Late-onset Attention-deficit/hyperactivity Disorder Research Articles

Attention-Deficit/Hyperactivity Disorder Symptoms as a Function of Arousal and Executive Vigilance: Testing Halperin and Schulz’s Neurodevelopmental Model in a Sample of Community Adults

Halperin and Schulz’s neurodevelopmental model postulates that the onset of attention-deficit/hyperactivity disorder (ADHD) in childhood is due to subcortical alterations, whereas the disorder’s trajectory into adulthood depends on the development of executive functions. Based on a dimensional framework of ADHD, Coll-Martín et al. (2021) found support for the model in an adult community sample assessed on arousal and executive vigilance. The present study is a preregistered (https://osf.io/tkdq7) close replication of Coll-Martín et al. expressly aimed to test the two predictions of the model. A sample of college students (N = 292 valid; 49% women; 18–30 years, M = 21.7) from a Spanish university completed self-reports of ADHD symptoms in childhood (retrospectively) and adulthood and performed the online version of an attentional task (the ANTI-Vea). Our preregistered hypotheses achieved an acceptable statistical power for the effects of interest, even after accounting for random measurement error. Despite this, none of them replicated the findings of the original study: Only the unexpected negative correlation between executive vigilance and symptoms in childhood was significant, thereby not supporting the theoretical predictions. The lack of support for the dissociation pattern hypothesized by the neurodevelopmental model was robust to multiverse and exploratory analyses. At least in terms of vigilance, ADHD symptoms seem to share altered neurocognitive pathways across the lifespan, regardless of their time of onset. This challenges the notion of late-onset ADHD as a condition neuropsychologically distinct from child-onset ADHD. Future studies need to include complementary assessment methods and clinical groups.

Compared Profile of Late-Onset Versus Childhood-Onset ADHD: A Case-Control Study Among Treatment-Seeking Adult Patients.

To compare the characteristics of childhood-onset versus late-onset Attention Deficit Hyperactivity Disorder (ADHD) in a sample of treatment-seeking patients. Among total of 101 adult patients who were recently diagnosed for ADHD, using the Diagnostic Interview for Adult ADHD (DIVA 2.0), 56 subjects exhibited childhood-onset ADHD, versus 45 displayed late-onset ADHD. Both groups were compared according to their sociodemographic, clinical, and neuropsychological features, providing crude (OR) and adjusted odds ratios (aOR), and their 95% confidence intervals [95% CI]. Compared to late-onset ADHD, patients with childhood-onset had a lower educational score, (OR = 0.52; 95% CI [0.35, 0.76]), a greater score of impulsivity (aOR = 1.09; 95% CI [1.03, 1.16]), an increased number of hyperactive-impulsive ADHD symptoms (aOR = 1.9; 95% CI [1.46, 2.47]), and higher rates childhood trauma (aOR = 1.07; 95% CI [1.01, 1.13]), cannabis use disorder (aOR = 1.07; 95% CI [1.01, 1.13]), and working memory impairment. No difference was observed concerning age, sex, psychiatric symptoms, quality of life, and autonomy. Childhood-onset adult ADHD displayed a more severe profile, relative to late-onset ADHD.

Attention-deficit/hyperactivity disorder has a state-dependent association with asthma: The role of systemic inflammation in a population-based birth cohort followed from childhood to adulthood

