HANDEDNESS SUBTYPES--BIOLOGICAL MARKERS IN AUTISM

拟议的目标有以下目标：(1)确定是否 在未选择的样本中，利手的分布发生了变化 自闭症儿童和成人；(2)如果是，确定其潜在的 构造；(3)确定构造是否为自闭症所特有 或者更广泛地说，它们与整体精神发育迟滞有关 与自闭症症状无关，以及(4)确定这些 表型提供了不同的潜在神经生物学标记 疾病内部或疾病之间的病因亚组。 受试者将由两个未经选择的自闭症样本组成，具体如下：(A) 加州大学洛杉矶分校样本(n=50)，包含更年轻和更高功能的 门诊组；(B)卡马里洛样本(n=80)，其中包括一名年长的和 低功能住院组。两个功能更低和更高的MR 非自闭症样本将从加州大学洛杉矶分校和卡马里洛州立大学挑选 医院作为对比，与两个目标样本匹配。 研究设计包括严格的一周测试-重测评估 对发育迟缓的SS使用多项常模的利手。 这些措施将被用来调查目标1-3，基本上 涉及识别不同的惯用手表型。独一无二的 这个项目的特点，包括对惯用手的评估，关注的问题 PLH模型的一个扩展(Satz，1972)以处理多手持手 表型。这个修订后的模型提供了一个概念性的和定量的 处理自闭症潜在病因亚群的框架 和/或MR对象。 子类型将首先根据外部行为标准进行验证 以确定它们是否与不同的神经行为结果相关 (例如，适应性行为、智力、家族性利手、营养 肢体的变化)。如果出现组内差异，初步确定 结果表明，然后每个表型的随机子集将被给予高 分辨率计算机断层扫描以确定这些表型 作为病原学亚型的生物标志物是否具有任何意义 婴儿自闭症。该提案试图解释一些已知的 长期困扰这种疾病研究的异质性(S)。

The proposed objectives have the following aims: (1) to determine whether a shift in the distribution of handedness exists in an unselected sample of autistic children and adults; (2) if so, to determine its underlying constructs; (3) to determine whether the constructs are specific to autism or whether they relate more generally to overall mental retardation irrespective of autistic symptomatology and (4) to determine whether these phenotypes provide potential neurobiological markers of different etiological subgroups within or between disorders. Subjects will consist of two unselected autistic samples as follows: (a) UCLA Sample (n=50) which comprises a younger and higher functioning outpatient group; (b) Camarillo Sample (n=80) which comprises an older and lower functioning inpatient group. Two lower and higher functioning MR non-autistic samples will be selected from UCLA and Camarillo State Hospital as comparison matches for the two target samples. The research design involves a rigorous one week test-retest assessment of handedness using multiple items normed for developmentally retarded Ss. These measures will be used to investigate Aims 1-3 which essentially involve the identification of various handedness phenotypes. A unique feature of this project, including the assessment of handedness, concerns an extension of the PLH model (Satz, 1972) to deal with multiple handedness phenotypes. This revised model provides a conceptual and quantitative framework for dealing with potential etiological subgroups of autistic and/or MR subjects. The subtypes will first be validated against external behavioral criteria to determine whether they correlate with different neurobehavioral outcomes (e.g., adaptive behavior, intelligence, familial handedness, trophic changes in extremities). If group differences occur, as preliminary results suggest, then a random subset of each phenotype will be given high resolution computerized tomography to determine whether these phenotypes confer any significance as biological markers of etiological subtypes in infantile autism. The proposal seeks to explain some of the known heterogeneity that has long plagued research in this disorder(s).