1,721,610 research outputs found
Here/in this issue and there/abstract thinking: the DSM-5 is here (and there)
No full textBackgroundA significant association between attention-deficit hyperactivity disorder (ADHD) and obesity has been reported. This study addresses unexplored aspects of this relationship.AimsTo evaluate the association between adult obesity and: (a) persistent, remitted or lifetime ADHD; (b) number of childhood ADHD symptoms, controlling for socioeconomic status and mood, anxiety and substance use disorders.MethodFace-to-face psychiatric interviews in 34 653 US adults from the National Epidemiologic Study on Alcohol and Related Conditions. Obesity was defined as a body mass index ?30.ResultsPersistent, lifetime or remitted ADHD were not associated with obesity after controlling for confounders. The number of childhood ADHD symptoms was significantly associated with adult obesity, even after adjustment, in women.ConclusionsChildhood ADHD symptoms are associated with obesity in women even after comorbid psychiatric disorders are accounted for. This provides a rationale for longitudinal studies assessing the impact of the treatment of childhood ADHD symptoms on obesity in women.<br/
Regional analysis of UK primary care prescribing and adult service referrals for young people with attention-deficit hyperactivity disorder: from little to very little
No full textDrawing on data from the Clinical Practice Research Datalink, Price et al reported UK regional variations in primary care prescribing and referral rates to adult mental health services for young people with attention-deficit hyperactivity disorder (ADHD) in transition from child and adolescent mental health services. Overall, considering that around 65% of young adults with childhood ADHD present with impairing ADHD symptoms and up to 90% of individuals with ADHD may benefit from ADHD medications, the study by Price et al shows that the rate of appropriate treatment for youngsters in the transition period varies from low to very low across the UK. As such, there is a continuous need for education and training for patients, their families, mental health professionals and commissioners, to eradicate the misconception that, in the majority of the cases, ADHD remits during adolescence and to support the devolvement of appropriate services for the evidence-based management of adult ADHD across the UK.</p
Pharmacologic treatment of Attention Deficit Hyperactivity Disorder
No full textAmphetamines and methylphenidate and, less often, nonstimulants (atomoxetine, clonidine, and guanfacine) are used to treat ADHD. Inattentiveness and restlessness are improved more than quality-of-life measures in short-term trials.https://www.nejm.org/doi/10.1056/NEJMra191706
Are the effects of methylphenidate uncertain?
No full textObjectives:A recent systematic review and meta-analysis of randomised controlled trials of methylphenidate (MPH) in children and adolescents by a Cochrane group, led by Storebø, raised concern around the level of evidence supporting the use of this medication for attention-deficit/hyperactivity disorder (ADHD) in children and adolescents. This led to several critical responses from a number of ADHD experts.Methods:This paper reviews the conclusions reached from the Storebø meta-analysis by a critical analysis of methodologies used along with drawing on extant literature.Results:The controversy raised by the Cochrane meta-analysis should lead to a balanced reflection on the research priorities and needs for the field.Conclusions:It is hoped the controversy will ultimately lead to improve the quality of the research on the efficacy, effectiveness and tolerability of MPH for ADHD.<br/
The neurobiology and genetics of attention-deficit/hyperactivity disorder (ADHD): what every clinician should know
No full textThis review, addressed mainly to clinicians, considers commonly asked questions related to the neuroimaging, neurophysiology, neurochemistry and genetics of Attention-Deficit/Hyperactivity Disorder (ADHD). It provides answers based on the most recent meta-analyses and systematic reviews, as well as additional relevant original studies. Empirical findings from neurobiological research into ADHD reflect a shift in the conceptualisation of this disorder from simple theoretical views of a few isolated dysfunctions to more complex models integrating the heterogeneity of the clinical manifestations of ADHD. Thus, findings from structural and functional neuroimaging suggest the involvement of developmentally abnormal brain networks related to cognition, attention, emotion and sensorimotor functions. Brain functioning alterations are confirmed by neurophysiological findings, showing that individuals with ADHD have elevated theta/beta power ratios, and less pronounced responses and longer latencies of event-related potentials, compared with controls. At a molecular level, alterations in any single neurotransmitter system are unlikely to explain the complexity of ADHD; rather, the disorder has been linked to dysfunctions in several systems, including the dopaminergic, adrenergic, serotoninergic and cholinergic pathways. Genetic studies showing a heritability of ?60–75% suggest that a plethora of genes, each one with a small but significant effect, interact with environmental factors to increase the susceptibility to ADHD. Currently, findings from neurobiological research do not have a direct application in daily clinical practice, but it is hoped that in the near future they will complement the diagnostic process and contribute to the long-term effective treatment of this impairing condition
