From the Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Helsinki, Finland (Salmela, Lahti); and the Department of Psychiatry, University of Helsinki and Helsinki University Hospital, Helsinki, Finland (Socada, Söderholm, Heikkilä, Ekelund, Isometsä).
J Psychiatry Neurosci. 2021 Mar 11;46(2):E222-E231. doi: 10.1503/jpn.200091.
Previous studies have suggested that processing of visual contrast information could be altered in major depressive disorder. To clarify the changes at different levels of the visual hierarchy, we behaviourally measured contrast perception in 2 centre-surround conditions, assessing retinal and cortical processing.
As part of a prospective cohort study, our sample consisted of controls (n = 29; 21 female) and patients with unipolar depression, bipolar disorder and borderline personality disorder who had baseline major depressive episodes (n = 111; 74 female). In a brightness induction test that assessed retinal processing, participants compared the perceived luminance of uniform patches (presented on a computer screen) as the luminance of the backgrounds was varied. In a contrast suppression test that assessed cortical processing, participants compared the perceived contrast of gratings, which were presented with collinearly or orthogonally oriented backgrounds.
Brightness induction was similar for patients with major depressive episodes and controls (p = 0.60, d = 0.115, Bayes factor = 3.9), but contrast suppression was significantly lower for patients than for controls (p < 0.006, d = 0.663, Bayes factor = 35.2). We observed no statistically significant associations between contrast suppression and age, sex, or medication or diagnostic subgroup. At follow-up (n = 74), we observed some normalization of contrast perception.
We assessed contrast perception using behavioural tests instead of electrophysiology.
The reduced contrast suppression we observed may have been caused by decreased retinal feedforward or cortical feedback signals. Because we observed intact brightness induction, our results suggest normal retinal but altered cortical processing of visual contrast during a major depressive episode. This alteration is likely to be present in multiple types of depression and to partially normalize upon remission.
先前的研究表明,在重度抑郁症中,视觉对比信息的处理可能会发生改变。为了明确在视觉层次的不同水平上的变化,我们在 2 种中心-环绕条件下对对比感知进行了行为测量,评估了视网膜和皮质处理。
作为一项前瞻性队列研究的一部分,我们的样本包括对照组(n=29;21 名女性)和有单相抑郁、双相障碍和边缘型人格障碍的患者,他们在基线时有重度抑郁发作(n=111;74 名女性)。在评估视网膜处理的亮度诱导测试中,参与者比较了均匀斑块的感知亮度,因为背景的亮度发生了变化。在评估皮质处理的对比抑制测试中,参与者比较了光栅的感知对比度,光栅与共线或正交定向的背景一起呈现。
有重度抑郁发作的患者和对照组的亮度诱导相似(p=0.60,d=0.115,贝叶斯因子=3.9),但患者的对比抑制明显低于对照组(p<0.006,d=0.663,贝叶斯因子=35.2)。我们没有观察到对比抑制与年龄、性别、药物或诊断亚组之间存在统计学上显著的关联。在随访时(n=74),我们观察到对比感知的一些正常化。
我们使用行为测试而不是电生理学来评估对比感知。
我们观察到的对比抑制减少可能是由于视网膜前馈或皮质反馈信号减少所致。由于我们观察到正常的亮度诱导,我们的结果表明在重度抑郁发作期间,视觉对比的正常视网膜处理,但皮质处理发生改变。这种改变可能存在于多种类型的抑郁症中,并在缓解时部分恢复正常。