Sagvolden T, Sergeant J A
Behav Brain Res. 1998 Jul;94(1):1-10.
This special issue represents an attempt to answer fundamental brain and behaviour issues in attention-deficit hyperactivity disorder (ADHD). The European network on hyperkinetic disorders (Eunethydis) is trying to develop a novel, testable theory of ADHD, giving an account of its causes, its development from brain dysfunctions to behavioural symptoms and co-morbidity and explaining why no current therapy produces long-lasting improvements. The combined insights of the articles presented here suggest that there is no brain damage in ADHD, but hypo-efficient dopamine systems which give rise to neurochemical imbalances. These cause behavioural problems: deficits in sustained attention, overactivity and impulsiveness. Impulsiveness is increasingly being seen as a key characteristic of the disorder. None of these symptoms are necessarily primary, but may be secondary to an underlying deficit in reinforcement processes seen particularly in a greater than normal sensitivity to variations in the timing of stimulus presentation. Other symptoms can also be seen: altered effects of reinforcers, increased behavioural variance and motor co-ordination problems. Medication produces temporary, plastic changes in cellular components like receptors and transduction mechanisms normalising dopamine functions and behaviour. reserved.
本期特刊旨在尝试解答注意力缺陷多动障碍(ADHD)中有关大脑和行为的基本问题。欧洲多动障碍网络(Eunethydis)正试图构建一种全新的、可验证的ADHD理论,阐述其成因、从大脑功能障碍到行为症状及共病的发展过程,并解释为何目前的治疗方法均无法带来持久改善。此处发表的文章综合见解表明,ADHD不存在脑损伤,而是多巴胺系统效率低下,导致神经化学失衡。这些失衡引发行为问题:持续注意力缺陷、多动和冲动。冲动越来越被视为该障碍的关键特征。这些症状不一定是原发性的,可能继发于强化过程中的潜在缺陷,尤其表现为对刺激呈现时间变化的超常敏感。还可观察到其他症状:强化物效果改变、行为变异性增加和运动协调问题。药物治疗会使细胞成分如受体和转导机制产生暂时的、可塑性变化,使多巴胺功能和行为正常化。保留。