Neurocognitive impairment in unaffected siblings of youth with bipolar disorder.

Neurocognitive impairment in unaffected siblings of youth with bipolar disorder.
复制标题

DOI:
10.1017/s0033291708004832
复制
发表时间:
2009-08
影响因子:
6.9
通讯作者:
Biederman, J.
Biederman, J.
中科院分区:
医学1区
文献类型:
--
作者:
Doyle, A. E.;Wozniak, J.;Wilens, T. E.;Henin, A.;Seidman, L. J.;Petty, C.;Fried, R.;Gross, L. M.;Faraone, S. V.;Biederman, J.

文献摘要

被引文献

相似文献

越来越多的证据表明,儿童双相情感障碍(BPD)及其与处理速度、语言学习和“执行”功能方面的损伤有关。目前的研究调查了这些神经认知障碍是否表明了诊断背后的家族风险。研究对象为170名患有BPD的青少年(平均年龄12.3岁),他们的118名无情绪障碍的兄弟姐妹和79名无情绪障碍的对照组。研究人员对各组进行了一系列神经心理测试,包括韦氏智力量表、Stroop测验、威斯康星卡片分类测验、Rey-Osterreith复杂图形测验、听觉工作记忆CPT测验和加州语言学习测验(儿童版)。为了减少数据,对措施进行了因素分析。所有的分析都控制了年龄、性别和注意力缺陷多动症。主成分分析与最大旋转得到三个因素反映:1)处理速度/语言学习;2)工作记忆/干扰控制和3)抽象问题解决。带干扰过滤要求的CPT工作记忆测试仅对12岁及以上的受试者进行,因此单独分析。与对照组和未受影响的亲属相比,BPD青年在所有三个因素和WM INT上都表现出损伤。与对照组相比,未受影响的亲属在抽象问题解决因素和WM INT上表现出损伤。他们在工作/记忆干扰控制因素上也表现出更差的统计趋势(p=.07)。执行功能中的神经认知障碍可能反映了儿童BPD的家族性神经生物学风险机制,并且可能在该疾病的分子遗传学研究中作为内表型具有实用价值。
There is growing evidence for the familiality of pediatric bipolar disorder (BPD) and its association with impairments on measures of processing speed, verbal learning and “executive” functions. The current study investigated whether these neurocognitive impairments index the familial risk underlying the diagnosis. Subjects were 170 youth with BPD (mean age 12.3 yrs), their 118 non-mood disordered siblings and 79 non mood-disordered controls. Groups were compared on a battery of neuropsychological tests from the Wechsler Intelligence Scales, the Stroop, the Wisconsin Card Sorting Test, the Rey-Osterreith Complex Figure, an auditory working memory CPT and the California Verbal Learning Test (Child Edition). Measures were factor analyzed for data reduction purposes. All analyses controlled for age, sex and ADHD. Principal components analyses with a promax rotation yielded three factors reflecting: 1) processing speed/verbal learning; 2) working memory/interference control and 3) abstract problem solving. A CPT working memory measure with interference filtering demands (WM INT) was only administered to subjects 12 and older and thus analyzed separately. BPD youth showed impairments versus controls and unaffected relatives on all three factors and the WM INT. Unaffected relatives exhibited impairments versus controls on the abstract problem-solving factor and the WM INT. They also showed a statistical trend (p=.07) toward worse performance on the working/memory interference control factor. Neurocognitive impairments in executive functions may reflect the familial neurobiological risk mechanisms underlying pediatric BPD and may have utility as endophenotypes in molecular genetic studies of the condition.