Assessment of age-at-onset criterion for adult attention-deficit hyperactivity disorder.
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ABSTRACT:
SUBMITTER: Riglin L
PROVIDER: S-EPMC7612274 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:Widening definitions of health conditions have the potential to affect millions of people and should only occur when there is strong evidence of benefit. In the last version of the Diagnostic and Statistical Manual of Mental Disorders (DSM), the DSM-5 Committee changed the Attention Deficit Hyperactivity Disorder (ADHD) age of onset criterion in two ways: raising the age of symptom onset and removing the requirement for symptoms to cause impairment. Given concerns about ADHD prevalence and treatment rates, we aimed to evaluate the evidence available to support these changes using a recently developed Checklist for Modifying Disease Definitions. METHODS:We identified and analysed research informing changes to the DSM-IV-TR ADHD age of onset criterion. We compared this evidence to the evidence recommended in the Checklist for Modifying Disease Definitions. RESULTS:The changes to the DSM-IV-TR age of onset criterion were based on a literature review (publicly available as a 2 page document with online table of included studies), which we appraised as at high risk of bias. Estimates of the change in ADHD prevalence resulting from change to the age of onset criterion were based on a single study that included only a small number of children with ADHD (n =?68) and only assessed the impact of change to the age component of the criterion. No evidence was used by, or available to the Committee regarding the impact on prevalence of removal of the requirement for impairment, or the effect of the criterion changes on diagnostic precision, the prognosis of, or the potential benefits or harms for individuals diagnosed by the new, but not old criterion. CONCLUSIONS:The changes to the age of onset criterion were based on minimal research evidence that suffered from either high risk of bias or poor applicability. The minimal documentation available makes it difficult to judge the rigor of the process behind the criterion changes. Use of the Checklist for Modifying Disease Definitions would assist future proposed modifications of the DSM ADHD criteria, provide guidance on the studies needed to inform potential changes and would improve the transparency and documentation of the process.
| S-EPMC6849294 | biostudies-literature
Project description:BackgroundSluggish cognitive tempo (SCT) is associated with-but distinct from-attention-deficit/hyperactivity disorder (ADHD). This study examined SCT rates in adult outpatients seeking an ADHD assessment, differences in rates based on ADHD status, impact of assessment method (i.e., reporting source, symptom count, and functional impairment), and age of SCT symptom onset.MethodsOutpatients (n = 124) completed an SCT measure (n = 120 other-reporters). SCT was based on reporting source (i.e., self-report, other-report, either reporting source ["or" rule], and both reporting sources ["and" rule]), symptom count (i.e., age-based norms at or near the 93rd percentile, and a higher symptom count threshold of five), and functional impairment (i.e., 0, 1, and ≥2 domains).ResultsSCT rates varied based on assessment method for the full sample (26%-82%) and among those with (32%-91%) and without (16%-66%) ADHD. Rates decreased with stricter functional impairment and symptom count criteria. SCT was higher in the ADHD group than the non-ADHD group based on other-reporters and the "or" rule, but not the "and" rule. Functional impairment and symptom count criteria did not impact these comparisons. For self-reported SCT rates, ADHD/non-ADHD group comparisons did not differ based on age-based symptom count threshold, but did with a symptom count threshold of five. Self-reported SCT symptom onset was 13.36 years-old and was significantly younger for the ADHD group (11.69 years) than the non-ADHD group (16.36 years).ConclusionsElevated SCT symptoms and related impairment are common among adults seeking an ADHD evaluation. These rates and ADHD/non-ADHD group differences vary substantially based on diagnostic methods.
| S-EPMC7983554 | biostudies-literature
Project description:Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable childhood-onset neuropsychiatric condition, often persisting into adulthood. The genetic architecture of ADHD, particularly in adults, is largely unknown. We performed an exome-wide scan of adult ADHD using the Illumina Human Exome Bead Chip, which interrogates over 250 000 common and rare variants. Participants were recruited by the International Multicenter persistent ADHD CollaboraTion (IMpACT). Statistical analyses were divided into 3 steps: (1) gene-level analysis of rare variants (minor allele frequency (MAF)<1%); (2) single marker association tests of common variants (MAF⩾1%), with replication of the top signals; and (3) pathway analyses. In total, 9365 individuals (1846 cases and 7519 controls) were examined. Replication of the most associated common variants was attempted in 9847 individuals (2077 cases and 7770 controls) using fixed-effects inverse variance meta-analysis. With a Bonferroni-corrected significance level of 1.82E-06, our analyses of rare coding variants revealed four study-wide significant loci: 6q22.1 locus (P=4.46E-08), where NT5DC1 and COL10A1 reside; the SEC23IP locus (P=6.47E-07); the PSD locus (P=7.58E-08) and ZCCHC4 locus (P=1.79E-06). No genome-wide significant association was observed among the common variants. The strongest signal was noted at rs9325032 in PPP2R2B (odds ratio=0.81, P=1.61E-05). Taken together, our data add to the growing evidence of general signal transduction molecules (NT5DC1, PSD, SEC23IP and ZCCHC4) having an important role in the etiology of ADHD. Although the biological implications of these findings need to be further explored, they highlight the possible role of cellular communication as a potential core component in the development of both adult and childhood forms of ADHD.
