QUANTITATIVE-CLINICAL STUDIES OF MINOR ANOMALIES IN ADHD

这个项目探讨了轻微的身体异常之间的关系 注意力缺陷多动障碍（ADHD）。 这些小 畸形特征可能具有重要的诊断意义，表明 形态发生改变或特定畸形的一般分类 综合征 我们的主要目标是应用定量和临床MPA ADHD男孩的诊断方法。 我们曾研究 选择单个MPA的组合以反映胚胎学因素。 由于脑和颅面形态起源于共同的原基， 是由共同的力量塑造的，假设一种病理性的 过程导致精神病理学和畸形学。 因此，在本发明中， 特定类型的畸形可以描述大脑发育不良， 多动症。 在这个项目的第一阶段，我们发现了具体的 ADHD中的胚胎学确定的MPA类别，反映了特定的 发展机制： (a)畸形发生的时间起源， (b)改变类型（畸形与变形），以及 (c)产生MPA的特定胚胎原基（“原基”）。 在下一阶段的研究中，我们建议将这些发现扩展到 回答以下问题： (1)ADHD患者的畸形表型是否因 对兴奋剂的反应 初步研究表明， 有利和不利的反应者是畸形的，但在 不同的生物学解释方式。 (2)ADHD畸形的模式和程度在男孩身上发现了吗 也出现在女孩身上？ 初步数据显示， 畸形 (3)ADHD患者的颅面MPAs和脑畸形是否相关， 就像它们的胚胎学关系所预测的那样 我们将 确定ADHD患者的大脑形态是否异常（a） 通常，或（B）作为药物反应函数，和（c） 大脑和颅面畸形的模式是否一致 在（a）和（B）中的受试者内。

This project explores the relationship between minor physical anomalies (MPAs) and Attention-deficit Hyperactivity Disorder (ADHD). These minor dysmorphic features may be of major diagnostic significance, indicating general classes of altered morphogenesis or specific malformation syndromes. Our primary goal has been to apply quantitative and clinical MPA diagnostic methods to a population of ADHD boys. We have examined combinations of individual MPAs chosen to reflect embryological factors. Since brain and craniofacial morphology arise from common primordia and are molded by shared forces, it is hypothesized that a pathological process results in both psychopathology and dysmorphology. Thus, specific classes of dysmorphology may delineate brain maldevelopment in ADHD. In the first stage of this project, we have found specific embryologically-determined classes of MPAs in ADHD, reflecting specific developmental mechanisms: (a) the chronological origin of dysmorphogenesis, (b) type of alteration (malformation versus deformation), and (c) specific embryonic primordia ("Anlagen") giving rise to MPAs. In our next stage of research, we propose to extend these findings to address the following questions: (1) Do dysmorphic phenotypes differ for ADHD patients as a function of response to stimulant medication? Pilot studies suggest that both favorable and non-favorable responders are dysmorphic, but in different, biologically interpretable ways. (2) Are the patterns and extent of ADHD dysmorphology found in boys also present in girls? Preliminary data suggest that they too are dysmorphic. (3) Are craniofacial MPAs and brain dysmorphology correlated in ADHD, as predicted by their embryological relationship? We will determine whether brain morphology is abnormal in ADHD patients (a) in general, or (b) as a function of medication response, and (c) whether patterns of brain and craniofacial dysmorphology cohere within subjects in (a) and (b).