Computer-based inhibitory control training in children with Attention-Deficit/Hyperactivity Disorder (ADHD): Evidence for behavioral and neural impact.

Attention-deficit hyperactivity disorder (ADHD) is the most commonly diagnosed psychological disorder of childhood. Medication and cognitive behavioral therapy are effective treatments for many children; however, adherence to medication and therapy regimens is low. Thus, identifying effective adjunct treatments is imperative. Previous studies exploring computerized training programs as supplementary treatments have targeted working memory or attention. However, many lines of research suggest inhibitory control (IC) plays a central role in ADHD pathophysiology, which makes IC a potential intervention target. In this randomized control trial (NCT03363568), we target IC using a modified stop-signal task (SST) training designed by NeuroScouting, LLC in 40 children with ADHD, aged 8 to 11 years. Children were randomly assigned to adaptive treatment (n = 20) or non-adaptive control (n = 20) with identical stimuli and task goals. Children trained at home for at least 5 days a week (about 15m/day) for 4-weeks. Relative to the control group, the treatment group showed decreased relative theta power in resting EEG and trending improvements in parent ratings of attention (i.e. decreases in inattentive behaviors). Both groups showed improved SST performance. There was not evidence for treatment effects on hyperactivity or teacher ratings of symptoms. Results suggest training IC alone has potential to positively impact symptoms of ADHD and provide evidence for neural underpinnings of this impact (change in theta power; change in N200 latency). This shows promising initial results for the use of computerized training of IC in children with ADHD as a potential adjunct treatment option for children with ADHD.

Amygdala response to negative stimuli predicts PTSD symptom onset following a terrorist attack.

OBJECTIVE: Individuals with posttraumatic stress disorder (PTSD) exhibit heightened amygdala reactivity and atypical activation patterns in the medial prefrontal cortex (mPFC) in response to negative emotional information. It is unknown whether these aspects of neural function are risk factors for PTSD or consequences of either trauma exposure or onset of the disorder. We had a unique opportunity to investigate this issue following the terrorist attacks at the 2013 Boston Marathon and the ensuing manhunt and shelter in place order. We examined associations of neural function measured prior to the attack with PTSD symptom onset related to these events. METHODS: A sample of 15 adolescents (mean age = 16.5 years) who previously participated in a neuroimaging study completed a survey assessing posttraumatic symptoms related to the terrorist attack. We examined blood oxygen level dependent (BOLD) response to viewing and actively down-regulating emotional responses to negative stimuli in regions previously associated with PTSD, including the amygdala, hippocampus, and mPFC, as prospective predictors of posttraumatic symptom onset. RESULTS: Increased BOLD signal to negative emotional stimuli in the left amygdala was strongly associated with posttraumatic symptoms following the attack. Reduced bilateral hippocampal activation during effortful attempts to down-regulate emotional responses to negative stimuli was also associated with greater posttraumatic symptoms. Associations of amygdala reactivity with posttraumatic symptoms were robust to controls for pre-existing depression, anxiety, and PTSD symptoms and prior exposure to violence. CONCLUSIONS: Amygdala reactivity to negative emotional information might represent a neurobiological marker of vulnerability to traumatic stress and, potentially, a risk factor for PTSD.