Stuart F. White

Dual neurocircuitry dysfunctions in disruptive behavior disorders: Emotional responding and response inhibition

BACKGROUNDnTo determine the functional integrity of the neural systems involved in emotional responding/regulation and response control/inhibition in youth (age 10-18 years) with disruptive behavioral disorders (DBDs: conduct disorder and/or oppositional defiant disorder) as a function of callous-unemotional (CU) traits.nnnMETHODnTwenty-eight healthy youths and 35 youths with DBD [high CU (HCU), n = 18; low CU (LCU), n = 17] performed the fMRI Affective Stroop task. Participants viewed positive, neutral, and negative images under varying levels of cognitive load. A 3-way ANOVA (group×emotion by task) was conducted on the BOLD response data.nnnRESULTSnYouth with DBD-HCU showed significantly less activation of ventromedial prefrontal cortex (vmPFC) and amygdala in response to negative stimuli, compared to healthy youth and youth with DBD-LCU. vmPFC responsiveness was inversely related to CU symptoms in DBD. Youth with DBD-LCU showed decreased functional connectivity between amygdala and regions including inferior frontal gyrus in response to emotional stimuli. Youth with DBD (LCU and HCU) additionally showed decreased insula responsiveness to high load (incongruent trials) compared to healthy youth. Insula responsiveness was inversely related to ADHD symptoms in DBD.nnnCONCLUSIONSnThese data reveal two forms of pathophysiology in DBD. One associated with reduced amygdala and vmPFC responses to negative stimuli and related to increased CU traits. Another associated with reduced insula responses during high load task trials and related to ADHD symptoms. Appropriate treatment will need to be individualized according to the patients specific pathophysiology.

Youth with substance abuse histories exhibit dysfunctional representation of expected value during a passive avoidance task

Individuals with substance abuse (SA) histories show impairment in the computations necessary for decision-making, including expected value (EV) and prediction error (PE). Neuroimaging findings, however, have been inconsistent. Sixteen youth with (SApositive) and 29 youth without (SAnegative) substance abuse histories completed a passive avoidance task while undergoing functional MRI. The groups did not significantly differ on age, gender composition or IQ. Behavioral results indicated that SApositive youth showed significantly less learning than SAnegative youth over the task. SApositive youth show problems representing EV information when attempting to avoid sub-optimal choices in bilateral inferior frontal gyrus and striatum. Furthermore, SApositive youth showed a significantly increased differential response to reward versus punishment feedback modulated by PE in posterior cingulate cortex relative to SAnegative youth. Disrupted decision-making is likely to exacerbate SA as a failure to represent EV during the avoidance of sub-optimal choices is likely to increase the likelihood of SA. With respect to the representation of PE, future work will be needed to clarify the impact of different substances on the neural systems underpinning PE representation. Moreover, interaction of age/development and substance abuse on PE signaling will need to be explored.

Adolescents show differential dysfunctions related to Alcohol and Cannabis Use Disorder severity in emotion and executive attention neuro-circuitries

Alcohol and cannabis are two substances that are commonly abused by adolescents in the United States and which, when abused, are associated with negative medical and psychiatric outcomes across the lifespan. These negative psychiatric outcomes may reflect the detrimental impact of substance abuse on neural systems mediating emotion processing and executive attention. However, work indicative of this has mostly been conducted either in animal models or adults with Alcohol and/or Cannabis Use Disorder (AUD/CUD). Little work has been conducted in adolescent patients. In this study, we used the Affective Stroop task to examine the relationship in 82 adolescents between AUD and/or CUD symptom severity and the functional integrity of neural systems mediating emotional processing and executive attention. We found that AUD symptom severity was positively related to amygdala responsiveness to emotional stimuli and negatively related to responsiveness within regions implicated in executive attention and response control (i.e., dorsolateral prefrontal cortex, anterior cingulate cortex, precuneus) as a function of task performance. In contrast, CUD symptom severity was unrelated to amygdala responsiveness but positively related to responsiveness within regions including precuneus, posterior cingulate cortex, and inferior parietal lobule as a function of task performance. These data suggest differential impacts of alcohol and cannabis abuse on the adolescent brain.

Moderation of prior exposure to trauma on the inverse relationship between callous-unemotional traits and amygdala responses to fearful expressions: an exploratory study

BACKGROUNDnPrevious work has shown that amygdala responsiveness to fearful expressions is inversely related to level of callous-unemotional (CU) traits (i.e. reduced guilt and empathy) in youth with conduct problems. However, some research has suggested that the relationship between pathophysiology and CU traits may be different in those youth with significant prior trauma exposure.nnnMETHODSnIn experiment 1, 72 youth with varying levels of disruptive behavior and trauma exposure performed a gender discrimination task while viewing morphed fear expressions (0, 50, 100, 150 fear) and Blood Oxygenation Level Dependent responses were recorded. In experiment 2, 66 of these youth performed the Social Goals Task, which measures self-reports of the importance of specific social goals to the participant in provoking social situations.nnnRESULTSnIn experiment 1, a significant CU traits-by-trauma exposure interaction was observed within right amygdala; fear intensity-modulated amygdala responses negatively predicted CU traits for those youth with low levels of trauma but positively predicted CU traits for those with high levels of trauma. In experiment 2, a bootstrapped model revealed that the indirect effect of fear intensity amygdala response on social goal importance through CU traits is moderated by prior trauma exposure.nnnCONCLUSIONSnThis study, while exploratory, indicates that the pathophysiology associated with CU traits differs in youth as a function of prior trauma exposure. These data suggest that prior trauma exposure should be considered when evaluating potential interventions for youth with high CU traits.