There is a high comorbidity between attention-deficit/hyperactivity disorder (ADHD) and asthma, and inflammation has been proposed as a potential pathophysiological mechanism behind this association. Most studies conducted so far have used a cross-sectional design, and none has evaluated the prevalence of asthma symptoms in patients with ADHD followed from childhood to adulthood. We relied on data from the 1993 Pelotas birth cohort to evaluate the association between ADHD and asthma in patients with distinct patterns of incidence, persistence and remission, and to explore the potential role of inflammatory markers in the comorbidity. We analyzed data from 3281 individuals from the 1993 Pelotas birth cohort collected at birth (1993), 11 years (2004), 18 years (2011), and 22 years (2015). Subjects were first classified according to their ADHD and asthma status as early-onset (EO) persistent (positive screening for ADHD at 11 years and diagnosis of ADHD according to DSM-5, except criterion E, at either 18 or 22 years), EO-remittent (positive screening for ADHD at 11 years only), late-onset (diagnosis of ADHD according to DSM-5, except criterion E, at 18 or 22 years only), or healthy subjects (negative for both conditions in all evaluation). After controlling for confounders, significant associations were observed between EO-remittent ADHD and EO-remittent asthma (OR 1.68, 95% CI 1.11–2.55), EO-persistent ADHD and EO-persistent asthma (OR 4.33, 95% CI 1.65–11.34), and between late-onset ADHD and late-onset asthma (OR 1.86, 95% CI 1.28–2.70), suggesting a state-dependent association. Serum interleukin-6 (IL-6) and C-reactive protein (CRP) were measured at the 18- and 22-year evaluations and compared between subjects positive for ADHD, asthma, and subjects with both or none conditions, regardless of the previously defined trajectories. Subjects with comorbid ADHD and asthma presented higher levels of IL-6 at the 18- and 22-year evaluations when compared to subjects negative for both conditions. Our results demonstrate a state-dependent association between ADHD and asthma despite underlying trajectories. Higher levels of serum IL-6 in patients with both conditions suggest that a pro-inflammatory environment might have a role in the pathophysiological mechanisms underlying the comorbidity.

Late-onset ADHD: does it exist?

According to current classification systems, attention-deficit/hyperactivity disorder (ADHD) cannot be diagnosed unless its symptoms have been present already in childhood. Recently, this view has begun to be challenged with the thesis that the disorder may have its onset later in life (adolescence or young adulthood). The Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnostic criteria for ADHD are more liberal than those of the International Classification of Disease (ICD). Moreover, reports have begun to emerge demonstrating a different clinical picture in patients diagnosed with ADHD according to current guidelines and in a cohort with the onset in adulthood. The symptomatology of the disease in adults differs from that presented by children. Additionally, theories on the different etiopathogenesis of these entities have been advanced. These data have led to the proposal of distinguishing late-onset ADHD. There are also critical voices in the literature that question the possibility of developing ADHD symptoms in adulthood. Despite insufficient data and arguments to support the thesis of late-onset ADHD, there is a need for discussion and further exploration of the age at which ADHD may appear.

Polygenic Risk and the Course of Attention-Deficit/Hyperactivity Disorder From Childhood to Young Adulthood: Findings From a Nationally Representative Cohort

ObjectiveTo understand whether genetic risk for attention-deficit/hyperactivity disorder (ADHD) is associated with the course of the disorder across childhood and into young adulthood.MethodParticipants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-based birth cohort of 2,232 twins. ADHD was assessed at ages 5, 7, 10, and 12 with mother- and teacher-reports and at age 18 with self-report. Polygenic risk scores (PRSs) were created using a genome-wide association study of ADHD case status. Associations with PRS were examined at multiple points in childhood and longitudinally from early childhood to adolescence. We investigated ADHD PRS and course to young adulthood, as reflected by ADHD remission, persistence, and late onset.ResultsParticipants with higher ADHD PRSs had increased risk for meeting ADHD diagnostic criteria (odds ratios ranging from 1.17 at age 10 to 1.54 at age 12) and for elevated symptoms at ages 5, 7, 10, and 12. Higher PRS was longitudinally associated with more hyperactivity/impulsivity (incidence rate ratio = 1.18) and inattention (incidence rate ratio = 1.14) from age 5 to age 12. In young adulthood, participants with persistent ADHD exhibited the highest PRS (mean PRS = 0.37), followed by participants with remission (mean PRS = 0.21); both groups had higher PRS than controls (mean PRS = −0.03), but did not significantly differ from one another. Participants with late-onset ADHD did not show elevated PRS for ADHD, depression, alcohol dependence, or marijuana use disorder.ConclusionGenetic risk scores derived from case-control genome-wide association studies may have relevance not only for incidence of mental health disorders, but also for understanding the longitudinal course of mental health disorders.

