ADHD affects you or your children

ADHD in childhood and adolescence. Update 2020

Summary

Attention Deficit Hyperactivity Disorder (ADHD) is a common, chronic neuropsychiatric disorder with a genetic background, multiple comorbidities, and a wide range of individual and social impairments. Despite numerous positive characteristics and mostly successful drug therapy, there are long-term, individual abnormalities and dysfunctions and cause a significant impairment of quality of life even in adulthood. Unsolved problems are mainly transgenerational social burdens, severe forms with comorbid disorder of social behavior, therapeutic failures and non-compliance as well as the question of effective prevention. The overview article tries to summarize the findings of the last 10 years and to give an insight into the complexity of the conditions, effects, diagnostics and therapy.

Abstract

Attention deficit hyperactivity disorder (ADHD) is a frequently observed, chronic neuropsychiatric condition with a genetic background, multiple comorbidities, and a wide spectrum of individual and social impairments. In spite of numerous positive characteristics and mostly successful medical treatment, long-term individual problems and deficits persist and cause significant impairment of quality of life, even in adulthood. In particular, unresolved problems consist of transgenerational social burdens, unfavorable trajectories with comorbid disturbance of social behavior, therapeutic failure, and non-compliance, as well as the question of effective prevention. In this review we try to summarize important research of the last 10 years and to provide an insight into the complexity of the conditions, impact, diagnostics and therapy.

Attention Deficit Hyperactivity Disorder (ADHD) is a genetic [21, 67, 111, 141, 233, 319] chronic disorder that is characterized by a wide range [212] of persistent attention problems, hyperactivity, impulsivity and a disorder of emotion regulation [64, 68, 111, 310] as well as various comorbid problems [222], e.g. B. Social behavior disorder (SSV), dysexecutive [266], cognitive [239] and partial performance problems, anxiety and tic disorders. Problems not only affect neural or intellectual function and performance, but also behavior and family and social integration [128, 154]. Twin studies, genetic linkage and genome-wide association studies confirm a heredity of about 72–80%, of which at least one third of those affected involve several genes.

According to the DSM-5 classification (314.00‑2; [10]) and the ICD-11 classification (6A05.0‑2; [350]), three types are distinguished according to the main symptoms: inattentive, hyperactive-impulsive and a combined type that includes the symptoms of both types. The hyperactive-impulsive type is seen as a preliminary stage of the combined type. The frequent combination, ADHD with disorder of social behavior, is also coded in both classification systems, with a lighter, oppositional (DSM ‑ 5 313.81 or ICD-11 6C9) and a more severe, dissocial behavior disorder (DSM ‑ 5 312.81,2,9 and ICD-11 6C91).

ADHD affects at least 3–6% of all school children [263] and has serious psychological and social consequences even in adulthood [136, 173]. There are phenotypic gender differences: in boys who are more likely to show the impulsive-hyperactive or combined type, ADHD is diagnosed about 3 times more often than in girls who are more likely to show the inattentive type. The background of these differences is unclear; methodological influences [346], influences of the Y chromosome and sex hormones on brain development [194], differences in the excitatory glutamate system [339] and gender-specific different stress processing [23] are discussed. There are also geographical differences in prevalence [297], although methodological (e.g. differences in the diagnostic criteria of the ICD and DSM classifications, clinical vs. epidemiological samples) than human genetic or environmental causes are likely to cause these differences. The combined clinical picture, ADHD with disorder of social behavior, causes a worse prognosis [40, 186, 254]. ADHD affects family and social life, school success, friendships [128, 175, 220], job prospects and subjective well-being [53], increases the likelihood of eating disorders (obesity and anorexia nervosa; [226, 232]) and causes considerable intra-family and economic costs [48, 313, 315]. Drug therapy brings clear advantages for quality of life [75, 87, 127] and future prospects and in any case also cost advantages [351]. There are also associated strengths of ADHD, such as diverse interests, energy, perseverance, humor, charm, authenticity, creativity, spontaneity, sensitivity, courage, willpower, emotional stress and prosocial behavior [195, 206, 285].

ADHD can be treated [22, 50, 60, 94, 132, 224, 244, 246]: stimulants, especially methylphenidate (MPH; [74]) as well as amphetamine and lisdexamphetamine [124, 304], the norepinephrine reuptake inhibitor, atomoxetine (ATX , [289]), and that α2Receptor-stimulating guanfacine ER [Hirota14] show different, medium to high potency, but also side effects (circulatory problems, poor appetite, occasionally increased aggressiveness, sleep disorders). However, these drugs are able to significantly improve the ADHD symptoms in around 80% of children. Alternative drug therapies, e.g. B. that α2-Sympathomimetic clonidine, have lower potency or are ineffective like omega-3 fatty acids or homeopathy, while additional therapies such as psychotherapy (e.g. the therapy program for children with hyperkinetic and oppositional problem behavior, THOP [100]), parental, partial performance training, Anti-aggression or occupational therapy can be helpful if there is a corresponding comorbid indication.

The thesis aims to provide a subjective, practice-oriented overview of recent developments on the subject of ADHD on the basis of selected literature citations.

Methods

The present work is based on a systematic literature search, using the PubMed database for the keyword ADHD (38,228 hits), restricted to the last 10 years (21,240 hits), review articles (2931 hits), "children" (1752 hits) and English ( 1576 hits) was searched. The remaining 1576 papers were screened with regard to their quality, topic relevance according to title or abstract (remaining papers 224) and supplemented by additional, topic-related researched papers (n = 199) added. Of these 423 papers, 360 were used in this article (Fig. 1).

