Sleep disturbance induces neuroinflammation and impairment of learning and memory.

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Zhu, Biao; Dong, Yuanlin; Xu, Zhipeng; Gompf, Heinrich S; Ward, Sarah A P; Xue, Zhanggang; Miao, Changhong; Zhang, Yiying; Chamberlin, Nancy L; Xie, Zhongcong

2012-12-01

Hospitalized patients can develop cognitive function decline, the mechanisms of which remain largely to be determined. Sleep disturbance often occurs in hospitalized patients, and neuroinflammation can induce learning and memory impairment. We therefore set out to determine whether sleep disturbance can induce neuroinflammation and impairment of learning and memory in rodents. Five to 6-month-old wild-type C57BL/6J male mice were used in the studies. The mice were placed in rocking cages for 24 h, and two rolling balls were present in each cage. The mice were tested for learning and memory function using the Fear Conditioning Test one and 7 days post-sleep disturbance. Neuroinflammation in the mouse brain tissues was also determined. Of the Fear Conditioning studies at one day and 7 days after sleep disturbance, twenty-four hour sleep disturbance decreased freezing time in the context test, which assesses hippocampus-dependent learning and memory; but not the tone test, which assesses hippocampus-independent learning and memory. Sleep disturbance increased pro-inflammatory cytokine IL-6 levels and induced microglia activation in the mouse hippocampus, but not the cortex. These results suggest that sleep disturbance induces neuroinflammation in the mouse hippocampus, and impairs hippocampus-dependent learning and memory in mice. Pending further studies, these findings suggest that sleep disturbance-induced neuroinflammation and impairment of learning and memory may contribute to the development of cognitive function decline in hospitalized patients. Copyright © 2012 Elsevier Inc. All rights reserved.

The short- and long-term proteomic effects of sleep deprivation on the cortical and thalamic synapses.

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Simor, Attila; Györffy, Balázs András; Gulyássy, Péter; Völgyi, Katalin; Tóth, Vilmos; Todorov, Mihail Ivilinov; Kis, Viktor; Borhegyi, Zsolt; Szabó, Zoltán; Janáky, Tamás; Drahos, László; Juhász, Gábor; Kékesi, Katalin Adrienna

2017-03-01

Acute total sleep deprivation (SD) impairs memory consolidation, attention, working memory and perception. Structural, electrophysiological and molecular experimental approaches provided evidences for the involvement of sleep in synaptic functions. Despite the wide scientific interest on the effects of sleep on the synapse, there is a lack of systematic investigation of sleep-related changes in the synaptic proteome. We isolated parietal cortical and thalamic synaptosomes of rats after 8h of total SD by gentle handling and 16h after the end of deprivation to investigate the short- and longer-term effects of SD on the synaptic proteome, respectively. The SD efficiency was verified by electrophysiology. Protein abundance alterations of the synaptosomes were analyzed by fluorescent two-dimensional differential gel electrophoresis and by tandem mass spectrometry. As several altered proteins were found to be involved in synaptic strength regulation, our data can support the synaptic homeostasis hypothesis function of sleep and highlight the long-term influence of SD after the recovery sleep period, mostly on cortical synapses. Furthermore, the large-scale and brain area-specific protein network change in the synapses may support both ideas of sleep-related synaptogenesis and molecular maintenance and reorganization in normal rat brain. Copyright © 2017 Elsevier Inc. All rights reserved.

Impaired sleep and allostatic load

DEFF Research Database (Denmark)

Clark, Alice Jessie; Dich, Nadya; Lange, Theis

2014-01-01

Objective: Understanding the mechanisms linking sleep impairment to morbidity and mortality is important for future prevention, but these mechanisms are far from elucidated. We aimed to determine the relation between impaired sleep, both in terms of duration and disturbed sleep, and allostatic load...... Biobank with comprehensive information on sleep duration, disturbed sleep, objective measures of an extensive range of biological risk markers, and physical conditions. Results: Long sleep (mean difference 0.23; 95% confidence interval, 0.13, 0.32) and disturbed sleep (0.14; 0.06, 0.22) were associated...... with higher AL as well as with high-risk levels of risk markers from the anthropometric, metabolic, and immune system. Sub-analyses suggested that the association between disturbed sleep and AL might be explained by underlying disorders. Whereas there was no association between short sleep and AL...

State-dependent changes in auditory sensory gating in different cortical areas in rats.

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Renli Qi

Full Text Available Sensory gating is a process in which the brain's response to a repetitive stimulus is attenuated; it is thought to contribute to information processing by enabling organisms to filter extraneous sensory inputs from the environment. To date, sensory gating has typically been used to determine whether brain function is impaired, such as in individuals with schizophrenia or addiction. In healthy subjects, sensory gating is sensitive to a subject's behavioral state, such as acute stress and attention. The cortical response to sensory stimulation significantly decreases during sleep; however, information processing continues throughout sleep, and an auditory evoked potential (AEP can be elicited by sound. It is not known whether sensory gating changes during sleep. Sleep is a non-uniform process in the whole brain with regional differences in neural activities. Thus, another question arises concerning whether sensory gating changes are uniform in different brain areas from waking to sleep. To address these questions, we used the sound stimuli of a Conditioning-testing paradigm to examine sensory gating during waking, rapid eye movement (REM sleep and Non-REM (NREM sleep in different cortical areas in rats. We demonstrated the following: 1. Auditory sensory gating was affected by vigilant states in the frontal and parietal areas but not in the occipital areas. 2. Auditory sensory gating decreased in NREM sleep but not REM sleep from waking in the frontal and parietal areas. 3. The decreased sensory gating in the frontal and parietal areas during NREM sleep was the result of a significant increase in the test sound amplitude.

Obstructive sleep apnea and cortical thickness in females and males.

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Macey, Paul M; Haris, Natasha; Kumar, Rajesh; Thomas, M Albert; Woo, Mary A; Harper, Ronald M

2018-01-01

Obstructive sleep apnea (OSA) affects approximately 10% of adults, and alters brain gray and white matter. Psychological and physiological symptoms of the disorder are sex-specific, perhaps related to greater injury occurs in female than male patients in white matter. Our objective was to identify influences of OSA separated by sex on cortical gray matter. We assessed cortical thickness in 48 mild-severe OSA patients (mean age±std[range] = 46.5±9.0[30.8-62.7] years; apnea-hypopnea index = 32.6±21.1[6-102] events/hour; 12 female, 36 male; OSA severity: 5 mild, 18 moderate, 25 severe) and 62 controls (mean age = 47.7±8.9[30.9-65.8] years; 22 female, 40 male). All OSA patients were recently-diagnosed via polysomnography, and control subjects screened and a subset assessed with sleep studies. We used high-resolution magnetic resonance imaging to identify OSA-related cortical thinning, based on a model with condition and sex as independent variables. OSA and OSA-by-sex interaction effects were assessed (Pfrontal lobe in female OSA vs. all other groups. Significant thinning within the pre- and post-central gyri and the superior temporal gyrus, extending into the insula, appeared between the general OSA populations vs. control subjects. No areas showed increased thickness in OSA vs. controls or positive female OSA interaction effects. Reduced cortical thickness likely represents tissue atrophy from long term injury, including death of neurons and supporting glia from repeated intermittent hypoxic exposure in OSA, although disease comordities may also contribute to thinning. Lack of polysomnography in all control subjects means results may be confounded by undiagnosed OSA. The greater cortical injury in cognitive areas of female OSA patients may underlie enhanced symptoms in that group. The thinning associated with OSA in male and females OSA patients may contribute to autonomic dysregulation and impaired upper airway sensori-motor function.

Mild Traumatic Brain Injury Chronically Impairs Sleep- and Wake-Dependent Emotional Processing.

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Mantua, Janna; Henry, Owen S; Garskovas, Nolan F; Spencer, Rebecca M C

2017-06-01

A single traumatic brain injury (TBI), even when mild (ie, concussion), can cause lasting consequences. Individuals with a history of chronic (>1-year prior) mild TBI have an increased risk of mood disturbances (eg, depression, suicide). This population also has lingering sleep alterations, including poor sleep quality and changes in sleep stage proportions. Given these sleep deficits, we aimed to test whether sleep-dependent emotional memory consolidation is reduced in this population. We utilized a mild TBI group (3.7 ± 2.9 years post injury) and an uninjured (non-TBI) population. Participants viewed negative and neutral images both before and after a 12-hour period containing sleep ("Sleep" group) or an equivalent period of time spent awake ("Wake" group). Participants rated images for valence/arousal at both sessions, and memory recognition was tested at session two. The TBI group had less rapid eye movement (REM), longer REM latency, and more sleep complaints. Sleep-dependent memory consolidation of nonemotional images was present in all participants. However, consolidation of negative images was only present in the non-TBI group. A lack of differentiation between the TBI Sleep and Wake groups was due to poor performance in the sleep group and, unexpectedly, enhanced performance in the wake group. Additionally, although the non-TBI participants habituated to negative images over a waking period, the TBI participants did not. We propose disrupted sleep- and wake-dependent emotional processing contributes to poor emotional outcomes following chronic, mild TBI. This work has broad implications, as roughly one-third of the US population will sustain a mild TBI during their lifetime. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Sleep impairment and prognosis of acute myocardial infarction

DEFF Research Database (Denmark)

Clark, Alice; Lange, Theis; Hallqvist, Johan

2014-01-01

STUDY OBJECTIVES: Impaired sleep is an established risk factor for the development of cardiovascular disease, whereas less is known about how impaired sleep affects cardiovascular prognosis. The aim of this study is to determine how different aspects of impaired sleep affect the risk of case fata...... assessment that could benefit secondary cardiovascular prevention. CITATION: Clark A, Lange T, Hallqvist J, Jennum P, Rod NH. Sleep impairment and prognosis of acute myocardial infarction: a prospective cohort study. SLEEP 2014;37(5):851-858....... registries. In women, disturbed sleep showed a consistently higher risk of long-term cardiovascular events: AMI (hazard ratio [HR] = 1.69; 95% confidence interval [CI] 0.95-3.00), stroke (HR = 2.61; 95% CI: 1.19-5.76), and heart failure (HR = 2.43; 95% CI: 1.18-4.97), whereas no clear effect of impaired...

Promoting Sleep Oscillations and Their Functional Coupling by Transcranial Stimulation Enhances Memory Consolidation in Mild Cognitive Impairment.

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Ladenbauer, Julia; Ladenbauer, Josef; Külzow, Nadine; de Boor, Rebecca; Avramova, Elena; Grittner, Ulrike; Flöel, Agnes

2017-07-26

Alzheimer's disease (AD) not only involves loss of memory functions, but also prominent deterioration of sleep physiology, which is already evident at the stage of mild cognitive impairment (MCI). Cortical slow oscillations (SO; 0.5-1 Hz) and thalamocortical spindle activity (12-15 Hz) during sleep, and their temporal coordination, are considered critical for memory formation. We investigated the potential of slow oscillatory transcranial direct current stimulation (so-tDCS), applied during a daytime nap in a sleep-state-dependent manner, to modulate these activity patterns and sleep-related memory consolidation in nine male and seven female human patients with MCI. Stimulation significantly increased overall SO and spindle power, amplified spindle power during SO up-phases, and led to stronger synchronization between SO and spindle power fluctuations in EEG recordings. Moreover, visual declarative memory was improved by so-tDCS compared with sham stimulation and was associated with stronger synchronization. These findings indicate a well-tolerated therapeutic approach for disordered sleep physiology and memory deficits in MCI patients and advance our understanding of offline memory consolidation. SIGNIFICANCE STATEMENT In the light of increasing evidence that sleep disruption is crucially involved in the progression of Alzheimer's disease (AD), sleep appears as a promising treatment target in this pathology, particularly to counteract memory decline. This study demonstrates the potential of a noninvasive brain stimulation method during sleep in patients with mild cognitive impairment (MCI), a precursor of AD, and advances our understanding of its mechanism. We provide first time evidence that slow oscillatory transcranial stimulation amplifies the functional cross-frequency coupling between memory-relevant brain oscillations and improves visual memory consolidation in patients with MCI. Copyright © 2017 the authors 0270-6474/17/377111-14$15.00/0.

Chronic caffeine treatment prevents sleep deprivation-induced impairment of cognitive function and synaptic plasticity.

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Alhaider, Ibrahim A; Aleisa, Abdulaziz M; Tran, Trinh T; Alzoubi, Karem H; Alkadhi, Karim A

2010-04-01

This study was undertaken to provide a detailed account of the effect of chronic treatment with a small dose of caffeine on the deleterious effects of sleep loss on brain function in rats. We investigated the effects of chronic (4 weeks) caffeine treatment (0.3 g/L in drinking water) on memory impairment in acutely (24 h) sleep-deprived adult male Wistar rats. Sleep deprivation was induced using the modified multiple platform model. The effects of caffeine on sleep deprivation-induced hippocampus-dependent learning and memory deficits were studied by 3 approaches: learning and memory performance in the radial arm water maze task, electrophysiological recording of early long-term potentiation (E-LTP) in area CA1 of the hippocampus, and levels of memory- and synaptic plasticity-related signaling molecules after E-LTP induction. The results showed that chronic caffeine treatment prevented impairment of hippocampus-dependent learning, shortterm memory and E-LTP of area CA1 in the sleep-deprived rats. In correlation, chronic caffeine treatment prevented sleep deprivation-associated decrease in the levels of phosphorylated calcium/calmodulin-dependent protein kinase II (P-CaMKII) during expression of E-LTP. The results suggest that long-term use of a low dose of caffeine prevents impairment of short-term memory and E-LTP in acutely sleep-deprived rats.

On-call work: To sleep or not to sleep? It depends.

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Ferguson, Sally A; Paterson, Jessica L; Hall, Sarah J; Jay, Sarah M; Aisbett, Brad

On-call working time arrangements are increasingly common, involve work only in the event of an unpredictable incident and exist primarily outside of standard hours. Like other non-standard working time arrangements, on-call work disrupts sleep and can therefore have negative effects on health, safety and performance. Unlike other non-standard working time arrangements, on-call work often allows sleep opportunities between calls. Any sleep obtained during on-call periods will be beneficial for waking performance. However, there is evidence that sleep while on call may be of substantially reduced restorative value because of the expectation of receiving the call and apprehension about missing the call. In turn, waking from sleep to respond to a call may be associated with temporary increases in performance impairment. This is dependent on characteristics of both the preceding sleep, the tasks required upon waking and the availability and utility of any countermeasures to support the transition from sleep to wake. In this paper, we critically evaluate the evidence both for and against sleeping during on-call periods and conclude that some sleep, even if it is of reduced quality and broken by repeated calls, is a good strategy. We also note, however, that organisations utilising on-call working time arrangements need to systematically manage the likelihood that on-call sleep can be associated with temporary performance impairments upon waking. Given that the majority of work in this area has been laboratory-based, there is a significant need for field-based investigations of the magnitude of sleep inertia, in addition to the utility of sleep inertia countermeasures. Field studies should include working with subject matter experts to identify the real-world impacts of changes in performance associated with sleeping, or not sleeping, whilst on call.

Influence of cued-fear conditioning and its impairment on NREM sleep.

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Kumar, Tankesh; Jha, Sushil K

2017-10-01

Many studies suggest that fear conditioning influences sleep. It is, however, not known if the changes in sleep architecture after fear conditioning are essentially associated with the consolidation of fearful memory or with fear itself. Here, we have observed that within sleep, NREM sleep consistently remained augmented after the consolidation of cued fear-conditioned memory. But a similar change did not occur after impairing memory consolidation by blocking new protein synthesis and glutamate transmission between glial-neuronal loop in the lateral amygdala (LA). Anisomycin (a protein synthesis inhibitor) and DL-α-amino-adipic acid (DL- α -AA) (a glial glutamine synthetase enzyme inhibitor) were microinjected into the LA soon after cued fear-conditioning to induce memory impairment. On the post-conditioning day, animals in both the groups exhibited significantly less freezing. In memory-consolidated groups (vehicle groups), NREM sleep significantly increased during 2nd to 5th hours after training compared to their baseline days. However, in memory impaired groups (anisomycin and DL- α -AA microinjected groups), similar changes were not observed. Our results thus suggest that changes in sleep architecture after cued fear-conditioning are indeed a consolidation dependent event. Copyright © 2017 Elsevier Inc. All rights reserved.

Amyloid burden and sleep blood pressure in amnestic mild cognitive impairment

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Tarumi, Takashi; Harris, Thomas S.; Hill, Candace; German, Zohre; Riley, Jonathan; Turner, Marcel; Womack, Kyle B.; Kerwin, Diana R.; Monson, Nancy L.; Stowe, Ann M.; Mathews, Dana; Cullum, C. Munro

2015-01-01

Objective: To determine whether cortical β-amyloid (Aβ) deposition is associated with circadian blood pressure (BP) profiles and dynamic cerebral blood flow (CBF) regulation in patients with amnestic mild cognitive impairment (aMCI). Methods: Forty participants with aMCI were included in this study. Cortical Aβ depositions were measured by 18F-florbetapir PET and expressed as the standardized uptake value ratio (SUVR) relative to the cerebellum. Circadian BP profiles were measured by 24-hour ambulatory monitoring during awake and sleep periods. The dipping status of sleep BP (i.e., the percent changes from the awake BP) was calculated and dichotomized into the dipper (≥10%) and nondipper (<10%) groups. Dynamic CBF regulation was assessed by a transfer function analysis between beat-to-beat changes in BP and CBF velocity measured from the middle cerebral artery during a repeated sit-stand maneuver. Results: Age was positively correlated with a greater Aβ deposition in the posterior cingulate, precuneus, and mean cortex. Accounting for the age effect, attenuated reductions in sleep systolic BP were associated with higher levels of posterior cingulate SUVR. Consistently, the nondippers exhibited a higher SUVR in the posterior cingulate than the dippers. Transfer function gain between changes in BP and CBF velocity was diminished in the nondippers, and moreover those individuals with a lower gain exhibited a higher SUVR in the posterior cingulate. Conclusions: Attenuated reductions in sleep BP are associated with a greater Aβ burden in the posterior cingulate and altered dynamic CBF regulation in patients with aMCI. PMID:26537049

Why Does Sleep Slow-Wave Activity Increase After Extended Wake? Assessing the Effects of Increased Cortical Firing During Wake and Sleep.

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Rodriguez, Alexander V; Funk, Chadd M; Vyazovskiy, Vladyslav V; Nir, Yuval; Tononi, Giulio; Cirelli, Chiara

2016-12-07

During non-rapid eye movement (NREM) sleep, cortical neurons alternate between ON periods of firing and OFF periods of silence. This bi-stability, which is largely synchronous across neurons, is reflected in the EEG as slow waves. Slow-wave activity (SWA) increases with wake duration and declines homeostatically during sleep, but the underlying mechanisms remain unclear. One possibility is neuronal "fatigue": high, sustained firing in wake would force neurons to recover with more frequent and longer OFF periods during sleep. Another possibility is net synaptic potentiation during wake: stronger coupling among neurons would lead to greater synchrony and therefore higher SWA. Here, we obtained a comparable increase in sustained firing (6 h) in cortex by: (1) keeping mice awake by exposure to novel objects to promote plasticity and (2) optogenetically activating a local population of cortical neurons at wake-like levels during sleep. Sleep after extended wake led to increased SWA, higher synchrony, and more time spent OFF, with a positive correlation between SWA, synchrony, and OFF periods. Moreover, time spent OFF was correlated with cortical firing during prior wake. After local optogenetic stimulation, SWA and cortical synchrony decreased locally, time spent OFF did not change, and local SWA was not correlated with either measure. Moreover, laser-induced cortical firing was not correlated with time spent OFF afterward. Overall, these results suggest that high sustained firing per se may not be the primary determinant of SWA increases observed after extended wake. A long-standing hypothesis is that neurons fire less during slow-wave sleep to recover from the "fatigue" accrued during wake, when overall synaptic activity is higher than in sleep. This idea, however, has rarely been tested and other factors, namely increased cortical synchrony, could explain why sleep slow-wave activity (SWA) is higher after extended wake. We forced neurons in the mouse cortex to fire

White Matter Structure in Older Adults Moderates the Benefit of Sleep Spindles on Motor Memory Consolidation.

