Journal of Psychiatry & Neuroscience最新文献

Background: Mindfulness-based stress reduction (MBSR) alleviates depression and anxiety in adults with autism spectrum disorder (ASD); however, underlying therapeutic neural mechanisms and mindfulness-specific effects have yet to be elucidated.

Methods: We randomly assigned adults with ASD to MBSR or social support/education (SE). They completed questionnaires that assessed depression, anxiety, mindfulness traits, autistic traits and executive functioning abilities as well as a self-reflection functional MRI task. We used repeated-measures analysis of covariance (ANCOVA) to evaluate behavioural changes. To identify task-specific connectivity changes, we performed a generalized psychophysiological interactions (gPPI) functional connectivity (FC) analysis on regions of interest (ROIs; insula, amygdala, cingulum and prefrontal cortex [PFC]). We used Pearson correlations to explore brain-behaviour relationships.

Results: Our final sample included 78 adults with ASD - 39 who received MBSR and 39 who received SE. Mindfulness-based stress reduction uniquely improved executive functioning abilities and increased mindfulness traits, whereas both MBSR and SE groups showed reductions in depression, anxiety and autistic traits. Decreases specific to MBSR in insula-thalamus FC were associated with anxiety reduction and increased mindfulness traits, including the trait "nonjudgment;" MBSR-specific decreases in PFC-posterior cingulate connectivity correlated with improved working memory. Both groups showed decreased amygdala-sensorimotor and medial-lateral PFC connectivity, which corresponded with reduced depression.

Limitations: Larger sample sizes and neuropsychological evaluations are needed to replicate and extend these findings.

Conclusion: Together, our findings suggest that MBSR and SE are similarly efficacious for depression, anxiety and autistic traits, whereas MBSR produced additional salutary effects related to executive functioning and mindfulness traits. Findings from gPPI identified shared and distinct therapeutic neural mechanisms, implicating the default mode and salience networks. Our results mark an early step toward the development of personalized medicine for psychiatric symptoms in ASD and offer novel neural targets for future neurostimulation research.

Clinical trial registration: ClinicalTrials.gov identifier NCT04017793.

Background: The pathophysiology of psychosis is complex, but a better understanding of stimulus binding windows (BWs) could help to improve our knowledge base. Previous studies have shown that dopamine release is associated with psychosis and widened BWs. We can probe BW mechanisms using drugs of specific interest to psychosis. Therefore, we were interested in understanding how manipulation of the dopamine or catecholamine systems affect psychosis and BWs. We aimed to investigate the effect of dexamphetamine, as a dopamine-releasing stimulant, on the BWs in a unimodal illusion: the tactile funneling illusion (TFI).

Methods: We conducted a randomized, double-blind, counterbalanced placebo-controlled crossover study to investigate funnelling and errors of localization. We administered dexamphetamine (0.45 mg/kg) to 46 participants. We manipulated 5 spatial (5-1 cm) and 3 temporal (0, 500 and 750 ms) conditions in the TFI.

Results: We found that dexamphetamine increased funnelling illusion (p = 0.009) and increased the error of localization in a delay-dependent manner (p = 0.03). We also found that dexamphetamine significantly increased the error of localization at 500 ms temporal separation and 4 cm spatial separation (p _interaction = 0.009; p _{500ms|4cm v. baseline} = 0.01).

Limitations: Although amphetamine-induced models of psychosis are a useful approach to understanding the physiology of psychosis related to dopamine hyperactivity, dexamphetamine is equally effective at releasing noradrenaline and dopamine, and, therefore, we were unable to tease apart the effects of the 2 systems on BWs in our study.

Conclusion: We found that dexamphetamine increases illusory perception on the unimodal TFI in healthy participants, which suggests that dopamine or other catecholamines have a role in increasing tactile spatial and temporal BWs.

Background: Signatures from the metabolome and microbiome have already been introduced as candidates for diagnostic and treatment support. The aim of this study was to investigate the utility of volatile organic compounds (VOCs) from the breath for detection of schizophrenia and depression.

Methods: Patients with a diagnosis of major depressive disorder (MDD) or schizophrenia, as well as healthy controls, were recruited to participate. After being clinically assessed and receiving instruction, each participant independently collected breath samples for subsequent examination by proton transfer-reaction mass spectrometry.