Results

etiology

ADHD is a spectrum disorder, i. H. there is a multitude of clinical manifestations, degrees of severity, comorbidities and courses as well as considerable aetiological heterogeneity [228, 315]. Structurally, there are global abnormalities, in particular delayed brain development with cortical mass reduction especially in the frontal lobe, further thalamic and cerebellar structural deficits, networking problems of long tracts [332] and microstructure anomalies frontal, temporal and parietal [7, 112, 267, 330]. Functional deficits affect activation and connectivity in these areas [125]. There is also overlap with autism spectrum disorder [319].

Genetically and epigenetically determined problems in the catecholamine neurotransmitter metabolism are seen as the cause, which cause a reduced dopaminergic inhibitory function of the (right-sided) prefrontal, cingulate and temporal cortex as well as in the striatum [148, 174, 219, 283]. The prefrontal cortex is responsible for executive (EF) and social functions, the cingulum for attention and selection control. Dopaminergic neurons are essentially responsible for motivation, learning, maintaining goal-oriented behavior and, in short-term memory [277], noradrenaline neurons for activating and controlling attention [18]. In addition, structural and functional deficits in the default mode network [29] and in the glutamate system [160] were described. Killeen et al. [172] see the basic pathology in an energy deficit of active neurons, whose lactate energy supply by noradrenaline-dependent glial cells functions only inadequately.

ADHD is inherited polygenically to a high degree (around 80% [88, 135, 141, 319])Footnote 1 [355]. Parents with ADHD have a greater than 50% chance of having a child with ADHD [109].

However, there are also clear indications of environmental risk factors [6, 210]. Pre- and perinatal factors (especially prematurity and perinatal complications; [119, 227, 264, 288, 298]) as well as questionable air pollution [96, 223], lead exposure [54, 105] and oxidative stress [327]. Changes in the microbiome [57] can also cause or intensify ADHD. For example, regardless of the genetic risk, the risk of the occurrence [95, 155, 159] of ADHD and more severe forms of ADHD [323] seems to increase in a dose-dependent manner. The fetal alcohol syndrome [92, 165] is associated with reduced growth of prefrontal and temporal areas, intrauterine oxygen and iron deficiency [32], hyperbilirubinemia [303], iodine deficiency and hypothyroxinemia [328] or treatment with thyroxine during pregnancy [121] possibly affect the dopaminergic system. Temporal and frontal brain damage or damage to the caudate nucleus or to the frontostriatal pathways can also cause ADHD in the context of apoplexy, bleeding, injuries or as a result of infections [153, 211]. Emotional neglect in early childhood [360] also represents an increased risk of ADHD, although the likely increased genetic risk in the examined population of Romanian orphans was not analyzed independently. Intelligence [265], socio-economic [270] and family factors [268] as well as breastfeeding [25] are seen as protective.

ADHD is characterized by phenotypic heterogeneity, the exact genetic and pathophysiological background of which is currently the subject of intensive research [83]. According to Barkley [26], the cardinal symptoms can be traced back to executive inhibition deficits, problems of working memory, perception [126], self-regulation, the internalization of language as well as behavior analysis and synthesis, whereby experimentally the inhibition of planned activities (stop or go - / no-go tasks) appears impaired. Above all, the deficient behavioral inhibition and problems in working memory are decisive [9]. This model has also been repeatedly confirmed experimentally (e.g. [348]). Another model [272] sees problems in the reward system (delayed reward) and the associated motivation difficulties as primary defects that cause numerous subsequent problems. Sonuga-Barke, et al. [299, 301] have developed a dual-pathway model from these two models, which addresses functional and motivational, but also environmental problems and adaptation processes (e.g. in the context of parent-child interaction or the behavior of parents [- share] with [untreated] ADHD [235]). Sonuga-Barke and Halperin [300] tried to develop prevention strategies based on this model. Singh [297] explains the diversity of ADHD from the perspective of a biopsychosocial model. Overall, increased genetic and environmental risk seem to complement each other: the greater the number of risk factors, the greater the degree of ADHD [41] as well as the number and severity of comorbid problems [201]; on the other hand, the greater the number of resilience factors, the better the prognosis.

Boys are represented much more strongly in clinical samples (around 9–10: 1), with the prevalence ratio in epidemiological field studies being 2–3: 1. This difference is probably due to the increased combination of ADHD with behavioral problems in boys (boys: girls = 20%: 8%; [38]) and the high number of unreported cases in girls because of the less noticeable clinical symptoms (predominantly inattentive type).

Clinic and comorbidities

In addition to the cardinal symptoms, the clinical diversity of ADHD is also influenced by age ([14, 118, 156, 314, 342]; Table 1 and environmental conditions; see Section 1).

Multiple comorbid, internalizing and externalizing problems as well as neurocognitive deficits [239] also determine the clinical picture. They should be carefully clarified and taken into account in therapy [12, 42, 326]. Only one third of the children of the 579 children in the Multimodal Treatment Study of Children with Attention Deficit Hyperactivity Disorder (MTA [297]) had no comorbid problemsFootnote 2 examined 500 children with ADHD [230] this was only 4%! The most common comorbid problems are dysexecutive [169]; 99.6% in their own clinical patient population, SI 6–16% [34]), partial performance (78% in own patient population), perception [126] and language development disorders (7% in own patient population), SSV of the oppositional type ( over 50%), severe depression and anxiety disorders (one third each) and tics (11–20%). Recent work [55] shows a link between ADHD, emotional or sexual trauma, and the development of borderline personality disorder. Individual patient groups have significantly higher ADHD prevalences: for example, ADHD and intelligence are negatively correlated [265], patients with chronic tic disorders (55% of children with chronic tic disorders have a comorbid diagnosis of ADHD [120], 20% of ADHD children develop a chronic tic disorder [45]), depressive episodes (70% [37]) and patients from the autism spectrum (about 36–50%; [149]). ADHD is a risk factor for accidents and injuries [269