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Mander, Bryce A; Zhu, Alyssa H; Lindquist, John R; Villeneuve, Sylvia; Rao, Vikram; Lu, Brandon; Saletin, Jared M; Ancoli-Israel, Sonia; Jagust, William J; Walker, Matthew P

2017-11-29

Sleep spindles promote the consolidation of motor skill memory in young adults. Older adults, however, exhibit impoverished sleep-dependent motor memory consolidation. The underlying pathophysiological mechanism(s) explaining why motor memory consolidation in older adults fails to benefit from sleep remains unclear. Here, we demonstrate that male and female older adults show impoverished overnight motor skill memory consolidation relative to young adults, with the extent of impairment being associated with the degree of reduced frontal fast sleep spindle density. The magnitude of the loss of frontal fast sleep spindles in older adults was predicted by the degree of reduced white matter integrity throughout multiple white matter tracts known to connect subcortical and cortical brain regions. We further demonstrate that the structural integrity of selective white matter fiber tracts, specifically within right posterior corona radiata, right tapetum, and bilateral corpus callosum, statistically moderates whether sleep spindles promoted overnight consolidation of motor skill memory. Therefore, white matter integrity within tracts known to connect cortical sensorimotor control regions dictates the functional influence of sleep spindles on motor skill memory consolidation in the elderly. The deterioration of white matter fiber tracts associated with human brain aging thus appears to be one pathophysiological mechanism influencing subcortical-cortical propagation of sleep spindles and their related memory benefits. SIGNIFICANCE STATEMENT Numerous studies have shown that sleep spindle expression is reduced and sleep-dependent motor memory is impaired in older adults. However, the mechanisms underlying these alterations have remained unknown. The present study reveals that age-related degeneration of white matter within select fiber tracts is associated with reduced sleep spindles in older adults. We further demonstrate that, within these same fiber tracts, the degree of

Validation of the PROMIS Sleep Disturbance and Sleep-Related Impairment item banks in Dutch adolescents.

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van Kooten, Jojanneke A M C; van Litsenburg, Raphaёle R L; Yoder, Whitney R; Kaspers, Gertjan J L; Terwee, Caroline B

2018-04-16

Sleep problems are common in adolescents and have a negative impact on daytime functioning. However, there is a lack of well-validated adolescent sleep questionnaires. The Patient-Reported Outcomes Measurement Information System (PROMIS) Sleep Disturbance and Sleep-Related Impairment item banks are well-validated instruments developed for and tested in adults. The aim of this study was to evaluate their structural validity in adolescents. Test and retest data were collected for the Dutch-Flemish V1.0 PROMIS Sleep Disturbance (27) and Sleep-Related Impairment (16 items) item banks from 1046 adolescents (11-19 years). Cross-validation methods, Confirmatory (CFA), and Exploratory Factor Analyses (EFA) were used. Fit indices and factor loadings were used to improve the models. The final models were assessed for model fit using retest data. The one-factor Sleep Disturbance (CFI = 0.795, TLI = 0.778, RMSEA = 0.117) and Sleep-Related Impairment (CFI = 0.897, TLI = 0.882, RMSEA = 0.156) models could not be replicated in adolescents. Cross-validation resulted in a final Sleep Disturbance model of 23 and a Sleep-Related Impairment model of 11 items. Retest data CFA showed adequate fit for the Sleep-Related Impairment-11 (CFI = 0.981, TLI = 0.976, RMSEA = 0.116). The Sleep Disturbance-23 model fit indices stayed below the recommended values (CFI = 0.895, TLI = 0.885, RMSEA = 0.105). While the PROMIS Sleep Disturbance-23 for adolescents and PROMIS Sleep-Related Impairment-11 for adolescents provide a framework to assess adolescent sleep, additional research is needed to replicate these findings in a larger and more diverse sample.

Cortical Spreading Depression Closes Paravascular Space and Impairs Glymphatic Flow: Implications for Migraine Headache.

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Schain, Aaron J; Melo-Carrillo, Agustin; Strassman, Andrew M; Burstein, Rami

2017-03-15

Functioning of the glymphatic system, a network of paravascular tunnels through which cortical interstitial solutes are cleared from the brain, has recently been linked to sleep and traumatic brain injury, both of which can affect the progression of migraine. This led us to investigate the connection between migraine and the glymphatic system. Taking advantage of a novel in vivo method we developed using two-photon microscopy to visualize the paravascular space (PVS) in naive uninjected mice, we show that a single wave of cortical spreading depression (CSD), an animal model of migraine aura, induces a rapid and nearly complete closure of the PVS around surface as well as penetrating cortical arteries and veins lasting several minutes, and gradually recovering over 30 min. A temporal mismatch between the constriction or dilation of the blood vessel lumen and the closure of the PVS suggests that this closure is not likely to result from changes in vessel diameter. We also show that CSD impairs glymphatic flow, as indicated by the reduced rate at which intraparenchymally injected dye was cleared from the cortex to the PVS. This is the first observation of a PVS closure in connection with an abnormal cortical event that underlies a neurological disorder. More specifically, the findings demonstrate a link between the glymphatic system and migraine, and suggest a novel mechanism for regulation of glymphatic flow. SIGNIFICANCE STATEMENT Impairment of brain solute clearance through the recently described glymphatic system has been linked with traumatic brain injury, prolonged wakefulness, and aging. This paper shows that cortical spreading depression, the neural correlate of migraine aura, closes the paravascular space and impairs glymphatic flow. This closure holds the potential to define a novel mechanism for regulation of glymphatic flow. It also implicates the glymphatic system in the altered cortical and endothelial functioning of the migraine brain. Copyright © 2017

Burden of impaired sleep quality on work productivity in functional dyspepsia.

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Matsuzaki, Juntaro; Suzuki, Hidekazu; Togawa, Koji; Yamane, Tsuyoshi; Mori, Hideki; Komori, Takahiro; Masaoka, Tatsuhiro; Kanai, Takanori

2018-04-01

Impaired sleep quality is common, and can reduce work productivity in patients with functional dyspepsia (FD). The objective of this article is to evaluate whether there is a direct association between the presence of FD and the severity of impaired sleep quality, and to calculate the economic loss due to the decreased work productivity associated with sleep quality. In Study 1, using a web-based survey completed by workers with and without FD, we evaluated impaired sleep quality, work and daily productivity, and the severity of reflux and bowel symptoms. In Study 2, the association between the presence of FD and the severity of impaired sleep quality was validated in a hospital-based cohort. In both Study 1 and 2, although impaired sleep quality was more frequent in participants with FD than in those without FD, the independent association between the presence of FD and the severity of impaired sleep quality was not observed after adjustment for the severity of reflux and bowel symptoms. FD participants with impaired sleep quality reported additional economic loss of 53,500 Japanese yen/month. Although the association between impaired sleep quality and FD was indirect, concomitant impaired sleep quality could worsen economic loss.

Sleep, Torpor and Memory Impairment

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Palchykova, S.; Tobler, I.

It is now well known that daily torpor induces a sleep deficit. Djungarian hamsters emerging from this hypometabolic state spend most of the time in sleep. This sleep is characterized by high initial values of EEG slow-wave activity (SWA) that monotonically decline during recovery sleep. These features resemble the changes seen in numerous species during recovery after prolonged wakefulness or sleep deprivation (SD). When hamsters are totally or partially sleep deprived immediately after emerging from torpor, an additional increase in SWA can be induced. It has been therefore postulated, that these slow- waves are homeostatically regulated, as predicted by the two-process model of sleep regulation, and that during daily torpor a sleep deficit is accumulated as it is during prolonged waking. The predominance of SWA in the frontal EEG observed both after SD and daily torpor provides further evidence for the similarity of these conditions. It has been shown in several animal and human studies that sleep can enhance memory consolidation, and that SD leads to memory impairment. Preliminary data obtained in the Djungarian hamster showed that both SD and daily torpor result in object recognition deficits. Thus, animals subjected to SD immediately after learning, or if they underwent an episode of daily torpor between learning and retention, displayed impaired recognition memory for complex object scenes. The investigation of daily torpor can reveal mechanisms that could have important implications for hypometabolic state induction in other mammalian species, including humans.

Differential effect of an anticholinergic antidepressant on sleep-dependent memory consolidation.

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Goerke, Monique; Cohrs, Stefan; Rodenbeck, Andrea; Kunz, Dieter

2014-05-01

Rapid eye movement (REM) sleep is considered critical to the consolidation of procedural memory - the memory of skills and habits. Many antidepressants strongly suppress REM sleep, however, and procedural memory consolidation has been shown to be impaired in depressed patients on antidepressant therapy. As a result, it is important to determine whether antidepressive therapy can lead to amnestic impairment. We thus investigated the effects of the anticholinergic antidepressant amitriptyline on sleep-dependent memory consolidation. Double-blind, placebo-controlled, randomized, parallel-group study. Sleep laboratory. Twenty-five healthy men (mean age: 26.8 ± 5.6 y). 75 mg amitriptyline versus placebo. To test memory consolidation, a visual discrimination task, a finger-tapping task, the Rey-Osterrieth Complex Figure Test, and the Rey Auditory-Verbal Learning Test were performed. Sleep was measured using polysomnography. Our findings show that amitriptyline profoundly suppressed REM sleep and impaired perceptual skill learning, but not motor skill or declarative learning. Our study is the first to demonstrate that an antidepressant can affect procedural memory consolidation in healthy subjects. Moreover, considering the results of a recent study, in which selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors were shown not to impair procedural memory consolidation, our findings suggest that procedural memory consolidation is not facilitated by the characteristics of REM sleep captured by visual sleep scoring, but rather by the high cholinergic tone associated with REM sleep. Our study contributes to the understanding of potentially undesirable behavioral effects of amitriptyline.

[Effect of intermittent hypoxia of sleep apnea on embryonic rat cortical neurons in vitro].

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Zhang, Chanjuan; Li, Yanzhong; Wang, Yan

2015-05-01

To investigate the effects of different pattens of intermittent hypoxia on the activity and apoptosis of primary cultured rat embryonic cortical neurons, and to evaluate the role of intermittent hypoxia in the mechanism of obstructive sleep syndrom induced cognitive function loss. The embryonic cerebral cortical neurons were cultured in vitro and were identified by immunofluorescence. Cultured neurons were randomly divided into intermittent hypoxia group, intermittent normal oxygen group, persistent hypoxia group and the control group, and intermittent hypoxia group was divided into five subgroups according to different frequency and time-bound. Neurons were exposed in different modes of hypoxia. MTT colorimetry was used to detect the viability of the neurons, and DAPI colorated measurement was used to calculate the percentages of neuron apoptosis. There were significantly different effects between all subgroups of intermittent hypoxia and the continued hypoxia group on neuronal activity and apoptosis (P Intermittent hypoxia groups with different frequency and time had no difference in neuronal activity and apoptosis (P > 0.05). The effect of intermittent hypoxia was more serious than that of continued hypoxia on neuronal activity and apoptosis; The impact of intermittent hypoxia on neuronal activity and apoptosis may be an important factor in obstructive sleep apnea related cognitive impairment.

The maturation of cortical sleep rhythms and networks over early development

OpenAIRE

Chu, Catherine Jean; Leahy, J.; Pathmanathan, Jay Sriram; Kramer, M.A.; Cash, Sydney S.

2014-01-01

Objective: Although neuronal activity drives all aspects of cortical development, how human brain rhythms spontaneously mature remains an active area of research. We sought to systematically evaluate the emergence of human brain rhythms and functional cortical networks over early development. Methods: We examined cortical rhythms and coupling patterns from birth through adolescence in a large cohort of healthy children (n=384) using scalp electroencephalogram (EEG) in the sleep state. ...

Some Sleep Drugs Can Impair Driving

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... For Consumers Home For Consumers Consumer Updates Some Sleep Drugs Can Impair Driving Share Tweet Linkedin Pin ... over-the-counter (OTC) drugs. Most Widely Used Sleep Drug Zolpidem—which has been on the market ...

Cortical Thinning and Altered Cortico-Cortical Structural Covariance of the Default Mode Network in Patients with Persistent Insomnia Symptoms.

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Suh, Sooyeon; Kim, Hosung; Dang-Vu, Thien Thanh; Joo, Eunyeon; Shin, Chol

2016-01-01

Recent studies have suggested that structural abnormalities in insomnia may be linked with alterations in the default-mode network (DMN). This study compared cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia (PI) and good sleepers (GS). The current study used a clinical subsample from the longitudinal community-based Korean Genome and Epidemiology Study (KoGES). Cortical thickness and structural connectivity linked to the DMN in patients with persistent insomnia symptoms (PIS; n = 57) were compared to good sleepers (GS; n = 40). All participants underwent MRI acquisition. Based on literature review, we selected cortical regions corresponding to the DMN. A seed-based structural covariance analysis measured cortical thickness correlation between each seed region of the DMN and other cortical areas. Association of cortical thickness and covariance with sleep quality and neuropsychological assessments were further assessed. Compared to GS, cortical thinning was found in PIS in the anterior cingulate cortex, precentral cortex, and lateral prefrontal cortex. Decreased structural connectivity between anterior and posterior regions of the DMN was observed in the PIS group. Decreased structural covariance within the DMN was associated with higher PSQI scores. Cortical thinning in the lateral frontal lobe was related to poor performance in executive function in PIS. Disrupted structural covariance network in PIS might reflect malfunctioning of antero-posterior disconnection of the DMN during the wake to sleep transition that is commonly found during normal sleep. The observed structural network alteration may further implicate commonly observed sustained sleep difficulties and cognitive impairment in insomnia. © 2016 Associated Professional Sleep Societies, LLC.

A single night of sleep loss impairs objective but not subjective working memory performance in a sex-dependent manner.

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Rångtell, Frida H; Karamchedu, Swathy; Andersson, Peter; Liethof, Lisanne; Olaya Búcaro, Marcela; Lampola, Lauri; Schiöth, Helgi B; Cedernaes, Jonathan; Benedict, Christian

2018-01-31

Acute sleep deprivation can lead to judgement errors and thereby increases the risk of accidents, possibly due to an impaired working memory. However, whether the adverse effects of acute sleep loss on working memory are modulated by auditory distraction in women and men are not known. Additionally, it is unknown whether sleep loss alters the way in which men and women perceive their working memory performance. Thus, 24 young adults (12 women using oral contraceptives at the time of investigation) participated in two experimental conditions: nocturnal sleep (scheduled between 22:30 and 06:30 hours) versus one night of total sleep loss. Participants were administered a digital working memory test in which eight-digit sequences were learned and retrieved in the morning after each condition. Learning of digital sequences was accompanied by either silence or auditory distraction (equal distribution among trials). After sequence retrieval, each trial ended with a question regarding how certain participants were of the correctness of their response, as a self-estimate of working memory performance. We found that sleep loss impaired objective but not self-estimated working memory performance in women. In contrast, both measures remained unaffected by sleep loss in men. Auditory distraction impaired working memory performance, without modulation by sleep loss or sex. Being unaware of cognitive limitations when sleep-deprived, as seen in our study, could lead to undesirable consequences in, for example, an occupational context. Our findings suggest that sleep-deprived young women are at particular risk for overestimating their working memory performance. © 2018 The Authors. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.

Sleep deprivation impairs object recognition in mice

NARCIS (Netherlands)

Palchykova, S; Winsky-Sommerer, R; Meerlo, P; Durr, R; Tobler, Irene

2006-01-01

Many studies in animals and humans suggest that sleep facilitates learning, memory consolidation, and retrieval. Moreover, sleep deprivation (SD) incurred after learning, impaired memory in humans, mice, rats, and hamsters. We investigated the importance of sleep and its timing in in object

Verbal memory impairments in schizophrenia associated with cortical thinning

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S. Guimond

2016-01-01

Full Text Available Verbal memory (VM represents one of the most affected cognitive domains in schizophrenia. Multiple studies have shown that schizophrenia is associated with cortical abnormalities, but it remains unclear whether these are related to VM impairments. Considering the vast literature demonstrating the role of the frontal cortex, the parahippocampal cortex, and the hippocampus in VM, we examined the cortical thickness/volume of these regions. We used a categorical approach whereby 27 schizophrenia patients with ‘moderate to severe’ VM impairments were compared to 23 patients with ‘low to mild’ VM impairments and 23 healthy controls. A series of between-group vertex-wise GLM on cortical thickness were performed for specific regions of interest defining the parahippocampal gyrus and the frontal cortex. When compared to healthy controls, patients with ‘moderate to severe’ VM impairments revealed significantly thinner cortex in the left frontal lobe, and the parahippocampal gyri. When compared to patients with ‘low to mild’ VM impairments, patients with ‘moderate to severe’ VM impairments showed a trend of thinner cortex in similar regions. Virtually no differences were observed in the frontal area of patients with ‘low to mild’ VM impairments relative to controls. No significant group differences were observed in the hippocampus. Our results indicate that patients with greater VM impairments demonstrate significant cortical thinning in regions known to be important in VM performance. Treating VM deficits in schizophrenia could have a positive effect on the brain; thus, subgroups of patients with more severe VM deficits should be a prioritized target in the development of new cognitive treatments.

[Clinical characteristics in Parkinson's disease patients with cognitive impairment and effects of cognitive impairment on sleep].

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Gong, Yan; Xiong, Kang-ping; Mao, Cheng-jie; Huang, Juan-ying; Hu, Wei-dong; Han, Fei; Chen, Rui; Liu, Chun-feng

2013-09-03

To analyze the clinical characteristics, correlation factors and clinical heterogeneities in Parkinson's disease (PD) patients with cognitive impairment and identify whether cognitive impairment could influence the aspect of sleep. A total of 130 PD outpatients and inpatients of sleep center at our hospital were eligible for participation. According to Montreal cognitive assessment (MOCA), they were divided into cognitive normal group (MOCA ≥ 26) (n = 51) and cognitive impairment group (MOCA cognitive impairment (MOCA cognitive impairment, the PD patients with cognitive impairment had significantly higher score of HAMD (10 ± 7 vs 7 ± 4), increased incidence of hallucinations (40.50% vs 19.60%) and REM behavior disorders (RBD) (63.29% vs 39.21%), significantly higher H-Y stage [2.5(2.0-3.0) vs 2.0 (2.0-2.5)] , United Kingdom Parkinson Disease Society (UPDRS) part III (22 ± 10 vs 19 ± 10) and levodopa-equivalent daily dose (LED) (511 ± 302vs 380 ± 272) (all P 0.05). Non-conditional Logistic regression analysis showed that PD duration, score of HAMD and H-Y stage were the major influencing factors of cognition. On PSG, significantly decreased sleep efficiency (57% ± 21% vs 66% ± 17%), higher percentage of non-REM sleep stage 1 (NREMS1) (37% ± 21% vs 27% ± 13%), lower percentage of NREMS2 (40% ± 17% vs 46% ± 13%) and REM sleep (39% ± 28% vs 54% ± 36%) were found for PD patients with cognitive impairment (all P cognitive impairment have more severe disease and partial nonmotor symptoms. And the severity of disease and depression is closely associated with cognitive impairment. Cognitive impairment may also affect sleep to cause decreased sleep efficiency and severe sleep structure disorder.

The Roles of Cortical Slow Waves in Synaptic Plasticity and Memory Consolidation.

