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IntroductionBehavioral addictions (with related behaviors often conducted online) constitute new categories within the Diagnostic and Statistical Manual (DSM) and International Classification of Diseases (ICD). In both, gambling disorder is listed as a formal clinical diagnosis whereas disorders related to videogaming exist in the DSM (research criteria) and ICD (clinical criteria). However, a broader range of disorders related to other behaviors (e.g., shopping/buying, social media use, pornography use) have been proposed as possible behavioral addictions.ObjectivesThis presentation will provide insight in efforts by major organizations (e.g., the World Health Organization) to consider behavioral addictions and how best to screen for, assess and intervene to help people with these conditions. Empirical data influencing the classification of the behaviors and disorders will be presented. Changes in online behaviors during the COVID-19 pandemic will be considered with respect to mental health concerns.MethodsMultiple methods ranging from results of neuroimaging studies, clinical trials, and longitudinal investigations will be presented.ResultsBrain imaging results suggest similarities between specific internet-use behaviors (especially internet gaming disorder) and substance use disorders, supporting a classification as behavioral addictions. Multiple types of internet use increased during the pandemic, particularly during the onset. Different patterns of mental concerns in relation to internet use behaviors were seen during the pandemic. Consensus guidances regarding how best to avoid and address problematic use of the internet were developed and disseminated. Clinical trials support the efficacy of behavioral and neuromodulatory approaches, although no treatments have regulatory approval for behavioral addictions.ConclusionsMultiple internet-use behaviors may form the basis of behavioral addictions. While considerable data exist for internet gaming disorder, other behaviors commonly performed on the internet also warrant consideration. Additional research is needed to develop, test and implement more effective prevention and treatment strategies.Disclosure of InterestNone Declared

Endocannabinoids and their attending cannabinoid type 1 (CB 1 ) receptor have been implicated in animal models of post-traumatic stress disorder (PTSD). However, their specific role has not been studied in people with PTSD. Herein, we present an in vivo imaging study using positron emission tomography (PET) and the CB 1 -selective radioligand [ 11 C]OMAR in individuals with PTSD, and healthy controls with lifetime histories of trauma (trauma-exposed controls (TC)) and those without such histories (healthy controls (HC)). Untreated individuals with PTSD ( N =25) with non-combat trauma histories, and TC ( N =12) and HC ( N =23) participated in a magnetic resonance imaging scan and a resting PET scan with the CB 1 receptor antagonist radiotracer [ 11 C]OMAR, which measures the volume of distribution ( V T ) linearly related to CB 1 receptor availability. Peripheral levels of anandamide, 2-arachidonoylglycerol, oleoylethanolamide, palmitoylethanolamide and cortisol were also assessed. In the PTSD group, relative to the HC and TC groups, we found elevated brain-wide [ 11 C]OMAR V T values (F(2,53)=7.96, P =0.001; 19.5% and 14.5% higher, respectively), which were most pronounced in women (F(1,53)=5.52, P =0.023). Anandamide concentrations were reduced in the PTSD relative to the TC (53.1% lower) and HC (58.2% lower) groups. Cortisol levels were lower in the PTSD and TC groups relative to the HC group. Three biomarkers examined collectively—OMAR V T , anandamide and cortisol—correctly classified nearly 85% of PTSD cases. These results suggest that abnormal CB 1 receptor-mediated anandamide signaling is implicated in the etiology of PTSD, and provide a promising neurobiological model to develop novel, evidence-based pharmacotherapies for this disorder.

IntroductionNumerous studies point to the comorbidity between gambling disorder (GD) and attention deficit hyperactivity disorder (ADHD). However, there is a lack of research exploring how ADHD symptoms might influence psychological treatment outcomes for GD.ObjectivesTherefore, we aimed to explore differences between patients with GD with and without ADHD symptoms regarding psychopathology, personality, sociodemographic and especially treatment outcome measures.MethodsThis longitudinal study included n=170 patients with GD receiving 16 sessions of cognitive behavioral therapy (CBT) in a specialized unit of a public hospital. Multiple self-reported instruments were used to assess GD severity, personality, ADHD and other symptoms and sociodemographic measures prior to treatment.ResultsA clinical profile characterized by greater GD severity, higher psychopathology and impulsivity, and less adaptive personality features was observed in patients with self-reported ADHD symptoms compared to those without. No significant differences in treatment response (measured by dropout and relapse rates) were reported between the two groups. However, patients with ADHD symptoms described more severe relapses (more money gambled) and GD patients who relapsed scored higher on measures of ADHD, particularly inattention.ConclusionsIndividuals with GD and ADHD may experience more severe relapses following treatment, suggesting a need for more vigilant follow-up and interventions for patients with this comorbidity.Disclosure of InterestC. Vintró-Alcaraz: None Declared, G. Mestre-Bach: None Declared, R. Granero: None Declared, M. Gómez-Peña: None Declared, L. Moragas: None Declared, F. Fernández-Aranda Consultant of: Novo Nordisk and editorial honoraria as EIC from Wiley, M. Potenza Consultant of: Opiant Pharmaceuticals, Idorsia Pharmaceuticals, AXA, Game Day Data, Baria-Tek and the Addiction Policy Forum; has been involved in a patent application with Yale University and Novartis; has received research support (to Yale) from Mohegan Sun Casino and Connecticut Council on Problem Gambling; and has consulted for and/or advised gambling and legal entities on issues related to impulse-control/addictive disorders, S. Jiménez-Murcia: None Declared