The neurodevelopmental nature of attention-deficit hyperactivity disorder in adults.

Population studies have suggested that most adults with attention-deficit hyperactivity disorder (ADHD) did not have the disorder in childhood, challenging the neurodevelopmental conceptualisation of ADHD. Arbitrary definitions of age at onset and lack of defined trajectories were accounted for the findings. The objective of this study was to assess the proportion of individuals presenting with either a neurodevelopmental trajectory or late-onset disorder, and to assess risk factors associated with them. Data of 4676 individuals from the 1993 Pelotas birth cohort at 11, 15, 18 and 22 years of age were used. Polythetic and latent class mixed model analyses were performed to define ADHD trajectories from childhood to adulthood, and characterise the neurodevelopmental or late-onset courses. Regression models were applied to assess factors associated with different trajectories. Classical polythetic analyses showed that 67% of those with ADHD at 22 years of age had a neurodevelopmental course of the disorder. Latent class mixed model analysis indicated that 78% of adults with ADHD had a trajectory of persistent symptoms, more common in males. The remaining adults with ADHD had an ascending symptom trajectory that occurred after puberty, with late-onset ADHD associated with female gender and higher IQ. Both polythetic and latent trajectories analyses provided empirical evidence supporting that the large majority of adults with ADHD had a neurodevelopmental disorder.

Neurocognitive markers of late‐onset ADHD: a 6‐year longitudinal study

There is an increased interest in 'late-onset' attention-deficit/hyperactivity disorder (ADHD), referring to the onset of clinically significant ADHD symptoms after the age of 12years. This study aimed to examine whether unaffected siblings with late-onset ADHD could be differentiated from stable unaffected siblings by their neurocognitive functioning in childhood. We report findings from a 6-year prospective, longitudinal study of the Dutch part of the International Multicenter ADHD Genetics (IMAGE) study, including individuals with childhood-onset (persistent) ADHD (n=193), their siblings with late-onset ADHD (n=34), their stable unaffected siblings (n=111) and healthy controls (n=186). At study entry (mean age: 11.3) and follow-up (mean age: 17.01), participants were assessed for ADHD by structured psychiatric interviews and multi-informant questionnaires. Several neurocognitive functions were assessed at baseline and after 6years, including time reproduction, timing variability (reaction time variability and time production variability), reaction time speed, motor control and working memory; intelligence was taken as a measure of overall neurocognitive functioning. Siblings with late-onset ADHD were similar to individuals with childhood-onset ADHD in showing longer reaction times and/or higher error rates on all neurocognitive measures at baseline and follow-up, when compared to healthy controls. They differed from stable unaffected siblings (who were similar to healthy controls) by greater reaction time variability and timing production variability at baseline. No significant group by time interaction was found for any of the tasks. For unaffected siblings of individuals with ADHD, reaction time variability and timing production variability may serve as neurocognitive marker for late-onset ADHD.

A Qualitative Analysis of Contextual Factors Relevant to Suspected Late-Onset ADHD

Objective: Recent studies suggest attention-deficit/hyperactivity disorder (ADHD) may emerge post-childhood. We integrate qualitative methods to systematically characterize contextual factors that may (a) delay identification of ADHD in childhood and (b) inform why ADHD symptoms emerge post-childhood. Method: Suspected late-onset ADHD cases from the local normative comparison group of the Multimodal Treatment Study of ADHD completed a qualitative interview (14 young adults and 7 caregivers). Interviews were qualitatively analyzed. Results: We identified five themes. Three themes may attenuate or delay identification of childhood ADHD: external factors (e.g., supportive adults), internal factors (e.g., strong intellectual functioning), and other factors (e.g., dismissive attitudes toward ADHD). Two themes may accompany an increase in ADHD symptoms post-childhood: external factors (e.g., increased external demands) and internal factors (e.g., perceived stress). Conclusion: Clinicians should probe these factors in suspected late-onset cases to address (a) whether, how, and to what extent ADHD was attenuated in childhood and (b) why symptoms emerge post-childhood.