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Miyamoto, Daisuke; Hirai, Daichi; Murayama, Masanori

2017-01-01

Sleep plays important roles in sensory and motor memory consolidation. Sleep oscillations, reflecting neural population activity, involve the reactivation of learning-related neurons and regulate synaptic strength and, thereby affect memory consolidation. Among sleep oscillations, slow waves (0.5-4 Hz) are closely associated with memory consolidation. For example, slow-wave power is regulated in an experience-dependent manner and correlates with acquired memory. Furthermore, manipulating slow waves can enhance or impair memory consolidation. During slow wave sleep, inter-areal interactions between the cortex and hippocampus (HC) have been proposed to consolidate declarative memory; however, interactions for non-declarative (HC-independent) memory remain largely uninvestigated. We recently showed that the directional influence in a slow-wave range through a top-down cortical long-range circuit is involved in the consolidation of non-declarative memory. At the synaptic level, the average cortical synaptic strength is known to be potentiated during wakefulness and depressed during sleep. Moreover, learning causes plasticity in a subset of synapses, allocating memory to them. Sleep may help to differentiate synaptic strength between allocated and non-allocated synapses (i.e., improving the signal-to-noise ratio, which may facilitate memory consolidation). Herein, we offer perspectives on inter-areal interactions and synaptic plasticity for memory consolidation during sleep.

The Roles of Cortical Slow Waves in Synaptic Plasticity and Memory Consolidation

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Daisuke Miyamoto

2017-11-01

Full Text Available Sleep plays important roles in sensory and motor memory consolidation. Sleep oscillations, reflecting neural population activity, involve the reactivation of learning-related neurons and regulate synaptic strength and, thereby affect memory consolidation. Among sleep oscillations, slow waves (0.5–4 Hz are closely associated with memory consolidation. For example, slow-wave power is regulated in an experience-dependent manner and correlates with acquired memory. Furthermore, manipulating slow waves can enhance or impair memory consolidation. During slow wave sleep, inter-areal interactions between the cortex and hippocampus (HC have been proposed to consolidate declarative memory; however, interactions for non-declarative (HC-independent memory remain largely uninvestigated. We recently showed that the directional influence in a slow-wave range through a top-down cortical long-range circuit is involved in the consolidation of non-declarative memory. At the synaptic level, the average cortical synaptic strength is known to be potentiated during wakefulness and depressed during sleep. Moreover, learning causes plasticity in a subset of synapses, allocating memory to them. Sleep may help to differentiate synaptic strength between allocated and non-allocated synapses (i.e., improving the signal-to-noise ratio, which may facilitate memory consolidation. Herein, we offer perspectives on inter-areal interactions and synaptic plasticity for memory consolidation during sleep.

Memory Reactivation during Rapid Eye Movement Sleep Promotes Its Generalization and Integration in Cortical Stores

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Sterpenich, Virginie; Schmidt, Christina; Albouy, Geneviève; Matarazzo, Luca; Vanhaudenhuyse, Audrey; Boveroux, Pierre; Degueldre, Christian; Leclercq, Yves; Balteau, Evelyne; Collette, Fabienne; Luxen, André; Phillips, Christophe; Maquet, Pierre

2014-01-01

Study Objectives: Memory reactivation appears to be a fundamental process in memory consolidation. In this study we tested the influence of memory reactivation during rapid eye movement (REM) sleep on memory performance and brain responses at retrieval in healthy human participants. Participants: Fifty-six healthy subjects (28 women and 28 men, age [mean ± standard deviation]: 21.6 ± 2.2 y) participated in this functional magnetic resonance imaging (fMRI) study. Methods and Results: Auditory cues were associated with pictures of faces during their encoding. These memory cues delivered during REM sleep enhanced subsequent accurate recollections but also false recognitions. These results suggest that reactivated memories interacted with semantically related representations, and induced new creative associations, which subsequently reduced the distinction between new and previously encoded exemplars. Cues had no effect if presented during stage 2 sleep, or if they were not associated with faces during encoding. Functional magnetic resonance imaging revealed that following exposure to conditioned cues during REM sleep, responses to faces during retrieval were enhanced both in a visual area and in a cortical region of multisensory (auditory-visual) convergence. Conclusions: These results show that reactivating memories during REM sleep enhances cortical responses during retrieval, suggesting the integration of recent memories within cortical circuits, favoring the generalization and schematization of the information. Citation: Sterpenich V, Schmidt C, Albouy G, Matarazzo L, Vanhaudenhuyse A, Boveroux P, Degueldre C, Leclercq Y, Balteau E, Collette F, Luxen A, Phillips C, Maquet P. Memory reactivation during rapid eye movement sleep promotes its generalization and integration in cortical stores. SLEEP 2014;37(6):1061-1075. PMID:24882901

Sleep impairment is a threat to good health

DEFF Research Database (Denmark)

Clark, Alice Jessie; Jørgensen, Thea Suldrup; Bonke, Jens

2016-01-01

sleep. A quiet, dark and well-tempered bedroom and physical activity during the day may have a positive impact on sleep. Impaired sleep may be related to stress and conditions at home or at work. Psychological sleep treatment is free of adverse side effects with effects comparable to effects of medical...

Novel experience induces persistent sleep-dependent plasticity in the cortex but not in the hippocampus

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Sidarta Ribeiro

2007-10-01

Full Text Available Episodic and spatial memories engage the hippocampus during acquisition but migrate to the cerebral cortex over time. We have recently proposed that the interplay between slow-wave (SWS and rapid eye movement (REM sleep propagates recent synaptic changes from the hippocampus to the cortex. To test this theory, we jointly assessed extracellular neuronal activity, local field potentials (LFP, and expression levels of plasticity-related immediate-early genes (IEG arc and zif-268 in rats exposed to novel spatio-tactile experience. Post-experience firing rate increases were strongest in SWS and lasted much longer in the cortex (hours than in the hippocampus (minutes. During REM sleep, firing rates showed strong temporal dependence across brain areas: cortical activation during experience predicted hippocampal activity in the first post-experience hour, while hippocampal activation during experience predicted cortical activity in the third post-experience hour. Four hours after experience, IEG expression was specifically upregulated during REM sleep in the cortex, but not in the hippocampus. Arc gene expression in the cortex was proportional to LFP amplitude in the spindle-range (10-14 Hz but not to firing rates, as expected from signals more related to dendritic input than to somatic output. The results indicate that hippocampo-cortical activation during waking is followed by multiple waves of cortical plasticity as full sleep cycles recur. The absence of equivalent changes in the hippocampus may explain its mnemonic disengagement over time.

The cortical signature of impaired gesturing: Findings from schizophrenia

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Petra Verena Viher

2018-01-01

Full Text Available Schizophrenia is characterized by deficits in gesturing that is important for nonverbal communication. Research in healthy participants and brain-damaged patients revealed a left-lateralized fronto-parieto-temporal network underlying gesture performance. First evidence from structural imaging studies in schizophrenia corroborates these results. However, as of yet, it is unclear if cortical thickness abnormalities contribute to impairments in gesture performance. We hypothesized that patients with deficits in gesture production show cortical thinning in 12 regions of interest (ROIs of a gesture network relevant for gesture performance and recognition. Forty patients with schizophrenia and 41 healthy controls performed hand and finger gestures as either imitation or pantomime. Group differences in cortical thickness between patients with deficits, patients without deficits, and controls were explored using a multivariate analysis of covariance. In addition, the relationship between gesture recognition and cortical thickness was investigated. Patients with deficits in gesture production had reduced cortical thickness in eight ROIs, including the pars opercularis of the inferior frontal gyrus, the superior and inferior parietal lobes, and the superior and middle temporal gyri. Gesture recognition correlated with cortical thickness in fewer, but mainly the same, ROIs within the patient sample. In conclusion, our results show that impaired gesture production and recognition in schizophrenia is associated with cortical thinning in distinct areas of the gesture network.

Cortical Thickness and Episodic Memory Impairment in Systemic Lupus Erythematosus.

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Bizzo, Bernardo Canedo; Sanchez, Tiago Arruda; Tukamoto, Gustavo; Zimmermann, Nicolle; Netto, Tania Maria; Gasparetto, Emerson Leandro

2017-01-01

The purpose of this study was to investigate differences in brain cortical thickness of systemic lupus erythematosus (SLE) patients with and without episodic memory impairment and healthy controls. We studied 51 patients divided in 2 groups (SLE with episodic memory deficit, n = 17; SLE without episodic memory deficit, n = 34) by the Rey Auditory Verbal Learning Test and 34 healthy controls. Groups were paired based on sex, age, education, Mini-Mental State Examination score, and accumulation of disease burden. Cortical thickness from magnetic resonance imaging scans was determined using the FreeSurfer software package. SLE patients with episodic memory deficits presented reduced cortical thickness in the left supramarginal cortex and superior temporal gyrus when compared to the control group and in the right superior frontal, caudal, and rostral middle frontal and precentral gyri when compared to the SLE group without episodic memory impairment considering time since diagnosis of SLE as covaried. There were no significant differences in the cortical thickness between the SLE without episodic memory and control groups. Different memory-related cortical regions thinning were found in the episodic memory deficit group when individually compared to the groups of patients without memory impairment and healthy controls. Copyright © 2016 by the American Society of Neuroimaging.

Sleep-dependent memory consolidation--what can be learnt from children?

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Wilhelm, I; Prehn-Kristensen, A; Born, J

2012-08-01

Extensive research has been accumulated demonstrating that sleep is essential for processes of memory consolidation in adults. In children and infants, a great capacity to learn and to memorize coincides with longer and more intense sleep. Here, we review the available data on the influence of sleep on memory consolidation in healthy children and infants, as well as in children with attention-deficit/hyperactivity disorder (ADHD) as a model of prefrontal impairment, and consider possible mechanisms underlying age-dependent differences. Findings indicate a major role of slow wave sleep (SWS) for processes of memory consolidation during early development. Importantly, longer and deeper SWS during childhood appears to produce a distinctly superior strengthening of hippocampus-dependent declarative memories, but concurrently prevents an immediate benefit from sleep for procedural memories, as typically observed in adults. Studies of ADHD children point toward an essential contribution of prefrontal cortex to the preferential consolidation of declarative memory during SWS. Developmental studies of sleep represent a particularly promising approach for characterizing the supra-ordinate control of memory consolidation during sleep by prefrontal-hippocampal circuitry underlying the encoding of declarative memory. Copyright © 2012 Elsevier Ltd. All rights reserved.

A preliminary investigation of sleep quality in functional neurological disorders: Poor sleep appears common, and is associated with functional impairment.

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Graham, Christopher D; Kyle, Simon D

2017-07-15

Functional neurological disorders (FND) are disabling conditions for which there are few empirically-supported treatments. Disturbed sleep appears to be part of the FND context; however, the clinical importance of sleep disturbance (extent, characteristics and impact) remains largely unknown. We described sleep quality in two samples, and investigated the relationship between sleep and FND-related functional impairment. We included a sample recruited online via patient charities (N=205) and a consecutive clinical sample (N=20). Participants completed validated measures of sleep quality and sleep characteristics (e.g. total sleep time, sleep efficiency), mood, and FND-related functional impairment. Poor sleep was common in both samples (89% in the clinical range), which was characterised by low sleep efficiency (M=65.40%) and low total sleep time (M=6.05h). In regression analysis, sleep quality was negatively associated with FND-related functional impairment, accounting for 16% of the variance and remaining significant after the introduction of mood variables. These preliminary analyses suggest that subjective sleep disturbance (low efficiency, short sleep) is common in FND. Sleep quality was negatively associated with the functional impairment attributed to FND, independent of depression. Therefore, sleep disturbance may be a clinically important feature of FND. Copyright © 2017 Elsevier B.V. All rights reserved.

The perilipin homologue, lipid storage droplet 2, regulates sleep homeostasis and prevents learning impairments following sleep loss.

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Matthew S Thimgan

2010-08-01

Full Text Available Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. Recently, two genes, brummer (bmm and Lipid storage droplet 2 (Lsd2, have been shown to modulate the response to starvation. bmm mutants have excess fat and are resistant to starvation, whereas Lsd2 mutants are lean and sensitive to starvation. Thus, we hypothesized that bmm and Lsd2 may play a role in sleep regulation. Indeed, bmm mutant flies display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking.

Impaired quality and efficiency of sleep impairs cognitive functioning in Addison's disease.

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Henry, Michelle; Ross, Ian Louis; Wolf, Pedro Sofio Abril; Thomas, Kevin Garth Flusk

2017-04-01

Standard replacement therapy for Addison's disease (AD) does not restore a normal circadian rhythm. Periods of sub- and supra- physiological cortisol levels experienced by patients with AD likely induce disrupted sleep. Given that healthy sleep plays an important role in memory consolidation, the novelty of the current study was to characterise, using objective measures, the relationship between sleep and memory in patients with AD, and to examine the hypothesis that poor sleep is a biological mechanism underlying memory impairment in those patients. We used a within-subjects design. Ten patients with AD and 10 matched healthy controls completed standardised neuropsychological tests assessing declarative memory (Rey Auditory Verbal Learning Test) and procedural memory (Finger Tapping Task) before and after a period of actigraphy-measured sleep, and before and after a period of waking. Relative to healthy controls, patients with AD experienced disrupted sleep characterised by poorer sleep efficiency and more time spent awake. Patients also showed impaired verbal learning and memory relative to healthy controls (p=0.007). Furthermore, whereas healthy controls' declarative memory performance benefited from a period of sleep compared to waking (p=0.032), patients with AD derived no such benefit from sleep (p=0.448). Regarding the procedural memory task, analyses detected no significant between-group differences (all p's<0.065), and neither group showed significant sleep-enhanced performance. We demonstrated, using actigraphy and standardized measures of memory performance, an association between sleep disturbances and cognitive deficits in patients with AD. These results suggest that, in patients with AD, the source of memory deficits is, at least to some extent, disrupted sleep patterns that interfere with optimal consolidation of previously-learned declarative information. Hence, treating the sleep disturbances that are frequently experienced by patients with AD may

Daily impaired detachment and short-term effects of impaired sleep quality on next-day commuting near-accidents - an ambulatory diary study.

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Pereira, Diana; Bucher, Sarah; Elfering, Achim

2016-08-01

This study investigated the short-term effects of daily recovery, that is, impaired psychological detachment from work and various actigraphical indicators of sleep quality, on near-accidents when commuting to work the next morning. Furthermore, the mediating effect of actigraphically assessed sleep quality on the relationship between impaired psychological detachment from work and near-accidents when commuting to work was analysed. Fifty-six full-time employees of a Swiss assurance company participated in the one-week study. Multilevel analyses revealed that impaired detachment was highly related to a decrease in sleep duration. Furthermore, impaired daily recovery processes, such as impaired psychological detachment from work and disturbed sleep quality, were related to commuting near-accidents. Impaired sleep quality mediated the effect of impaired psychological detachment from work on these near-accidents. Our results show that occupational safety interventions should address both impaired psychological detachment from work and sleep quality in order to prevent near accidents when commuting to work. Practitioner Summary: Commuting accidents occur frequently and have detrimental effects on employees, organisations and society. This study shows that daily lack of recovery, that is, impaired psychological detachment and impaired sleep quality, is related to near-accidents when commuting to work the next morning. Primary prevention of commuting accidents should therefore address daily lack of recovery.

Sleep: A Novel Mechanistic Pathway, Biomarker, and Treatment Target in the Pathology of Alzheimer's Disease?

Energy Technology Data Exchange (ETDEWEB)

Mander, Bryce A. [Univ. of California, Berkeley, CA (United States). Sleep and Neuroimaging Laboratory; Winer, Joseph R. [Univ. of California, Berkeley, CA (United States). Sleep and Neuroimaging Laboratory; Jagust, William J. [Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute; Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States). Molecular Biophysics and Bioimaging Div.; Walker, Matthew P. [Univ. of California, Berkeley, CA (United States). Sleep and Neuroimaging Laboratory; Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Institute

2016-06-17

Sleep disruption appears to be a major component of Alzheimer's disease (AD) and its pathophysiology. Signature abnormalities of sleep emerge before clinical onset of AD. Moreover, insufficient sleep facilitates accumulation of amyloid-β (Aβ), potentially triggering earlier cognitive decline and conversion to AD. Building on such findings, this review has four goals: evaluating (i) associations and plausible mechanisms linking non-rapid-eye-movement (NREM) sleep disruption, Aβ, and AD; (ii) a role for NREM sleep disruption as a novel factor linking cortical Aβ to impaired hippocampus-dependent memory consolidation; (iii) the potential diagnostic utility of NREM sleep disruption as a new biomarker of AD; and (iv) the possibility of sleep as a new treatment target in aging, affording preventative and therapeutic benefits.

Neurological impairments and sleep-wake behaviour among the mentally retarded.

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Lindblom, N; Heiskala, H; Kaski, M; Leinonen, L; Nevanlinna, A; Iivanainen, M; Laakso, M L

2001-12-01

The objective of the present study was to evaluate the relationship between the sleep-wake behaviour and neurological impairments among mentally retarded people. The sleep-wake behaviour of 293 mentally retarded subjects living in a rehabilitation center was studied by a standardized observation protocol carried out by trained staff members. The protocol consisted of brief check-ups of the subjects' sleep-wake status at 20-min intervals for five randomly chosen 24-h periods during 4 months. From the raw data five sleep-wake behaviour variables were formed. The data concerning the subject characteristics (age, body mass index (BMI), gender, degree of mental retardation, presence of locomotor disability, that of epilepsy, blindness or deafness and the usage of psychotropic medications) were collected from the medical records. Two main findings emerged: (1) severe locomotor disability, blindness and active epilepsy were found to be independent predictors of increased daytime sleep and increased number of wake-sleep transitions and (2) the subjects with a combination of two or all three of these impairments had a significantly more fragmented and abnormally distributed sleep than those with none or milder forms of these impairments. Age, BMI, degree of mental retardation and the studied medications played a minor role in the sleep disturbances of the study population. Finally, deafness was not found to be associated with any of the measured sleep-wake variables.

Retrosplenial cortical thinning as a possible major contributor for cognitive impairment in HIV patients

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Shin, Na-Young [The Catholic University of Korea, Department of Radiology, College of Medicine, Seoul (Korea, Republic of); Hong, Jinwoo; Yoon, Uicheul [Catholic University of Daegu, Department of Biomedical Engineering, College of Health and Medical Science, Gyeongsan-si, Gyeongbuk (Korea, Republic of); Choi, Jun Yong [Yonsei University College of Medicine, Department of Internal Medicine and AIDS Research Institute, Seoul (Korea, Republic of); Lee, Seung-Koo [Yonsei University College of Medicine, Department of Radiology, Seoul (Korea, Republic of); Lim, Soo Mee [Ewha Womans University, School of Medicine, Department of Radiology, Seoul (Korea, Republic of)

2017-11-15

To identify brain cortical regions relevant to HIV-associated neurocognitive disorder (HAND) in HIV patients. HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness. Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills. This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment. (orig.)

Retrosplenial cortical thinning as a possible major contributor for cognitive impairment in HIV patients

International Nuclear Information System (INIS)

Shin, Na-Young; Hong, Jinwoo; Yoon, Uicheul; Choi, Jun Yong; Lee, Seung-Koo; Lim, Soo Mee

2017-01-01

To identify brain cortical regions relevant to HIV-associated neurocognitive disorder (HAND) in HIV patients. HIV patients with HAND (n = 10), those with intact cognition (HIV-IC; n = 12), and age-matched, seronegative controls (n = 11) were recruited. All participants were male and underwent 3-dimensional T1-weighted imaging. Both vertex-wise and region of interest (ROI) analyses were performed to analyse cortical thickness. Compared to controls, both HIV-IC and HAND showed decreased cortical thickness mainly in the bilateral primary sensorimotor areas, extending to the prefrontal and parietal cortices. When directly comparing HIV-IC and HAND, HAND showed cortical thinning in the left retrosplenial cortex, left dorsolateral prefrontal cortex, left inferior parietal lobule, bilateral superior medial prefrontal cortices, right temporoparietal junction and left hippocampus, and cortical thickening in the left middle occipital cortex. Left retrosplenial cortical thinning showed significant correlation with slower information processing, declined verbal memory and executive function, and impaired fine motor skills. This study supports previous research suggesting the selective vulnerability of the primary sensorimotor cortices and associations between cortical thinning in the prefrontal and parietal cortices and cognitive impairment in HIV-infected patients. Furthermore, for the first time, we propose retrosplenial cortical thinning as a possible major contributor to HIV-associated cognitive impairment. (orig.)