Increased cognitive control and reduced emotional interference is associated with reduced PTSD symptom severity in a trauma-exposed sample: A preliminary longitudinal study

Individuals with posttraumatic stress disorder (PTSD) show deficits in recruiting neural regions associated with cognitive control. In contrast, trauma exposed individuals (TEIs) show increased recruitment of these regions. While many individuals who experience a trauma exhibit some PTSD symptoms, relatively few develop PTSD. Despite this, no work has examined the relationship between changes in PTSD symptoms and changes in neural functioning in TEIs longitudinally. This study examined the neural correlates of changing PTSD symptom levels in TEIs. Twenty-one military service members completed the affective stroop task while undergoing fMRI within 2 months of returning from deployment and a second scan 6-12 months later. Participants with PTSD or depression at baseline were excluded. PTSD symptom improvement was associated with greater increase in response to incongruent relative to congruent negative stimuli in dorsal anterior cingulate cortex and inferior frontal gyrus/anterior insula and increased BOLD response over time to emotional relative to neutral stimuli in inferior parietal cortex. Improvement in PTSD symptoms were not associated with changes in amygdala responsiveness to emotional stimuli. In short, the current data indicate that TEIs who become more able to recruit regions implicated in cognitive control show greater reductions in PTSD symptom levels.

Applying a Cognitive Neuroscience Perspective to Disruptive Behavior Disorders: Implications for Schools

ABSTRACT A cognitive neuroscience perspective seeks to understand behavior, in this case disruptive behavior disorders (DBD), in terms of dysfunction in cognitive processes underpinned by neural processes. While this type of approach has clear implications for clinical mental health practice, it also has implications for school-based assessment and intervention with children and adolescents who have disruptive behavior and aggression. This review articulates a cognitive neuroscience account of DBD by discussing the neurocognitive dysfunction related to emotional empathy, threat sensitivity, reinforcement-based decision-making, and response inhibition. The potential implications for current and future classroom-based assessments and interventions for students with these deficits are discussed.

The processing of animacy information is disrupted as a function of callous-unemotional traits in youth with disruptive behavior disorders

Atypical amygdala responses to emotional stimuli have been consistently reported in youth with Disruptive Behavior Disorders (DBDs; Conduct Disorder/Oppositional Defiant Disorder). However, responding to animacy stimuli has not been systematically investigated. Yet, the amygdala is known to be responsive to animacy stimuli and impairment in responsiveness to animacy information may have implications for social cognitive development. Twenty-nine youth with DBDs and 20 typically developing youth, matched for IQ, age (Mage = 14.45, SD = 2.05) and gender, completed a dot probe task during fMRI. Stimuli consisted of negative/faces, negative/objects, neutral/faces and neutral/objects images. Youth with DBDs, relative to typically developing youth, showed: i) reduced amygdala and lateral temporal cortex responses to faces relative to objects. Moreover, within the group of youth with DBDs, increasing callous-unemotional traits were associated with lesser amygdala responses to faces relative to objects. These data suggest that youth with DBDs, particularly those with high levels of CU traits exhibit dysfunction in animacy processing in the amygdala. This dysfunction may underpin the asociality reported in these youth.

Neurodevelopmental Changes in Social Reinforcement Processing: A Functional Magnetic Resonance Imaging Study

Objective In the current study we investigated neurodevelopmental changes in response to social and non-social reinforcement. Methods Fifty-three healthy participants including 16 early adolescents (age, 10–15 years), 16 late adolescents (age, 15–18 years), and 21 young adults (age, 21–25 years) completed a social/non-social reward learning task while undergoing functional magnetic resonance imaging. Participants responded to fractal image stimuli and received social or non-social reward/non-rewards according to their accuracy. ANOVAs were conducted on both the blood oxygen level dependent response data and the product of a context-dependent psychophysiological interaction (gPPI) analysis involving ventromedial prefrontal cortex (vmPFC) and bilateral insula cortices as seed regions. Results Early adolescents showed significantly increased activation in the amygdala and anterior insula cortex in response to non-social monetary rewards relative to both social reward/non-reward and monetary non-rewards compared to late adolescents and young adults. In addition, early adolescents showed significantly more positive connectivity between the vmPFC/bilateral insula cortices seeds and other regions implicated in reinforcement processing (the amygdala, posterior cingulate cortex, insula cortex, and lentiform nucleus) in response to non-reward and especially social non-reward, compared to late adolescents and young adults. Conclusion It appears that early adolescence may be marked by: (i) a selective increase in responsiveness to non-social, relative to social, rewards; and (ii) enhanced, integrated functioning of reinforcement circuitry for non-reward, and in particular, with respect to posterior cingulate and insula cortices, for social non-reward.