Amsterdam UMC location University of Amsterdam, Endocrinology and Metabolism, Amsterdam, The Netherlands.
Amsterdam Gastroenterology Endocrinology Metabolism, Endocrinology, Metabolism and Nutrition, Amsterdam, The Netherlands.
Eur J Endocrinol. 2022 Nov 4;187(6):809-821. doi: 10.1530/EJE-22-0527. Print 2022 Dec 1.
Pituitary tumours that compress the optic chiasm are associated with long-term alterations in sleep-wake rhythm. This may result from damage to intrinsically photosensitive retinal ganglion cells (ipRGCs) projecting from the retina to the hypothalamic suprachiasmatic nucleus via the optic chiasm to ensure photoentrainment (i.e. synchronisation to the 24-h solar cycle through light). To test this hypothesis, we compared the post-illumination pupil response (PIPR), a direct indicator of ipRGC function, between hypopituitarism patients with and without a history of optic chiasm compression.
Observational study, comparing two predefined groups.
We studied 49 patients with adequately substituted hypopituitarism: 25 patients with previous optic chiasm compression causing visual disturbances (CC+ group) and 24 patients without (CC- group). The PIPR was assessed by chromatic pupillometry and expressed as the relative change between baseline and post-blue-light stimulus pupil diameter. Objective and subjective sleep parameters were obtained using polysomnography, actigraphy, and questionnaires.
Post-blue-light stimulus pupillary constriction was less sustained in CC+ patients compared with CC- patients, resulting in a significantly smaller extended PIPR (mean difference: 8.1%, 95% CI: 2.2-13.9%, P = 0.008, Cohen's d = 0.78). Sleep-wake timing was consistently later in CC+ patients, without differences in sleep duration, efficiency, or other rest-activity rhythm features. Subjective sleep did not differ between groups.
Previous optic chiasm compression due to a pituitary tumour in patients with hypopituitarism is associated with an attenuated PIPR and delayed sleep timing. Together, these data suggest that ipRGC function and consequently photoentrainment of the central biological clock is impaired in patients with a history of optic chiasm compression.
压迫视交叉的垂体肿瘤与睡眠-觉醒节律的长期改变有关。这可能是由于损伤了从视网膜投射到下丘脑视交叉上核的内在感光性视网膜神经节细胞（ipRGC），通过视交叉投射到下丘脑视交叉上核，以确保光适应（即通过光使 24 小时太阳周期同步）。为了验证这一假设，我们比较了有和无视交叉压迫史的垂体功能减退症患者的光照后瞳孔反应（PIPR），这是 ipRGC 功能的直接指标。
观察性研究，比较两个预定义的组。
我们研究了 49 例垂体功能减退症患者：25 例有引起视觉障碍的视交叉压迫史（CC+组），24 例无视交叉压迫史（CC-组）。通过色度瞳孔计评估 PIPR，并表示为基线和蓝光刺激后瞳孔直径之间的相对变化。使用多导睡眠图、活动记录仪和问卷调查获得客观和主观睡眠参数。
与 CC-组相比，CC+组患者在蓝光刺激后瞳孔收缩的持续时间更短，导致扩展 PIPR 明显较小（平均差异：8.1%，95%CI：2.2-13.9%，P=0.008，Cohen's d=0.78）。CC+组患者的睡眠-觉醒时间始终较晚，睡眠时间、效率或其他休息-活动节律特征无差异。两组的主观睡眠无差异。
在垂体功能减退症患者中，由于垂体肿瘤引起的视交叉压迫与 PIPR 减弱和睡眠时间延迟有关。这些数据表明，有视交叉压迫史的患者的 ipRGC 功能和中央生物钟的光适应受损。