Sleep and its associations with perceived and objective cognitive impairment in individuals with multiple sclerosis.

Science.gov (United States)

Hughes, Abbey J; Parmenter, Brett A; Haselkorn, Jodie K; Lovera, Jesus F; Bourdette, Dennis; Boudreau, Eilis; Cameron, Michelle H; Turner, Aaron P

2017-08-01

Problems with sleep and cognitive impairment are common among people with multiple sclerosis (MS). The present study examined the relationship between self-reported sleep and both objective and perceived cognitive impairment in MS. Data were obtained from the baseline assessment of a multi-centre intervention trial (NCT00841321). Participants were 121 individuals with MS. Nearly half (49%) of participants met the criteria for objective cognitive impairment; however, cognitively impaired and unimpaired participants did not differ on any self-reported sleep measures. Nearly two-thirds (65%) of participants met the criteria for 'poor' sleep, and poorer sleep was significantly associated with greater levels of perceived cognitive impairment. Moreover, the relationships between self-reported sleep and perceived cognitive impairment were significant beyond the influence of clinical and demographic factors known to influence sleep and cognitive functioning (e.g. age, sex, education level, disability severity, type of MS, disease duration, depression and fatigue). However, self-reported sleep was not associated with any measures of objective cognitive impairment. Among different types of perceived cognitive impairment, poor self-reported sleep was most commonly related to worse perceived executive function (e.g. planning/organization) and prospective memory. Results from the present study emphasize that self-reported sleep is significantly and independently related to perceived cognitive impairment in MS. In terms of clinical implications, interventions focused on improving sleep may help improve perceived cognitive function and quality of life in this population; however, the impact of improved sleep on objective cognitive function requires further investigation. © 2017 European Sleep Research Society.

Both oophorectomy and obesity impaired solely hippocampal-dependent memory via increased hippocampal dysfunction.

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Mantor, Duangkamol; Pratchayasakul, Wasana; Minta, Wanitchaya; Sutham, Wissuta; Palee, Siripong; Sripetchwandee, Jirapas; Kerdphoo, Sasiwan; Jaiwongkum, Thidarat; Sriwichaiin, Sirawit; Krintratun, Warunsorn; Chattipakorn, Nipon; Chattipakorn, Siriporn C

2018-04-17

Our previous study demonstrated that obesity aggravated peripheral insulin resistance and brain dysfunction in the ovariectomized condition. Conversely, the effect of obesity followed by oophorectomy on brain oxidative stress, brain apoptosis, synaptic function and cognitive function, particularly in hippocampal-dependent and hippocampal-independent memory, has not been investigated. Our hypothesis was that oophorectomy aggravated metabolic impairment, brain dysfunction and cognitive impairment in obese rats. Thirty-two female rats were fed with either a normal diet (ND, n = 16) or a high-fat diet (HFD, n = 16) for a total of 20 weeks. At week 13, rats in each group were subdivided into sham and ovariectomized subgroups (n = 8/subgroup). At week 20, all rats were tested for hippocampal-dependent and hippocampal-independent memory by using Morris water maze test (MWM) and Novel objective recognition (NOR) tests, respectively. We found that the obese-insulin resistant condition occurred in sham-HFD-fed rats (HFS), ovariectomized-ND-fed rats (NDO), and ovariectomized-HFD-fed rats (HFO). Increased hippocampal oxidative stress level, increased hippocampal apoptosis, increased hippocampal synaptic dysfunction, decreased hippocampal estrogen level and impaired hippocampal-dependent memory were observed in HFS, NDO, and HFO rats. However, the hippocampal-independent memory, cortical estrogen levels, cortical ROS production, and cortical apoptosis showed no significant difference between groups. These findings suggested that oophorectomy and obesity exclusively impaired hippocampal-dependent memory, possibly via increased hippocampal dysfunction. Nonetheless, oophorectomy did not aggravate these deleterious effects under conditions of obesity. Copyright © 2017. Published by Elsevier Inc.

EEG-guided transcranial magnetic stimulation reveals rapid shifts in motor cortical excitability during the human sleep slow oscillation

DEFF Research Database (Denmark)

Bergmann, Til O; Mölle, Matthias; Schmidt, Marlit A

2012-01-01

Evoked cortical responses do not follow a rigid input–output function but are dynamically shaped by intrinsic neural properties at the time of stimulation. Recent research has emphasized the role of oscillatory activity in determining cortical excitability. Here we employed EEG-guided transcranial......, closely resembling a spontaneous SO. However, both MEPs and TEPs were consistently larger when evoked during SO up-states than during down-states, and ampliudes within each SO state depended on the actual EEG potential at the time and site of stimulation. These results provide first-time evidence...... magnetic stimulation (TMS) during non-rapid eye movement sleep to examine whether the spontaneous

PROMIS Sleep Disturbance and Sleep-Related Impairment in Adolescents: Examining Psychometrics Using Self-Report and Actigraphy.

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Hanish, Alyson E; Lin-Dyken, Deborah C; Han, Joan C

The National Institutes of Health Patient-Reported Outcomes Measurement Information System (PROMIS) has self-reported health measures available for both pediatric and adult populations, but no pediatric measures are available currently in the sleep domains. The purpose of this observational study was to perform preliminary validation studies on age-appropriate, self-reported sleep measures in healthy adolescents. This study examined 25 healthy adolescents' self-reported daytime sleepiness, sleep disturbance, sleep-related impairment, and sleep patterns. Healthy adolescents completed a physical exam at the National Institutes of Health Clinical Center (Bethesda, MD), had no chronic medical conditions, and were not taking any chronic medications. The Cleveland Adolescent Sleepiness Questionnaire (CASQ), PROMIS Sleep Disturbance (v. 1.0; 8a), and PROMIS Sleep-Related Impairment (v. 1.0; 8b) questionnaires were completed, and sleep patterns were assessed using actigraphy. Total scores on the three sleep questionnaires were correlated (all Spearman's r > .70, p psychometrically sound sleep questionnaires. Findings suggest the potential research and clinical utility of adult versions of PROMIS sleep measures in adolescents. Future studies should include larger, more diverse samples and explore additional psychometric properties of PROMIS sleep measures to provide age-appropriate, validated, and reliable measures of sleep in adolescents.

Emotional bias of sleep-dependent processing shifts from negative to positive with aging.

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Jones, Bethany J; Schultz, Kurt S; Adams, Sydney; Baran, Bengi; Spencer, Rebecca M C

2016-09-01

Age-related memory decline has been proposed to result partially from impairments in memory consolidation over sleep. However, such decline may reflect a shift toward selective processing of positive information with age rather than impaired sleep-related mechanisms. In the present study, young and older adults viewed negative and neutral pictures or positive and neutral pictures and underwent a recognition test after sleep or wake. Subjective emotional reactivity and affect were also measured. Compared with waking, sleep preserved valence ratings and memory for positive but not negative pictures in older adults and negative but not positive pictures in young adults. In older adults, memory for positive pictures was associated with slow wave sleep. Furthermore, slow wave sleep predicted positive affect in older adults but was inversely related to positive affect in young adults. These relationships were strongest for older adults with high memory for positive pictures and young adults with high memory for negative pictures. Collectively, these results indicate preserved but selective sleep-dependent memory processing with healthy aging that may be biased to enhance emotional well-being. Copyright © 2016 Elsevier Inc. All rights reserved.

When Thinking Impairs Sleep: Trait, Daytime and Nighttime Repetitive Thinking in Insomnia.

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Lancee, Jaap; Eisma, Maarten C; van Zanten, Kristopher B; Topper, Maurice

2017-01-01

We performed two studies in individuals with sleep problems to investigate trait, daytime, and nighttime repetitive thinking as risk factors for insomnia. In Study 1, 139 participants completed questionnaires on worry, rumination, insomnia, anxiety, depression, and a sleep diary. Trait rumination and trait worry were not associated with sleep impairment. In Study 2, 64 participants completed similar measures and a daytime and nighttime sleep-related worry diary. Only nighttime sleep-related worry was consistently associated with sleep impairment. Overall, results indicate that nighttime sleep-related worry is important in the maintenance of insomnia, whereas effects of trait and daytime repetitive thinking are more benign. Treatment for insomnia can potentially be improved by focusing more on nighttime sleep-related worry.

Cortical dendritic activity correlates with spindle-rich oscillations during sleep in rodents.

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Seibt, Julie; Richard, Clément J; Sigl-Glöckner, Johanna; Takahashi, Naoya; Kaplan, David I; Doron, Guy; de Limoges, Denis; Bocklisch, Christina; Larkum, Matthew E

2017-09-25

How sleep influences brain plasticity is not known. In particular, why certain electroencephalographic (EEG) rhythms are linked to memory consolidation is poorly understood. Calcium activity in dendrites is known to be necessary for structural plasticity changes, but this has never been carefully examined during sleep. Here, we report that calcium activity in populations of neocortical dendrites is increased and synchronised during oscillations in the spindle range in naturally sleeping rodents. Remarkably, the same relationship is not found in cell bodies of the same neurons and throughout the cortical column. Spindles during sleep have been suggested to be important for brain development and plasticity. Our results provide evidence for a physiological link of spindles in the cortex specific to dendrites, the main site of synaptic plasticity.Different stages of sleep, marked by particular electroencephalographic (EEG) signatures, have been linked to memory consolidation, but underlying mechanisms are poorly understood. Here, the authors show that dendritic calcium synchronisation correlates with spindle-rich sleep phases.

L-carnitine prevents memory impairment induced by chronic REM-sleep deprivation.

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Alzoubi, Karem H; Rababa'h, Abeer M; Owaisi, Amani; Khabour, Omar F

2017-05-01

Sleep deprivation (SD) negatively impacts memory, which was related to oxidative stress induced damage. L-carnitine is a naturally occurring compound, synthesized endogenously in mammalian species and known to possess antioxidant properties. In this study, the effect of L-carnitine on learning and memory impairment induced by rapid eye movement sleep (REM-sleep) deprivation was investigated. REM-sleep deprivation was induced using modified multiple platform model (8h/day, for 6 weeks). Simultaneously, L-carnitine was administered (300mg/kg/day) intraperitoneally for 6 weeks. Thereafter, the radial arm water maze (RAWM) was used to assess spatial learning and memory. Additionally, the hippocampus levels of antioxidant biomarkers/enzymes: reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratio, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) and thiobarbituric acid reactive substance (TBARS) were assessed. The results showed that chronic REM-sleep deprivation impaired both short- and long-term memory (Psleep deprivation induced reduction in the hippocampus ratio of GSH/GSSG, activity of catalase, GPx, and SOD. No change was observed in TBARS among tested groups (P>0.05). In conclusion, chronic REM-sleep deprivation induced memory impairment, and treatment with L-carnitine prevented this impairment through normalizing antioxidant mechanisms in the hippocampus. Copyright © 2017 Elsevier Inc. All rights reserved.

Polysomnographic Sleep Dysregulation in Cocaine Dependence

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Edwin M. Valladares

2007-01-01

Full Text Available Insomnia and sleep disturbance are associated with declines in health functioning, alongwith increases in mortality risk. Given the prominence of reported sleep disturbance incocaine-dependent subjects and persistence into recovery, understanding the natureand severity of these disturbances in this population may help to identify relevantpathways that contribute to the increased mortality in cocaine dependence. Polysomnography provides a means of objectively characterizing sleep and, in turn, sleep disturbances. Few studies have used polysomnography to evaluate sleep incocaine-dependent persons, yet these studies have the potential to advance treatmentsthat will ultimately reduce morbidity in cocaine-dependent subjects.

[Sleep disorders and impaired sleep as adverse drug reactions of psychotropic drugs: an evaluation of data of summaries of product characteristics].

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Gahr, Maximilian; Connemann, Bernhard J; Zeiss, René; Fröhlich, Albrecht

2018-03-02

 Psychopharmacotherapy is essential in the treatment of many mental disorders. Adverse drug reactions (ADR) have impact on compliance and tolerability. Sleep disorders or impaired sleep may occur as ADRs of psychopharmacotherapy. Sleep disorders are associated with an increased risk for physical and mental illness and may impair cognition, impulse control, emotion regulation and mood. Objective of the following study was the systematic presentation of type and risk of sleep disorders/impairments of sleep of frequently prescribed psychotropic drugs.  Psychotropic agents that are most frequently prescribed in Germany were identified by using the Arzneiverordnungs-Report 2016. Summaries of product characteristics (SmPC) of corresponding original products were analyzed regarding presence and frequency of sleep disorders/impairments of sleep according to the International Classification of Sleep Disorders 3 (ICSD-3).  N = 64 SmPCs were analyzed. In most of the analyzed SmPCs, at least one sleep disorder (50/64; 78 %) was listed. At least one SmPC with a corresponding ADR was found in the categories insomnia (52 %), parasomnias (33 %), and sleep-related movement disorders (20 %); sleep-related breathing disorders (6 %) and central disorders of hypersomnolence (5 %) were rarely listed; circadian rhythm sleep-wake disorder was not found. The SmPCs of the four most frequently prescribed agents (citalopram > venlafaxine > mirtazapine > sertraline) listed insomnia as an ADR. Nearly all analysed hypnotics (except chloral hydrate) were associated with nightmares.  Most of the psychotropic agents frequently prescribed in Germany may induce sleep disorders/impairments of sleep. The four most frequently prescribed agents were antidepressants and all of the corresponding SmPCs listed insomnia as a possible ADR. Sleep disorders should be taken seriously as possible ADRs of psychopharmacotherapy. © Georg Thieme Verlag KG Stuttgart · New York.

Repeated Sleep Restriction in Adolescent Rats Altered Sleep Patterns and Impaired Spatial Learning/Memory Ability

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Yang, Su-Rong; Sun, Hui; Huang, Zhi-Li; Yao, Ming-Hui; Qu, Wei-Min

2012-01-01

Study Objectives: To investigate possible differences in the effect of repeated sleep restriction (RSR) during adolescence and adulthood on sleep homeostasis and spatial learning and memory ability. Design: The authors examined electroencephalograms of rats as they were subjected to 4-h daily sleep deprivation that continued for 7 consecutive days and assessed the spatial learning and memory by Morris water maze test (WMT). Participants: Adolescent and adult rats. Measurements and Results: Adolescent rats exhibited a similar amount of rapid eye movement (REM) and nonrapid eye movement (NREM) sleep with higher slow wave activity (SWA, 0.5-4 Hz) and fewer episodes and conversions with prolonged durations, indicating they have better sleep quality than adult rats. After RSR, adult rats showed strong rebound of REM sleep by 31% on sleep deprivation day 1; this value was 37% on sleep deprivation day 7 in adolescents compared with 20-h baseline level. On sleep deprivation day 7, SWA in adult and adolescent rats increased by 47% and 33%, and such elevation lasted for 5 h and 7 h, respectively. Furthermore, the authors investigated the effects of 4-h daily sleep deprivation immediately after the water maze training sessions on spatial cognitive performance. Adolescent rats sleep-restricted for 7 days traveled a longer distance to find the hidden platform during the acquisition training and had fewer numbers of platform crossings in the probe trial than those in the control group, something that did not occur in the sleep-deprived adult rats. Conclusions: Repeated sleep restriction (RSR) altered sleep profiles and mildly impaired spatial learning and memory capability in adolescent rats. Citation: Yang SR; Sun H; Huang ZL; Yao MH; Qu WM. Repeated sleep restriction in adolescent rats altered sleep patterns and impaired spatial learning/memory ability. SLEEP 2012;35(6):849-859. PMID:22654204

Impaired bed mobility and disordered sleep in Parkinson's disease.

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Stack, Emma L; Ashburn, Ann M

2006-09-01

The contribution of impaired mobility to disordered sleep in Parkinson's disease (PD) remains uncertain. We evaluated the sleep of 38 people with PD and observed their turning strategies. Most reported difficulty maintaining sleep and difficulty turning. Those who hip-hitched rated themselves more disabled and those who sat up had more severe PD than those who used support. Using multiple strategies was associated with sleep disturbance. As the ability to turn deteriorates, we recommend patients identify the single strategy least disruptive to sleep. Research must address whether improving mobility improves sleep quality. (c) 2006 Movement Disorder Society.

Sleep deprivation and daily torpor impair object recognition in Djungarian hamsters

NARCIS (Netherlands)

Palchykova, S; Crestani, F; Meerlo, P; Tobler, Irene

2006-01-01

Sleep has been shown to play a facilitating role in memory consolidation, whereas sleep deprivation leads to performance impairment both in humans and rodents. The effects of 4-h sleep deprivation on recognition memory were investigated in the Djungarian hamster (Phodopus sungorus). Because sleep

Effects of sleep deprivation on cognition.

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Killgore, William D S

2010-01-01

Sleep deprivation is commonplace in modern society, but its far-reaching effects on cognitive performance are only beginning to be understood from a scientific perspective. While there is broad consensus that insufficient sleep leads to a general slowing of response speed and increased variability in performance, particularly for simple measures of alertness, attention and vigilance, there is much less agreement about the effects of sleep deprivation on many higher level cognitive capacities, including perception, memory and executive functions. Central to this debate has been the question of whether sleep deprivation affects nearly all cognitive capacities in a global manner through degraded alertness and attention, or whether sleep loss specifically impairs some aspects of cognition more than others. Neuroimaging evidence has implicated the prefrontal cortex as a brain region that may be particularly susceptible to the effects of sleep loss, but perplexingly, executive function tasks that putatively measure prefrontal functioning have yielded inconsistent findings within the context of sleep deprivation. Whereas many convergent and rule-based reasoning, decision making and planning tasks are relatively unaffected by sleep loss, more creative, divergent and innovative aspects of cognition do appear to be degraded by lack of sleep. Emerging evidence suggests that some aspects of higher level cognitive capacities remain degraded by sleep deprivation despite restoration of alertness and vigilance with stimulant countermeasures, suggesting that sleep loss may affect specific cognitive systems above and beyond the effects produced by global cognitive declines or impaired attentional processes. Finally, the role of emotion as a critical facet of cognition has received increasing attention in recent years and mounting evidence suggests that sleep deprivation may particularly affect cognitive systems that rely on emotional data. Thus, the extent to which sleep deprivation

Altered Regional Brain Cortical Thickness in Pediatric Obstructive Sleep Apnea

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Paul M. Macey

2018-01-01

Full Text Available RationaleObstructive sleep apnea (OSA affects 2–5% of all children and is associated with cognitive and behavioral deficits, resulting in poor school performance. These psychological deficits may arise from brain injury, as seen in preliminary findings of lower gray matter volume among pediatric OSA patients. However, the psychological deficits in OSA are closely related to functions in the cortex, and such brain areas have not been specifically assessed. The objective was to determine whether cortical thickness, a marker of possible brain injury, is altered in children with OSA.MethodsWe examined regional brain cortical thicknesses using high-resolution T1-weighted magnetic resonance images in 16 pediatric OSA patients (8 males; mean age ± SD = 8.4 ± 1.2 years; mean apnea/hypopnea index ± SD = 11 ± 6 events/h and 138 controls (8.3 ± 1.1 years; 62 male; 138 subjects from the NIH Pediatric MRI database to identify cortical thickness differences in pediatric OSA subjects.ResultsCortical thinning occurred in multiple regions including the superior frontal, ventral medial prefrontal, and superior parietal cortices. The left side showed greater thinning in the superior frontal cortex. Cortical thickening was observed in bilateral precentral gyrus, mid-to-posterior insular cortices, and left central gyrus, as well as right anterior insula cortex.ConclusionChanges in cortical thickness are present in children with OSA and likely indicate disruption to neural developmental processes, including maturational patterns of cortical volume increases and synaptic pruning. Regions with thicker cortices may reflect inflammation or astrocyte activation. Both the thinning and thickening associated with OSA in children may contribute to the cognitive and behavioral dysfunction frequently found in the condition.