Annual Research Review: Does late-onset attention-deficit/hyperactivity disorder exist?

Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as an early onset childhood neurodevelopmental disorder. Prevalence in adults is around two-thirds that in childhood, yet longitudinal outcome studies of children with ADHD found a minority continue to meet full criteria in adulthood. This suggests that not all adult cases meet ADHD criteria as children, a conclusion supported by earlier studies relying on retrospective recall in adolescent and adult samples. More recently prospective follow-up of population and control samples suggest that adolescent and young adult ADHD is not always a continuation of childhood ADHD. Here, we review the literature on age of onset, to explore whether late-onset ADHD exists, and if so, examine the evidence for whether this should be considered the same or a different disorder as childhood onset ADHD. We conclude that current evidence supports the view that a significant proportion of young adults meeting criteria for ADHD would not have met full diagnostic criteria for ADHD as children. However, many in the late-onset group show some ADHD symptoms in childhood, or an externalizing disorder such as oppositional defiant disorder. Furthermore, the current studies suggest that most (but not all) cases of late-onset ADHD develop the disorder between the ages of 12-16 and can therefore be considered adolescent or early adult onset ADHD. There is a relative lack of data spanning young to older adulthood to address the question of adult-onset. Currently, there is insufficient data to clarify the extent to which early and late onset ADHD reflect a different balance of genetic and environmental risks or share the same underlying neural mechanisms. Clinicians should be aware that significantly impairing forms of ADHD can emerge beyond the age of 12years, although perhaps rarely in the context of a complete absence of precursors. The current evidence on treatment responses is limited.

Little evidence for late-onset ADHD in a longitudinal sample of women.

Individuals with late-onset symptoms of attention-deficit/hyperactivity disorder (ADHD) are presenting to providers at increasing rates. Recent birth-cohort studies reveal evidence for late-onset ADHD, but conclusions are challenged by measurement methods as well as presence of participant impairment and psychiatric comorbidities. We examined the occurrence of late-onset ADHD in a small but thoroughly investigated group of diverse (47% white) women followed from childhood to adulthood. From a larger, 16-year longitudinal study, a subsample of young women without childhood ADHD (N = 87) was assessed at four time points between childhood and adulthood via a multimethod, multiinformant approach. We used a stepped diagnostic procedure to identify those who initially met symptom criteria for ADHD after childhood and then evaluated them for remaining DSM ADHD diagnostic criteria, including impairment, cross-situational symptoms, and comorbid diagnoses. Of 87 participants, 17 met ADHD symptom criteria after childhood. Fifteen showed no evidence of childhood onset, 10 showed clear evidence of impairment, and nine had cross-situational symptoms. Of these nine, all but one showed clinically significant co-occurring or preexisting psychiatric diagnoses and/or substance use that might account for ADHD symptoms. Although 19.5% of women from our subsample without childhood ADHD met symptom criteria for ADHD during adolescence/adulthood, only one showed the needed combination of impairment and cross-situational symptoms without significant co-occurring mental health problems. It is possible that uncomplicated cases of adult ADHD do arise, yet we find little supporting evidence herein. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Heritability of Attention-Deficit Hyperactivity Disorder Across The Lifespan

