Executive functioning, memory, and learning in phenylketonuria
Executive functioning, memory, and learning in phenylketonuria
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DOI：
10.1037/0894-4105.18.4.613
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发表时间：
2004-10-01
期刊：
影响因子：
2.4
通讯作者：
Lee, P
中科院分区：
文献类型：
--
作者：
Channon, S;German, E;Lee, P
治疗苯丙酮尿症（PKU）的执行缺陷假说表明，外侧前额叶皮质多巴胺能耗竭导致选择性执行障碍。通过比较终生饮食的PKU成人与匹配的健康对照组来检查这一点。PKU患者的选择性和持续性注意力、工作记忆（自我排序指向）和字母流畅性受损。然而，他们未能表现出不同的敏感性，增加认知负荷的注意和工作记忆任务，他们没有显着差异，其余的执行任务（规则发现，抑制和多任务）。他们在回忆或识别记忆方面也没有显着差异。总体而言，研究结果提供了很少的支持执行赤字假说。一个可能的解释在信息处理速度减慢的方面进行了探讨。
The executive deficit hypothesis of treated phenylketonuria (PKU) suggests that dopaminergic depletion in the lateral prefrontal cortex leads to selective executive impairment. This was examined by comparing adults with PKU on a lifelong diet with a matched healthy control group. Those with PKU were impaired on selective and sustained attention, working memory (Self-Ordered Pointing), and letter fluency. However, they failed to show differential sensitivity to increased cognitive load on the attentional and working memory tasks, and they did not differ significantly on the remaining executive tasks (rule finding, inhibition, and multitasking). Nor did they differ significantly on recall or recognition memory. Overall, the findings provided little support for the executive deficit hypothesis. A possible explanation in terms of slowed information processing speed is explored.