Functional Neuroimaging Evidence for Distinct Neurobiological Pathways in Attention-Deficit/Hyperactivity Disorder.

Functional Neuroimaging Evidence for Distinct Neurobiological Pathways in Attention-Deficit/Hyperactivity Disorder.
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DOI:
10.1016/j.bpsc.2017.09.005
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发表时间:
2018-08
期刊:
Biological psychiatry. Cognitive neuroscience and neuroimaging
影响因子:
--
通讯作者:
Bessette KL
Bessette KL
中科院分区:
其他
文献类型:
--
作者:
Stevens MC;Pearlson GD;Calhoun VD;Bessette KL

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临床神经科学家面临的一个挑战是,如何最好地将精神疾病中发现的神经心理缺陷和脑系统功能障碍的各种证据(有时是不一致的证据)综合到指导病因学和治疗研究的模型中。多通路模型提示精神症状可能是由不同神经系统的病理生理引起的。本研究测试了“双通路”模型对注意缺陷多动障碍(ADHD)的预测,即奖励和执行功能认知缺陷应该与相应功能特异性神经系统的异常有关。对N=251名年龄在12-18岁、诊断为DSM-IV合并亚型ADHD或非ADHD对照的青春期男孩和女孩进行行为抑制和对即时奖励的偏好评估。在对测试表现进行分类分析后,对结果亚组进行了fMRI货币激励延迟任务探测奖励预期和运动反应抑制的Go/NoGo任务的比较。三个ADHD亚组被确定为符合不同的建议途径- ADHD伴有执行功能/运动抑制缺陷,ADHD伴有执行和奖励缺陷,以及ADHD具有相对正常的测试表现。正如预期的那样,每个认知领域都映射到不同的ADHD脑功能障碍特征。然而,没有发现所有ADHD亚组都有共同的大脑异常,尽管事实上他们有几乎相同的ADHD相关临床特征。结果表明,合并亚型ADHD是一系列离散的疾病,其相似的行为终点是通过不同的神经生物学途径产生的。研究结果提出了将共同原因、单一缺陷概念模型应用于个体ADHD患者的警告,并应促使研究人员考虑将生物学定义的多因素病因模型应用于其他精神疾病诊断。
A challenge facing clinical neuroscientists is how best to synthesize diverse and sometimes inconsistent evidence for neuropsychological deficits and brain system dysfunction found in psychiatric disorders into models that guide etiological and treatment research. Multiple pathway models suggest psychiatric symptoms might arise from pathophysiology in different neural systems. This study tested “dual pathway” model predictions for Attention Deficit Hyperactivity Disorder (ADHD) that reward and executive function cognitive deficits should be related to abnormalities in corresponding functionally-specialized neural systems. Behavioral inhibition and preference for immediate rewards were assessed in N=251 adolescent boys and girls ages 12–18 diagnosed with DSM-IV Combined-subtype ADHD or non-ADHD controls. Following taxometric analyses of test performance, the resulting subgroups were compared on an fMRI Monetary Incentive Delay task probing reward anticipation and Go/NoGo task of motor response inhibition. Three ADHD subgroups were identified consistent with different proposed pathways – ADHD with executive function/motor inhibition deficits, ADHD with both executive and reward deficits, and ADHD with relatively normal test performance. Each cognitive domain mapped to different ADHD brain dysfunction features as expected. However, no brain abnormalities were found common to all ADHD subgroups despite the fact they had nearly identical ADHD-related clinical characteristics. The results suggest Combined-subtype ADHD is a collection of discrete disorders for which a comparable behavioral endpoint arises through different neurobiological pathways. The findings raise caution about applying common cause, single-deficit conceptual models to individual ADHD patients and should prompt researchers to consider biologically-defined, multifactorial etiological models for other psychiatric diagnoses.
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