Results indicate a severe and pervasive pattern of temporal aberrations in SZ (specifically, being “stuck” in a state of weak connectivity), that distinguishes SZ participants from both ASD and HC, and is associated with clinical symptoms.

The results suggest that H-coil deep-TMS administered continuation treatment can help maintain an antidepressant effect for 18 weeks, following 4 weeks of acute treatment.

Treatment for negative symptoms and cognitive deficits, core elements of schizophrenia, remains inadequate. Stimulation of the prefrontal cortex via transcranial magnetic stimulation (TMS) yields only moderate results, possibly due to limited stimulation depth. Deep-TMS enables deeper and wider stimulation than before. This preliminary study is the first to examine deep-TMS as a possible add-on treatment for negative symptoms and cognitive deficits of schizophrenia. The effect of 20 daily deep-TMS sessions (20 Hz, 120% motor threshold) over the prefrontal cortex of 15 patients indicated improvement in cognition and negative symptoms that was maintained at 2-wk post-treatment follow-up.

Negative symptoms and cognitive deficits are considered core symptoms of schizophrenia, yet treatment for them remains inadequate. Deep-transcranial magnetic stimulation (TMS) is a novel technology that enables non-invasive stimulation of deep layers of the prefrontal cortex. Preliminary evidence suggests that deep-TMS could be effective in the treatment of negative symptoms and cognitive deficits. The current study is the first double-blind, randomized sham-controlled study to examine the feasibility of deep-TMS add-on treatment for negative symptoms and cognitive deficits in schizophrenia. Twenty daily H1 deep-TMS treatments (20Hz, 120% MT) were delivered, in a double-blind, randomized sham-controlled design (n=30). Extensive clinical and cognitive assessments were carried out throughout the study and for an additional one month follow-up period. The results indicate that at the end of the treatment period, negative symptoms (as indicated by the Scale for the Assessment of Negative Symptoms (SANS)) significantly reduced in the TMS group (-7.7), but not in the sham group (-1.9). Differences between the groups were not statistically significant.

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Highlights Autism spectrum disorder (ASD) & schizophrenia (SZ) have mentalizing deficits. Spatially constrained ICA reveals shared deficits in mentalizing default mode activity. Mentalizing-related temporoparietal junction activity correlated with ADOS scores in ASD. Mentalizing-related precuneus activity correlated with tendency to fantasize in SZ. Both categorical and RDoC approaches to study neural deficits in SZ & ASD are supported.

Generalized anxiety disorder (GAD) and social anxiety disorder (SAD) are currently considered distinct diagnostic categories. Accumulating data suggest the study of anxiety disorders may benefit from the use of dimensional conceptualizations. One such dimension of shared dysfunction is emotion regulation (ER). The current study evaluated dimensional (ER) and categorical (diagnosis) neurocorrelates of resting-state functional connectivity (rsFC) in participants with GAD and SAD and healthy controls (HC). Functional magnetic resonance imaging (fMRI) rsFC was estimated between all regions of the default mode network (DMN), salience network (SN), and bilateral amygdala (N = 37: HC-19; GAD-10; SAD-8). Thereafter, rsFC was predicted by both ER, (using the Difficulties in Emotion Regulation Scale [DERS]), and diagnosis (DSM-5) within a single unified analysis of covariance (ANCOVA). For the ER dimension, there was a significant association between impaired ER abilities and anticorrelated rsFC of amygdala and DMN (L.amygdala-ACC: p = 0.011, beta = -0.345), as well as amygdala and SN (L.amygdala-posterior cingulate cortex [PCC]: p = 0.032, beta = -0.409). Diagnostic status was significantly associated with rsFC differences between the SAD and HC groups, both within the DMN (PCC-MPFC: p = 0.009) and between the DMN and SN (R.LP-ACC: p = 0.010). Although preliminary, our results exemplify the potential contribution of the dimensional approach to the study of GAD and SAD and support a combined categorical and dimensional model of rsFC of anxiety disorders.

CDSS structure indicated of two separate factors, i.e., depression-hopelessness and guilt, suggesting separate underlying processes. The validity of the scale might benefit from a two-fold structure and the removal/replacement of item #7 (early waking). A noteworthy inverse correlation was found between the depression factor and negative symptoms, as well as a positive correlation between depression factor and neuroleptic side effects.