Results: The sample consisted of 104 participants: 36 patients with MDD, 34 patients with schizophrenia and 34 healthy controls. Through mixed-model and deep learning analyses, 5 VOCs contained in the participants' breath samples were detected that significantly differentiated between diagnostic groups and healthy controls, namely VOCs with mass-to-charge ratios (m/z) 60, 69, 74, 88 and 90, which had classification accuracy of 76.8% to distinguish participants with MDD from healthy controls, 83.6% to distinguish participants with schizophrenia from healthy controls and 80.9% to distinguish participants with MDD from those with schizophrenia. No significant associations with medication, illness duration, age of onset or time in hospital were detected for these VOCs.

Limitations: The sample size did not allow generalization, and confounders such as nutrition and medication need to be tested.

Conclusion: This study established promising results for the use of human breath gas for detection of schizophrenia and MDD. Two VOCs, 1 with m/z 60 (identified as trimethylamine) and 1 with m/z 90 (identified as butyric acid) could then be further connected to the interworking of the microbiota-gut-brain axis.

Background: Risk-taking behaviours are observed among adults with attention-deficit/hyperactivity disorder (ADHD). We sought to evaluate altered neural processing of stimuli values associated with risk-taking decision behaviour, distinct from learning requirements, among adults with ADHD.

Methods: Overall, 32 adults with ADHD and 32 healthy controls without ADHD underwent a lottery choice task in a functional magnetic resonance imaging (fMRI) experiment. Participants accepted or rejected stakes with explicit information about variable probabilities of winning or losing points at different magnitudes. Outcomes were independent across trials, circumventing reward learning. Data analysis explored group differences in neurobehavioural responses to stimuli values during choice decision-making processing and outcome feedback.

Results: Compared with healthy controls, adults with ADHD had slower response times and tended to accept more stakes with a middle-to-low probability of winning. Adults with ADHD had evidence of lower dorsolateral prefrontal cortex (DLPFC) activity and reduced sensitivity in the ventromedial prefrontal cortex (VMPFC) region of interest in response to linear changes in probability, compared with healthy controls. Lower DLPFC responses were associated with lower VMPFC probability sensitivity and greater risk-taking among healthy controls but not adults with ADHD. Compared with health controls, adults with ADHD showed higher responses to loss outcomes in the putamen and hippocampus.

Limitations: Assessments of real-life decision behaviours are required to further validate the experimental findings.

Conclusions: Our findings explore tonic and phasic neural processing of value-related information that modulates risk-taking behaviours among adults with ADHD. Dysregulated neural computation of the values of behavioural actions and outcomes in the frontostriatal circuits may underlie decision processing distinct from reward learning differences among adults with ADHD.

Clinical trial registration: NCT02642068.

Background: There is growing evidence that the striatum plays a central role in cognitive dysfunction. However, it remains unclear whether and how the striatum contributes specifically to executive deficits in Alzheimer disease (AD). We sought to elucidate aberrations in the striatal subregion associated with executive function and its metabolic connectivity with the cortical regions to investigate its role in the pathogenesis of executive deficits in patients with AD.

Methods: Patients with AD and healthy controls underwent a neuropsychological assessment battery, including assessment of executive function, and a hybrid positron emission tomography/magnetic resonance imaging (PET/MRI) scan. We performed voxel-wise analyses of cerebral metabolism between patients and controls, focusing on the executive subregion of the striatum according to the Oxford-GSK-Imanova Striatal Connectivity Atlas. We assessed the correlation between the [¹⁸F]-fluorodeoxyglucose standardized uptake value ratio of the striatal executive subregion and clinical variables, and we analyzed seed-based metabolic connectivity of the striatal executive subregion with the dorsolateral prefrontal cortex (DLPFC) using [¹⁸F]-fluorodeoxyglucose PET.

Results: We included 50 patients with AD and 33 controls in our analyses. The patterns of striatal hypometabolism in patients with AD were specific to executive and caudal motor subregions. Metabolic activity in the executive subregion of the striatum correlated negatively with the severity of executive dysfunction, as measured with the Trial-Making Test (TMT) part B and the difference score TMT B-A, and correlated positively with Digit Span (backward) and Verbal Fluency Test scales, particularly on the left side. Compared with controls, patients with AD showed reduced metabolic connectivity between striatal executive subregions and the dorsolateral prefrontal cortex (DLPFC).

Limitations: Our study was limited by small sample sizes and cross-sectional findings.

Conclusion: Our findings show that patients with AD have impairments in the executive subregion of the striatum, and these deficits may be associated with a disconnection between the executive striatum and DLPFC, providing valuable insight into the pathogenesis of this disease.