Here/In this issue and There/Abstract thinking: neurosciences and (child) psychiatry
No full textThis issue of the Journal features 3 neuroimaging studies aimed at advancing our understanding of the neurobiological bases of common psychiatric disorders.The first article focuses on the neurodevelopmental underpinnings of schizophrenia and bipolar disorder. There is evidence that the 2 disorders are related to neurodevelopmental abnormalities. However, the timing and impact of such neurodevelopmental alterations might differ in the 2 disorders. To address this hypothesis, Sugranyes and colleagues (p. 677) conducted the first magnetic resonance imaging study comparing gray matter volume in 38 offspring of patients with schizophrenia (SzO), 77 offspring of patients with bipolar disorder (BdO), and 83 offspring of community controls (CcO) who were 6 to 17 years old. As evaluated by clinicians blinded to parental status, none of the SzO or BdO offspring presented with psychosis, bipolar disorder, or prodromal syndrome, although some of them presented with other Axis I disorders. CcO offspring were excluded if they had a personal or first-degree family history of schizophrenia or bipolar spectrum disorders. The investigators found that total cerebral gray volume was significantly reduced in SzO compared with CcO offspring. Compared with BdO and CcO offspring, SzO offspring presented with significantly reduced volume in the left inferior frontal cortex/anterior insula. There were no significant brain volume differences between BdO and CcO offspring. These findings suggest that the neurodevelopmental correlates of premorbid schizophrenia and bipolar disorder are likely to differ. SzO offspring would be characterized by more evident and earlier neurodevelopmental alterations related to genetic and early environmental influences. In contrast, gray matter alterations in BdO offspring might emerge at a later stage.The second study, by Schweren and colleagues (p. 660), was carried out to gain insight into the neurobiology of attention-deficit/hyperactivity disorder (ADHD), in particular, its brain structural correlates. Importantly, the study also addressed the effect of psychostimulants on the brains of children with ADHD, which is not yet fully understood. The investigators compared measurements of brain cortical thickness in 308 youths with ADHD and 184 controls (8–28 years old) from the European NeuroIMAGE sample. Eighty-eight percent of participants with ADHD had received psychostimulants at some point in their lives, on average for approximately 5 years. Of note, the investigators obtained detailed information on type, dose, and duration of treatment with psychostimulants for each participant. They found that, compared with controls, youths with ADHD had significantly decreased cortical thickness in the medial temporal cortex, bilaterally, which persisted even after controlling for psychiatric comorbidities and regardless of the age of the participants. Of note, there were no significant differences in cortical thickness between psychostimulant-treated and psychostimulant-naive participants with ADHD. In addition, neither treatment duration nor mean dose was related to cortical thickness. These findings are in line with recent evidence showing that networks other than the frontostriatal one, classically believed to underpin ADHD, are relevant in the pathophysiology of the disorder. This study does not support previous evidence of brain structural normalization after treatment with psychostimulants. It is worthy of note that, although medication effects would ideally be tested in a long-term controlled trial in which participants are randomly assigned to psychostimulant treatment or placebo, this is clearly unethical.The third study, by Bos and colleagues (p. 668), combined the assessment of 2 different brain features estimated by structural neuroimaging, namely cortical gyrification and white matter structure, to advance our knowledge of the brain structural correlates of autism spectrum disorder (ASD). The study tested the hypothesis that decreased cortical gyrification is related to altered white matter connectivity in a sample of 30 children with ASD and 29 typically developing controls 8 to 18 years of age. Compared with controls, participants with ASD showed a decrease in the gyrification index in the left prefrontal and parietal cortex. Importantly, a similar result was found in the analysis of an independent, free, and publicly released large neuroimaging dataset on ASD, the Autism Brain Imaging Data Exchange (ABIDE). This is a crucial result that is particularly relevant in light of inconsistent findings that characterized the early wave of neuroimaging studies in (child) psychiatry. The use of the ABIDE dataset to replicate study findings highlights the value, for the scientific community, of free data sharing as a way to overcome the challenge of recruiting large samples in neuroimaging research.Consistent with their hypothesis, the investigators also found that radial diffusivity (a diffusion tensor imaging parameter that allows estimation of structural connectivity) in the forceps minor was inversely related to prefrontal gyrification in children with ASD. Overall, this study suggests that, in addition to abnormal brain size, altered gyrification and structural connectivity might be relevant neurobiological correlates of ASD.<br/
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