Although ADHD is the most frequently diagnosed psychiatric disorder in childhood, the majority of adults with ADHD are not diagnosed and 90% of the cases remain untreated. One of the main reasons that may lead to the missed diagnosis of ADHD in adults may be the high rate of comorbid psychiatric conditions masking the main symptoms.

In this study, it was aimed to present a case who was followed up with the diagnosis of ADHD since childhood and developed psychosis after a recent traumatic life event.

A 19-year-old male patient was consulted because of his complaints of persecution delusions, and disorganized speech that started 2 years ago. IIt was learned that the first psychiatry application of the patient was 10 years ago with complaints of impulsivity, aggression, increased psychomotor movements, and methylphenidate treatment was started during this period. The patient, whose current clinical picture was evaluated as psychosis, was discharged after the symptoms subsided with paliperidone depot 100mg/month treatment after hospitalization. It is understood that his psychotic complaints completely regressed in the follow-ups.

It is stated that approximately 80% of adult ADHD cases have at least one accompanying psychiatric disorder. However, there are limited studies in the literature on the relationship between psychotic disorders and ADHD.

Recent studies indicate that beyond the fact that ADHD is a feature of the schizophrenia prodrome, ADHD diagnosis may be associated with an increased risk of psychosis in the future. Therefore, this association can be better clarified in further studies on comorbidities.

No significant relationships.

Better evaluation and understanding of the core symptoms have key importance both in clinical practice and the research of attention-deficit hyperactivity disorder (ADHD). One hallmark neurocognitive feature of ADHD is impaired inhibition, related to impulsivity. Given the high heritability of ADHD, the assessment of genetic background of impaired inhibition may contribute to our knowledge about the genetic background of the disorder.

In our study we investigated whether different forms of impulsivity (attentive, motor, and nonplanning) and polymorphisms in genes of the noradrenergic, serotonergic, and dopaminergic neurotransmission, i.e. dopamine transporter-1 (DAT1), cathecoloamin-O-metiltransferase (COMT), and serotonin receptor-1B (HTR1B genes show association.

208 aADHD patients diagnosed according to DSM-5 criteria from a clinical sample and 142 individuals from a population sample who screened positive for aADHD were included in the study. DNA samples were genotyped for the HTR-1B gene rs1321041 and the COMT gene rs4680 SNPs, moreover the DAT-1 VNTR polymorphism. Dimensional variables for impulsivity were compared between genotypes with the Generalized Linear Model procedure corrected for sex and age, using the PLINK 1.9 statistical software.

The 9 repeat polymorphism in DAT1 was associated with the severity of hyperactivity, moreover, all impulsivity factors. The A allele in COMT was associated with hyperactivity and better motor inhibition activity. In carriers of the G allele in HTR1B we detected significantly higher inattention scores and increased reaction time.

Our results support the putative role of the investigated genetic polymorphisms in the etiology of impulsivity. Nevertheless, these polymorphisms demonstrate a heterogeneous associations.

No significant relationships.

Symptoms of attention deficit hyperactivity disorder (ADHD) and trait impulsivity have been associated with disordered eating but are seldom assessed in community studies, or longitudinally and little is known about the mediating mechanisms.

We tested associations between ADHD symptoms and disordered eating cross-sectionally and between trait impulsivity and disordered eating longitudinally. We utilised data from a normative cohort of young adults (642 participants: 65% female, Mage = 23 years). Participants were classified as high risk or low risk for disordered eating using the SCOFF instrument. In the first two steps of both cross-sectional and longitudinal hierarchical logistic regression models, demographics and covariates were entered. For the cross-sectional regression, Adult ADHD self-report scale (ASRS) scores, separated into inattentive and hyperactive/impulsive symptoms, were entered in the third step. In a separate longitudinal model, Barratt impulsivity scale subscales (attentional, motor and non-planning impulsivity) were entered in the third step. Depression, as assessed by the moods and feelings questionnaire (MFQ), was examined as a mediator.

Cross-sectionally, sex, MFQ score and inattentive symptoms predicted disordered eating risk (model R2 = 20%). Longitudinally, sex, MFQ score and attentional impulsivity predicted disordered eating risk (model R2 = 16%). The relationship between inattentive symptoms and the disordered eating risk was partially mediated by MFQ score, whereas the relationship between attentional impulsivity and the disordered eating risk was fully mediated by MFQ scores.

These data highlight (1) a specific role for inattentive symptoms of ADHD and (2) the importance of both depression and impulsivity in predicting eating disorder risk.

A growing body of evidence suggests that child aggression is likely to be driven by multiple developmental pathways. However, little is known about the complex interactions between developmental trajectories of child psychological factors (such as anxiety, irritability, and hyperactivity/impulsivity dimensions) and their associations with aggression from childhood to adolescence. Therefore, the current study aimed to identify clusters of individuals with different developmental multi-trajectory, investigate their early risk factors, and describe their longitudinal associations with physical aggression.

