Tournikioti K, Dikeos D, Alevizaki M, Michopoulos I, Ferentinos P, Porichi E, Soldatos C R, Douzenis A
Second Department of Psychiatry, Attikon General Hospital, University of Athens, Medical School, Athens.
First Department of Psychiatry, Eginition Hospital, University of Athens, Medical School, Athens.
Psychiatriki. 2018 Jul-Sep;29(3):199-208. doi: 10.22365/jpsych.2018.293.199.
Bipolar disorder is associated with neurocognitive impairment but the etiology of such impairment remains largely unknown. The present study aimed at investigating the performance of bipolar patients in various neuropsychological tasks within the framework of HPA axis hyperactivity model and also the impact of disease characteristics on neuropsychological functioning. Cognitive performance of 60 bipolar-I patients and 30 healthy controls was evaluated by using tasks from the CANTAB battery targeting visual memory, executive function and inhibitory control. Current symptoms were evaluated via administration of the Hamilton Depression Rating Scale (HAMD) and Young Mania Rating Scale (YMRS) whereas assessment of functioning was performed with the Global Assessment of Functioning (GAF). Basal cortisol levels were determined and all patients were administered the Dexamethasone Suppression Test (DST). Statistically significant differences between patients and controls were found in visuo-spatial associative learning and memory, planning, attentional set shifting and inhibitory control. Worse performance in visuospatial associative memory correlated with longer duration of illness and higher levels of basal cortisol. Poorer attentional set shifting was related to higher number of manic episodes. We found no relationship of neurocognitive measures with DST suppression status, current symptom severity or history of psychosis. The results of our study confirm the presence of cognitive deficits in bipolar disorder and provide evidence on the relation of cortisol with neuropsychological functioning, especially visuo-spatial associative memory. Moreover, we have found that number of previous manic episodes and duration of illness is associated with worse cognitive performance. It is known that neurocognitive deficits are evident in many patients with bipolar disorder. These deficits are often a cause of considerable distress and can lead to impairment of psychosocial and occupational functioning. The role of HPA axis needs to be further examined in bipolar disorder. Nevertheless, the identification of factors affecting neurocognitive functioning, like basal cortisol and number of manic episodes, may contribute to the implementation of more appropriate prevention strategies.
双相情感障碍与神经认知功能损害有关,但这种损害的病因在很大程度上仍不清楚。本研究旨在探讨双相情感障碍患者在HPA轴功能亢进模型框架内各种神经心理学任务中的表现,以及疾病特征对神经心理功能的影响。通过使用剑桥神经心理测试自动化成套系统(CANTAB)中针对视觉记忆、执行功能和抑制控制的任务,对60例双相I型患者和30名健康对照者的认知表现进行了评估。通过汉密尔顿抑郁量表(HAMD)和杨氏躁狂量表(YMRS)评估当前症状,而功能评估则采用功能总体评定量表(GAF)。测定基础皮质醇水平,并对所有患者进行地塞米松抑制试验(DST)。患者与对照者在视觉空间联想学习与记忆、计划、注意力转换和抑制控制方面存在统计学显著差异。视觉空间联想记忆表现较差与病程较长和基础皮质醇水平较高相关。注意力转换较差与躁狂发作次数较多有关。我们发现神经认知指标与DST抑制状态、当前症状严重程度或精神病病史无关。我们的研究结果证实了双相情感障碍患者存在认知缺陷,并提供了皮质醇与神经心理功能,特别是视觉空间联想记忆之间关系的证据。此外,我们发现既往躁狂发作次数和病程与较差的认知表现有关。众所周知,许多双相情感障碍患者存在明显的神经认知缺陷。这些缺陷往往是相当大痛苦的根源,并可能导致心理社会和职业功能受损。双相情感障碍中HPA轴的作用需要进一步研究。然而,识别影响神经认知功能的因素,如基础皮质醇和躁狂发作次数,可能有助于实施更合适的预防策略。