Sleep Restriction Impairs Vocabulary Learning when Adolescents Cram for Exams: The Need for Sleep Study

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Huang, Sha; Deshpande, Aadya; Yeo, Sing-Chen; Lo, June C.; Chee, Michael W.L.; Gooley, Joshua J.

2016-01-01

Study Objectives: The ability to recall facts is improved when learning takes place at spaced intervals, or when sleep follows shortly after learning. However, many students cram for exams and trade sleep for other activities. The aim of this study was to examine the interaction of study spacing and time in bed (TIB) for sleep on vocabulary learning in adolescents. Methods: In the Need for Sleep Study, which used a parallel-group design, 56 adolescents aged 15–19 years were randomly assigned to a week of either 5 h or 9 h of TIB for sleep each night as part of a 14-day protocol conducted at a boarding school. During the sleep manipulation period, participants studied 40 Graduate Record Examination (GRE)-type English words using digital flashcards. Word pairs were presented over 4 consecutive days (spaced items), or all at once during single study sessions (massed items), with total study time kept constant across conditions. Recall performance was examined 0 h, 24 h, and 120 h after all items were studied. Results: For all retention intervals examined, recall of massed items was impaired by a greater amount in adolescents exposed to sleep restriction. In contrast, cued recall performance on spaced items was similar between sleep groups. Conclusions: Spaced learning conferred strong protection against the effects of sleep restriction on recall performance, whereas students who had insufficient sleep were more likely to forget items studied over short time intervals. These findings in adolescents demonstrate the importance of combining good study habits and good sleep habits to optimize learning outcomes. Citation: Huang S, Deshpande A, Yeo SC, Lo JC, Chee MW, Gooley JJ. Sleep restriction impairs vocabulary learning when adolescents cram for exams: the Need for Sleep Study. SLEEP 2016;39(9):1681–1690. PMID:27253768

Chronic Low Quality Sleep Impairs Postural Control in Healthy Adults.

Science.gov (United States)

Furtado, Fabianne; Gonçalves, Bruno da Silva B; Abranches, Isabela Lopes Laguardia; Abrantes, Ana Flávia; Forner-Cordero, Arturo

2016-01-01

The lack of sleep, both in quality and quantity, is an increasing problem in modern society, often related to workload and stress. A number of studies have addressed the effects of acute (total) sleep deprivation on postural control. However, up to date, the effects of chronic sleep deficits, either in quantity or quality, have not been analyzed. Thirty healthy adults participated in the study that consisted of registering activity with a wrist actigraph for more than a week before performing a series of postural control tests. Sleep and circadian rhythm variables were correlated and the sum of activity of the least active 5-h period, L5, a rhythm variable, obtained the greater coefficient value with sleep quality variables (wake after sleep onset WASO and efficiency sleep). Cluster analysis was performed to classify subjects into two groups based on L5 (low and high). The balance tests scores used to asses postural control were measured using Biodex Balance System and were compared between the two groups with different sleep quality. The postural tests were divided into dynamic (platform tilt with eyes open, closed and cursor) and static (clinical test of sensory integration). The results showed that during the tests with eyes closed, the group with worse sleep quality had also worse postural control performance. Lack of vision impairs postural balance more deeply in subjects with chronic sleep inefficiency. Chronic poor sleep quality impairs postural control similarly to total sleep deprivation.

Chronic Low Quality Sleep Impairs Postural Control in Healthy Adults.

Directory of Open Access Journals (Sweden)

Fabianne Furtado

Full Text Available The lack of sleep, both in quality and quantity, is an increasing problem in modern society, often related to workload and stress. A number of studies have addressed the effects of acute (total sleep deprivation on postural control. However, up to date, the effects of chronic sleep deficits, either in quantity or quality, have not been analyzed. Thirty healthy adults participated in the study that consisted of registering activity with a wrist actigraph for more than a week before performing a series of postural control tests. Sleep and circadian rhythm variables were correlated and the sum of activity of the least active 5-h period, L5, a rhythm variable, obtained the greater coefficient value with sleep quality variables (wake after sleep onset WASO and efficiency sleep. Cluster analysis was performed to classify subjects into two groups based on L5 (low and high. The balance tests scores used to asses postural control were measured using Biodex Balance System and were compared between the two groups with different sleep quality. The postural tests were divided into dynamic (platform tilt with eyes open, closed and cursor and static (clinical test of sensory integration. The results showed that during the tests with eyes closed, the group with worse sleep quality had also worse postural control performance. Lack of vision impairs postural balance more deeply in subjects with chronic sleep inefficiency. Chronic poor sleep quality impairs postural control similarly to total sleep deprivation.

Transient decoupling of cortical EEGs following arousals during NREM sleep in middle-aged and elderly women.

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Ramanand, Pravitha; Bruce, Margaret C; Bruce, Eugene N

2010-08-01

Spontaneous cortical arousals in non-REM sleep increase with age and contribute to sleep fragmentation in the elderly. EEG spectral power in the faster frequencies exhibits well-described shifts during arousals. On the other hand, EEG activities also exhibit correlations, which are interpreted as an index of interdependence between distant cortical neural activities. The possibility of changes to the interdependence between cortical regions due to an arousal has not been considered. In this work, using previously recorded C3A2 and C4A1 EEG signals from two groups of adults, middle-aged (42-50 years) and elderly (71-86 years) women, we examined the effects of spontaneous arousals in NREM sleep on cortical interdependence. We quantified the auto- and cross-correlations in these signals using mutual information and characterized these correlations in periods before the onset and following the end of arousals. The pre-arousal period exhibited significantly higher interdependence between central regions than that following the arousal in both age groups (middle-aged: p=0.004, elderly: ppower changes characteristic of an arousal are no longer visible. The findings suggest that the state following an arousal characterized by lower interdependence may resemble a more vigilant period during which the system may be vulnerable to more arousals. Copyright 2010 Elsevier B.V. All rights reserved.

Night Sleep Duration and Risk of Cognitive Impairment in a Chinese Population: A Cross-sectional Study.

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Song, Qiao Feng; Liu, Xiao Xue; Hu, Wan Ning; Han, Xiao Chen; Zhou, Wen Hua; Lu, Ai Dong; Wang, Xi Zhu; Wu, Shou Ling

2017-10-01

Although sleep is one of the most important health-related behavioral factors, the association between night sleep duration and cognitive impairment has not been fully understood. A cross-sectional study was conducted with a random sample of 2,514 participants (⋝ 40 years of age; 46.6% women) in China to examine the association between night sleep duration and cognitive impairment. Night sleep duration was categorized as ⋜ 5, 6, 7, 8, or ⋝ 9 h per night. Cognitive function was measured using the Mini-Mental State Examination. A multivariate regression analysis was used to analyze the association of night sleep duration with cognitive impairment. A total of 122 participants were diagnosed with cognitive impairment. A U-shaped association between night sleep duration and cognitive impairment was found. The odds ratios (95% confidence intervals) of cognitive impairment (with 7 h of daily sleep being considered as the reference) for individuals reporting ⋜ 5, 6, 8, and ⋝ 9 h were 2.14 (1.20-3.83), 1.13 (0.67-1.89), 1.51 (0.82-2.79), and 5.37 (1.62-17.80), respectively (P ⋜ 0.01). Short or long night sleep duration was an important sleep-related factor independently associated with cognitive impairment and may be a useful marker for increased risk of cognitive impairment.. Copyright © 2017 The Editorial Board of Biomedical and Environmental Sciences. Published by China CDC. All rights reserved.

Acute Kynurenine Challenge Disrupts Sleep-Wake Architecture and Impairs Contextual Memory in Adult Rats.

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Pocivavsek, Ana; Baratta, Annalisa M; Mong, Jessica A; Viechweg, Shaun S

2017-11-01

Tryptophan metabolism via the kynurenine pathway may represent a key molecular link between sleep loss and cognitive dysfunction. Modest increases in the kynurenine pathway metabolite kynurenic acid (KYNA), which acts as an antagonist at N-methyl-d-aspartate and α7 nicotinic acetylcholine receptors in the brain, result in cognitive impairments. As glutamatergic and cholinergic neurotransmissions are critically involved in modulation of sleep, our current experiments tested the hypothesis that elevated KYNA adversely impacts sleep quality. Adult male Wistar rats were treated with vehicle (saline) and kynurenine (25, 50, 100, and 250 mg/kg), the direct bioprecursor of KYNA, intraperitoneally at zeitgeber time (ZT) 0 to rapidly increase brain KYNA. Levels of KYNA in the brainstem, cortex, and hippocampus were determined at ZT 0, ZT 2, and ZT 4, respectively. Analyses of vigilance state-related parameters categorized as wake, rapid eye movement (REM), and non-REM (NREM) as well as spectra power analysis during NREM and REM were assessed during the light phase. Separate animals were tested in the passive avoidance paradigm, testing contextual memory. When KYNA levels were elevated in the brain, total REM duration was reduced and total wake duration was increased. REM and wake architecture, assessed as number of vigilance state bouts and average duration of each bout, and theta power during REM were significantly impacted. Kynurenine challenge impaired performance in the hippocampal-dependent contextual memory task. Our results introduce kynurenine pathway metabolism and formation of KYNA as a novel molecular target contributing to sleep disruptions and cognitive impairments. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Reduction in Cortical Gamma Synchrony during Depolarized State of Slow Wave Activity in Mice

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EUNJIN eHWANG

2013-12-01

Full Text Available EEG gamma band oscillations have been proposed to account for the neural synchronization crucial for perceptual integration. While increased gamma power and synchronization is generally observed during cognitive tasks performed during wake, several studies have additionally reported increased gamma power during sleep or anesthesia, raising questions about the characteristics of gamma oscillation during impaired consciousness and its role in conscious processing. Phase-amplitude modulation has been observed between slow wave activity (SWA, 0.5–4 Hz and gamma oscillations during ketamine/xylazine anesthesia or sleep, showing increased gamma activity corresponding to the depolarized (ON state of SWA. Here we divided gamma activity into its ON and OFF (hyperpolarized state components based on the phase of SWA induced by ketamine/xylazine anesthesia and compared their power and synchrony with wake state levels in mice. We further investigated the state-dependent changes in both gamma power and synchrony across primary motor and primary somatosensory cortical regions and their interconnected thalamic regions throughout anesthesia and recovery. As observed previously, gamma power was as high as during wake specifically during the ON state of SWA. However, the synchrony of this gamma activity between somatosensory-motor cortical regions was significantly reduced compared to the baseline wake state. In addition, the somatosensory-motor cortical synchrony of gamma oscillations was reduced and restored in an anesthetic state-dependent manner, reflecting the changing depth of anesthesia. Our results provide evidence that during anesthesia changes in long-range information integration between cortical regions might be more critical for changes in consciousness than changes in local gamma oscillatory power.

Sensitivity and validity of psychometric tests for assessing driving impairment: effects of sleep deprivation.

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Jongen, Stefan; Perrier, Joy; Vuurman, Eric F; Ramaekers, Johannes G; Vermeeren, Annemiek

2015-01-01

To assess drug induced driving impairment, initial screening is needed. However, no consensus has been reached about which initial screening tools have to be used. The present study aims to determine the ability of a battery of psychometric tests to detect performance impairing effects of clinically relevant levels of drowsiness as induced by one night of sleep deprivation. Twenty four healthy volunteers participated in a 2-period crossover study in which the highway driving test was conducted twice: once after normal sleep and once after one night of sleep deprivation. The psychometric tests were conducted on 4 occasions: once after normal sleep (at 11 am) and three times during a single night of sleep deprivation (at 1 am, 5 am, and 11 am). On-the-road driving performance was significantly impaired after sleep deprivation, as measured by an increase in Standard Deviation of Lateral Position (SDLP) of 3.1 cm compared to performance after a normal night of sleep. At 5 am, performance in most psychometric tests showed significant impairment. As expected, largest effect sizes were found on performance in the Psychomotor Vigilance Test (PVT). Large effects sizes were also found in the Divided Attention Test (DAT), the Attention Network Test (ANT), and the test for Useful Field of View (UFOV) at 5 and 11 am during sleep deprivation. Effects of sleep deprivation on SDLP correlated significantly with performance changes in the PVT and the DAT, but not with performance changes in the UFOV. From the psychometric tests used in this study, the PVT and DAT seem most promising for initial evaluation of drug impairment based on sensitivity and correlations with driving impairment. Further studies are needed to assess the sensitivity and validity of these psychometric tests after benchmark sedative drug use.

Sensitivity and validity of psychometric tests for assessing driving impairment: effects of sleep deprivation.

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Stefan Jongen

Full Text Available To assess drug induced driving impairment, initial screening is needed. However, no consensus has been reached about which initial screening tools have to be used. The present study aims to determine the ability of a battery of psychometric tests to detect performance impairing effects of clinically relevant levels of drowsiness as induced by one night of sleep deprivation.Twenty four healthy volunteers participated in a 2-period crossover study in which the highway driving test was conducted twice: once after normal sleep and once after one night of sleep deprivation. The psychometric tests were conducted on 4 occasions: once after normal sleep (at 11 am and three times during a single night of sleep deprivation (at 1 am, 5 am, and 11 am.On-the-road driving performance was significantly impaired after sleep deprivation, as measured by an increase in Standard Deviation of Lateral Position (SDLP of 3.1 cm compared to performance after a normal night of sleep. At 5 am, performance in most psychometric tests showed significant impairment. As expected, largest effect sizes were found on performance in the Psychomotor Vigilance Test (PVT. Large effects sizes were also found in the Divided Attention Test (DAT, the Attention Network Test (ANT, and the test for Useful Field of View (UFOV at 5 and 11 am during sleep deprivation. Effects of sleep deprivation on SDLP correlated significantly with performance changes in the PVT and the DAT, but not with performance changes in the UFOV.From the psychometric tests used in this study, the PVT and DAT seem most promising for initial evaluation of drug impairment based on sensitivity and correlations with driving impairment. Further studies are needed to assess the sensitivity and validity of these psychometric tests after benchmark sedative drug use.

Work stressors and impaired sleep: rumination as a mediator.

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Berset, Martial; Elfering, Achim; Lüthy, Stefan; Lüthi, Simon; Semmer, Norbert K

2011-04-01

An association between stress at work and impaired sleep is theoretically plausible and supported by empirical evidence. The current study's main aim was to investigate how the influence of stressors is carried over into the evening and the night. We assume that this relationship is mediated by perseverative cognitions. We tested this assumption in two cross-sectional samples with structural equation modeling, using bootstrapped standard errors to test for significance. Effort–reward imbalance and time pressure were used as stressors, and rumination as a measure for perseverative cognitions. Results show that the stressors are related to perseverative cognitions, and these are related to impaired sleep in both samples. Indirect effects are significant in both samples. With rumination controlled, direct effects of stressors on sleep are only significant in one out of four cases. Thus, there is full mediation in three out of four cases, and partial mediation in the fourth one. Our results underscore the notion that perseverative cognitions are crucial for transferring negative effects of work stressors into private life, including sleep, thus hindering individuals to successfully recover.

Sleep discontinuity and impaired sleep continuity affect transition to and from obesity over time: results from the Alameda county study.

Science.gov (United States)

Nordin, Maria; Kaplan, Robert M

2010-03-01

To investigate the impact of development in sleep continuity on transition to and from obesity over time. The study used self-reported sleep and body mass index (BMI) measures from the 1965, 1974, 1983, and 1994 waves of the longitudinal Alameda County Study. Sleep continuity was assessed by a question on whether the participants had any troubles falling or staying asleep. Change in sleep and BMI were estimated from the sleep and BMI questions in 1965 and 1994 respectively. Multinomial regression analyses were used to examine the risk/chance for a transition to and from obesity (BMI >or=30 kg/m(2)) due to development in sleep continuity. After adjustment for confounding variables, consistent sleep discontinuity both increases the risk for a transition to obesity and reduces the chance of losing weight, whereas impaired sleep continuity lowers the chance for weight loss. Effects for obesity were non-significant for those with improved sleep continuity. Consistent sleep discontinuity and impaired sleep continuity increases the risk of transition to obesity or of remaining obese.

TMS-induced cortical potentiation during wakefulness locally increases slow wave activity during sleep.

Directory of Open Access Journals (Sweden)

Reto Huber

2007-03-01

Full Text Available Sleep slow wave activity (SWA is thought to reflect sleep need, increasing in proportion to the length of prior wakefulness and decreasing during sleep. However, the process responsible for SWA regulation is not known. We showed recently that SWA increases locally after a learning task involving a circumscribed brain region, suggesting that SWA may reflect plastic changes triggered by learning.To test this hypothesis directly, we used transcranial magnetic stimulation (TMS in conjunction with high-density EEG in humans. We show that 5-Hz TMS applied to motor cortex induces a localized potentiation of TMS-evoked cortical EEG responses. We then show that, in the sleep episode following 5-Hz TMS, SWA increases markedly (+39.1+/-17.4%, p<0.01, n = 10. Electrode coregistration with magnetic resonance images localized the increase in SWA to the same premotor site as the maximum TMS-induced potentiation during wakefulness. Moreover, the magnitude of potentiation during wakefulness predicts the local increase in SWA during sleep.These results provide direct evidence for a link between plastic changes and the local regulation of sleep need.

[Poststroke cognitive, emotional impairment and sleep quality: efficience of treatment with melaxen].

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Kulesh, A A; Shestakov, V V

2014-01-01

To study melatonin secretion and its correlations with poststroke cognitive, emotional impairment and sleep quality in the acute period of stroke and to assess treatment efficacy of melaxen. We studied 96 patients with acute stroke. A battery of tests and scales for assessment of neurological deficit, neuropsychological status and emotional impairment was used. The night urinary level of 6-sulfatoxymelatonin was assessed. The relationship between 6-sulfatoxymelatonin and cognitive, emotional status and sleep parameters was analyzed. The level of 6-sulfatoxymelatonin was decreased in the night urine. Patients with dysexecutive poststroke cognitive impairment had higher level of 6-sulfatoxymelatonin and patients with dysmnestic and mixed cognitive impairment had lower level of 6-sulfatoxymelatonin in comparison with patients with normal cognitive functions. Melaxen improved cognitive function and sleep parameters, reduced the level of anxiety in the early recovery period of stroke. A role of chronobiological processes in the development of clinical signs of stroke in the aspect of cognitive impairment is discussed.

Association between Visual Impairment and Low Vision and Sleep Duration and Quality among Older Adults in South Africa.

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Peltzer, Karl; Phaswana-Mafuya, Nancy

2017-07-19

This study aims to estimate the association between visual impairment and low vision and sleep duration and poor sleep quality in a national sample of older adults in South Africa. A national population-based cross-sectional Study of Global Ageing and Adults Health (SAGE) wave 1 was conducted in 2008 with a sample of 3840 individuals aged 50 years or older in South Africa. The interviewer-administered questionnaire assessed socio-demographic characteristics, health variables, sleep duration, quality, visual impairment, and vision. Results indicate that 10.0% of the sample reported short sleep duration (≤5 h), 46.6% long sleep (≥9 h), 9.3% poor sleep quality, 8.4% self-reported and visual impairment (near and/or far vision); and 43.2% measured low vision (near and/or far vision) (0.01-0.25 decimal) and 7.5% low vision (0.01-0.125 decimal). In fully adjusted logistic regression models, self-reported visual impairment was associated with short sleep duration and poor sleep quality, separately and together. Low vision was only associated with long sleep duration and poor sleep quality in unadjusted models. Self-reported visual impairment was related to both short sleep duration and poor sleep quality. Population data on sleep patterns may want to include visual impairment measures.

