The temporal binding deficit hypothesis of autism

Frith has argued that people with autism show “weak central coherence,” an unusual bias toward piecemeal rather than configurational processing and a reduction in the normal tendency to process information in context. However, the precise cognitive and neurological mechanisms underlying weak central coherence are still unknown. We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication

Network destabilization and transition in depression : new methods for studying the dynamics of therapeutic change

The science of dynamic systems is the study of pattern formation and system change. Dynamic systems theory can provide a useful framework for understanding the chronicity of depression and its treatment. We propose a working model of therapeutic change with potential to organize findings from psychopathology and treatment research, suggest new ways to study change, facilitate comparisons across studies, and stimulate treatment innovation. We describe a treatment for depression that we developed to apply principles from dynamic systems theory and then present a program of research to examine the utility of this application. Recent methodological and technological developments are also discussed to further advance the search for mechanisms of therapeutic change

Subanesthetic ketamine treatment promotes abnormal interactions between neural subsystems and alters the properties of functional brain networks

Acute treatment with subanesthetic ketamine, a non-competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist, is widely utilized as a translational model for schizophrenia. However, how acute NMDA receptor blockade impacts on brain functioning at a systems level, to elicit translationally relevant symptomatology and behavioral deficits, has not yet been determined. Here, for the first time, we apply established and recently validated topological measures from network science to brain imaging data gained from ketamine-treated mice to elucidate how acute NMDA receptor blockade impacts on the properties of functional brain networks. We show that the effects of acute ketamine treatment on the global properties of these networks are divergent from those widely reported in schizophrenia. Where acute NMDA receptor blockade promotes hyperconnectivity in functional brain networks, pronounced dysconnectivity is found in schizophrenia. We also show that acute ketamine treatment increases the connectivity and importance of prefrontal and thalamic brain regions in brain networks, a finding also divergent to alterations seen in schizophrenia. In addition, we characterize how ketamine impacts on bipartite functional interactions between neural subsystems. A key feature includes the enhancement of prefrontal cortex (PFC)-neuromodulatory subsystem connectivity in ketamine-treated animals, a finding consistent with the known effects of ketamine on PFC neurotransmitter levels. Overall, our data suggest that, at a systems level, acute ketamine-induced alterations in brain network connectivity do not parallel those seen in chronic schizophrenia. Hence, the mechanisms through which acute ketamine treatment induces translationally relevant symptomatology may differ from those in chronic schizophrenia. Future effort should therefore be dedicated to resolve the conflicting observations between this putative translational model and schizophrenia

High-frequency neural oscillations and visual processing deficits in schizophrenia

Visual information is fundamental to how we understand our environment, make predictions, and interact with others. Recent research has underscored the importance of visuo-perceptual dysfunctions for cognitive deficits and pathophysiological processes in schizophrenia. In the current paper, we review evidence for the relevance of high frequency (beta/gamma) oscillations towards visuo-perceptual dysfunctions in schizophrenia. In the first part of the paper, we examine the relationship between beta/gamma band oscillations and visual processing during normal brain functioning. We then summarize EEG/MEG-studies which demonstrate reduced amplitude and synchrony of high-frequency activity during visual stimulation in schizophrenia. In the final part of the paper, we identify neurobiological correlates as well as offer perspectives for future research to stimulate further inquiry into the role of high-frequency oscillations in visual processing impairments in the disorder

Mapping dynamic interactions among cognitive biases in depression

Depression is theorized to be caused in part by biased cognitive processing of emotional information. Yet, prior research has adopted a reductionist approach that does not characterize how biases in cognitive processes such as attention and memory work together to confer risk for this complex multifactorial disorder. Grounded in affective and cognitive science, we highlight four mechanisms to understand how attention biases, working memory difficulties, and long-term memory biases interact and contribute to depression. We review evidence for each mechanism and highlight time- and context-dependent dynamics. We outline methodological considerations and recommendations for research in this area. We conclude with directions to advance the understanding of depression risk, cognitive training interventions, and transdiagnostic properties of cognitive biases and their interactions

