期刊
NEUROLOGY
卷 59, 期 6, 页码 834-840出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.59.6.834
关键词
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资金
- NICHD NIH HHS [HD35469] Funding Source: Medline
- NIMH NIH HHS [MH01433, MH42969, MH01727] Funding Source: Medline
- NINDS NIH HHS [NS33355] Funding Source: Medline
Objective: To test the hypothesis that deficits in spatial working memory in autism are due to abnormalities in prefrontal circuitry. Methods: Functional MRI (fMRI) at 3 T was performed in 11 rigorously diagnosed non-mentally retarded autistic and six healthy volunteers while they performed an oculomotor spatial working memory task and a visually guided saccade task. Results: Autistic subjects demonstrated significantly less task-related activation in dorsolateral prefrontal cortex (Brodmann area [BA] 9/46) and posterior cingulate cortex (BA 23) in comparison with healthy subjects during a spatial working memory task. In contrast, activation of autistic individuals was not reduced in other regions comprising the neural circuitry for spatial working memory including the cortical eye fields, anterior cingulate cortex, insula, basal ganglia, thalamus, and lateral cerebellum. Autistic subjects also did not demonstrate reduced activation in any brain regions while performing visually guided saccades. Conclusion: Impairments in executive cognitive processes in autism may be subserved by abnormalities in neocortical circuitry as evidenced by decreased activation in prefrontal and posterior cingulate circuitry during a spatial working memory task.
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