Rehabilitation of cortical blindness secondary to stroke.

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Gaber, Tarek A-Z K

2010-01-01

Cortical blindness is a rare complication of posterior circulation stroke. However, its complex presentation with sensory, physical, cognitive and behavioural impairments makes it one of the most challenging. Appropriate approach from a rehabilitation standpoint was never reported. Our study aims to discuss the rehabilitation methods and outcomes of a cohort of patients with cortical blindness. The notes of all patients with cortical blindness referred to a local NHS rehabilitation service in the last 6~years were examined. Patients' demographics, presenting symptoms, scan findings, rehabilitation programmes and outcomes were documented. Seven patients presented to our service, six of them were males. The mean age was 63. Patients 1, 2 and 3 had total blindness with severe cognitive and behavioural impairments, wandering and akathisia. All of them failed to respond to any rehabilitation effort and the focus was on damage limitation. Pharmacological interventions had a modest impact on behaviour and sleep pattern. The 3 patients were discharged to a nursing facility. Patients 4, 5, 6 and 7 had partial blindness with variable severity. All of them suffered from significant memory impairment. However, none suffered from any behavioural, physical or other cognitive impairment. Rehabilitation efforts on 3 patients were carried out collaboratively between brain injury occupational therapists and sensory disability officers. All patients experienced significant improvement in handicap and they all maintained community placements. This small cohort of patients suggests that the rehabilitation philosophy and outcomes of these 2 distinct groups of either total or partial cortical blindness differ significantly.

Sleep deprivation specifically impairs short-term olfactory memory in Drosophila.

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Li, Xinjian; Yu, Feng; Guo, Aike

2009-11-01

Sleep is crucial to memory consolidation in humans and other animals; however, the effect of insufficient sleep on subsequent learning and memory remains largely elusive. Learning and memory after 1-day sleep deprivation (slpD) was evaluated using Pavlovian olfactory conditioning in Drosophila, and locomotor activity was measured using the Drosophila Activity Monitoring System in a 12:12 light-dark cycle. We found that slpD specifically impaired 1-h memory in wild type Canton-S flies, and this effect could persist for at least 2 h. However, alternative stresses (heat stress, oxidative stress, starvation, and rotation stress) did not result in a similar effect and left the flies' memory intact. Mechanistic studies demonstrated that flies with either silenced transmission of the mushroom body (MB) during slpD or down-regulated cAMP levels in the MB demonstrated no slpD-induced 1-h memory impairment. We found that slpD specifically impaired 1-h memory in Drosophila, and either silencing of MB transmission during slpD or down-regulation of the cAMP level in the MB protected the flies from slpD-induced impairment.

Lithium prevents REM sleep deprivation-induced impairments on memory consolidation.

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Ota, Simone M; Moreira, Karin Di Monteiro; Suchecki, Deborah; Oliveira, Maria Gabriela M; Tiba, Paula A

2013-11-01

Pre-training rapid eye movement sleep (REMS) deprivation affects memory acquisition and/or consolidation. It also produces major REMS rebound at the cost of waking and slow wave sleep (SWS). Given that both SWS and REMS appear to be important for memory processes, REMS rebound after training may disrupt the organization of sleep cycles, i.e., excessive amount of REMS and/or little SWS after training could be harmful for memory formation. To examine whether lithium, a drug known to increase SWS and reduce REMS, could prevent the memory impairment induced by pre-training sleep deprivation. Animals were divided in 2 groups: cage control (CC) and REMS-deprived (REMSDep), and then subdivided into 4 subgroups, treated either with vehicle or 1 of 3 doses of lithium (50, 100, and 150 mg/kg) 2 h before training on the multiple trial inhibitory avoidance task. Animals were tested 48 h later to make sure that the drug had been already metabolized and eliminated. Another set of animals was implanted with electrodes and submitted to the same experimental protocol for assessment of drug-induced sleep-wake changes. Wistar male rats weighing 300-400 g. Sleep deprived rats required more trials to learn the task and still showed a performance deficit during test, except from those treated with 150 mg/kg of lithium, which also reduced the time spent in REM sleep during sleep recovery. Lithium reduced rapid eye movement sleep and prevented memory impairment induced by sleep deprivation. These results indicate that these phenomena may be related, but cause-effect relationship cannot be ascertained.

Postnatal Ablation of Synaptic Retinoic Acid Signaling Impairs Cortical Information Processing and Sensory Discrimination in Mice.

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Park, Esther; Tjia, Michelle; Zuo, Yi; Chen, Lu

2018-06-06

Retinoic acid (RA) and its receptors (RARs) are well established essential transcriptional regulators during embryonic development. Recent findings in cultured neurons identified an independent and critical post-transcriptional role of RA and RARα in the homeostatic regulation of excitatory and inhibitory synaptic transmission in mature neurons. However, the functional relevance of synaptic RA signaling in vivo has not been established. Here, using somatosensory cortex as a model system and the RARα conditional knock-out mouse as a tool, we applied multiple genetic manipulations to delete RARα postnatally in specific populations of cortical neurons, and asked whether synaptic RA signaling observed in cultured neurons is involved in cortical information processing in vivo Indeed, conditional ablation of RARα in mice via a CaMKIIα-Cre or a layer 5-Cre driver line or via somatosensory cortex-specific viral expression of Cre-recombinase impaired whisker-dependent texture discrimination, suggesting a critical requirement of RARα expression in L5 pyramidal neurons of somatosensory cortex for normal tactile sensory processing. Transcranial two-photon imaging revealed a significant increase in dendritic spine elimination on apical dendrites of somatosensory cortical layer 5 pyramidal neurons in these mice. Interestingly, the enhancement of spine elimination is whisker experience-dependent as whisker trimming rescued the spine elimination phenotype. Additionally, experiencing an enriched environment improved texture discrimination in RARα-deficient mice and reduced excessive spine pruning. Thus, RA signaling is essential for normal experience-dependent cortical circuit remodeling and sensory processing. SIGNIFICANCE STATEMENT The importance of synaptic RA signaling has been demonstrated in in vitro studies. However, whether RA signaling mediated by RARα contributes to neural circuit functions in vivo remains largely unknown. In this study, using a RARα conditional

Onset of impaired sleep as a predictor of change in health-related behaviours

DEFF Research Database (Denmark)

Clark, Alice Jessie; Salo, Paula; Lange, Theis

2015-01-01

BACKGROUND: Changes in health-related behaviour may be a key mechanism linking impaired sleep to poor health, but evidence on this is limited. In this study, we analysed observational data to determine whether onset of impaired sleep is followed by changes in health-related behaviours. METHODS: W...

[Pilot study to investigate sleep disorders in the blind and persons with relevant visual impairment].

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Dirks, C; Grünewald, D; Young, P; Heidbreder, A

2018-05-22

Sleep disorders are associated with serious health problems in blind and visually impaired persons. Loss of light perception may result in a shift of sleep-wake pattern, which may lead to significant impairments in daily life--the so-called non-24-hour sleep-wake disorder. To date, epidemiologic data on non-24 only exist for the USA. This pilot study was conducted to provide first epidemiologic data for the prevalence of non-24 and other sleep disorders among blind and visually impaired persons in Germany. Recruited were 111 blind and visually impaired subjects (36 subjects without light perception; male [m] = 56, 27-85 years, average [Mx] = 59.53, standard deviation [SD] = 14.69) and 111 sighted controls (m = 41, 27-88 years, Mx = 58.32, SD = 14.21), who answered a set of validated questionnaires referring to general health status (SF-36), sleep characteristics (PSQI), and daytime sleepiness (ESS). In addition, a questionnaire to predict non-24-hour sleep-wake disorder, which is not yet validated in German, was provided. The prevalence of 72.2% for the non-24-hour sleep-wake disorder in blind people is in accordance with results from the USA. In contrast, our results indicated non-24 in only 21.3% of the subjects with residual light perception. Furthermore, other sleep disorders like problems falling asleep (100% vs. 79.9%), maintaining sleep (90% vs. 88.1%), sleep-disordered breathing (19.4% vs. 32%), or sleep-related movement disorders (28.1% vs. 32.9%) were also common in the group of blind or visually impaired persons. The non-24-hour sleep-wake disorder is a frequent problem among people with no light perception, associated with problems falling asleep, maintaining sleep, and daytime sleepiness. The perception of light as an external cue for our circadian rhythm plays a key role. However, sleep disruption is not fully explained by non-24, making a detailed sleep history essential.

Bombesin administration impairs memory and does not reverse memory deficit caused by sleep deprivation.

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Ferreira, L B T; Oliveira, S L B; Raya, J; Esumi, L A; Hipolide, D C

2017-07-28

Sleep deprivation impairs performance in emotional memory tasks, however this effect on memory is not completely understood. Possible mechanisms may involve an alteration in neurotransmission systems, as shown by the fact that many drugs that modulate neural pathways can prevent memory impairment by sleep loss. Gastrin releasing peptide (GRP) is a neuropeptide that emerged as a regulatory molecule of emotional memory through the modulation of other neurotransmission systems. Thus, the present study addressed the effect of intraperitoneal (IP) administration of bombesin (BB) (2.5, 5.0 and 10.0μg/kg), a GRP agonist, on the performance of Wistar rats in a multiple trail inhibitory avoidance (MTIA) task, after sleep deprivation, using the modified multiple platforms method (MMPM). Sleep deprived animals exhibited acquisition and retention impairment that was not prevented by BB injection. In addition, non-sleep deprived animals treated with BB before and after the training session, but not before the test, have shown a retention deficit. In summary, BB did not improve the memory impairment by sleep loss and, under normal conditions, produced a memory consolidation deficit. Copyright © 2017 Elsevier B.V. All rights reserved.

Olfactory insights into sleep-dependent learning and memory.

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Shanahan, Laura K; Gottfried, Jay A

2014-01-01

Sleep is pervasive throughout most of the animal kingdom-even jellyfish and honeybees do it. Although the precise function of sleep remains elusive, research increasingly suggests that sleep plays a key role in memory consolidation. Newly formed memories are highly labile and susceptible to interference, and the sleep period offers an optimal window in which memories can be strengthened or modified. Interestingly, a small but growing research area has begun to explore the ability of odors to modulate memories during sleep. The unique anatomical organization of the olfactory system, including its intimate overlap with limbic systems mediating emotion and memory, and the lack of a requisite thalamic intermediary between the nasal periphery and olfactory cortex, suggests that odors may have privileged access to the brain during sleep. Indeed, it has become clear that the long-held assumption that odors have no impact on the sleeping brain is no longer tenable. Here, we summarize recent studies in both animal and human models showing that odor stimuli experienced in the waking state modulate olfactory cortical responses in sleep-like states, that delivery of odor contextual cues during sleep can enhance declarative memory and extinguish fear memory, and that olfactory associative learning can even be achieved entirely within sleep. Data reviewed here spotlight the emergence of a new research area that should hold far-reaching implications for future neuroscientific investigations of sleep, learning and memory, and olfactory system function. © 2014 Elsevier B.V. All rights reserved.

Bistability breaks-off deterministic responses to intracortical stimulation during non-REM sleep

Directory of Open Access Journals (Sweden)

Andrea Pigorini

2015-04-01

These results point to bistability as the underlying critical mechanism that prevents the emergence of complex interactions in human thalamocortical networks during NREM sleep. Besides sleep, the same basic neurophysiological dynamics may play a role in pathological conditions(Casali et al., 2013; Rosanova et al., 2012 where cortico-cortical communication and consciousness are impaired in spite of preserved neuronal activity.

Associations of Subjective Sleep Quality and Daytime Sleepiness With Cognitive Impairment in Adults and Elders With Heart Failure.

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Byun, Eeeseung; Kim, Jinyoung; Riegel, Barbara

2017-01-01

This study examined the association of subjective nighttime sleep quality and daytime sleepiness with cognitive impairment in 105 adults (sleep quality and daytime sleepiness were measured by the Pittsburgh Sleep Quality Index and the Epworth Sleepiness Scale. Cognitive impairment was assessed using a neuropsychological battery measuring attention, memory, and processing speed. Multivariate logistic regression was used. In adults, daytime sleepiness was associated with cognitive impairment, whereas poor nighttime sleep quality was associated with cognitive impairment in elders. Age may play an important role in how sleep impacts cognition in persons with heart failure. Improving nighttime sleep quality and daytime sleepiness in this population may improve cognition.

Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

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Trksak, George H.; Bracken, Bethany K.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

2013-01-01

In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent [31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, [31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse. PMID:24250276

The maturation of cortical sleep rhythms and networks over early development.

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Chu, C J; Leahy, J; Pathmanathan, J; Kramer, M A; Cash, S S

2014-07-01

Although neuronal activity drives all aspects of cortical development, how human brain rhythms spontaneously mature remains an active area of research. We sought to systematically evaluate the emergence of human brain rhythms and functional cortical networks over early development. We examined cortical rhythms and coupling patterns from birth through adolescence in a large cohort of healthy children (n=384) using scalp electroencephalogram (EEG) in the sleep state. We found that the emergence of brain rhythms follows a stereotyped sequence over early development. In general, higher frequencies increase in prominence with striking regional specificity throughout development. The coordination of these rhythmic activities across brain regions follows a general pattern of maturation in which broadly distributed networks of low-frequency oscillations increase in density while networks of high frequency oscillations become sparser and more highly clustered. Our results indicate that a predictable program directs the development of key rhythmic components and physiological brain networks over early development. This work expands our knowledge of normal cortical development. The stereotyped neurophysiological processes observed at the level of rhythms and networks may provide a scaffolding to support critical periods of cognitive growth. Furthermore, these conserved patterns could provide a sensitive biomarker for cortical health across development. Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Sleep Restriction Impairs Blood–Brain Barrier Function

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He, Junyun; Hsuchou, Hung; He, Yi; Kastin, Abba J.; Wang, Yuping

2014-01-01

The blood–brain barrier (BBB) is a large regulatory and exchange interface between the brain and peripheral circulation. We propose that changes of the BBB contribute to many pathophysiological processes in the brain of subjects with chronic sleep restriction (CSR). To achieve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disruption in mice by a week of consecutive sleep recording. We then tested the hypothesis that CSR compromises microvascular function. CSR not only diminished endothelial and inducible nitric oxide synthase, endothelin1, and glucose transporter expression in cerebral microvessels of the BBB, but it also decreased 2-deoxy-glucose uptake by the brain. The expression of several tight junction proteins also was decreased, whereas the level of cyclooxygenase-2 increased. This coincided with an increase of paracellular permeability of the BBB to the small tracers sodium fluorescein and biotin. CSR for 6 d was sufficient to impair BBB structure and function, although the increase of paracellular permeability returned to baseline after 24 h of recovery sleep. This merits attention not only in neuroscience research but also in public health policy and clinical practice. PMID:25355222

Onset of Impaired Sleep and Cardiovascular Disease Risk Factors

DEFF Research Database (Denmark)

Clark, Alice Jessie; Salo, Paula; Lange, Theis

2016-01-01

, and dyslipidemia). METHODS: In a longitudinal cohort study with 3 survey waves (2000, 2004, 2008) from the Finnish Public Sector study we used repeated information on sleep duration and disturbances to determine onset of impaired sleep. Information on development of CVD risk factors, as indicated by initiation...... of medication for hypertension, diabetes, and dyslipidemia was derived from electronic medical records within 8 years of follow-up. Data on 45,647 participants was structured as two data-cycles to examine the effect of change in sleep (between two waves) on incident CVD events. We applied strict inclusion...... and exclusion criteria to determine temporality between changes in sleep and the outcomes. RESULTS: While we did not find consistent effects of onset of short or long sleep, we found onset of disturbed sleep to predict subsequent risk of hypertension (hazard ratio = 1.22, 95% CI: 1.04-1.44) and dyslipidemia (HR...

Cortical Visual Impairment

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... resolves by one year of life. Is “cortical blindness” the same thing as CVI? Cortical blindness is ... What visual characteristics are associated with CVI? • Distinct color preferences • Variable level of vision loss, often demonstrating ...

Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment.

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Eckert, Danny J; Younes, Magdy K

2014-02-01

Historically, brief awakenings from sleep (cortical arousals) have been assumed to be vitally important in restoring airflow and blood-gas disturbances at the end of obstructive sleep apnea (OSA) breathing events. Indeed, in patients with blunted chemical drive (e.g., obesity hypoventilation syndrome) and in instances when other defensive mechanisms fail, cortical arousal likely serves an important protective role. However, recent insight into the pathogenesis of OSA indicates that a substantial proportion of respiratory events do not terminate with a cortical arousal from sleep. In many cases, cortical arousals may actually perpetuate blood-gas disturbances, breathing instability, and subsequent upper airway closure during sleep. This brief review summarizes the current understanding of the mechanisms mediating respiratory-induced cortical arousal, the physiological factors that influence the propensity for cortical arousal, and the potential dual roles that cortical arousal may play in OSA pathogenesis. Finally, the extent to which existing sedative agents decrease the propensity for cortical arousal and their potential to be therapeutically beneficial for certain OSA patients are highlighted.

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation.

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Holst, Sebastian C; Sousek, Alexandra; Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich; Tafti, Mehdi; Landolt, Hans-Peter

2017-10-05

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep.

Cerebral mGluR5 availability contributes to elevated sleep need and behavioral adjustment after sleep deprivation

Science.gov (United States)

Hefti, Katharina; Saberi-Moghadam, Sohrab; Buck, Alfred; Ametamey, Simon M; Scheidegger, Milan; Franken, Paul; Henning, Anke; Seifritz, Erich

2017-01-01

Increased sleep time and intensity quantified as low-frequency brain electrical activity after sleep loss demonstrate that sleep need is homeostatically regulated, yet the underlying molecular mechanisms remain elusive. We here demonstrate that metabotropic glutamate receptors of subtype 5 (mGluR5) contribute to the molecular machinery governing sleep-wake homeostasis. Using positron emission tomography, magnetic resonance spectroscopy, and electroencephalography in humans, we find that increased mGluR5 availability after sleep loss tightly correlates with behavioral and electroencephalographic biomarkers of elevated sleep need. These changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-induced modifications downstream of mGluR5 signaling. Knock-out mice without functional mGluR5 exhibit severe dysregulation of sleep-wake homeostasis, including lack of recovery sleep and impaired behavioral adjustment to a novel task after sleep deprivation. The data suggest that mGluR5 contribute to the brain's coping mechanisms with sleep deprivation and point to a novel target to improve disturbed wakefulness and sleep. PMID:28980941

Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback

Science.gov (United States)

Whitney, Paul; Hinson, John M.; Jackson, Melinda L.; Van Dongen, Hans P.A.

2015-01-01

Study Objectives: To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Design: Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Setting: Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Subjects: Twenty-six subjects (22–40 y of age; 10 women). Interventions: Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Results: Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Conclusions: Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback

Sleep restriction impairs blood-brain barrier function.

Science.gov (United States)

He, Junyun; Hsuchou, Hung; He, Yi; Kastin, Abba J; Wang, Yuping; Pan, Weihong

2014-10-29

The blood-brain barrier (BBB) is a large regulatory and exchange interface between the brain and peripheral circulation. We propose that changes of the BBB contribute to many pathophysiological processes in the brain of subjects with chronic sleep restriction (CSR). To achieve CSR that mimics a common pattern of human sleep loss, we quantified a new procedure of sleep disruption in mice by a week of consecutive sleep recording. We then tested the hypothesis that CSR compromises microvascular function. CSR not only diminished endothelial and inducible nitric oxide synthase, endothelin1, and glucose transporter expression in cerebral microvessels of the BBB, but it also decreased 2-deoxy-glucose uptake by the brain. The expression of several tight junction proteins also was decreased, whereas the level of cyclooxygenase-2 increased. This coincided with an increase of paracellular permeability of the BBB to the small tracers sodium fluorescein and biotin. CSR for 6 d was sufficient to impair BBB structure and function, although the increase of paracellular permeability returned to baseline after 24 h of recovery sleep. This merits attention not only in neuroscience research but also in public health policy and clinical practice. Copyright © 2014 the authors 0270-6474/14/3414697-10$15.00/0.