Attention-Deficit Hyperactivity Disorder (ADHD) is a common neurodevelopmental disorder affecting around 5-10% of children and 2.5-5% of adults worldwide. Research addressing the heritability of ADHD have yielded inconsistent findings, with studies in children suggesting higher heritability (75–90%) compared to studies in adults (30–50% )(Brikell, Kuja-Halkola, and Larsson 2015). To review the role of rater effects on the observed differences in heritability between children and adults, and to address the role of genetic and environmental influences on stability and change of ADHD over the life-span, we conducted a literature review of cross-sectional and longitudinal studies addressing the heritability of ADHD across ages, or in adulthood. We identified quantitative genetic studies published up until May 2017 by searching the NCBI's PubMed database using a combination of the keywords heritability, attention-deficit hyperactivity disorder, attention problems, ADHD, adult, genetic, self-report, twin, longitudinal and family studies.Based on the reviewed cross-sectional studies, the heritability of self-rated ADHD symptoms in adults ranged between 30%-44% and the heritability of self-rated symptoms in adolescent between 34%-54%. Cross-sectional studies including multiple informants showed that heritability estimates based on ratings from different informants (i.e., self-ratings and different parents/teachers rating each twin in a pair) consistently yield lower heritability estimates compared to studies based on ratings from a single informant. This effect appears to be independent of age. One study using cross-informant data in adults (combined parent and self-ratings) and two studies using register based clinical diagnoses in twin and family data reported the heritability of ADHD in adults to be 70–80%. The reviewed longitudinal twin studies suggest that stability in ADHD is largely due to genetic factors. In addition, longitudinal studies also provide evidence that new genetic effects for ADHD come online at different developmental stages and that these genetic factors are partly independent of those contributing to baseline symptoms. We identified one study assessing late-onset adult ADHD, which reported the heritability of both self-reported and co-informant (mother or co-twin) reported clinically relevant ADHD at age 18 to be around 35%.Together, the reviewed cross-sectional studies suggest that the reported lower heritability of ADHD in adults is likely to be at least partly explained by the switch from relying one rater (parent/teacher) in childhood, to relying on self-ratings (where each twin rates themselves) of ADHD symptoms in adulthood. When rater effects are addressed using cross-informant data or clinical diagnoses, the heritability of ADHD in adulthood appears to be comparable to the heritability of ADHD in childhood. Longitudinal studies show evidence for the role of genetic factors in both the stability and change in ADHD across ages. Emerging evidence suggest that the genes implicated in the onset of childhood ADHD are in part distinct from those associated with the developmental course of ADHD. Such findings raise new questions as to whether the heterogeneity in heritability estimates of ADHD across ages may be related to differential developmental trajectories of ADHD.

Young adult mental health and functional outcomes among individuals with remitted, persistent and late-onset ADHD.

Attention-deficit hyperactivity disorder (ADHD) is associated with mental health problems and functional impairment across many domains. However, how the longitudinal course of ADHD affects later functioning remains unclear.AimsWe aimed to disentangle how ADHD developmental patterns are associated with young adult functioning. The Environmental Risk (E-Risk) Longitudinal Twin Study is a population-based cohort of 2232 twins born in England and Wales in 1994-1995. We assessed ADHD in childhood at ages 5, 7, 10 and 12 years and in young adulthood at age 18 years. We examined three developmental patterns of ADHD from childhood to young adulthood - remitted, persistent and late-onset ADHD - and compared these groups with one another and with non-ADHD controls on functioning at age 18 years. We additionally tested whether group differences were attributable to childhood IQ, childhood conduct disorder or familial factors shared between twins. Compared with individuals without ADHD, those with remitted ADHD showed poorer physical health and socioeconomic outcomes in young adulthood. Individuals with persistent or late-onset ADHD showed poorer functioning across all domains, including mental health, substance misuse, psychosocial, physical health and socioeconomic outcomes. Overall, these associations were not explained by childhood IQ, childhood conduct disorder or shared familial factors. Long-term associations of childhood ADHD with adverse physical health and socioeconomic outcomes underscore the need for early intervention. Young adult ADHD showed stronger associations with poorer mental health, substance misuse and psychosocial outcomes, emphasising the importance of identifying and treating adults with ADHD.Declaration of interestNone.

Is late-onset Attention Deficit Hyperactivity Disorder (ADHD) a valid diagnosis in adults?

