Biological psychiatry. Cognitive neuroscience and neuroimaging最新文献

Background: The mechanisms that link neural and behavioral indices of reduced reward sensitivity in depression, particularly in children, remain unclear. Reward positivity (RewP), a neural index of reward processing, has been consistently associated with depression. Separately, recent studies using the drift-diffusion model on behavioral data have delineated computational indices of reward sensitivity. Therefore, in the current study, we examined whether RewP is a neural mediator of drift-diffusion model-based indices of reward processing in predicting pediatric depression across varying levels of symptom severity.

Methods: A community sample of 166 girls, ages 8 to 14 years, completed 2 tasks. The first was a reward guessing task from which RewP was computed using electroencephalography; the second was a probabilistic reward-based decision-making task. On this second task, drift-diffusion model analysis was applied to behavioral data to quantify the efficiency of accumulating reward-related evidence (drift rate) and potential baseline bias (starting point) toward the differently rewarded choices. Depression severity was measured using the self-report Children's Depression Inventory.

Results: RewP was correlated with drift rate, but not starting point bias, toward the more rewarded choice. Furthermore, RewP completely mediated the association between a slower drift rate toward the more rewarded option and higher depression symptom severity.

Conclusions: Our findings suggest that reduced neural sensitivity to reward feedback may be a neural mechanism that underlies behavioral insensitivity to reward in children and adolescents with higher depression symptom severity, offering novel insights into the relationship between neural and computational indices of reward processing in this context.

Background: Binge-eating disorder (BED) is thought of as a disorder of cognitive control, but evidence regarding its neurocognitive mechanisms is inconclusive. Key limitations of previous research include a lack of consistent separation between effects of BED and obesity and a disregard for self-report evidence suggesting that neurocognitive alterations may emerge primarily in loss- or harm-avoidance contexts.

Methods: To address these gaps, in this longitudinal study we investigated behavioral flexibility and its underlying neurocomputational processes in reward-seeking and loss-avoidance contexts. Obese participants with BED, obese participants without BED, and healthy normal-weight participants (n = 96) performed a probabilistic reversal learning task during functional imaging, with different blocks focused on obtaining wins or avoiding losses. They were reinvited for a 6-month follow-up assessment.

Results: Analyses informed by computational models of reinforcement learning showed that unlike obese participants with BED, obese participants without BED performed worse in the win than in the loss condition. Computationally, this was explained by differential learning sensitivities in the win versus loss conditions in the groups. In the brain, this was echoed in differential neural learning signals in the ventromedial prefrontal cortex per condition. The differences were subtle but scaled with BED symptoms, such that more severe BED symptoms were associated with increasing bias toward improved learning from wins versus losses. Across conditions, obese participants with BED switched more between choice options than healthy normal-weight participants. This was reflected in diminished representation of choice certainty in the ventromedial prefrontal cortex.

Conclusions: Our study highlights the importance of distinguishing between obesity with and without BED to identify unique neurocomputational alterations underlying different styles of maladaptive eating behavior.

Recent neuroimaging studies and publicly disseminated analytic tools suggest that regional morphometric analyses covary for global thickness. We empirically demonstrated that this statistical approach severely underestimates regional thickness dysmorphology in psychiatric disorders. Study 1 included 90 healthy control participants, 51 participants at clinical high risk for psychosis, and 78 participants with early-illness schizophrenia. Study 2 included 56 healthy control participants, 83 participants with nonaffective psychosis, and 30 participants with affective psychosis. We examined global and regional thickness correlations, global thickness group differences, and regional thickness group differences with and without global thickness covariation. Global and regional thickness were strongly correlated across groups. Global thickness was lower in the schizophrenia spectrum groups than the other groups. Regional thickness deficits in schizophrenia spectrum groups were attenuated or eliminated with global thickness covariation. Eliminating the variation that regional thickness shares with global thickness eliminated disease-related effects. This statistical approach results in erroneous conclusions that regional thickness is normal in disorders like schizophrenia or clinical high risk syndrome.

Background: Restricted scan path mode is hypothesized to explain abnormal scanning patterns in patients with schizophrenia. Here, we calculated entropy scores (drawing on gaze data to measure the statistical randomness of eye movements) to quantify how strategical and random participants were when processing image stimuli.

Methods: Eighty-six patients with first-episode schizophrenia (FES), 124 individuals at clinical high risk (CHR) for psychosis, and 115 healthy control participants (HCs) completed an eye-tracking examination while freely viewing 35 static images (each presented for 10 seconds) and cognitive assessments. We compared group differences in the overall entropy score, as well as entropy scores under various conditions. We also investigated the correlations between entropy scores and symptoms and cognitive function.

Results: Increased overall entropy scores were noted in the FES and CHR groups compared with the HC group, and these differences were already apparent within 0 to 2.5 seconds. In addition, the CHR group exhibited higher entropy than the HC group when viewing low-meaning images. Moreover, the entropy within 0 to 2.5 seconds showed significant correlations with negative symptoms in the FES group, attention/vigilance scores in the CHR group, and speed of processing and attention/vigilance scores across all 3 groups.

Conclusions: The results indicate that individuals with FES and those at CHR scanned pictures more randomly and less strategically than HCs. These patterns also correlated with clinical symptoms and neurocognition. The current study highlights the potential of the eye movement entropy measure as a neurophysiological marker for early psychosis.

Background: Risk for bipolar disorder (BD) is increased among individuals with a family history or subthreshold mood symptoms. However, the brain structural developments associated with these BD risks remain unknown.

