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Previous studies have reported associations between aggression and Internet addiction disorder (IAD), which has also been linked with anxiety, depression, and impulsiveness. However, the causal relationship between aggression and IAD has thus far not been clearly demonstrated. This study was designed to (a) examine the association between aggression and IAD and (b) investigate the mediating effects of anxiety, depression, and impulsivity in cases in which IAD predicts aggression or aggression predicts IAD. A total of 714 middle school students in Seoul, South Korea, were asked to provide demographic information and complete the

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Study objectivesTo examine the resting-state functional connectivity (FC) between subcortical regions in relation to whole-brain activity in patients with psychophysiological insomnia (PI) and changes following cognitive–behavioral therapy for insomnia (CBTi).MethodsThe FC between subcortical seed regions (caudate, putamen, pallidum, amygdala, thalamus, and hippocampus) and whole-brain voxels were compared between the PI group (n = 13, mean age: 51.0 ± 10.2 years) and good sleepers (GS, n = 18, mean age: 42.7 ± 12.3 years). Also, in the PI group, FC was compared before and after 5 weeks of CBTi.ResultsCompared to the GS group, the PI group exhibited stronger FC between the thalamus and prefrontal cortex and between the pallidum and precuneus but weaker FC between the pallidum and angular gyrus, the caudate and orbitofrontal cortex, and the hippocampus and fusiform gyrus. After CBTi, the PI group exhibited decreased FC between the thalamus and parietal cortex, the putamen and motor cortices, and the amygdala and lingual gyrus, but increased FC between the caudate and supramarginal gyrus, the pallidum and orbitofrontal cortex, and the hippocampus and frontal/parietal gyri.ConclusionsThe present findings demonstrate different FC in PI patients compared to GS and provide insight into the neurobiological rationale for CBTi.

BackgroundInternet addiction (IA) is considered as one of behavioral addictions. Although common neurobiological mechanisms have been suggested to underlie behavioral addiction and substance dependence, few studies have directly compared IA with substance dependence, such as alcohol dependence (AD).MethodsWe compared patients with IA, AD, and healthy controls (HC) in terms of the Five Factor Model of personality and with regard to impulsiveness, anger expression, and mood to explore psychological factors that are linked to aggression. All patients were treatment-seeking and had moderate-to-severe symptoms.ResultsThe IA and AD groups showed a lower level of agreeableness and higher levels of neuroticism, impulsivity, and anger expression compared with the HC group, which are characteristics related to aggression. The addiction groups showed lower levels of extraversion, openness to experience, and conscientiousness and were more depressive and anxious than the HCs, and the severity of IA and AD symptoms was positively correlated with these types of psychopathology.ConclusionsIA and AD are similar in terms of personality, temperament, and emotion, and they share common characteristics that may lead to aggression. Our findings suggest that strategies to reduce aggression in patients with IA are necessary and that IA and AD are closely related and should be dealt with as having a close nosological relationship.

Psychophysiological insomnia (PI) includes arousal to sleep-related stimuli (SS), which can be treated by cognitive behavioral therapy for insomnia (CBT-I). The present study was an exploratory, prospective intervention study that aimed to explore brain response to visual SS in PI before and after CBT-I. Blood oxygen level dependent (BOLD) signal differences in response to SS and neutral stimuli (NS) were compared between 14 drug-free PI patients and 18 good sleepers (GS) using functional magnetic resonance imaging (fMRI). BOLD changes after CBT-I in patients were also examined. PI patients showed higher BOLD activation to SS in the precentral, prefrontal, fusiform, and posterior cingulate cortices before CBT-I. The increased responses to SS were reduced after CBT-I. The increased response to SS in the precentral cortex was associated with longer wake time after sleep onset (WASO), and its reduction after CBT-I was associated with improvements in WASO. Clinical improvements after CBT-I were correlated with BOLD reduction in the right insula and left paracentral cortex in response to SS. PI showed hyper-responses to SS in the precentral cortex, prefrontal cortex, and default mode network and these brain hyper-responses were normalized after CBT-I. CBT-I may exert its treatment effects on PI by reducing hyper-responses to SS in the precentral cortex and insula.

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