Insomnia with objective short sleep duration is associated with deficits in neuropsychological performance: a general population study.
ABSTRACT To examine the joint effect of insomnia and objective short sleep duration on neuropsychological performance.
Representative cross-sectional study.
1,741 men and women randomly selected from central Pennsylvania.
Insomnia (n = 116) was defined by a complaint of insomnia with a duration > or = 1 year and the absence of sleep disordered breathing (SDB), while normal sleep (n = 562) was defined as the absence of insomnia, excessive daytime sleepiness, and SDB. Both groups were split according to polysomnographic sleep duration into 2 categories: > or = 6 h of sleep ("normal sleep duration") and < 6 h of sleep ("short sleep duration"). We compared the groups' performance on a comprehensive neuropsychological battery that measured processing speed, attention, visual memory, and verbal fluency, while controlling for age, race, gender, education, body mass index, and physical and mental health.
No significant differences were detected between insomniacs and controls. However, the insomnia with short sleep duration group compared to the control with normal or short sleep duration groups showed poorer neuropsychological performance in variables such as processing speed, set-switching attention, and number of visual memory errors and omissions. In contrast, the insomnia with normal sleep duration group showed no significant deficits.
Insomnia with objective short sleep duration is associated with deficits in set-switching attentional abilities, a key component of the "executive control of attention." These findings suggest that objective sleep duration may predict the severity of chronic insomnia, including its effect on neurocognitive function.
Full-textDOI: · Available from: Julio Fernandez-Mendoza, May 16, 2015
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ABSTRACT: Previous studies have suggested that insomnia with objective short sleep duration is associated with a higher risk of hypertension, and it has been speculated that the underlying mechanism is physiological hyperarousal. In this study, we tested whether insomnia with physiological hyperarousal measured by Multiple Sleep Latency Test (MSLT), a standard test of sleepiness/alertness, is associated with increased risk of hypertension. Two hundred nineteen chronic insomniacs and 96 normal sleepers were included in this study. Chronic insomnia was defined based on standard diagnostic criteria with symptoms lasting ≥6 months. All subjects underwent 1 night in laboratory polysomnography followed by a standard MSLT. We used the median mean MSLT value (ie, >14 minutes) and the 75th percentile of mean MSLT value (ie, >17 minutes) to define hyperarousal. Hypertension was defined based either on blood pressure measures or on diagnosis treatment by a physician. After controlling for age, sex, body mass index, apnea-hypopnea index, diabetes mellitus, smoking, alcohol, and caffeine use, insomnia combined with MSLT >14 minutes increased the odds of hypertension by 300% (odds ratio=3.27; 95% confidence interval=1.20-8.96), whereas insomnia combined with MSLT >17 minutes increased even further the odds of hypertension by 400% (odds ratio=4.33; 95% confidence interval=1.48-12.68) compared with normal sleepers with MSLT ≤14 minutes. Insomnia associated with physiological hyperarousal is associated with a significant risk of hypertension. Long MSLT values may be a reliable index of the physiological hyperarousal and biological severity of chronic insomnia. © 2015 American Heart Association, Inc.Hypertension 03/2015; 65(3):644-650. DOI:10.1161/HYPERTENSIONAHA.114.04604 · 7.63 Impact Factor
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ABSTRACT: Despite compelling evidence from animal studies indicating hippocampal subfield-specific vulnerability to poor sleep quality and related cognitive impairment, there have been no human magnetic resonance imaging (MRI) studies investigating the relationship between hippocampal subfield volume and sleep disturbance. Our aim was to investigate the pattern of volume changes across hippocampal subfields in patients with primary insomnia relative to controls.Sleep 07/2014; 37(7):1189-98. DOI:10.5665/sleep.3836 · 5.06 Impact Factor
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ABSTRACT: The main mystery about sleep is why we do not do more of it. Almost every type of human function or dysfunction involves sleep disruption, from our perception of sleep as an impediment to our social and professional lives, thus direct- ing our schedules to restrict the time we allocate for sleep; to psychiatric disorders, the majority of which interfere with sleep patterns. This is even more enigmatic consider- ing the overlap between sleep regulatory mechanisms and reward systems, as will be outlined here. Like the major- ity of psychiatric disorders, sleep disturbances are a central feature of addictions, with different substances associated with divergent effects on sleep regulation and subjective sleep quality. Clearly, the long- and short-term pharmaco- logical effects of a psychoactive drug alter the functional- ity of brain systems associated with arousal states; hence, it would be expected that continued use of such substances would impact sleep patterns. However, the links between the motivational effects of drug use and sleep are far more complex. I propose a model that will demonstrate that key mechanisms involved in the susceptibility to engage in drug-seeking behaviors and to develop an addiction are linked to sleep and sleep disruption. The emerging model suggests that the same systems that reinforce drug-seeking behaviors are also activated during sleep. As replay patterns during sleep have been linked to consolidation of memories, sleep, per se, may have a role in the creation of addiction. With this in mind, the proposed model may also provide a tentative answer to the questions posed, suggesting that sleep deprivation, at least in a mild form, is reinforcing.Modulation of Sleep by Obesity, Diabetes, Age, and Diet, 1st edited by R. Watson, 01/2015: chapter 37: pages 337-347; Elsevier., ISBN: 9780124201682