Methods: This longitudinal cohort study examined the brain gray matter volume (GMV) developmental features of familial and symptomatic risks for BD and their associations with participants' global function levels. We recruited unaffected BD offspring with (n = 26, 14 female, mean ± SD age = 14.9 ± 2.9 years) or without (n = 35, 19 female, age = 15.3 ± 2.7 years) subthreshold manic or depressive symptoms and unaffected non-BD offspring with (n = 49, 30 female, age = 14.5 ± 2.2 years) or without (n = 68, 37 female, age = 15.0 ± 2.3 years) symptoms. The offspring had no mood disorder diagnosis prior to the study. The average follow-up duration was 2.63 ± 1.63 years.

Results: At baseline, we found significant interactive effects of familial risk and subthreshold symptoms that indicated that the symptomatic offspring exhibited markedly large GMV in the brain affective and cognitive circuitries. During follow-up, the combined group of BD offspring (symptomatic and nonsymptomatic) displayed a more accelerated GMV decrease than BD nonoffspring in the hippocampus and anterior cingulate cortex. In contrast, the combined group of symptomatic participants (offspring and nonoffspring) displayed a slower GMV decrease than nonsymptomatic participants in the ventromedial prefrontal cortex. Larger GMV at baseline and accelerated GMV decrease during follow-up prospectively and longitudinally predicted positive global function changes. All results survived multiple testing correction.

Conclusions: These findings indicated that familial and symptomatic risks of BD are associated with distinct brain structural developments and unraveled key brain developmental features of particularly vulnerable high-risk individuals to subsequent functional deterioration.

Background: Nonsuicidal self-injury (NSSI) behavior is significantly prevalent in both adolescents and psychiatric populations, particularly in individuals with major depressive disorder. NSSI can be considered a result of risky decision making in response to negative emotions, where individuals choose self-harm over other less harmful alternatives, suggesting a potential decision-making deficit in those engaging in NSSI. This study delves into the complex relationship between NSSI and depression severity in decision making and its cognitive underpinnings.

Methods: We assessed decision behaviors in 57 patients with major depressive disorder and NSSI, 42 patients with major depressive disorder without NSSI, and 142 healthy control participants using the Balloon Analog Risk Task, which involves risk taking, learning, and exploration in uncertain scenarios. Using computational modeling, we dissected the nuanced cognitive dimensions influencing decision behaviors. A novel statistical method was developed to elucidate interaction effects between NSSI and depression severity.

Results: Contrary to common perceptions, we found that individuals with NSSI behaviors were typically more risk averse. There was also a complex interaction between NSSI and depression severity in shaping risk-taking behaviors. As depressive symptoms intensified, the individuals with NSSI began to perceive less risk and behave more randomly.

Conclusions: This research provides new insights into the cognitive aspects of NSSI and depression, highlighting the importance of considering the influence of comorbid mental disorders when investigating the cognitive underpinnings of such behaviors, especially in the context of prevalent cross-diagnostic phenomena such as NSSI behaviors.

Background: Internet gaming disorder (IGD) involves an imbalance in the brain's dual system, characterized by heightened reward seeking and diminished cognitive control, which lead to decision-making challenges. The exploration-exploitation strategy is key to decision making, but how IGD affects this process is unclear.

Methods: To investigate the impact of IGD on decision making, a modified version of the 2-armed bandit task was employed. Participants included 41 individuals with IGD and 44 healthy control individuals. The study assessed the strategies used by participants in the task, particularly focusing on the exploitation-exploration strategy. Additionally, functional magnetic resonance imaging was used to examine brain activation patterns during decision-making and estimation phases.

Results: The study found that individuals with IGD demonstrated greater reliance on exploitative strategies in decision making due to their elevated value-seeking tendencies and decreased cognitive control. Individuals with IGD also displayed heightened activation in the presupplementary motor area and the ventral striatum compared with the healthy control group in both decision-making and estimation phases. Meanwhile, the prefrontal cortex showed more inhibition in individuals with IGD than in the healthy control group during exploitative strategies. This inhibition decreased as cognitive control diminished.

Conclusions: The imbalance in the development of the dual system in individuals with IGD may lead to an overreliance on exploitative strategies. This imbalance, marked by increased reward seeking and reduced cognitive control, contributes to difficulties in decision making and value-related behavioral processes in individuals with IGD.

Background: Repetitive negative thinking (RNT) symptoms, which are characterized by pervasive, uncontrollable negative thoughts, are common in individuals with mood, anxiety, and traumatic stress disorders. Inability to regulate the contents of working memory is a hypothesized etiological factor in RNT, which suggests that training to improve working memory may be beneficial. This study examined the effects of working memory training on resting-state functional connectivity (rsFC) in individuals with elevated RNT and whether such changes would be associated with clinical improvement.

Methods: We conducted a secondary analysis of pre-post resting-state data collected as part of a randomized controlled trial (NCT04912089) of working memory training interventions (n = 42) compared with a waitlist control group (n = 23). We hypothesized that individuals who completed training would show increased rsFC between the 2 key intrinsic connectivity networks-the default mode network (posterior cingulate cortex) and the frontoparietal network (dorsolateral prefrontal cortex). We explored whether the magnitude of rsFC change was associated with change in RNT symptom severity.

Results: rsFC increased between the posterior cingulate cortex and regions including the frontal and parietal cortex in the training group compared with the waitlist group. Increased connectivity between the posterior cingulate cortex and superior frontal cortex was associated with RNT symptom reduction.

Conclusions: These data provide evidence that working memory training can modulate neural circuitry at rest in individuals with RNT. Results are consistent with accounts of working memory training effects on large-scale neurocircuitry changes and suggest that these changes may contribute to clinical promise of this type of intervention on transdiagnostic RNT symptoms.