Neurobiologische Grundlagen der Aufmerksamkeitsdefizit-/Hyperaktivitätsstörung

Abstract

The origin of ADHD is multifactorial and both the aetiology and pathophysiology of ADHD are as yet incompletely understood. The monoamine deficit hypothesis of ADHD postulates a dysbalance in the interaction of the neurotransmitters dopamine, noradrenaline and serotonin. Pathophysiological mechanisms involved in ADHD include alterations in fronto-striatal circuits. The currently proposed animal models of ADHD are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. Some evidence points to a genetic basis for ADHD which is likely to involve many genes of small individual effects. In summary, specific neurobiological substrates of ADHD are unknown and multiple genetic and environmental factors appear to act together to create a spectrum of neurobiological liability.

Attention-deficit/hyperactivity disorder associated with KChIP1 rs1541665 in Kv channels accessory proteins

“…KCNIP1 gene (also known with its alias name KChIP1 ) encodes the potassium channel-interacting protein 1 (KChIP1), which is expressed predominantly in the brain, with relative abundance in cerebellum, hippocampus, striatum, and the reticular thalamic and medial habenular nuclei [ 43 ]. Abnormal function in cerebellum, hippocampus, and striatum has been known to be involved in ADHD risk [ 44 ]. KChIP1 was traditionally thought an auxiliary subunit of the protein complex Kv4.2 and Kv4.3 channels in neurons, and it has been reported to be able to dramatically increase the surface expression and slow the turnover of the Kv 4 protein, as well as increase the rate of recovery from the inactive state of Kv 4.2/4.3 channels, thereby reducing neuronal excitability [ 45 , 46 ].…”

Spektrum und Häufigkeit von ADHS-Syndromen und Teilleistungsstörungen bei Patienten in der psychosomatischen Rehabilitation

“…Die Daten zeigen zunächst einmal die Probleme in der Diagnostik von ADHS und Teilleistungsstörungen und machen nachvollziehbar, warum dieser Störungstyp seit etwa 100 Jahren die Psychiatrie und Neurologie und speziell auch die Kinder-und Jugendpsychiatrie beschäftigt und warum seine Existenz immer infrage gestellt wurde, um dann unter jeweils neuem Namen wieder aufgegriffen zu werden, wie bspw. als "komplexe Teilleistungsstörung" [32], "Minimale Zerebrale Dysfunktion" [33], "Minimal Brain Dysfunction" [34,35], "leichtes organisches Psychosyndroms" [36,37], "psychoorganisches Achsensyndrom [38], "mild cognitive impairment" [39], "Entwicklungsstörung" [40] oder "entwicklungsbiologische Störung" [41]. Zunächst stellt sich die Frage, ab wann eine Beschwerde als Krankheitssymptom zu werten ist.…”

“…Ggf. sind dann auch zusätzliche diagnostische Untersuchungen angezeigt, einschließlich detaillierten neuropsychologischen [43,44], -physiologischen [41,45], -radiologischen [41] oder neurologischen Untersuchungen [46,47].…”

Yoga and the Therapy of Children with Attention Deficit Hyperactivity Disorder

“…The etiology of ADHD is unknown and appears to be multifactorial. Specific neurobiological correlates of ADHD or biomarkers have not been identified and multiple factors including genetics and environment appear to interact and cause neurobiological liability [4,5]. Some evidence points to a genetic basis of ADHD which is likely to involve many genes with minor individual effects [6].…”