Kate M Edwards1, Rujvi Kamat2, Lianne M Tomfohr2, Sonia Ancoli-Israel3, Joel E Dimsdale3. 1. University of Sydney, Exercise Health and Performance Research Group, Lidcombe, Australia; Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA. Electronic address: kate.edwards@sydney.edu.au. 2. San Diego State University, Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA; University of California, San Diego, Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA. 3. Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA; San Diego State University, Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA; University of California, San Diego, Joint Doctoral Program in Clinical Psychology, San Diego, CA, USA.
Abstract
BACKGROUND: Obstructive sleep apnea (OSA) is a prevalent disorder with multiple consequences including negative effects on neurocognitive function. Several domains of cognitive function are impaired in OSA patients, but the mechanisms through which this sleep disorder results in impairment are not clear. Given the well-known effects of cortisol on cognitive function, in particular memory, the dysregulating effects of OSA on cortisol levels are hypothesized as a potential pathway leading to cognitive impairment. METHODS: Fifty-five participants with OSA (mean apnea-hypopnea index [AHI], 30.3) were assessed over 2 days. Over a 24-h period, blood samples were collected every 2h to examine cortisol levels. The following night, sleep was monitored with polysomnography (PSG). Participants were given a battery of neurocognitive tests, which assessed seven cognitive domains. RESULTS: OSA severity assessed by oxygen desaturation index (ODI) was associated with 24-h cortisol levels. AHI, ODI, and nighttime cortisol levels were associated with global deficit scores (GDS) in cognitive functioning, particularly in domains of learning, memory, and working memory (P<.05 for all). Hierarchical linear regression analysis revealed that nighttime cortisol accounted for 9-16% of variance in learning (P=.018), memory (P=.003), and working memory (P=.016) domains, though apnea severity did not significantly predict any additional variance. CONCLUSIONS: In our sample of patients with OSA, nocturnal cortisol levels were associated with neuropsychologic functioning above and beyond the influence of covariates and apnea severity. These findings suggest that OSA-related alterations in cortisol activity may partially explain the pathophysiology of neuropsychologic impairments in sleep apnea.
BACKGROUND:Obstructive sleep apnea (OSA) is a prevalent disorder with multiple consequences including negative effects on neurocognitive function. Several domains of cognitive function are impaired in OSA patients, but the mechanisms through which this sleep disorder results in impairment are not clear. Given the well-known effects of cortisol on cognitive function, in particular memory, the dysregulating effects of OSA on cortisol levels are hypothesized as a potential pathway leading to cognitive impairment. METHODS: Fifty-five participants with OSA (mean apnea-hypopnea index [AHI], 30.3) were assessed over 2 days. Over a 24-h period, blood samples were collected every 2h to examine cortisol levels. The following night, sleep was monitored with polysomnography (PSG). Participants were given a battery of neurocognitive tests, which assessed seven cognitive domains. RESULTS: OSA severity assessed by oxygen desaturation index (ODI) was associated with 24-h cortisol levels. AHI, ODI, and nighttime cortisol levels were associated with global deficit scores (GDS) in cognitive functioning, particularly in domains of learning, memory, and working memory (P<.05 for all). Hierarchical linear regression analysis revealed that nighttime cortisol accounted for 9-16% of variance in learning (P=.018), memory (P=.003), and working memory (P=.016) domains, though apnea severity did not significantly predict any additional variance. CONCLUSIONS: In our sample of patients with OSA, nocturnal cortisol levels were associated with neuropsychologic functioning above and beyond the influence of covariates and apnea severity. These findings suggest that OSA-related alterations in cortisol activity may partially explain the pathophysiology of neuropsychologic impairments in sleep apnea.
Authors: A J Rothschild; F Benes; N Hebben; B Woods; M Luciana; E Bakanas; J A Samson; A F Schatzberg Journal: Biol Psychiatry Date: 1989-10 Impact factor: 13.382
Authors: Arun S Karlamangla; Burton H Singer; Joshua Chodosh; Bruce S McEwen; Teresa E Seeman Journal: Neurobiol Aging Date: 2005-11-08 Impact factor: 4.673