Neurocognitive function in pediatric bipolar disorder: 3-year follow-up shows cognitive development lagging behind healthy youths.

Neurocognitive function in pediatric bipolar disorder: 3-year follow-up shows cognitive development lagging behind healthy youths.
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DOI:
10.1097/chi.0b013e318196b907
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发表时间:
2009-03
影响因子:
13.3
通讯作者:
Sweeney JA
Sweeney JA
中科院分区:
医学1区
文献类型:
--
作者:
Pavuluri MN;West A;Hill SK;Jindal K;Sweeney JA

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对儿童双相情感障碍(PBD)患者的神经认知功能进行了纵向跟踪,以表征该障碍中认知障碍的发展轨迹。PBD患者(n=26)和对照组(n=17,平均年龄11.66±2.70岁)在基线时完成认知测试,然后在3年随访时再次进行认知测试。这些组在年龄、性别、种族、父母的社会经济地位、一般智力和单字阅读能力方面进行了基线匹配。在3年的时间里,PBD组接受了标准化药物算法指导的治疗。在基线和随访时,进行了一系列神经心理学测试,以评估注意力、执行功能、工作记忆、言语记忆、视觉记忆和视觉空间知觉。在基线和随访时,患者在所有被检查的领域都显示出缺陷。在3年的随访中,PBD患者在执行功能和言语记忆方面的发展进展明显低于HC患者。PBD患者在注意力、工作记忆、视觉记忆和视觉空间知觉任务方面的改善与HC相当,但PBD患者在所有领域都与HC相比仍有损害。PBD患者一些神经认知功能的发育延迟表明,这种疾病扰乱了认知发展,可能会对功能能力下降产生终生影响。治疗躁郁症似乎并不能阻止认知发展的滞后。这种不成熟可能是疾病对大脑功能的直接影响,也可能是精神病理学或药物对认知发展的间接后果。
Longitudinal follow-up of neurocognitive functioning in people with pediatric bipolar disorder (PBD) was conducted to characterize the developmental trajectory of cognitive disabilities in this disorder. Patients with PBD (n = 26) and controls (HC; n = 17; mean age 11.66 ± 2.70 years) completed cognitive testing at baseline and then again at a 3-year follow-up. Groups were matched at baseline on age, sex, race, parental socioeconomic status, general intelligence, and single-word reading ability. The PBD group received treatment guided by a standardized medication algorithm during the 3-year period. A battery of neuropsychological tests was administered to assess attention, executive function, working memory, verbal memory, visual memory, and visuospatial perception at baseline and follow-up. At baseline and follow-up, the patients showed deficits in all of the examined domains. At 3-year follow-up, developmental progress in executive functions and verbal memory was significantly less in the patients with PBD than in the HC. Improvement on attention, working memory, visual memory, and visuospatial perception tasks in the patients with PBD was comparable to that of the HC, but the patients with PBD remained impaired in all domains relative to the HC. The developmental delay in some neurocognitive functioning in PBD suggests that the illness disrupts cognitive development with potential lifelong implications for reduced functional ability. Treating bipolar symptoms does not seem to prevent the lag in cognitive development. This dysmaturation may be a direct effect of the illness on brain function, or it may represent indirect consequences of psychopathology or medications on cognitive development.