INTRODUCTION: The current Attention Deficit Hyperactivity Disorder (ADHD) paradigm understands it as a childhood-onset neurodevelopmental disorder that can persist into adult life. However, it has been raised the possibility of a late-onset ADHD syndrome. OBJECTIVE: Evaluate the current state of knowledge regarding late-onset (i.e. age-of-onset > 12 years) ADHD. MATERIAL AND METHODS: Systematic literature review using PubMed (MEDLINE) and SCOPUS databases. RESULTS: We found six studies reporting data offering some support for the existence of late-onset ADHD: five from the PubMed search and one from the non-overlapping articles in the SCOPUS search. DISCUSSION: Despite the small number of studies, the differences in methodology among them and the presence of limitations in all of them, data regarding clinical aspects offer some support for the content validity of late-onset ADHD diagnosis in adults. CONCLUSIONS: Although many controversies still exist and studies supporting its construct validity are needed, late-onset ADHD may be a valid diagnosis in adults. Thus, clinicians should consider diagnosing and treating late-onset ADHD in adults, instead of just neglecting this possibility because of the age-of-onset criterion.

Late-Onset ADHD: Understanding the Evidence and Building Theoretical Frameworks.

The traditional definition of Attention-Deficit/Hyperactivity Disorder (ADHD), assuming onset in childhood, has been challenged by evidence from four recent birth-cohort studies that reported most adults with ADHD lacked a childhood categorical ADHD diagnosis. Late onset of symptoms was evaluated in the long-term follow-up of the Multimodal Treatment study of ADHD (MTA). In most cases, other factors were present that discounted the late onset of ADHD symptoms and excluded the diagnosis of ADHD. We offer two theoretical frameworks for understanding the ADHD trajectory throughout the life cycle: (1) the complex phenotype model, and (2) the restricted phenotype model. We conclude that (a) late onset (after age 12) is a valid trajectory for ADHD symptoms, (b) the percentage of these cases with onset after adolescence is yet uncertain, and

Late-Onset ADHD Reconsidered With Comprehensive Repeated Assessments Between Ages 10 and 25.

Adolescents and young adults without childhood attention deficit hyperactivity disorder (ADHD) often present to clinics seeking stimulant medication for late-onset ADHD symptoms. Recent birth-cohort studies support the notion of late-onset ADHD, but these investigations are limited by relying on screening instruments to assess ADHD, not considering alternative causes of symptoms, or failing to obtain complete psychiatric histories. The authors address these limitations by examining psychiatric assessments administered longitudinally to the local normative comparison group of the Multimodal Treatment Study of ADHD. Individuals without childhood ADHD (N=239) were administered eight assessments from comparison baseline (mean age=9.89 years) to young adulthood (mean age=24.40 years). Diagnostic procedures utilized parent, teacher, and self-reports of ADHD symptoms, impairment, substance use, and other mental disorders, with consideration of symptom context and timing. Approximately 95% of individuals who initially screened positive on symptom checklists were excluded from late-onset ADHD diagnosis. Among individuals with impairing late-onset ADHD symptoms, the most common reason for diagnostic exclusion was symptoms or impairment occurring exclusively in the context of heavy substance use. Most late-onset cases displayed onset in adolescence and an adolescence-limited presentation. There was no evidence for adult-onset ADHD independent of a complex psychiatric history. Individuals seeking treatment for late-onset ADHD may be valid cases; however, more commonly, symptoms represent nonimpairing cognitive fluctuations, a comorbid disorder, or the cognitive effects of substance use. False positive late-onset ADHD cases are common without careful assessment. Clinicians should carefully assess impairment, psychiatric history, and substance use before treating potential late-onset cases.

Evaluation of the Persistence, Remission, and Emergence of Attention-Deficit/Hyperactivity Disorder in Young Adulthood.

