Official websites use. Share sensitive information only on official, secure websites. This article is based on publications retrieved by a selective search in PubMed with an emphasis on pertinent guidelines and systematic reviews. The etiology of ADHD is complex and heterogeneous, involving a major genetic component and diverse neurobiological alterations. Prenatal environmental factors also seem to elevate the risk of ADHD. The mainstays of treatment are psychoeducation, behavioral therapy, and psychoactive drugs, which generally have only mild side effects, such as insomnia or decreased appetite.
The indication for treatment in the individual case is based on severity, comorbidity, previous therapy attempts, and the familial, social, and educational framework conditions. Translational research is needed to clarify the etiology of ADHD. Epidemiological studies published since do not reveal any increase in the prevalence of ADHD among children and adolescents. Improved diagnosis necessitates an evidence-based and need-adapted approach to treatment.
To diagnose the disorder, clinically relevant functional psychosocial impairment must be present in different settings, e. In the general population, these core symptoms are dimensionally distributed along a continuum, the upper end of which constitutes clinically relevant ADHD symptoms e1. In this selective review, we focus on meta-analyses, systematic reviews, large registry studies, and randomized controlled trials. The aim is to provide the reader with an evidence-based overview of the developmental trajectories in ADHD, the various and often controversial treatment options, and the current state of etiological research.
The two most commonly used nosological classification systems worldwide, the ICD and the DSM-5, are broadly consistent in their operationalizations of the various symptoms of ADHD, but differ with respect to subtypes and additional criteria. The DSM-5 is the first classification system to define specific features of ADHD in adults, reducing the number of symptoms necessary for diagnosis from the age of 17, due to the fact that functional impairment can persist or worsen with age despite an age-dependent reduction of symptoms e3 , e4.
Moreover, the age of onset criterion has been raised to 12 in the DSM-5, as an older age of onset between 7 and 12 years was found to show no effect on clinical manifestation, symptom severity, nature and extent of comorbid disorders, neuropsychological findings and functional impairment, progression or treatment response e5. The higher prevalence in males is more pronounced in clinical samples 3β4 : 1 than in epidemiological studies 2 : 1. ADHD is associated with a lower socio-economic status e9.