IntroductionThe neurobiology of gambling disorder (GD) is not yet fully understood. Although dysfunctional signalling involved in energy homeostasis has been studied in substance use disorders, it should be examined in detail in GD.ObjectivesTo compare different endocrine and neuropsychological factors between individuals with GD and healthy controls (HC), and to explore endocrine interactions with neuropsychological and clinical variables.MethodsA case-control design was performed in 297 individuals with GD and 41 HC, assessed through a semi-structured clinical interview and a psychometric battery, adding 38 HC in the evaluation of endocrine and anthropometric variables.ResultsIndividuals with GD presented higher fasting plasma ghrelin (p<.001) and lower LEAP2 and adiponectin concentrations (p<.001) than HC adjusting for body mass index (BMI). The GD group reported higher cognitive impairment regarding cognitive flexibility and decision-making strategies, a worse psychological state, higher impulsivity levels, and a more dysfunctional personality profile. Despite failing to find significant associations between endocrine factors and either neuropsychological or clinical aspects in GD, some impaired cognitive dimensions and lower LEAP2 concentrations significantly predicted GD presence.ConclusionsThis study suggests distinctive neuropsychological and endocrine dysfunctions may operate in individuals with GD, predicting GD presence. Further exploration of endophenotypic vulnerability pathways in GD appear warranted, especially with respect to etiological and therapeutic potentials.Disclosure of InterestF. Fernandez-Aranda Consultant of: Novo Nordisk , Employee of: editorial honoraria as EIC from Wiley, I. Baenas: None Declared, M. Etxandi : None Declared, B. Mora-Maltas: None Declared, R. Granero : None Declared, S. Tovar : None Declared, C. Diéguez: None Declared, M. Potenza Grant / Research support from: Mohegan Sun Casino and Connecticut Council on Problem Gambling, Consultant of: Opiant Pharmaceuticals, Idorsia Pharmaceuticals, Baria-Tek, AXA, Game Day Data and the Addiction Policy Forum; has participated in surveys, mailings or telephone consultations related to drug addiction, impulse control disorders or other health topics; and has consulted for law offices and gambling entities on issues related to impulse control or addictive disorders, Employee of: patent application in Yale University and Novartis, S. Jiménez-Murcia: None Declared.

Rationale Individuals with a family history of alcoholism (family history positive [FHP]) show higher alcoholism rates and are more impulsive than those without such a family history (family history negative [FHN]), possibly due to altered N -methyl- d -aspartate (NMDA) receptor function. Objectives We investigated whether memantine, an NMDA receptor antagonist, differentially influences impulsivity measures and Go/No-Go behavior and fMRI activity in matched FHP and FHN individuals. Methods On separate days, participants received a single dose of 40 mg memantine or identical-appearing placebo. Results No group performance differences were observed on placebo for Go correct hit or No-Go false alarm reaction time on the Go/No-Go task. During fMRI, right cingulate activation differed for FHP vs. FHN subjects during No-Go correct rejects. Memantine had attenuated effects in FHP vs. FHN subjects: For No-Go false alarms, memantine was associated with limited reduction in subcortical, cingulate, and temporal regions in FHP subjects and reduced activity in fronto-striatal–parietal networks in FHN subjects. For No-Go correct rejects, memantine (relative to placebo) reduced activity in left cingulate and caudate in FHP but not FHN subjects. Conclusions Lower sensitivity to the effects of memantine in FHP subjects is consistent with greater NMDA receptor function in this group.

Background The use of video games, a hobby for many teenagers in their leisure time, has brought with it a new potential for concerns. Internet gaming disorder (IGD) is a mental condition classified as a disorder due to addictive behaviors. It may include use of video games, both online and offline. Consequences of IGD may include introversion, social anxiety, mood swings, loneliness, sleep problems, behavioral problems, depression, low self-esteem, and increased violence. In order to design an app-based intervention for adolescents, a transtheoretical model (TTM) has been used. This widely used model in the field of behavioral change is also practical for health education programs. In addition, cognitive-behavioral therapy (CBT) has been used to make people more aware of their behaviors, feelings and thoughts and how to achieve behavioral change. The present study seeks to determine the effectiveness of this app-based intervention in in the treatment of IGD among adolescents. Method In this single-blinded, randomized, controlled trial, 206 high-school adolescents aged 13 to 18 years in Qazvin city will be recruited. Eligible adolescents will be randomly assigned into intervention and control groups. Eight consecutive sessions delivered over 2 months and based on the TTM and CBT will be delivered through the `app (named HAPPYTEEN) to the intervention group. The control group will receive a sleep hygiene intervention (8 consecutive sessions for 2 months) via the app. Data collection tools include the Internet Gaming Disorder Scale, Insomnia Severity Index, Depression, Anxiety, and Stress Scales, Stages of Change Questionnaire, Decision Balance, and Self-Efficacy. The study measures will be completed at baseline, post intervention, and 1 month and 3 months after the intervention. Discussion The results of this intervention could be used as adjunct therapy for adolescents with IGD. Trial registration Clinical Trial Registration Center of Iran (IRCT) IRCT20181226042140N1 . Registered on June 9, 2020.

