Kerner Nancy A, Roose Steven P, Pelton Gregory H, Ciarleglio Adam, Scodes Jennifer, Lentz Cody, Sneed Joel R, Devanand D P
Department of Psychiatry, College of Physicians and Surgeons of Columbia University / Columbia University Medical Center, New York, NY; The Late-life Depression Clinic and the Memory Disorders Clinic, Division of Geriatric Psychiatry, New York State Psychiatric Institute, New York, NY.
Department of Psychiatry, College of Physicians and Surgeons of Columbia University / Columbia University Medical Center, New York, NY; The Late-life Depression Clinic and the Memory Disorders Clinic, Division of Geriatric Psychiatry, New York State Psychiatric Institute, New York, NY.
Am J Geriatr Psychiatry. 2017 Mar;25(3):316-325. doi: 10.1016/j.jagp.2016.11.009. Epub 2016 Nov 17.
To evaluate the impact of obstructive sleep apnea (OSA) on neurocognitive function and brain morphology in older adults with depression and cognitive impairment.
We prospectively screened OSA with the STOP-Bang questionnaire in the last 25 patients enrolled into the Donepezil Treatment of Cognitive Impairment and Depression (DOTCODE) trial. High and low probability of OSA were defined as a STOP-Bang score of ≥5 (h-OSA) and of <5 (l-OSA), respectively. Baseline magnetic resonance imaging (MRI) was used to evaluate brain morphology. The initial 16 weeks of antidepressant treatment were part of the DOTCODE trial.
After 16 weeks of antidepressant treatment, the h-OSA group performed significantly worse on the Selective Reminding Test delayed recall task than the l-OSA group, controlling for baseline performance (F = 19.1, df = 1,22, p < 0.001). In 19 of 25 participants who underwent brain MRI, the h-OSA group had significantly greater volumes of MRI hyperintensities in deep white matter, periventricular white matter, and subcortical gray matter compared with the l-OSA group. There was no significant association between OSA and hippocampal or entorhinal cortex volumes in our sample, even after controlling for intracranial volume.
OSA is associated with impaired verbal episodic memory and microvascular damage in older adults with depression and cognitive impairment. One possibility is that by contributing to cerebral microvascular damage, OSA may exacerbate progressive memory decline.
评估阻塞性睡眠呼吸暂停（OSA）对患有抑郁症和认知障碍的老年人神经认知功能和脑形态的影响。
我们在最后25名纳入多奈哌齐治疗认知障碍和抑郁症（DOTCODE）试验的患者中，使用STOP-Bang问卷对OSA进行前瞻性筛查。OSA高概率和低概率分别定义为STOP-Bang评分≥5（高OSA）和<5（低OSA）。使用基线磁共振成像（MRI）评估脑形态。抗抑郁治疗的最初16周是DOTCODE试验的一部分。
抗抑郁治疗16周后，在控制基线表现的情况下，高OSA组在选择性提醒测试延迟回忆任务上的表现明显比低OSA组差（F = 19.1，自由度= 1,22，p <0.001）。在接受脑部MRI检查的25名参与者中的19名中，与低OSA组相比，高OSA组在深部白质、脑室周围白质和皮质下灰质中的MRI高信号体积明显更大。即使在控制颅内体积后，我们样本中OSA与海马体或内嗅皮质体积之间也没有显著关联。
OSA与患有抑郁症和认知障碍的老年人的言语情景记忆受损和微血管损伤有关。一种可能性是，通过导致脑微血管损伤，OSA可能会加剧进行性记忆衰退。