Attention-deficit/hyperactivity disorder (ADHD) is now recognized to occur in adulthood and is associated with a range of negative outcomes. However, less is known about the prospective course of ADHD into adulthood, the risk factors for its persistence, and the possibility of its emergence in young adulthood in nonclinical populations. To investigate childhood risk factors and young adult functioning of individuals with persistent, remitted, and late-onset young adult ADHD. The study sample was the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of 2232 twins born in England and Wales from January 1, 1994, to December 4, 1995. Evaluation of childhood ADHD (ages 5, 7, 10, and 12 years) included prenatal and perinatal factors, clinical characteristics, and aspects of the family environment. Among participants aged 18 years, ADHD symptoms and associated impairment, overall functioning, and other mental health disorders were examined. Data analysis was conducted from February 19 to September 10, 2015. Attention-deficit/hyperactivity disorder according to DSM-IV diagnostic criteria in childhood and DSM-5 diagnostic criteria in young adulthood. Of 2232 participants in the E-Risk Study, 2040 were included in the present analysis. In total, 247 individuals met diagnostic criteria for childhood ADHD; of these, 54 (21.9%) also met diagnostic criteria for the disorder at age 18 years. Persistence was associated with more symptoms (odds ratio [OR], 1.11 [95% CI, 1.04-1.19]) and lower IQ (OR, 0.98 [95% CI, 0.95-1.00]). At age 18 years, individuals with persistent ADHD had more functional impairment (school/work: OR, 3.30 [95% CI, 2.18-5.00], home/with friends: OR, 6.26 [95% CI, 3.07-12.76]), generalized anxiety disorder (OR, 5.19 [95% CI, 2.01-13.38]), conduct disorder (OR, 2.03 [95% CI, 1.03-3.99]), and marijuana dependence (OR, 2.88 [95% CI, 1.07-7.71]) compared with those whose ADHD remitted. Among 166 individuals with adult ADHD, 112 (67.5%) did not meet criteria for ADHD at any assessment in childhood. Results from logistic regressions indicated that individuals with late-onset ADHD showed fewer externalizing problems (OR, 0.93 [95% CI, 0.91-0.96]) and higher IQ (OR, 1.04 [95% CI, 1.02-1.07]) in childhood compared with the persistent group. However, at age 18 years, those with late-onset ADHD demonstrated comparable ADHD symptoms and impairment as well as similarly elevated rates of mental health disorders. We identified heterogeneity in the DSM-5 young adult ADHD population such that this group consisted of a large, late-onset ADHD group with no childhood diagnosis, and a smaller group with persistent ADHD. The extent to which childhood-onset and late-onset adult ADHD may reflect different causes has implications for genetic studies and treatment of ADHD.

Validation of DSM-5 age-of-onset criterion of attention deficit/hyperactivity disorder (ADHD) in adults: Comparison of life quality, functional impairment, and family function

The newly published Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) elevates the threshold of the ADHD age-of-onset criterion from 7 to 12 years. This study evaluated the quality of life and functional impairment of adults with ADHD who had symptoms onset by or after 7 years and examined the mediation effect of family function and anxiety/depression symptoms between ADHD diagnosis and quality of life and functional impairment. We assessed 189 adults with ADHD and 153 non-ADHD controls by psychiatric interview and self-administered reports on the Adult ADHD Quality of Life Scale, Weiss Functional Impairment Rating Scale, Family APGAR, and Adult Self Report Inventory-4. The ADHD group was divided into early-onset ADHD (onset <7 years, n=147) and late-onset ADHD (onset between 7 and 12 years, n=42). The mediation analysis was conducted to verify the mediating factors from ADHD to functional impairment and quality of life. The late-onset ADHD had more severe functional impairment at work and poorer family support than early-onset ADHD while they had comparable impairment at other domains. Less perceived family support and current anxiety/depressive symptoms partially mediated the link between ADHD diagnosis and quality of life/functional impairment both in early- and late-onset ADHD. Our data support decreased quality of life and increased functional impairment in adult ADHD, regardless of age of onset, and these adverse outcomes may be mediated by family support and anxiety/depression at adulthood. Our findings also imply that the new DSM-5 ADHD criteria do not over-include individuals without impairment.

