الفهرس 
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Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a neuropsychiatric conditioncharacterized by core symptoms of inattentiveness, hyperactivity, andimpulsivity. The impact of ADHD in children is widely recognized; however,only recently has ADHD in adults become the focus of clinical attention.Approximately 50% to 75% of children with ADHD continue to meet diagnosticcriteria in later life, as both adolescents and adults.
This work aims to verify that adult ADHD is a life span disorder, also trying to illustrate the overlapping with other psychiatric disorders,to illustrate the overlap between ADHD and bipolar disorders and to clarify the genetic burden of ADHD in adolescence and adults, to highlight a new modality of treatment.
ADHD is characterized by age inappropriate symptoms of inattention and/or hyperactivity or impulsivity which occur for at least 6 months in at least two domains of life and begin prior to the age of 7. It is estimated that ADHD affects approximately 8% to 12%of school-aged (6–12 years) children and 5%of adults. Impairments associated with ADHD have been found across the life span in areas such as academics, socioeconomic status and employment, family life, and mental health, including greater rates of disruptive behaviors, oppositional and conduct disorders, and substance use disorders.
Molecular genetic studies have predominantly focused on dopamine genes, including dopamine receptor and transporter genes, because of animal and human studies indicating the importance of dopaminergic attention systems. The recent clinical use of noradrenergic reuptake inhibitors has also increased interest in noradrenergic genes. Adult ADHD and age-related genetic effects, in addition to “reading” genes, are reviewed in relation to comorbidity and developmental effects.
Behavioural genetic investigations using family, twin, and adoption studies suggest that the persistent form of ADHD is familial and that it is more familial than the non-persistent form.
The adult, or persistent form of ADHD appears to have an even stronger genetic component than the child form based on the significantly higher genotype relative risk of 19 to 26.
The epigenetic aspect to ADHD involves a multiplicity of complex genotyped entities, environmental realities, and endophenotypes that interact to express the gene structural material, the symptom-profiles inherent to disorder pathophysiology, and the eventual responses to the therapeutic intervention, namely methylphenidate.
Separating BD from ADHD in adults is often understood by looking for the periodic nature of BD as opposed to the rather consistent symptomatic representation seen in ADHD. One of the main challenges to this diagnostic strategy relates to the fact that juvenile BD follows a different developmental course than in adults. In children, BD is often described as a continuous, non-episodic irritable mood, which contrasts from the clinical presentation seen in adult BD. When these symptoms are accepted as signs of bipolar disorder in children and teenagers, the prevalence reaches 0.3%.