Attention-deficit/hyperactivity disorder (ADHD) behaviour explained by dysfunctioning reinforcement and extinction processes

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Abstract

Inattentiveness, overactivity and impulsiveness are presently regarded as the main clinical symptoms of attention-deficit/hyperactivity disorder (ADHD). Inattention is, however, a characteristic of most psychiatric disorders. It is argued that the ADHD Inattentive subtype may have heterogeneous origins and be qualitatively different from the ADHD Hyperactive/Impulsive subtype. At the neurobiological level, ADHD symptoms may to a large extent be caused by a dysfunctioning dopamine system: A dysfunctioning meso-limbo-cortical dopamine branch will produce altered reinforcement and extinction processes, on a behavioural level giving rise to deficient sustained attention, hyperactivity, motor and cognitive impulsiveness. A dysfunctioning nigro-striatal dopamine branch will cause ‘extrapyramidal’ symptoms. Our model disentangles the behaviours usually explained by ‘executive functions’ into cognitive impulsiveness, motor impulsiveness and deficient motor control. The various dopaminergic branches may not be equally dysfunctional in all individuals with ADHD. Etiologically, dopamine dysfunctioning will probably mainly be genetically determined while sometimes be induced by environmental factors like drugs of abuse or pollutants, which may explain geographical differences in prevalence rates.

Introduction

Attention-deficit/hyperactivity disorder (ADHD) [1] is a seemingly heterogeneous group of behaviour disorders affecting between 2 and 5% of grade-school children [65], [69]. The disorder usually manifests itself before the child is 7 years old. In childhood, the disorder is more common in boys than in girls, but during adolescence and young adulthood relatively more females are affected [4]. Of children diagnosed with ADHD, 50–70% will have problems related to social adjustment and functioning and/or psychiatric problems as adolescents and young adults [6], [76] while the full ADHD syndrome is found in only 4% of the adult population [30].

Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms of ADHD [1]. Although there is considerable overlap between these symptoms, impulsiveness is increasingly seen as the symptom of greatest significance [69]. Admittedly, the symptoms are not that well defined and requirements vary somewhat between the ICD and DSM taxonomies [65], [69]. According to DSM-IV criteria, it is possible to have ‘ADHD’ without being inattentive. Inattentiveness is, however, a necessary requirement for a hyperkinetic disorder according to ICD-10 criteria [69].

ADHD is associated with altered dopamine function [15], [21], [28]. We will argue that the ADHD symptoms, to a large extent, are caused by dysfunctioning dopamine branches impairing non-dopaminergic signal transmission (Fig. 1):

  • 1

    A dysfunctioning meso-limbo-cortical dopamine branch will produce altered reinforcement and extinction processes, on a behavioural level giving rise to deficient sustained attention, hyperactivity, behavioural variability, motor and cognitive impulsiveness.

  • 2

    A dysfunctioning nigro-striatal dopamine branch will cause poor motor control.

Section snippets

Deficient sustained attention

It seems that perceptual processes are not altered in ADHD [58]. The attention problems of children with ADHD are typically described as ‘distractibility’ and trouble with ‘sustaining attention’ [18]. It is not convincingly established, however, that children with ADHD have attention problems in the same sense as seen in non-hyperactive, rather dreamy, inert children with attention problems [69].

The problems related to sustained attention occur in situations where stimuli are widely spaced in

Reinforcement, extinction, and the role of dopamine

The behaviour of children with ADHD and normal children is differently affected by reinforcement contingencies [20], [27], [63], [74]. It has been argued that the key features of ADHD, deficient sustained attention, overactivity, and impulsiveness, may all be due to altered reinforcement mechanisms and a shorter delay-of-reinforcement gradient [46], [48].

A stimulus is a positive reinforcer if its presentation increases the probability of future occurrence of the responses that produced it. The

Behaviour explained by dysfunctioning dopamine systems

Dopamine, like the other monoamines, is a neuromodulator that modulates the actions of neurotransmitters like glutamate. The dopaminergic system has two main branches: the meso-limbo-cortical originating in the ventral tegmental area and projecting to the prefrontal cortex, the nucleus accumbens septi, and the olfactory tubercle; and the nigro-striatal branch originating in the substantia nigra and projecting mainly to the neostriatum (the caudate–putamen complex). There are five distinct

Aetiology

Family and twin studies provide convincing evidence for a genetic component in ADHD (for a review see [51]). There are, however, geographic variations in the percentage of children receiving an ADHD diagnosis [69]. Some of this variation could be due to different referral practises and different diagnostic criteria [65], but this might not be the whole story.

As argued above, it is likely that dopamine dysfunction plays a pivotal role in the neurobiology of ADHD (Fig. 1). Therefore, ADHD-like

Conclusions

At the neurobiological level, ADHD symptoms may to a large extent be caused by a dysfunctioning dopamine system [48]. A dysfunctioning meso-limbo-cortical dopamine branch will produce altered reinforcement and extinction processes that, on a behavioural level, give rise to deficient sustained attention, hyperactivity, increased behavioural variability, and impulsiveness. A dysfunctioning nigro-striatal dopamine branch will cause poor motor control. Etiologically, dopamine dysfunctioning will

Acknowledgements

This work was supported by grants from Dr Letten F. Saugstad's Fund (Espen Borgå Johansen), The National Council for Mental Health-Norway (Heidi Aase), and The Norwegian Council of Development Research and Education (Anneke Meyer).

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