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Attention-deficit/hyperactivity disorder (ADHD) is a pervasive neurodevelopmental disorder of executive functions, which affects the social, occupational, educational, and personal life of the individuals concerned. The main characteristics of this disorder are age inappropriate inattention, impulsivity and hyperactivity. The research on adult ADHD is still scarce, especially concerning the neural networks of attention. Childhood ADHD has been associated with impairment in two of the attentional network subsystems alerting and executive control, leaving the third subsystem, orienting of attention, intact. Research on adult ADHD and the subsystems of attentional network is contradicting. The aim of this study was to investigate neural activation of these attentional networks during highly demanding attentional tasks in adults with ADHD. The first hypothesis was that the ADHD group have decreased activity in the frontoparietal network during orienting of attention in contrast to the control group. The second hypothesis was that the ADHD group have decreased activity in the dorsolateral prefrontal cortex, anterior cingulate gyrus, and precuneus during divided attention in contrast to the control group. Both the ADHD group and the control group included 16 participants, aged 25 – 56 across all participants, whose brain activation was measured with functional magnetic resonance imaging during the attentional tasks. The tasks included divided and selective attention. Both conditions included task-irrelevant novel distractors. The results supported both hypotheses. The ADHD group had decreased brain activity in the frontoparietal network during top-down controlled and bottom-up triggered attention. Decreased activation in the dorsolateral prefrontal cortex, anterior cingulate gyrus and precuneus was observed during divided attention in the ADHD group. Furthermore, the default-mode network was hyperactivated in the ADHD group. Activation of this network has been related to increasing task demands and failure of maintaining an alert state. Thus, adult ADHD seems to associate with abnormally functioning attention networks. Moreover, the results indicated that in addition to dysfunctional alerting and executive control, adults with ADHD have also impaired orienting of attention. These dysfunctional attentional networks may have a connection with the inattentive symptoms of adult ADHD.

Objectives. Exposure to maternal stress during pregnancy has been associated with a variety of adverse outcomes in the offspring, ranging from restrictions on fetal growth to long-term psychological impairments. Growing evidence suggests that prenatal maternal stress may also play a role in the onset of attention deficit hyperactivity disorder (ADHD). However, results from previous studies have not been uniform and methodological shortcomings may have impacted the findings. The aim of this study is to examine whether exposure to prenatal maternal stress is associated with higher levels of ADHD symptoms in the children, and whether the associations are timing-specific and independent of postnatal maternal and paternal stress. Methods. The current study sample consisted of 2,304 mother-child dyads participating in the PREDO project who were recruited from maternity clinics at 12 + 0 to 13 + 6 weeks of gestation. The women filled out a reliable and valid stress self-report questionnaire, the Perceived Stress Scale (PSS), every two weeks throughout pregnancy, a total of 14 times. Child ADHD symptoms were reported by the mothers at child age of 1–5 years with the Conners' 10-item scale, concurrently with a repeated assessment of maternal stress. Paternal stress was evaluated with the PSS at child age of six months. The associations between prenatal stress and child ADHD symptoms were analyzed statistically using multiple linear regression, controlling for multiple sociodemographic and perinatal confounders and for postnatal levels of maternal and paternal stress. Results and conclusions. Prenatal maternal stress was associated with significantly higher levels of ADHD symptoms in the offspring. Mid- to late-pregnancy stress had the strongest associations with child ADHD symptoms, while early-pregnancy stress showed a slightly weaker, yet significant, effect. The associations between prenatal stress and child ADHD symptoms were partially mediated by postnatal maternal stress. Nevertheless, even after controlling for postnatal maternal stress, the independent effects of prenatal stress remained significant. Adjusting for postnatal paternal stress had no impact on the effect sizes. The sex of the child moderated the association between first trimester prenatal stress and child ADHD symptoms, so that prenatal stress during the first trimester independently predicted higher levels of ADHD symptoms among boys, whereas, among girls, no significant associations were found for early-pregnancy stress after postnatal maternal stress was accounted for. Overall, the current findings are in line with the fetal programming hypothesis and highlight the importance of prenatal environmental factors in the etiology of childhood ADHD.