The sample comprised 4898 children derived from the Fragile Families and Child Wellbeing Study. A parallel process growth mixture model was used to identify developmental multi-trajectory groups at 5, 9 and 15 years old. Associations between multi-trajectory group membership and physical aggression were examined with Generalized Estimating Equations models. Finally, multinomial logistic regression was performed to assess perinatal and early risk factors for multi-trajectory groups.

Multi-trajectory groups differed in the magnitude of risk for exhibiting physical aggression, compared to typically developing children. The risk for physical aggression was the most prominent in children who were hyperactive/impulsive and irritable [odds ratio (OR) 6.47; 95% confidence interval (CI) 5.44–7.70] and hyperactive/impulsive, irritable, and anxious (OR 7.68; CI 6.62–8.91). Furthermore, maternal cigarette and alcohol use during pregnancy and maternal depression consistently predicted multi-trajectory groups characterized by problematic levels of at least two co-occurrent psychological symptoms.

Identified combinations of developmental trajectories of psychological characteristics were associated with different magnitude in risk for exhibiting physical aggression. These results may highlight the heterogeneity of developmental trajectories associated with childhood aggression.

Replicated evidence indicates that children with attention-deficit/hyperactivity disorder (ADHD) show disproportionate increases in hyperactivity/physical movement when their underdeveloped executive functions are taxed. However, our understanding of hyperactivity’s relation with set shifting is limited, which is surprising given set shifting’s importance as the third core executive function alongside working memory and inhibition. The aim of this study was to experimentally examine the effect of imposing set shifting and inhibition demands on objectively measured activity level in children with and without ADHD.

The current study used a validated experimental manipulation to differentially evoke set shifting, inhibition, and general cognitive demands in a carefully phenotyped sample of children aged 8–13 years with ADHD (n = 43) and without ADHD (n = 34). Activity level was sampled during each task using multiple, high-precision actigraphs; total hyperactivity scores (THS) were calculated.

Results of the 2 × 5 Bayesian ANOVA for hyperactivity revealed strong support for a main effect of task (BF10 = 1.79 × 1018, p < .001, ω2 = .20), such that children upregulated their physical movement in response to general cognitive demands and set shifting demands specifically, but not in response to increased inhibition demands. Importantly, however, this manipulation did not disproportionally increase hyperactivity in ADHD as demonstrated by significant evidence against the task × group interaction (BF01 = 18.21, p = .48, ω2 = .002).

Inhibition demands do not cause children to upregulate their physical activity. Set shifting produces reliable increases in children’s physical movement/hyperactivity over and above the effects of general cognitive demands but cannot specifically explain hyperactivity in children with ADHD.

This is a comprehensive, non-systematic review of the literature addressing the following issues:

1. a) differentiation normality/presence of the disorder;

2. b) clinical relevance of the age-of-onset of impairment criterion;

3. c) frontiers with Bipolar Disorders (BD);

4. d) guidelines for treatment when the disorder is associated with comorbidities.

Clinical tips are presented to make the diagnosis without significantly increasing the proportion of false positives, as well as to help in both the differential diagnosis with BD and the pharmacological management of the disorder associated to comorbidities.

The precise diagnosis, avoiding very flexible criteria, is crucial in a disorder with a dimensional construct in the population, as well as the adequate use of medication for a highly comorbid disorder.

Internet gaming disorder (IGD) has been included in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Currently, associations between IGD in early adolescence and mental health are largely unexplained. In the present study, the relation of IGD with adolescent and parental mental health was investigated for the first time.

We surveyed 1095 family dyads (an adolescent aged 12–14 years and a related parent) with a standardized questionnaire for IGD as well as for adolescent and parental mental health. We conducted linear (dimensional approach) and logistic (categorical approach) regression analyses.

Both with dimensional and categorical approaches, we observed statistically significant associations between IGD and male gender, a higher degree of adolescent antisocial behavior, anger control problems, emotional distress, self-esteem problems, hyperactivity/inattention and parental anxiety (linear regression model: corrected R2 = 0.41, logistic regression model: Nagelkerke's R2 = 0.41).

IGD appears to be associated with internalizing and externalizing problems in adolescents. Moreover, the findings of the present study provide first evidence that not only adolescent but also parental mental health is relevant to IGD in early adolescence. Adolescent and parental mental health should be considered in prevention and intervention programs for IGD in adolescence.

Childhood disruptive behaviors are highly prevalent and associated with adverse long-term social and economic outcomes. Trajectories of welfare receipt in early adulthood and the association of childhood behaviors with high welfare receipt trajectories have not been examined.

