Sagvolden Terje, Johansen Espen Borgå, Aase Heidi, Russell Vivienne Ann
Department of Physiology, University of Oslo, NO-0317 Oslo, Norway.
Behav Brain Sci. 2005 Jun;28(3):397-419; discussion 419-68. doi: 10.1017/S0140525X05000075.
Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to "inhibit" responses ("disinhibition"). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological "soft signs," and a "failure to inhibit" responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns.
注意力缺陷多动障碍（ADHD）目前被定义为一种认知/行为发育障碍，其所有临床标准均为行为性的。注意力不集中、多动和冲动目前被视为主要临床症状。动态发育行为理论基于这样一种假设，即多巴胺能功能改变通过未能适当调节非多巴胺能（主要是谷氨酸和γ-氨基丁酸）信号传递而发挥关键作用。中脑边缘多巴胺分支功能低下会导致行为强化改变以及先前强化行为的消退不足。这会导致延迟厌恶、在新情境中多动的发展、冲动、持续注意力不足、行为变异性增加以及无法“抑制”反应（“去抑制”）。中脑皮质多巴胺分支功能低下会导致注意力反应缺陷（定向反应不足、扫视眼动受损以及对目标的注意力反应较差）和行为规划不佳（执行功能差）。黑质纹状体多巴胺分支功能低下会导致运动功能调节受损以及非陈述性习惯学习和记忆不足。这些损伤会导致明显的发育延迟、笨拙、神经学“软体征”以及在需要快速反应时无法“抑制”反应。多巴胺分支功能低下是当前理论中的主要个体易患因素。该理论预测，ADHD中的行为和症状是个体易患因素与周围环境相互作用的结果。在生命中的特定时间，确切的ADHD症状会有所不同，并受到对症状发展有正面或负面影响的因素影响。学习和运动功能的改变或不足会对最佳育儿和社会方式产生特殊需求。药物治疗将在一定程度上使潜在的多巴胺功能障碍正常化，并减少这些儿童的特殊需求。该理论描述了个体易患因素如何与这些情况相互作用，以产生可转变为相对稳定行为模式的行为、情感和认知效应。