The surge in mobile gaming, fueled by smartphone and internet accessibility, lacks a comprehensive understanding of physiological changes during gameplay. This study, involving 93 participants (average age 21.75 years), categorized them into Problematic Mobile Gaming (PMG) and non-problematic Mobile Gaming (nPMG) groups based on Problematic Mobile Gaming Questionnaire (PMGQ) scores. The PMGQ is a 12-item scale developed in Taiwan to assess symptoms of problematic mobile gaming. The research delved into heart rate variability (HRV) alterations during real-time mobile gaming and self-gaming video viewing. Results showed that the PMG group significantly presents a lower root mean square of successive differences (RMSSD), and High Frequency (lnHF) than does the nPMG group (F=4.73, =0.03; F=10.65, =0.002, respectively) at the baseline. In addition, the PMG group significantly displayed elevated HF and low-frequency to high-frequency (LF/HF) in the mobile-gaming (F=7.59, =0.007; F=9.31, =0.003) condition as well as in the watching self-gaming videos (F=9.75, =0.002; F=9.02, =0.003) than did the nPMG. The study suggests targeted interventions to mitigate autonomic arousal, offering a potential avenue to address adverse effects associated with problematic mobile gaming behavior. The PMG group displayed increased craving scores after real-time mobile gaming and watching self-gaming video excerpts, unlike the nPMG group. Elevated LF/HF ratios in frequent gaming cases heightened autonomic arousal, presenting challenges in relaxation after mobile gaming. These findings contribute to a nuanced understanding of the complex interplay between mobile gaming activities, physiological responses, and potential intervention strategies.

Transcranial direct current stimulation (tDCS) of the dorsolateral prefrontal cortex (dlPFC) may reduce substance use and other addictive behaviours. However, the cognitive mechanisms that underpin such effects remain unclear. Impaired inhibitory control linked to hypoactivation of the prefrontal cortex may allow craving-related motivations to lead to compulsive addictive behaviours. However, very few studies have examined whether increasing the activation of the dlPFC via anodal tDCS could enhance inhibitory control over addiction-related distractors. The current study aimed to enrich empirical evidence related to this issue. Thirty-three males with Internet gaming disorder underwent active (1.5 mA for 20 minutes) and sham tDCS 1 week apart, in randomized order. We assessed inhibitory control over gaming-related distractors and craving pre- and post-stimulation. Relative to sham treatment, active tDCS reduced interference from gaming-related (versus non-gaming) distractors and attenuated background craving, but did not affect cue-induced craving. This study was limited by its relatively small sample size and the fact that it lacked assessments of tDCS effects on addictive behaviour. Future tDCS studies with multiple sessions in larger samples are warranted to examine the effects on addictive behaviours of alterations in addiction-related inhibitory control. These findings demonstrate that stimulation of the dlPFC influences inhibitory control over addiction-related cues and addiction-related motivation. This is the first empirical study to suggest that enhanced inhibitory control may be a cognitive mechanism underlying the effects of tDCS on addictions like Internet gaming disorder. Our finding of attenuated background craving replicated previous tDCS studies. Intriguingly, our finding of distinct tDCS effects on 2 forms of craving suggests that they may have disparate underlying mechanisms or differential sensitivity to tDCS. NCT03352973

This study used functional magnetic resonance imaging (fMRI) to examine the association between brain activation during exposure to cocaine-related cues and relapse to drug use in cocaine-dependent (CD) patients. We imaged 17 CD subjects during a 2-week in-patient stay. The subjects then entered a 10-week outpatient placebo-controlled, double-blind randomized clinical trial where urine toxicologies were assessed three times weekly to calculate the treatment effectiveness score (TES). Worse TES correlated with BOLD activation in the left precentral, superior temporal, and posterior cingulate cortices (PCC), and right middle temporal and lingual cortices (R>0.65; P<0.005). The left PCC activation also distinguished eight nonrelapsers (TES above mean and completed treatment) from nine relapsers. Cocaine-free urines were significantly greater in the nonrelapsers (92%) than in the relapsers (66%), who also remained in treatment for an average of only 3.2 weeks. Self-reports of craving during fMRI did not differ between nonrelapsers and relapsers and did not correlate with TES. Relapse to cocaine abuse was associated with increased activation in the sensory association cortex, the motor cortex, and PCC while viewing images of cocaine-related cues. These results suggest that relapse to cocaine abuse is associated with increased brain activation to cocaine cues in sensory, motor, and cognitive-emotional processing areas. This physiological activation was a better predictor of relapse than subjective reports of craving, and may be a useful target for treatment development.