BRAIN BEHAVIOR CORRELATES OF ATTENTION DEFICIT IN AUTISM
BRAIN BEHAVIOR CORRELATES OF ATTENTION DEFICIT IN AUTISM
批准号:
2033601
负责人:
ERIC COURCHESNE
金额:
$34.14万
依托单位国家:
美国
项目类别:
财政年份:
1990
资助国家:
美国
项目状态:
已结题
起止时间:
1990-08-01 至 1999-11-30
中文摘要
描述(摘自申请者的摘要):儿童自闭症
是一种神经生物学疾病,在这种疾病中,许多高等
认知、情感和交际功能严重受损
被打乱,导致语言、社会和综合缺陷。
直到最近,神经解剖异常可能会
自闭症的神经功能缺陷并不是
系统地调查了。一种强大而又非侵入性的
活体成像方法--磁共振成像--组合
凭借训练有素的定量测量算法,已经取得了
有可能从生活中获得准确和有意义的神经解剖学数据
病人。用这种方法获得的神经解剖学数据的比较
来自同一自闭症患者神经功能研究的数据
对这种疾病有了重要的新见解。
调查人员通过核磁共振成像研究透露,特定的
解剖异常的部位出现在顶叶和
年轻时确诊的自闭症患者的小脑
作为5岁。磁共振成像定量分析及临床应用
神经功能数据表明,这些特定部位的大小
异常与特定注意缺陷的程度有关
行动。例如,顶上区的体积损失量
大脑皮质与行为障碍的程度高度相关
检测位于视觉注意的主要焦点之外的刺激;
这种刺激还会引起视觉神经生理学异常减退
顶叶数目最多的自闭症患者的反应
体积损失。他们的其他研究发现,患有自闭症的患者
最严重的蠕虫异常引导注意力的速度比那些
有较少的蠕虫异常。自闭症患者的平行研究
获得性小脑局灶性病变的患者已经表明,
患者群体在视觉和视觉之间转移注意力的速度异常缓慢
听觉信息,并异常地降低了大脑对
暗示注意力转移的信号。这些发现显示出很大的希望
自闭症患者脑部位与功能关系的研究
在正常的大脑中,但需要仔细确认
设计了这项提案中概述的大脑行为研究。
探讨解剖异常部位与临床表现的关系。
自闭症患者特定注意操作的缺陷,研究人员
建议在自闭症和正常受试者中获得行为和
三种特定手术的神经生理测量--定向,
转移和分散注意力--这是一个统计上的相关性
测量各种大脑、小脑和皮质下的大小
结构。他们还提议获得功能性磁共振成像手段。
为了更直接地识别其缺陷的解剖结构
自闭症患者注意力转移障碍的潜在原因。完成
这项研究将进一步推动他们阐明
自闭症患者神经功能缺陷的解剖学基础。
英文摘要
DESCRIPTION (Adapted from the applicant's abstract): Infantile autism
is a neurobiological disorder in which the development of many higher
cognitive, affective, and communicative functions are severely
disrupted, resulting in language, social, and integrative deficits.
Until recently, the concept that neuroanatomical abnormalities may
underlie the neurofunctional deficits in autism has not been
systematically investigated. The advent of a powerful, yet non-invasive
in vivo imaging method -- magnetic resonance (MR) imaging -- combined
with disciplined quantitative measurement algorithms, has made it
possible to obtain accurate and meaningful neuroanatomic data from living
patients. Comparison of neuroanatomical data obtained in this manner
with data from neurofunctional studies in the same patients with autism
has yielded important new insights into the disorder.
The investigator has disclosed through MR imaging research that specific
sites of anatomical abnormalities are present in the parietal lobe and
in the cerebellum in diagnostically confirmed autistic patients as young
as 5 years of age. Quantitative analysis of MR imaging and
neurofunctional data indicate that the size of these specific sites of
abnormality is related to the degree of deficit in specific attention
operations. For example, the amount of volume loss in superior parietal
cortex is highly correlated with the degree of behavioral impairment in
detecting stimuli located outside a principal focus of visual attention;
such stimuli also elicit abnormally reduced visual neurophysiological
responses in autistic patients with the greatest amount of parietal
volume loss. Their other studies have found that autistic patients with
the most vermian abnormality orient attention more slowly than those who
have less vermian abnormality. Parallel studies of patients with autism
and patients with acquired focal cerebellar lesions have shown that both
patient groups are abnormally slow to shift attention between visual and
auditory information, and have abnormally reduced brain responses to
cues signalling attention shifts. These findings show great promise in
elucidating the relationship between brain site and function in autism
and in the normal brain, but require confirmation in the carefully
designed brain-behavior studies outlined in this proposal.
To explore the relationship between sites of anatomical abnormality and
deficits in specific attention operations in autism, the investigator
proposes to acquire in autistic and normal subjects behavioral and
neurophysiological measures of three specific operations -- orienting,
shifting, and distributing attention -- a statistically correlate these
measures with the size of various cerebral, cerebellar, and subcortical
structures. They also propose to acquire functional MR imaging measures
in order to more directly identify anatomical structures whose deficits
underlie impairment in shifting attention in autism. The completion of
this study will further their long-term objective of elucidating the
anatomical substrate of neurofunctional deficits in autism.
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