Samenvatting ADD, ODD/CD artikelen
https://bb.vu.nl/bbcswebdav/pid-2971617-dt-content-rid-
6834522_2/courses/FGB_P_BPEDNEU_2016_140/ADHD_Faraone_2015_NatureReviews.pdf
1. Attention-deficit/hyperactivity disorder – Faraone (2015)
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder that
affects 5% of children and adolescents and 2.5% of adults worldwide. Throughout an individual’s
lifetime, ADHD can increase the risk of other psychiatric disorders, educational and occupational
failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or
sufficient to cause ADHD. In most cases ADHD arises from several genetic and environmental risk
factors that each have a small individual effect and act together to increase susceptibility. The
multifactorial causation of ADHD is consistent with the heterogeneity of the disorder, which is shown
by its extensive psychiatric co-morbidity, its multiple domains of neurocognitive impairment and the
wide range of structural and functional brain anomalies associated with it. The diagnosis of ADHD is
reliable and valid when evaluated with standard criteria for psychiatric disorders. Rating scales and
clinical interviews facilitate diagnosis and aid screening. The expression of symptoms varies as a
function of patient developmental stage and social and academic contexts. Although there are no
curative treatments for ADHD, evidenced-based treatments can markedly reduce its symptoms and
associated impairments. For example, medications are efficacious and normally well tolerated, and
various non-pharmacological approaches are also valuable. Ongoing clinical and neurobiological
research holds the promise of advancing diagnostic and therapeutic approaches to ADHD.
Attention-deficit/hyperactivity disorder (ADHD; also known as hyperkinetic disorder) is a common
disorder characterized by inattention or hyperactivity– impulsivity, or both.
ADHD also affects adults. Although the majority of children with ADHD will not continue to meet the
full set of criteria for ADHD as adults, the persistence of either functional impairment or subthreshold
(three or fewer) impairing symptoms into adulthood is high.
Recent alterations to diagnostic criteria have had an impact on ADHD prevalence measures in both
young and adult populations. In 2013, DSM-5 included three important changes:
1) Increasing the age of onset from 7 years to 12 years
2) Decreasing the symptom threshold for patients ≥17 years of age from six to five symptoms
3) Enabling ADHD to be diagnosed in the presence of an autism spectrum disorder.
Sociodemographic factors
In children and adolescents, ADHD predominantly affects males and exhibits a male-to-female sex
ratio of 4:1 in clinical studies and 2.4:1 in population studies.
Although the true prevalence of ADHD does not vary with ethnicity, some studies have inconsistently
associated ethnicity with ADHD owing to referral patterns and barriers to care that
disproportionately affect particular ethnic groups.
Mechanisms/pathophysiology
ADHD runs in families, with parents and siblings of patients with ADHD showing between a fivefold
and tenfold increased risk of developing the disorder compared with the general population.
Environmental risk factors play their greatest part in the non-shared familial environment and/or act
through interactions with genes and DNA variants that regulate gene expression.
1
https://bb.vu.nl/bbcswebdav/pid-2971617-dt-content-rid-
6834522_2/courses/FGB_P_BPEDNEU_2016_140/ADHD_Faraone_2015_NatureReviews.pdf
1. Attention-deficit/hyperactivity disorder – Faraone (2015)
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a persistent neurodevelopmental disorder that
affects 5% of children and adolescents and 2.5% of adults worldwide. Throughout an individual’s
lifetime, ADHD can increase the risk of other psychiatric disorders, educational and occupational
failure, accidents, criminality, social disability and addictions. No single risk factor is necessary or
sufficient to cause ADHD. In most cases ADHD arises from several genetic and environmental risk
factors that each have a small individual effect and act together to increase susceptibility. The
multifactorial causation of ADHD is consistent with the heterogeneity of the disorder, which is shown
by its extensive psychiatric co-morbidity, its multiple domains of neurocognitive impairment and the
wide range of structural and functional brain anomalies associated with it. The diagnosis of ADHD is
reliable and valid when evaluated with standard criteria for psychiatric disorders. Rating scales and
clinical interviews facilitate diagnosis and aid screening. The expression of symptoms varies as a
function of patient developmental stage and social and academic contexts. Although there are no
curative treatments for ADHD, evidenced-based treatments can markedly reduce its symptoms and
associated impairments. For example, medications are efficacious and normally well tolerated, and
various non-pharmacological approaches are also valuable. Ongoing clinical and neurobiological
research holds the promise of advancing diagnostic and therapeutic approaches to ADHD.
Attention-deficit/hyperactivity disorder (ADHD; also known as hyperkinetic disorder) is a common
disorder characterized by inattention or hyperactivity– impulsivity, or both.
ADHD also affects adults. Although the majority of children with ADHD will not continue to meet the
full set of criteria for ADHD as adults, the persistence of either functional impairment or subthreshold
(three or fewer) impairing symptoms into adulthood is high.
Recent alterations to diagnostic criteria have had an impact on ADHD prevalence measures in both
young and adult populations. In 2013, DSM-5 included three important changes:
1) Increasing the age of onset from 7 years to 12 years
2) Decreasing the symptom threshold for patients ≥17 years of age from six to five symptoms
3) Enabling ADHD to be diagnosed in the presence of an autism spectrum disorder.
Sociodemographic factors
In children and adolescents, ADHD predominantly affects males and exhibits a male-to-female sex
ratio of 4:1 in clinical studies and 2.4:1 in population studies.
Although the true prevalence of ADHD does not vary with ethnicity, some studies have inconsistently
associated ethnicity with ADHD owing to referral patterns and barriers to care that
disproportionately affect particular ethnic groups.
Mechanisms/pathophysiology
ADHD runs in families, with parents and siblings of patients with ADHD showing between a fivefold
and tenfold increased risk of developing the disorder compared with the general population.
Environmental risk factors play their greatest part in the non-shared familial environment and/or act
through interactions with genes and DNA variants that regulate gene expression.
1