| S-EPMC5315553 | biostudies-literature
Project description:Attention-deficit hyperactivity disorder (ADHD), like other psychiatric disorders, represents an evolving construct that has been refined and developed over the past several decades in response to research into its clinical nature and structure. The clinical presentation and course of the disorder have been extensively characterised. Efficacious medication-based treatments are available and widely used, often alongside complementary psychosocial approaches. However, their effectiveness has been questioned because they might not address the broader clinical needs of many individuals with ADHD, especially over the longer term. Non-pharmacological approaches to treatment have proven less effective than previously thought, whereas scientific and clinical studies are starting to fundamentally challenge current conceptions of the causes of ADHD in ways that might have the potential to alter clinical approaches in the future. In view of this, we first provide an account of the diagnosis, epidemiology, and treatment of ADHD from the perspective of both the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders and the eleventh edition of the International Classification of Diseases. Second, we review the progress in our understanding of the causes and pathophysiology of ADHD on the basis of science over the past decade or so. Finally, using these discoveries, we explore some of the key challenges to both the current models and the treatment of ADHD, and the ways in which these findings can promote new perspectives.
| S-EPMC7880081 | biostudies-literature
Project description:Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with a long-term impact on functioning, productivity and quality of life of patients. This impact is largely due to the symptoms of inattentiveness. However, despite its impairing role in the lives of ADHD patients, inattentiveness has been studied relatively less frequently than have symptoms of impulsivity/hyperactivity and problems with executive function. This review therefore seeks to integrate the neuropsychological theories and current findings in the research fields of neuropsychology, neurophysiology, and neuroimaging, in an attempt to gain a more complete understanding of the role that inattentiveness plays in ADHD, as well as to suggest directions for future studies. The need for a more comprehensive understanding of inattentiveness and ADHD, which integrates findings from each of the three disciplines mentioned above, is emphasized.
| S-EPMC4440572 | biostudies-other
Project description:Genes encoding endocannabinoid and sphingolipid metabolism pathways were suggested to contribute to the genetic risk towards attention deficit hyperactivity disorder (ADHD). The present pilot study assessed plasma concentrations of candidate endocannabinoids, sphingolipids and ceramides in individuals with adult ADHD in comparison with healthy controls and patients with affective disorders. Targeted lipid analyses of 23 different lipid species were performed in 71 mental disorder patients and 98 healthy controls (HC). The patients were diagnosed with adult ADHD (n = 12), affective disorder (major depression, MD n = 16 or bipolar disorder, BD n = 6) or adult ADHD with comorbid affective disorders (n = 37). Canonical discriminant analysis and CHAID analyses were used to identify major components that predicted the diagnostic group. ADHD patients had increased plasma concentrations of sphingosine-1-phosphate (S1P d18:1) and sphinganine-1-phosphate (S1P d18:0). In addition, the endocannabinoids, anandamide (AEA) and arachidonoylglycerol were increased. MD/BD patients had increased long chain ceramides, most prominently Cer22:0, but low endocannabinoids in contrast to ADHD patients. Patients with ADHD and comorbid affective disorders displayed increased S1P d18:1 and increased Cer22:0, but the individual lipid levels were lower than in the non-comorbid disorders. Sphingolipid profiles differ between patients suffering from ADHD and affective disorders, with overlapping patterns in comorbid patients. The S1P d18:1 to Cer22:0 ratio may constitute a diagnostic or prognostic tool.
| S-EPMC8467584 | biostudies-literature
Project description:Attention-deficit/hyperactivity disorder (ADHD) and childhood-onset psychosis (COP) are chronic, heterogeneous disorders with symptoms that frequently co-occur, but the etiology of their comorbidity is unknown. Studies of each disorder indicate that both ADHD and COP are associated with a range of neuropsychological weaknesses, but few neuropsychological studies have directly compared groups with ADHD and COP.Groups with ADHD only (32 F, 48 M), COP only (5 F, 5 M), ADHD + COP (9 F, 21 M), and a control group with neither disorder (25 F, 44 M) completed a neuropsychological battery that included measures of verbal working memory, response inhibition, response speed and variability, and selective attention.All three clinical groups exhibited significantly lower performance versus the control group on all neuropsychological measures, whereas the only significant difference between the clinical groups was a significantly larger weakness in verbal working memory in the groups with COP.The frequent co-occurrence between COP and ADHD may reflect shared neuropsychological weaknesses that are most pronounced on measures of working memory and response variability.
| S-EPMC4065620 | biostudies-literature
Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder
| PRJNA1114309 | ENA
Project description:Genetic Investigations of Attention-Deficit/Hyperactivity Disorder
| PRJNA1114310 | ENA
Project description:Despite not being part of the core diagnostic criteria for attention-deficit/hyperactivity disorder (ADHD), emotion dysregulation is a highly prevalent and clinically important component of (adult) ADHD. Emotionally dysregulated behaviors such as reactive aggression have a significant impact on the functional outcome in ADHD. However, little is known about the mechanisms underlying reactive aggression in ADHD. In this study, we aimed to identify the neural correlates of reactive aggression as a measure of emotionally dysregulated behavior in adults with persistent ADHD during implicit emotion regulation processes. We analyzed associations of magnetic resonance imaging-based whole-brain activity during a dynamic facial expression task with levels of reactive aggression in 78 adults with and 78 adults without ADHD, and also investigated relationships of reactive aggression with symptoms and impairments. While participants with ADHD had higher reactive aggression scores than controls, the neural activation patterns of both groups to processing of emotional faces were similar. However, investigating the brain activities associated with reactive aggression in individuals with and without ADHD showed an interaction of diagnosis and reactive aggression scores. We found high levels of activity in the right insula, the hippocampus, and middle and superior frontal areas to be particularly associated with high reactive aggression scores within the ADHD group. Furthermore, the limbic activity was associated with more hyperactivity/impulsivity symptoms. These results suggest a partly differential mechanism associated with reactive aggression in ADHD as compared to controls. Emotional hyper-reactivity in the salience network as well as more effortful top-down regulation from the self-regulation network might contribute to emotionally dysregulated behavior as measured by reactive aggression.
| S-EPMC9160326 | biostudies-literature