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  • In the general concept of self-disturbances in schizophrenia and schizophrenia spectrum disorders, somatopsychic depersonalization (SPD) occupies a special place as it constitutes a syndrome that comprises feelings of detachment from one's own body and mental processes. However, apart from clinical descriptions, to date the pathophysiology of SPD is not fully understood due to the rareness of the syndrome and a lack of experimental studies. In a case study of one patient with schizotypal disorder, we applied a multimodal approach to understanding the SPD phenomena. The patient's clinical profile was identified as disruption of implicit bodily function, accompanied by depressive symptoms. On a neuropsychological level, the patient exhibited impairment in executive functioning, intact tactile perception and kinesthetic praxis. Behavioral tests revealed an altered sense of time but unimpaired self-agency. Furthermore, the patient exhibited a lack of empathy and he had autistic traits, although with a sufficient ability to verbalize his feelings. On the neurobiological level using an active and passive touch paradigm during functional magnetic resonance imaging (fMRI), we found a hyperconnectivity of the default-mode network and salience network and a hypoconnectivity of the central executive brain networks in the performance of the touch task as well as intact perceptual touch processing emerging from the direct comparisons of the touch conditions. Our data provide evidence for the important role of altered large-brain network functioning in SPD that corresponds to the specific behavioral and neurocognitive phenomena.

  • BACKGROUND: Nearly half of individuals with substance use disorders relapse in the year after treatment. A diagnostic tool to help clinicians make decisions regarding treatment does not exist for psychiatric conditions. Identifying individuals with high risk for relapse to substance use following abstinence has profound clinical consequences. This study aimed to develop neuroimaging as a robust tool to predict relapse. METHODS: 68 methamphetamine-dependent adults (15 female) were recruited from 28-day inpatient treatment. During treatment, participants completed a functional MRI scan that examined brain activation during reward processing. Patients were followed 1 year later to assess abstinence. We examined brain activation during reward processing between relapsing and abstaining individuals and employed three random forest prediction models (clinical and personality measures, neuroimaging measures, a combined model) to generate predictions for each participant regarding their relapse likelihood. RESULTS: 18 individuals relapsed. There were significant group by reward-size interactions for neural activation in the left insula and right striatum for rewards. Abstaining individuals showed increased activation for large, risky relative to small, safe rewards, whereas relapsing individuals failed to show differential activation between reward types. All three random forest models yielded good test characteristics such that a positive test for relapse yielded a likelihood ratio 2.63, whereas a negative test had a likelihood ratio of 0.48. CONCLUSIONS: These findings suggest that neuroimaging can be developed in combination with other measures as an instrument to predict relapse, advancing tools providers can use to make decisions about individualized treatment of substance use disorders.

  • There is some evidence that neuroimaging can be used to predict relapse among abstinent methamphetamine-dependent (MD) individuals. However, it remains unclear what cognitive and neural processes contribute to relapse. This investigation examined whether insula activation during risk-taking decisions-a process shown to be disrupted in MD-is able to predict susceptibility for relapse. Sixty-eight MD enrolled in a treatment program during early abstinence completed a risk-taking task during functional magnetic resonance imaging. Sixty-three of the sixty-eight individuals were followed up 1 year after the study. Of these, 18 MD reported relapse. The 45 abstinent MD showed patterns of insula activation during risky decisions that resembled those found in prior studies of healthy controls, consisting of lower insula activation during safe decisions paired with higher activation during risky decisions. In contrast, the 18 relapsed MD showed similar insula activation during safe and risky decisions. An increase in one standard deviation in the difference in insula activation between risky and safe choices was associated with a 0.34 odds ratio for relapse at any given time. A median split of insula activation (difference between risky and safe) showed that individuals in the bottom half were two times more likely to relapse. In addition, a model that included several other brain regions increased prediction accuracy compared with insula-based model alone. These results suggest that failure to differentially activate the insula as a function of risk is a part of an altered risk-processing network associated with an increased susceptibility to relapse.

  • Several studies provide empirical evidence for the association between impulsivity and time perception. However, little is known about the neural substrates underlying this function. This investigation examined the influence of impulsivity on neural activation patterns during the encoding and reproduction of intervals with durations of 3, 9 and 18s using event-related functional magnetic resonance imaging (fMRI). Twenty-seven subjects participated in this study, including 15 high impulsive subjects that were classified based on their self-rating. FMRI activation during the duration reproduction task was correlated with measures of two self-report questionnaires related to the concept of impulsivity (Barratt Impulsiveness Scale, BIS; Zimbardo Time Perspective Inventory, ZTPI). Behaviorally, those individuals who under-reproduced temporal intervals also showed lower scores on the ZTPI future perspective subscale and higher scores on the BIS. FMRI activation revealed an accumulating pattern of neural activity peaking at the end of the 9- and 18-s intervals within right posterior insula. Activations of brain regions during the reproduction phase of the timing task, such as those related to motor execution as well as to the 'core control network' - encompassing the inferior frontal and medial frontal cortices, the anterior insula as well as the inferior parietal cortex - were significantly correlated with reproduced duration, as well as with BIS and ZTPI subscales. In particular, the greater activation in these regions the shorter were the reproduced intervals, the more impulsive was an individual and the less pronounced the future perspective. Activation in the core control network, thus, may form a biological marker for cognitive time management and for impulsiveness.

  • Analyses of neural mechanisms of duration processing are essential for the understanding of psychological phenomena which evolve in time. Different mechanisms are presumably responsible for the processing of shorter (below 500 ms) and longer (above 500 ms) events but have not yet been a subject of an investigation with functional magnetic resonance imaging (fMRI). In the present study, we show a greater involvement of several brain regions - including right-hemispheric midline structures and left-hemispheric lateral regions - in the processing of visual stimuli of shorter as compared to longer duration. We propose a greater involvement of lower-level cognitive mechanisms in the processing of shorter events as opposed to higher-level mechanisms of cognitive control involved in longer events.

Last update from database: 04.06.25, 15:35 (UTC)

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