The effect of preinjury sleep difficulties on neurocognitive impairment and symptoms after sport-related concussion.

Science.gov (United States)

Sufrinko, Alicia; Pearce, Kelly; Elbin, R J; Covassin, Tracey; Johnson, Eric; Collins, Michael; Kontos, Anthony P

2015-04-01

Researchers have reported that sleep duration is positively related to baseline neurocognitive performance. However, researchers have yet to examine the effect of preinjury sleep difficulties on postconcussion impairments. To compare neurocognitive impairment and symptoms of athletes with preinjury sleep difficulties to those without after a sport-related concussion (SRC). Cohort study; Level of evidence, 3. The sample included 348 adolescent and adult athletes (age, mean ± SD, 17.43 ± 2.34 years) with a diagnosed SRC. The sample was divided into 2 groups: (1) 34 (10%) participants with preinjury sleep difficulties (sleeping less as well as having trouble falling asleep; SLEEP SX) and (2) 231 (66%) participants without preinjury sleep difficulties (CONTROL). The remaining 84 (24%) participants with minimal sleep difficulties (1 symptom) were excluded. Participants completed the Immediate Postconcussion Assessment and Cognitive Test (ImPACT) and Postconcussion Symptom Scale (PCSS) at baseline and 3 postinjury intervals (2, 5-7, and 10-14 days after injury). A series of repeated-measures analyses of covariance with Bonferroni correction, controlling for baseline non-sleep-related symptoms, were conducted to compare postinjury neurocognitive performance between groups. Follow-up exploratory t tests examined between-group differences at each time interval. A series of analyses of variance were used to examine total PCSS score, sleep-related, and non-sleep-related symptoms across time intervals between groups. Groups differed significantly in PCSS scores across postinjury intervals for reaction time (P SLEEP SX group performing worse than controls at 5-7 days (mean ± SD, 0.70 ± 0.32 [SLEEP SX], 0.60 ± 0.14 [CONTROL]) and 10-14 days (0.61 ± 0.17 [SLEEP SX]; 0.57 ± 0.10 [CONTROL]) after injury. Groups also differed significantly on verbal memory performance (P = .04), with the SLEEP SX (68.21 ± 18.64) group performing worse than the CONTROL group (76.76 ± 14

Obstructive sleep apnea-hypopnea syndrome and cognitive impairments in the elderly

Directory of Open Access Journals (Sweden)

Song Shuling

2017-01-01

Full Text Available Obstructive sleep apnea-hypopnea syndrome (OSAHS is a common sleep-related breathing disorder that is associated with significant morbidity and mortality. It has received increasing attention that neurocognitive deficits occur with a high frequency in OSAHS. However, it is rarely known that OSAHS impacts on cognition in the elderly in whom an increased prevalence of OSAHS is present. In this review we consider recent studies in the association between OSAHS and cognitive impairments, with specific interest in the older population. Firstly, we elucidate the characteristics of OSAHS and OSAHS-related cognitive impairments in the older patients. Many studies have showed that the prevalence of OSAHS increases with age and it is higher in the elderly than other population. Moreover, OSAHS is associated with higher incidence of comorbidities and increased risk of clinical deterioration in the elderly, especially the neurocognitive impairments which even can develop dementia. Subsequently, we discuss the possible reasons of cognitive impairments that caused or aggravated by OSAHS in the elderly. The intermittent hypoxia (IH-related disturbances of homeostasis such as oxidative stress, inflammation, and age-related changes such as the changes of sleep architecture, the declined expression level of anti-aging gene, medical comorbidities and polypharmacy, may be both contribute to the increased risk of cognitive impairments in the older patients with OSAHS.

Oculomotor impairment during chronic partial sleep deprivation.

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Russo, M; Thomas, M; Thorne, D; Sing, H; Redmond, D; Rowland, L; Johnson, D; Hall, S; Krichmar, J; Balkin, T

2003-04-01

The effects of chronic partial sleep (sleep deprivation) and extended sleep (sleep augmentation) followed by recovery sleep on oculomotor function were evaluated in normal subjects to explore the usefulness of oculomotor assessment for alertness monitoring in fitness-for-duty testing. Sixty-six commercial drivers (24-62 years, 50m/16f) participated in a 15 day study composed of 3 training days with 8h time in bed per night, 7 experimental days with subjects randomly assigned to either 3, 5, 7, or 9h time in bed, and 3 recovery nights with 8h time in bed. Data from 57 subjects were used. Saccadic velocity (SV), initial pupil diameter (IPD), latency to pupil constriction (CL), and amplitude of pupil constriction (CA) were assessed and correlated with the sleep latency test (SLT), the Stanford sleepiness scale (SSS), and simulated driving performance. Regression analyses showed that SV slowed significantly in the 3 and 5h groups, IPD decreased significantly in the 9h group, and CL increased significantly in the 3h group. SLT and SSS significantly correlated with SV, IPD, CL, and driving accidents for the 3h group, and with CL for the 5h group. Analyses also showed a significant negative correlation between decreasing SV and increasing driving accidents in the 3h group and a significant negative correlation between IPD and driving accidents for the 7h group. The results demonstrate a sensitivity primarily of SV to sleepiness, and a correlation of SV and IPD to impaired simulated driving performance, providing evidence for the potential utility of oculomotor indicators in the detection of excessive sleepiness and deterioration of complex motor performance with chronic partial sleep restriction. This paper shows a relationship between sleep deprivation and oculomotor measures, and suggests a potential utility for oculometrics in assessing operational performance readiness under sleep restricted conditions.

Genetic deletion of melanin-concentrating hormone neurons impairs hippocampal short-term synaptic plasticity and hippocampal-dependent forms of short-term memory.

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Le Barillier, Léa; Léger, Lucienne; Luppi, Pierre-Hervé; Fort, Patrice; Malleret, Gaël; Salin, Paul-Antoine

2015-11-01

The cognitive role of melanin-concentrating hormone (MCH) neurons, a neuronal population located in the mammalian postero-lateral hypothalamus sending projections to all cortical areas, remains poorly understood. Mainly activated during paradoxical sleep (PS), MCH neurons have been implicated in sleep regulation. The genetic deletion of the only known MCH receptor in rodent leads to an impairment of hippocampal dependent forms of memory and to an alteration of hippocampal long-term synaptic plasticity. By using MCH/ataxin3 mice, a genetic model characterized by a selective deletion of MCH neurons in the adult, we investigated the role of MCH neurons in hippocampal synaptic plasticity and hippocampal-dependent forms of memory. MCH/ataxin3 mice exhibited a deficit in the early part of both long-term potentiation and depression in the CA1 area of the hippocampus. Post-tetanic potentiation (PTP) was diminished while synaptic depression induced by repetitive stimulation was enhanced suggesting an alteration of pre-synaptic forms of short-term plasticity in these mice. Behaviorally, MCH/ataxin3 mice spent more time and showed a higher level of hesitation as compared to their controls in performing a short-term memory T-maze task, displayed retardation in acquiring a reference memory task in a Morris water maze, and showed a habituation deficit in an open field task. Deletion of MCH neurons could thus alter spatial short-term memory by impairing short-term plasticity in the hippocampus. Altogether, these findings could provide a cellular mechanism by which PS may facilitate memory encoding. Via MCH neuron activation, PS could prepare the day's learning by increasing and modulating short-term synaptic plasticity in the hippocampus. © 2015 Wiley Periodicals, Inc.

The Hypocretin/Orexin Antagonist Almorexant Promotes Sleep Without Impairment of Performance in Rats

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Stephen R Morairty

2014-01-01

Full Text Available The hypocretin receptor (HcrtR antagonist almorexant (ALM has potent hypnotic actions but little is known about neurocognitive performance in the presence of ALM. HcrtR antagonists are hypothesized to induce sleep by disfacilitation of wake-promoting systems whereas GABAA receptor modulators such as zolpidem (ZOL induce sleep through general inhibition of neural activity. To test the hypothesis that less functional impairment results from HcrtR antagonist-induced sleep, we evaluated the performance of rats in the Morris Water Maze in the presence of ALM vs. ZOL. Performance in spatial reference memory (SRM and spatial working memory (SWM tasks were assessed during the dark period after equipotent sleep-promoting doses (100 mg/kg, po following undisturbed and sleep deprivation (SD conditions. ALM-treated rats were indistinguishable from vehicle (VEH-treated rats for all SRM performance measures (distance travelled, latency to enter, time within, and number of entries into, the target quadrant after both the undisturbed and 6 h SD conditions. In contrast, rats administered ZOL showed impairments in all parameters measured compared to VEH or ALM in the undisturbed conditions. Following SD, ZOL-treated rats also showed impairments in all measures. ALM-treated rats were similar to VEH-treated rats for all SWM measures (velocity, time to locate the platform and success rate at finding the platform within 60 s after both the undisturbed and SD conditions. In contrast, ZOL-treated rats showed impairments in velocity and in the time to locate the platform. Importantly, ZOL rats only completed the task 23-50% of the time while ALM and VEH rats completed the task 79-100% of the time. Thus, following equipotent sleep-promoting doses, ZOL impaired rats in both memory tasks while ALM rats performed at levels comparable to VEH rats. These results are consistent with the hypothesis that less impairment results from HcrtR antagonism than from GABAA

cGMP-dependent protein kinase I, the circadian clock, sleep and learning.

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Feil, Robert; Hölter, Sabine M; Weindl, Karin; Wurst, Wolfgang; Langmesser, Sonja; Gerling, Andrea; Feil, Susanne; Albrecht, Urs

2009-07-01

The second messenger cGMP controls cardiovascular and gastrointestinal homeostasis in mammals. However, its physiological relevance in the nervous system is poorly understood.1 Now, we have reported that the cGMP-dependent protein kinase type I (PRKG1) is implicated in the regulation of the timing and quality of sleep and wakefulness.2Prkg1 mutant mice showed altered distribution of sleep and wakefulness as well as reduction in rapid-eye-movement sleep (REMS) duration and in non-REMS consolidation. Furthermore, the ability to sustain waking episodes was compromised. These observations were also reflected in wheel-running and drinking activity. A decrease in electroencephalogram power in the delta frequency range (1-4 Hz) under baseline conditions was observed, which was normalized after sleep deprivation. Together with the finding that circadian clock amplitude is reduced in Prkg1 mutants these results indicate a decrease of the wake-promoting output of the circadian system affecting sleep. Because quality of sleep might affect learning we tested Prkg1 mutants in several learning tasks and find normal spatial learning but impaired object recognition memory in these animals. Our findings indicate that Prkg1 impinges on circadian rhythms, sleep and distinct aspects of learning.

Commonly used stimulants: Sleep problems, dependence and psychological distress.

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Ogeil, Rowan P; Phillips, James G

2015-08-01

Caffeine and nicotine are commonly used stimulants that enhance alertness and mood. Discontinuation of both stimulants is associated with withdrawal symptoms including sleep and mood disturbances, which may differ in males and females. The present study examines changes in sleep quality, daytime sleepiness and psychological distress associated with use and dependence on caffeine and nicotine. An online survey comprising validated tools to assess sleep quality, excessive daytime sleepiness and psychological distress was completed by 166 participants (74 males, 96 females) with a mean age of 28 years. Participants completed the study in their own time, and were not offered any inducements to participate. Sleep quality was poorer in those dependent upon caffeine or nicotine, and there were also significant interaction effects with gender whereby females reported poorer sleep despite males reporting higher use of both stimulants. Caffeine dependence was associated with poorer sleep quality, increased daytime dysfunction, and increased levels of night time disturbance, while nicotine dependence was associated with poorer sleep quality and increased use of sleep medication and sleep disturbances. There were strong links between poor sleep and diminished affect, with psychological distress found to co-occur in the context of disturbed sleep. Stimulants are widely used to promote vigilance and mood; however, dependence on commonly used drugs including caffeine and nicotine is associated with decrements in sleep quality and increased psychological distress, which may be compounded in female dependent users. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Changes of cortical excitability as markers of antidepressant response in bipolar depression: preliminary data obtained by combining transcranial magnetic stimulation (TMS) and electroencephalography (EEG).

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Canali, Paola; Sferrazza Papa, Giovanna; Casali, Adenauer G; Schiena, Giandomenico; Fecchio, Matteo; Pigorini, Andrea; Smeraldi, Enrico; Colombo, Cristina; Benedetti, Francesco

2014-12-01

It is still unclear which biological changes are needed to recover from a major depressive episode. Current perspectives focus on cortical synaptic neuroplasticity. Measures of cortical responses evoked by transcranial magnetic stimulation (TMS) change with sleep homeostasic pressure in humans and approximate measures of synaptic strength in animal models. Using repeated total sleep deprivation as a model of antidepressant treatment, we aimed to correlate recovery from depression with these measures of cortical excitability. We recorded electroencephalographic responses to TMS in the prefrontal cortex of 21 depressed inpatients with bipolar disorder treated with repeated sleep deprivation combined with light therapy. We performed seven TMS/electroencephalography sessions during one week and calculated three measures of cortical excitability. Cortical excitability progressively increased during the antidepressant treatment and as a function of time awake. Higher values differentiated responders from non-responders at baseline and during and after treatment on all measures. Changes in measures of cortical excitability parallel and predict antidepressant response to combined sleep deprivation and light therapy. Data suggest that promoting cortical plasticity in bipolar depression could be a major effect of successful antidepressant treatments, and that patients not responding could suffer a persistent impairment in their neuroplasticity mechanisms. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

State-dependent intrinsic predictability of cortical network dynamics.

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Leila Fakhraei

Full Text Available The information encoded in cortical circuit dynamics is fleeting, changing from moment to moment as new input arrives and ongoing intracortical interactions progress. A combination of deterministic and stochastic biophysical mechanisms governs how cortical dynamics at one moment evolve from cortical dynamics in recently preceding moments. Such temporal continuity of cortical dynamics is fundamental to many aspects of cortex function but is not well understood. Here we study temporal continuity by attempting to predict cortical population dynamics (multisite local field potential based on its own recent history in somatosensory cortex of anesthetized rats and in a computational network-level model. We found that the intrinsic predictability of cortical dynamics was dependent on multiple factors including cortical state, synaptic inhibition, and how far into the future the prediction extends. By pharmacologically tuning synaptic inhibition, we obtained a continuum of cortical states with asynchronous population activity at one extreme and stronger, spatially extended synchrony at the other extreme. Intermediate between these extremes we observed evidence for a special regime of population dynamics called criticality. Predictability of the near future (10-100 ms increased as the cortical state was tuned from asynchronous to synchronous. Predictability of the more distant future (>1 s was generally poor, but, surprisingly, was higher for asynchronous states compared to synchronous states. These experimental results were confirmed in a computational network model of spiking excitatory and inhibitory neurons. Our findings demonstrate that determinism and predictability of network dynamics depend on cortical state and the time-scale of the dynamics.

Association between visual impairment and sleep duration: analysis of the 2009 National Health Interview Survey (NHIS).

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Ramos, Alberto R; Wallace, Douglas M; Williams, Natasha J; Spence, David Warren; Pandi-Perumal, Seithikurippu Ratnas; Zizi, Ferdinand; Jean-Louis, Girardin

2014-10-01

Visual impairment (VI) is associated with increased mortality and health factors such as depression and cardiovascular disease. Epidemiologic studies consistently show associations between sleep duration with adverse health outcomes, but these have not systematically considered the influence of VI. The aim of this study was to ascertain the independent association between VI and sleep duration using the National Health Interview Survey (NHIS) data. We also examined whether race/ethnicity influenced these associations independently of sociodemographic and medical characteristics. Our analysis was based on the 2009 NHIS, providing valid sleep and vision data for 29,815 participants. The NHIS is a cross-sectional household interview survey utilizing a multistage area probability design. Trained personnel from the US census bureau gathered data during face-to-face interview and obtained socio-demographic, self-reported habitual sleep duration and physician-diagnosed chronic conditions. The mean age of the sample was 48 years and 56% were female. Short sleep and long sleep durations were reported by 49% and 23% of the participants, respectively. Visual impairment was observed in 10%. Multivariate-adjusted logistic regression models showed significant associations between VI and short sleep (OR = 1.6, 95% CI = 1.5-1.9 and long sleep durations (OR = 1.6, 95% CI = 1.3-1.9). These associations persisted in multivariate models stratified by race-ethnic groups. Visual impairment was associated with both short and long sleep durations. Analysis of epidemiologic sleep data should consider visual impairment as an important factor likely to influence the amount of sleep experienced habitually.

Olfactory impairment is related to REM sleep deprivation in rotenone model of Parkinson's disease

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Mariana F. Aurich

Full Text Available Introduction: Olfactory dysfunction affects about 85-90% of Parkinson's disease (PD patients with severe deterioration in the ability of discriminate several types of odors. In addition, studies reported declines in olfactory performances during a short period of sleep deprivation. Besides, PD is also known to strongly affect the occurrence and maintenance of rapid eye movement (REM sleep. Methods: Therefore, we investigated the mechanisms involved on discrimination of a social odor (dependent on the vomeronasal system and a non-social odor (related to the main olfactory pathway in the rotenone model of PD. Also, a concomitant impairment in REM sleep was inflicted with the introduction of two periods (24 or 48 h of REM sleep deprivation (REMSD. Rotenone promoted a remarkable olfactory impairment in both social and non-social odors, with a notable modulation induced by 24 h of REMSD for the non-social odor. Results: Our findings demonstrated the occurrence of a strong association between the density of nigral TH-ir neurons and the olfactory discrimination capacity for both odorant stimuli. Specifically, the rotenone-induced decrease of these neurons tends to elicit reductions in the olfactory discrimination ability. Conclusions: These results are consistent with the participation of the nigrostriatal dopaminergic system mainly in the olfactory discrimination of a non-social odor, probably through the main olfactory pathway. Such involvement may have produce relevant impact in the preclinical abnormalities found in PD patients.

Parietal Fast Sleep Spindle Density Decrease in Alzheimer's Disease and Amnesic Mild Cognitive Impairment

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Gorgoni, Maurizio; Lauri, Giulia; Truglia, Ilaria; Cordone, Susanna; Sarasso, Simone; Scarpelli, Serena; Mangiaruga, Anastasia; D'Atri, Aurora; Tempesta, Daniela; Ferrara, Michele; Marra, Camillo; Rossini, Paolo Maria; De Gennaro, Luigi

2016-01-01

Several studies have identified two types of sleep spindles: fast (13–15 Hz) centroparietal and slow (11–13 Hz) frontal spindles. Alterations in spindle activity have been observed in Alzheimer's disease (AD) and Mild Cognitive Impairment (MCI). Only few studies have separately assessed fast and slow spindles in these patients showing a reduction of fast spindle count, but the possible local specificity of this phenomenon and its relation to cognitive decline severity are not clear. Moreover, fast and slow spindle density have never been assessed in AD/MCI. We have assessed fast and slow spindles in 15 AD patients, 15 amnesic MCI patients, and 15 healthy elderly controls (HC). Participants underwent baseline polysomnographic recording (19 cortical derivations). Spindles during nonrapid eye movements sleep were automatically detected, and spindle densities of the three groups were compared in the derivations where fast and slow spindles exhibited their maximum expression (parietal and frontal, resp.). AD and MCI patients showed a significant parietal fast spindle density decrease, positively correlated with Minimental State Examination scores. Our results suggest that AD-related changes in spindle density are specific for frequency and location, are related to cognitive decline severity, and may have an early onset in the pathology development. PMID:27066274

Memory suppression trades prolonged fear and sleep-dependent fear plasticity for the avoidance of current fear

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Kuriyama, Kenichi; Honma, Motoyasu; Yoshiike, Takuya; Kim, Yoshiharu

2013-07-01

Sleep deprivation immediately following an aversive event reduces fear by preventing memory consolidation during homeostatic sleep. This suggests that acute insomnia might act prophylactically against the development of posttraumatic stress disorder (PTSD) even though it is also a possible risk factor for PTSD. We examined total sleep deprivation and memory suppression to evaluate the effects of these interventions on subsequent aversive memory formation and fear conditioning. Active suppression of aversive memory impaired retention of event memory. However, although the remembered fear was more reduced in sleep-deprived than sleep-control subjects, suppressed fear increased, and seemed to abandon the sleep-dependent plasticity of fear. Active memory suppression, which provides a psychological model for Freud's ego defense mechanism, enhances fear and casts doubt on the potential of acute insomnia as a prophylactic measure against PTSD. Our findings bring into question the role of sleep in aversive-memory consolidation in clinical PTSD pathophysiology.