P03-548 - Late onset adult attention deficit hyperactivity disorder

Attention-deficit hyperactivity disorder (ADHD) is a common, genetically transmitted neurological disorder, with onset in childhood, probably mediated in part by decreased brain dopaminergic functioning. Prevalence and natural history data suggest that of the 3–10% of children diagnosed with ADHD, one-to two-thirds continue to manifest appreciable ADHD symptoms as adults, interfering in academic, professional, affective and social life. Recently, several studies have challenged DSM-IV's requirement of ADHD onset before age 7 with the questioning of the validity of the age-at onset criterion.Based on the description of a late onset ADHD clinical case (onset after the age of 7), this presentation shows a review on the recent literature about ADHD, addressing how ADHD in adults can be readily diagnosed and treated using the Wender Utah diagnostic criteria to identify adult characteristics of the disorder. This work also addresses core hypotheses of etiology and treatment. The study was based on a revision of articles from Medline/PubMed, PsycINFO and from books published in the last years.

Attention‐Deficit‐Hyperactivity Disorder: An Update

Attention-deficit-hyperactivity disorder (ADHD) is a common neuropsychiatric disorder that impairs social, academic, and occupational functioning in children, adolescents, and adults. In patients with ADHD, neurobiologic research has shown a lack of connectivity in key brain regions, inhibitory control deficits, delayed brain maturation, and noradrenergic and dopaminergic dysfunction in multiple brain regions. The prevalence of this disorder in the United States is 6-9% in youth (i.e., children and adolescents) and 3-5% in adults. Prevalence rates for youth are similar worldwide. Children with ADHD are at greater risk than children without ADHD for substance abuse and delinquency whether or not they receive drug therapy; however, early treatment with psychoeducation as well as drug therapy and/or behavioral intervention may decrease negative outcomes of ADHD, including the rate of conduct disorder and adult antisocial personality disorder. Drug therapy is effective for all age groups, even preschoolers, and for late-onset ADHD in adults. Stimulants, such as methylphenidate and amphetamine, are the most effective therapy and have a good safety profile; although recent concerns of sudden unexplained death, psychiatric adverse effects, and growth effects have prompted the introduction of other therapies. Atomoxetine, a nonstimulant, has no abuse potential, causes less insomnia than stimulants, and poses minimal risk of growth effects. Other drug options include clonidine and guanfacine, but both can cause bradycardia and sedation. Polyunsaturated fatty acids (fish oil), acetyl-L-carnitine, and iron supplements (for youth with low ferritin levels) show promise in improving ADHD symptoms. As long-term studies show that at least 50% of youth are nonadherent with their drug therapy as prescribed over a 1-year period, long-acting formulations (administered once/day) may improve adherence. Comorbid conditions are common in patients with ADHD, but this patient population can be treated effectively with individualized treatment regimens of stimulants, atomoxetine, or bupropion, along with close monitoring.

Late-onset ADHD in adults: Milder, but still dysfunctional

Objective The requirement in classificatory systems that some impairment from attention-deficit/hyperactivity disorder (ADHD) symptoms starts before 7 years of age (age of onset of impairment criteria – AOC) has been harshly criticized. Although there is evidence that late-onset ADHD is a valid diagnosis, little is known about the role of age of onset of impairment on the clinical profile of adult patients. Methods The diagnoses of 349 adults with ADHD followed DSM-IV criteria. ADHD and oppositional defiant disorder (ODD) were evaluated with the K-SADS-E, and other comorbidities with the SCID-IV and the MINI. Subjects were divided in early and late-onset groups (age of onset of impairment between 7 and 12 years old). The effect of age of onset over clinical and demographic characteristics was tested by regression models. Results Late-onset subjects were diagnosed later ( P = 0.04), had a lower frequency of problems with authority and discipline ( P = 0.004), and lower scores in SNAP-IV ( P < 0.001) and in Barkley’s scale for problems in areas of life activities ( P = 0.03). On the other hand, late-onset patients presented a higher prevalence of comorbid general anxiety disorder (GAD) ( P = 0.01). Both groups had a similar profile in the remaining comorbidities and sociodemographic characteristics. Conclusions This study provides initial evidence that adults with late-onset ADHD have less severity, lower frequency of externalizing symptoms and increased comorbidity with GAD, but similar profile in other comorbidities. In addition, the data suggest that late-onset patients have a higher probability of delayed diagnosis despite the significant impairment of their condition.