Examining Patterns of Executive Functioning Across Dimensions of Psychopathology

Executive functioning is a multifaceted collection of higher-order cognitive processes used to perform goal-oriented tasks. Although this construct is heavily researched, a major issue regarding the current literature stems from the influence of task impurity, which interferes with how executive functioning performance is interpreted. Additionally, while executive functioning has been previously explored in clinical populations, less work has evaluated this topic measuring dimensional psychopathology. The present study sought to examine the role of executive functioning, as it relates to dimensional psychopathology. Data was analyzed from a total of 731 individuals between the age of 18-59 years who took part in the Nathan Kline Institute (NKI)-Rockland project. A three-factor model of executive functioning (i.e., inhibition, shifting, and fluency) proposed by Karr et al. (2018) using scores primarily from the Delis-Kaplan Executive Function System (D-KEFS) and an original three-factor model of dimensional psychopathology (i.e., internalizing, externalizing, and thought disorder symptoms) using the Adult Self-Report (ASR) and Peter’s et al. Delusions Inventory (PDI) were constructed with confirmatory factor analyses and then compared using structural equation modeling. Results supported both three-factor models as having adequate fit for this sample and indicated that internalizing and externalizing psychopathology had positive and negative relationships with different factors of executive functioning, while thought disorders traits were not related to executive functioning. Implications for future work are discussed

Spontaneous thought and vulnerability to mood disorders : the dark side of the wandering mind

There is increasing interest in spontaneous thought, namely task-unrelated or rest-related mental activity. Spontaneous thought is an umbrella term for processes like mind-wandering, involuntary autobiographical memory, and daydreaming, with evidence elucidating adaptive and maladaptive consequences. In this theoretical framework, we propose that, apart from its positive functions, spontaneous thought is a precursor for cognitive vulnerability in individuals who are at risk for mood disorders. It is important that spontaneous thought mostly focuses on unattained goals and evaluates the discrepancy between current and desired status. In individuals who stably (i.e., trait negative affectivity) or transitorily (i.e., stress) experience negative emotions in reaction to goal-discrepancy, spontaneous thought fosters major cognitive vulnerabilities (e.g., rumination, hopelessness, low self-esteem, and cognitive reactivity), which, in turn, enhance depression. Furthermore, we also highlight preliminary links between spontaneous thought and bipolar disorder. The evidence for this framework is reviewed, and we discuss theoretical and clinical implications of our proposal

Residual negative symptoms differentiate cognitive performance in clinically stable patients with schizophrenia and bipolar disorder

Cognitive deficits in various domains have been shown in patients with bipolar disorder and schizophrenia. The purpose of the present study was to examine if residual psychopathology explained the difference in cognitive function between clinically stable patients with schizophrenia and bipolar disorder. We compared the performance on tests of attention, visual and verbal memory and executive function of 25 patients with schizophrenia in remission and 25 euthymic bipolar disorder patients with that of 25 healthy controls. Mediation analysis was used to see if residual psychopathology could explain the difference in cognitive function between the patient groups. Both patient groups performed significantly worse than healthy controls on most cognitive tests. Patients with bipolar disorder displayed cognitive deficits that were milder but qualitatively similar to those of patients with schizophrenia. Residual negative symptoms mediated the difference in performance on cognitive tests between the two groups. Neither residual general psychotic symptoms nor greater antipsychotic doses explained this relationship. The shared variance explained by the residual negative and cognitive deficits that the difference between patient groups may be explained by greater frontal cortical neurophysiological deficits in patients with schizophrenia, compared to bipolar disorder. Further longitudinal work may provide insight into pathophysiological mechanisms that underlie these deficits

Social interactions, emotion and sleep: a systematic review and research agenda

Sleep and emotion are closely linked, however the effects of sleep on socio-emotional task performance have only recently been investigated. Sleep loss and insomnia have been found to affect emotional reactivity and social functioning, although results, taken together, are somewhat contradictory. Here we review this advancing literature, aiming to 1) systematically review the relevant literature on sleep and socio-emotional functioning, with reference to the extant literature on emotion and social interactions, 2) summarize results and outline ways in which emotion, social interactions, and sleep may interact, and 3) suggest key limitations and future directions for this field. From the reviewed literature, sleep deprivation is associated with diminished emotional expressivity and impaired emotion recognition, and this has particular relevance for social interactions. Sleep deprivation also increases emotional reactivity; results which are most apparent with neuro-imaging studies investigating amygdala activity and its prefrontal regulation. Evidence of emotional dysregulation in insomnia and poor sleep has also been reported. In general, limitations of this literature include how performance measures are linked to self-reports, and how results are linked to socio-emotional functioning. We conclude by suggesting some possible future directions for this field