Boys (n = 1000) from low socioeconomic backgrounds were assessed by kindergarten teachers for inattention, hyperactivity, aggression, opposition, and prosociality, and prospectively followed up for 30 years. We used group-base trajectory modeling to estimate trajectories of welfare receipt from age 19–36 years using government tax return records, then examined the association between teacher-rated behaviors and trajectory group membership using mixed effects multinomial regression models.

Three trajectories of welfare receipt were identified: low (70.8%), declining (19.9%), and chronic (9.3%). The mean annual personal employment earnings (US$) for the three groups at age 35/36 years was $36 500 (s.d. = $24 000), $15 600 (s.d. = $16 275), and $1700 (s.d. = $4800), respectively. Relative to the low welfare receipt group, a unit increase in inattention (mean = 2.64; s.d. = 2.32, range = 0–8) at age 6 was associated with an increased risk of being in the chronic group (relative risk ratio; RRR = 1.16, 95% CI 1.03–1.31) and in the declining group (RRR = 1.13, 95% CI 1.03–1.23), after adjustment for child IQ and family adversity, and independent of other behaviors. Family adversity was more strongly associated with trajectories of welfare receipt than any behavior.

Boys from disadvantaged backgrounds exhibiting high inattention in kindergarten are at elevated risk of chronic welfare receipt during adulthood. Screening and support for inattentive behaviors beginning in kindergarten could have long-term social and economic benefits for individuals and society.

In 2013, Internet gaming disorder (IGD) was incorporated in the current version of the DSM-5. IGD refers to a problematic use of video games. Longitudinal studies on the etiology of IGD are lacking. Furthermore, it is currently unclear to which extent associated psychopathological problems are causes or consequences of IGD. In the present survey, longitudinal associations between IGD and adolescent and parental mental health were investigated for the first time, as well as the temporal stability of IGD.

In a cross-lagged panel design study, family dyads (adolescent with a parent each) were examined in 2016 (t1) and again 1 year later (2017, t2). Overall, 1095 family dyads were assessed at t1 and 985 dyads were re-assessed at t2 with standardized measures of IGD and several aspects of adolescent and parental mental health. Data were analyzed with structural equation modeling (SEM).

Male gender, a higher level of hyperactivity/inattention, self-esteem problems and IGD at t1 were predictors of IGD at t2. IGD at t1 was a predictor for adolescent emotional distress at t2. Overall, 357 out of the 985 adolescents received a diagnosis of IGD at t1 or t2: 142 (14.4%) at t1 and t2, 100 (10.2%) only at t1, and 115 (11.7%) only at t2.

Hyperactivity/inattention and self-esteem problems seem to be important for the development of IGD. We found first empirical evidence that IGD could prospectively contribute to a deterioration of adolescent mental health. Only a subgroup of affected adolescents showed IGD consistently over 1 year.

Prenatal maternal obesity has been linked to adverse childhood neuropsychiatric outcomes, including increased symptoms of attention deficit hyperactivity disorder (ADHD), internalizing and externalizing problems, affective disorders and neurodevelopmental problems but few studies have studied neuropsychiatric outcomes among offspring born to very severely obese women or assessed potential familial confounding by maternal psychological distress.

We evaluated neuropsychiatric symptoms in 112 children aged 3–5 years whose mothers had participated in a longitudinal study of obesity in pregnancy (50 very severe obesity, BMI ⩾40 kg/m2, obese class III and 62 lean, BMI 18.5–25 kg/m2). The mothers completed the Conners’ Hyperactivity Scale, Early Symptomatic Syndrome Eliciting Neurodevelopmental Clinical Examination Questionnaire (ESSENCE-Q), Child's Sleep Habits Questionnaire (CSHQ), Strengths and Difficulties Questionnaire (SDQ), and Child Behavior Checklist (CBCL) to assess child neuropsychiatric symptoms. Covariates included child's sex, age, birthweight, gestational age, socioeconomic deprivation levels, maternal age, parity, smoking status during pregnancy, gestational diabetes and maternal concurrent symptoms of anxiety and depression assessed using State Anxiety of Spielberger State-Trait Anxiety Index (STAI) and General Health Questionnaire (GHQ), respectively.

Children exposed to prenatal maternal very severe obesity had significantly higher scores in the Conners’ Hyperactivity Scale; ESSENCE-Q; total sleep problems in CSHQ; hyperactivity, conduct problems and total difficulties scales of the SDQ; higher externalizing and total problems, anxious/depressed, aggressive behaviour and other problem syndrome scores and higher DSM-oriented affective, anxiety and ADHD problems in CBCL. Prenatal maternal very severe obesity remained a significant predictor of child neuropsychiatric problems across multiple scales independent of demographic factors, prenatal factors and maternal concurrent symptoms of anxiety and depression.

Prenatal maternal very severe obesity is a strong predictor of increased neuropsychiatric problems in early childhood.