Insomnia with Objective Short Sleep Duration: the Most Biologically Severe Phenotype of the Disorder

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Vgontzas, Alexandros N.; Fernandez-Mendoza, Julio; Liao, Duanping; Bixler, Edward O.

2013-01-01

Summary Until recently, the association of chronic insomnia with significant medical morbidity was not established and its diagnosis was based solely on subjective complaints. We present evidence that insomnia with objective short sleep duration is the most biologically severe phenotype of the disorder, as it is associated with cognitive-emotional and cortical arousal, activation of both limbs of the stress system, and a higher risk for hypertension, impaired heart rate variability, diabetes, neurocognitive impairment, and mortality. Also, it appears that objective short sleep duration is a biological marker of genetic predisposition to chronic insomnia. In contrast, insomnia with objective normal sleep duration is associated with cognitive-emotional and cortical arousal and sleep misperception but not with signs of activation of both limbs of the stress system or medical complications. Furthermore, the first phenotype is associated with unremitting course, whereas the latter is more likely to remit. We propose that short sleep duration in insomnia is a reliable marker of the biological severity and medical impact of the disorder. Objective measures of sleep obtained in the home environment of the patient would become part of the routine assessment of insomnia patients in a clinician’s office setting. We speculate that insomnia with objective short sleep duration has primarily biological roots and may respond better to biological treatments, whereas insomnia with objective normal sleep duration has primarily psychological roots and may respond better to psychological interventions alone. PMID:23419741

Insomnia with objective short sleep duration: the most biologically severe phenotype of the disorder.

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Vgontzas, Alexandros N; Fernandez-Mendoza, Julio; Liao, Duanping; Bixler, Edward O

2013-08-01

Until recently, the association of chronic insomnia with significant medical morbidity was not established and its diagnosis was based solely on subjective complaints. We present evidence that insomnia with objective short sleep duration is the most biologically severe phenotype of the disorder, as it is associated with cognitive-emotional and cortical arousal, activation of both limbs of the stress system, and a higher risk for hypertension, impaired heart rate variability, diabetes, neurocognitive impairment, and mortality. Also, it appears that objective short sleep duration is a biological marker of genetic predisposition to chronic insomnia. In contrast, insomnia with objective normal sleep duration is associated with cognitive-emotional and cortical arousal and sleep misperception but not with signs of activation of both limbs of the stress system or medical complications. Furthermore, the first phenotype is associated with unremitting course, whereas the latter is more likely to remit. We propose that short sleep duration in insomnia is a reliable marker of the biological severity and medical impact of the disorder. Objective measures of sleep obtained in the home environment of the patient would become part of the routine assessment of insomnia patients in a clinician's office setting. We speculate that insomnia with objective short sleep duration has primarily biological roots and may respond better to biological treatments, whereas insomnia with objective normal sleep duration has primarily psychological roots and may respond better to psychological interventions alone. Copyright © 2012 Elsevier Ltd. All rights reserved.

Cortical visual impairment: Characteristics and treatment

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Vučinić Vesna

2014-01-01

Full Text Available According to the latest studies, Cortical visual impairment – CVI is one of the most common causes of problems and difficulties in visual functioning. It results from the impairment of the central part of visual system, i.e. visual cortex, posterior visual pathway, or both. The diagnosis is usually made in the first three years of life. The aim of this paper is to present the characteristics of children with CVI, and the strategies used for treatment. CVI has a negative impact on almost all developmental domains, visual-perceptive skills, motor skills, cognitive skills, and social skills. In children with CVI, vision ranges from the total inability to see to minimal visual perceptive difficulties, while more than 50% have multiple disabilities. Due to the progress in understanding the patterns of neuron activity and neuroplasticity, as well as the intensive studies of strengths and weaknesses of children with CVI, special treatment has been designed and performed in the last few decades, which provides optimal visual functioning in everyday life for these children.

Cortical Gamma-Aminobutyric Acid and Glutamate in Posttraumatic Stress Disorder and Their Relationships to Self-Reported Sleep Quality

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Meyerhoff, Dieter J.; Mon, Anderson; Metzler, Thomas; Neylan, Thomas C.

2014-01-01

Study Objectives: To test if posttraumatic stress disorder (PTSD) is associated with low brain gamma-aminobutyric acid (GABA) levels and if reduced GABA is mediated by poor sleep quality. Design: Laboratory study using in vivo proton magnetic resonance spectroscopy (1H MRS) and behavioral testing. Setting: VA Medical Center Research Service, Psychiatry and Radiology. Patients or Participants: Twenty-seven patients with PTSD (PTSD+) and 18 trauma-exposed controls without PTSD (PTSD−), recruited from United States Army reservists, Army National Guard, and mental health clinics. Interventions: None. Measurements and Results: 1H MRS at 4 Tesla yielded spectra from three cortical brain regions. In parieto-occipital and temporal cortices, PTSD+ had lower GABA concentrations than PTSD−. As expected, PTSD+ had higher depressive and anxiety symptom scores and a higher Insomnia Severity Index (ISI) score. Higher ISI correlated with lower GABA and higher glutamate levels in parieto-occipital cortex and tended to correlate with lower GABA in the anterior cingulate. The relationship between parieto-occipital GABA and PTSD diagnosis was fully mediated through insomnia severity. Lower N-acetylaspartate and glutamate concentrations in the anterior cingulate cortex correlated with higher arousal scores, whereas depressive and anxiety symptoms did generally not influence metabolite concentrations. Conclusions: Low brain gamma-aminobutyric acid (GABA) concentration in posttraumatic stress disorder (PTSD) is consistent with most findings in panic and social anxiety disorders. Low GABA associated with poor sleep quality is consistent with the hyperarousal theory of both primary insomnia and PTSD. Our data demonstrate that poor sleep quality mediates low parieto-occipital GABA in PTSD. The findings have implications for PTSD treatment approaches. Citation: Meyerhoff DJ, Mon A, Metzler T, Neylan TC. Cortical gamma-aminobutyric acid and glutamate in posttraumatic stress disorder and

REM Sleep Behavior Disorder and Cognitive Impairment in Parkinson's Disease.

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Jozwiak, Natalia; Postuma, Ronald B; Montplaisir, Jacques; Latreille, Véronique; Panisset, Michel; Chouinard, Sylvain; Bourgouin, Pierre-Alexandre; Gagnon, Jean-François

2017-08-01

REM sleep behavior disorder (RBD) is a parasomnia affecting 33% to 46% of patients with Parkinson's disease (PD). The existence of a unique and specific impaired cognitive profile in PD patients with RBD is still controversial. We extensively assessed cognitive functions to identify whether RBD is associated with more severe cognitive deficits in nondemented patients with PD. One hundred sixty-two participants, including 53 PD patients with RBD, 40 PD patients without RBD, and 69 healthy subjects, underwent polysomnography, a neurological assessment and an extensive neuropsychological exam to assess attention, executive functions, episodic learning and memory, visuospatial abilities, and language. PD patients with RBD had poorer and clinically impaired performance in several cognitive tests compared to PD patients without RBD and healthy subjects. These two latter groups were similar on all cognitive measures. Mild cognitive impairment (MCI) diagnosis frequency was almost threefold higher in PD patients with RBD compared to PD patients without RBD (66% vs. 23%, p < .001). Moreover, subjective cognitive decline was reported in 89% of PD patients with RBD compared to 58% of PD patients without RBD (p = .024). RBD in PD is associated with a more impaired cognitive profile and higher MCI diagnosis frequency, suggesting more severe and widespread neurodegeneration. This patient subgroup and their caregivers should receive targeted medical attention to better detect and monitor impairment and to enable the development of management interventions for cognitive decline and its consequences. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Disrupted sleep without sleep curtailment induces sleepiness and cognitive dysfunction via the tumor necrosis factor-α pathway

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Ramesh Vijay

2012-05-01

Full Text Available Abstract Background Sleepiness and cognitive dysfunction are recognized as prominent consequences of sleep deprivation. Experimentally induced short-term sleep fragmentation, even in the absence of any reductions in total sleep duration, will lead to the emergence of excessive daytime sleepiness and cognitive impairments in humans. Tumor necrosis factor (TNF-α has important regulatory effects on sleep, and seems to play a role in the occurrence of excessive daytime sleepiness in children who have disrupted sleep as a result of obstructive sleep apnea, a condition associated with prominent sleep fragmentation. The aim of this study was to examine role of the TNF-α pathway after long-term sleep fragmentation in mice. Methods The effect of chronic sleep fragmentation during the sleep-predominant period on sleep architecture, sleep latency, cognitive function, behavior, and inflammatory markers was assessed in C57BL/6 J and in mice lacking the TNF-α receptor (double knockout mice. In addition, we also assessed the above parameters in C57BL/6 J mice after injection of a TNF-α neutralizing antibody. Results Mice subjected to chronic sleep fragmentation had preserved sleep duration, sleep state distribution, and cumulative delta frequency power, but also exhibited excessive sleepiness, altered cognitive abilities and mood correlates, reduced cyclic AMP response element-binding protein phosphorylation and transcriptional activity, and increased phosphodiesterase-4 expression, in the absence of AMP kinase-α phosphorylation and ATP changes. Selective increases in cortical expression of TNF-α primarily circumscribed to neurons emerged. Consequently, sleepiness and cognitive dysfunction were absent in TNF-α double receptor knockout mice subjected to sleep fragmentation, and similarly, treatment with a TNF-α neutralizing antibody abrogated sleep fragmentation-induced learning deficits and increases in sleep propensity. Conclusions Taken together

The association of cognitive impairment with gray matter atrophy and cortical lesion load in clinically isolated syndrome.

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Diker, Sevda; Has, Arzu Ceylan; Kurne, Aslı; Göçmen, Rahşan; Oğuz, Kader Karlı; Karabudak, Rana

2016-11-01

Multiple sclerosis can impair cognition from the early stages and has been shown to be associated with gray matter damage in addition to white matter pathology. To investigate the profile of cognitive impairment in clinically isolated syndrome (CIS), and the contribution of cortical inflammation, cortical and deep gray matter atrophy, and white matter lesions to cognitive decline. Thirty patients with clinically isolated syndrome and twenty demographically- matched healthy controls underwent neuropsychologic assessment through the Rao Brief Repeatable Battery, and brain magnetic resonance imaging with double inversion recovery using a 3T scanner. Patients with clinically isolated syndrome performed significantly worse than healthy controls on tests that evaluated verbal memory, visuospatial learning and memory, and verbal fluency. Significant deep gray matter atrophy was found in the patients but cortical volume was not lower than the controls. Visual memory tests correlated with the volume of the hippocampus, cerebral white matter and deep gray matter structures and with cerebellar cortical atrophy. Cortical or white matter lesion load did not affect cognitive test results. In our patients with CIS, it was shown that cognitive impairment was mainly related to cerebral white matter, cerebellar cortical and deep gray matter atrophy, but not with cortical inflammation, at least in the early stage of disease. Copyright © 2016 Elsevier B.V. All rights reserved.

Sleep fragmentation alters brain energy metabolism without modifying hippocampal electrophysiological response to novelty exposure.

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Baud, Maxime O; Parafita, Julia; Nguyen, Audrey; Magistretti, Pierre J; Petit, Jean-Marie

2016-10-01

Sleep is viewed as a fundamental restorative function of the brain, but its specific role in neural energy budget remains poorly understood. Sleep deprivation dampens brain energy metabolism and impairs cognitive functions. Intriguingly, sleep fragmentation, despite normal total sleep duration, has a similar cognitive impact, and in this paper we ask the question of whether it may also impair brain energy metabolism. To this end, we used a recently developed mouse model of 2 weeks of sleep fragmentation and measured 2-deoxy-glucose uptake and glycogen, glucose and lactate concentration in different brain regions. In order to homogenize mice behaviour during metabolic measurements, we exposed them to a novel environment for 1 h. Using an intra-hippocampal electrode, we first showed that hippocampal electroencephalograph (EEG) response to exploration was unaltered by 1 or 14 days of sleep fragmentation. However, after 14 days, sleep fragmented mice exhibited a lower uptake of 2-deoxy-glucose in cortex and hippocampus and lower cortical lactate levels than control mice. Our results suggest that long-term sleep fragmentation impaired brain metabolism to a similar extent as total sleep deprivation without affecting the neuronal responsiveness of hippocampus to a novel environment. © 2016 European Sleep Research Society.

Sleep fragmentation alters brain energy metabolism without modifying hippocampal electrophysiological response to novelty exposure

KAUST Repository

Baud, Maxime O.

2016-05-03

© 2016 European Sleep Research Society. Sleep is viewed as a fundamental restorative function of the brain, but its specific role in neural energy budget remains poorly understood. Sleep deprivation dampens brain energy metabolism and impairs cognitive functions. Intriguingly, sleep fragmentation, despite normal total sleep duration, has a similar cognitive impact, and in this paper we ask the question of whether it may also impair brain energy metabolism. To this end, we used a recently developed mouse model of 2 weeks of sleep fragmentation and measured 2-deoxy-glucose uptake and glycogen, glucose and lactate concentration in different brain regions. In order to homogenize mice behaviour during metabolic measurements, we exposed them to a novel environment for 1 h. Using an intra-hippocampal electrode, we first showed that hippocampal electroencephalograph (EEG) response to exploration was unaltered by 1 or 14 days of sleep fragmentation. However, after 14 days, sleep fragmented mice exhibited a lower uptake of 2-deoxy-glucose in cortex and hippocampus and lower cortical lactate levels than control mice. Our results suggest that long-term sleep fragmentation impaired brain metabolism to a similar extent as total sleep deprivation without affecting the neuronal responsiveness of hippocampus to a novel environment.

Feedback Blunting: Total Sleep Deprivation Impairs Decision Making that Requires Updating Based on Feedback.

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Whitney, Paul; Hinson, John M; Jackson, Melinda L; Van Dongen, Hans P A

2015-05-01

To better understand the sometimes catastrophic effects of sleep loss on naturalistic decision making, we investigated effects of sleep deprivation on decision making in a reversal learning paradigm requiring acquisition and updating of information based on outcome feedback. Subjects were randomized to a sleep deprivation or control condition, with performance testing at baseline, after 2 nights of total sleep deprivation (or rested control), and following 2 nights of recovery sleep. Subjects performed a decision task involving initial learning of go and no go response sets followed by unannounced reversal of contingencies, requiring use of outcome feedback for decisions. A working memory scanning task and psychomotor vigilance test were also administered. Six consecutive days and nights in a controlled laboratory environment with continuous behavioral monitoring. Twenty-six subjects (22-40 y of age; 10 women). Thirteen subjects were randomized to a 62-h total sleep deprivation condition; the others were controls. Unlike controls, sleep deprived subjects had difficulty with initial learning of go and no go stimuli sets and had profound impairment adapting to reversal. Skin conductance responses to outcome feedback were diminished, indicating blunted affective reactions to feedback accompanying sleep deprivation. Working memory scanning performance was not significantly affected by sleep deprivation. And although sleep deprived subjects showed expected attentional lapses, these could not account for impairments in reversal learning decision making. Sleep deprivation is particularly problematic for decision making involving uncertainty and unexpected change. Blunted reactions to feedback while sleep deprived underlie failures to adapt to uncertainty and changing contingencies. Thus, an error may register, but with diminished effect because of reduced affective valence of the feedback or because the feedback is not cognitively bound with the choice. This has important

Sleep Restriction Impairs Vocabulary Learning when Adolescents Cram for Exams: The Need for Sleep Study.

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Huang, Sha; Deshpande, Aadya; Yeo, Sing-Chen; Lo, June C; Chee, Michael W L; Gooley, Joshua J

2016-09-01

The ability to recall facts is improved when learning takes place at spaced intervals, or when sleep follows shortly after learning. However, many students cram for exams and trade sleep for other activities. The aim of this study was to examine the interaction of study spacing and time in bed (TIB) for sleep on vocabulary learning in adolescents. In the Need for Sleep Study, which used a parallel-group design, 56 adolescents aged 15-19 years were randomly assigned to a week of either 5 h or 9 h of TIB for sleep each night as part of a 14-day protocol conducted at a boarding school. During the sleep manipulation period, participants studied 40 Graduate Record Examination (GRE)-type English words using digital flashcards. Word pairs were presented over 4 consecutive days (spaced items), or all at once during single study sessions (massed items), with total study time kept constant across conditions. Recall performance was examined 0 h, 24 h, and 120 h after all items were studied. For all retention intervals examined, recall of massed items was impaired by a greater amount in adolescents exposed to sleep restriction. In contrast, cued recall performance on spaced items was similar between sleep groups. Spaced learning conferred strong protection against the effects of sleep restriction on recall performance, whereas students who had insufficient sleep were more likely to forget items studied over short time intervals. These findings in adolescents demonstrate the importance of combining good study habits and good sleep habits to optimize learning outcomes. © 2016 Associated Professional Sleep Societies, LLC.

Shorter sleep duration is associated with social impairment and comorbidities in ASD.

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Veatch, Olivia J; Sutcliffe, James S; Warren, Zachary E; Keenan, Brendan T; Potter, Melissa H; Malow, Beth A

2017-07-01

Sleep disturbance, particularly insomnia, is common in children with autism spectrum disorders (ASD). Furthermore, disturbed sleep affects core symptoms and other related comorbidities. Understanding the causes and consequences of sleep disturbances in children with ASD is an important step toward mitigating these symptoms. To better understand the connection between sleep duration and ASD severity, we analyzed ASD-related symptoms using the Autism Diagnostic Interview-Revised (ADI-R), Autism Diagnostic Observation Schedule (ADOS), IQ scores, and parent reports of the average amount of time slept per night that were available in the medical histories of 2,714 children with ASD in the Simons Simplex Collection (SSC). The mean (SD) sleep duration was 555 minutes. Sleep duration and severity of core ASD symptoms were negatively correlated, and sleep duration and IQ scores were positively correlated. Regression results indicated that more severe social impairment, primarily a failure to develop peer relationships, is the core symptom most strongly associated with short sleep duration. Furthermore, increased severity for numerous maladaptive behaviors assessed on the Child Behavior Checklist, as well as reports of attention deficit disorder, depressive disorder, and obsessive compulsive disorder were associated with short sleep duration. Severity scores for social/communication impairment and restricted and repetitive behaviors (RRB) were increased, and IQ scores were decreased, for children reported to sleep ≤420 minutes per night (lower 5th percentile) compared to children sleeping ≥660 minutes (upper 95th percentile). Our results indicate that reduced amounts of sleep are related to more severe symptoms in children with ASD. Autism Res 2017. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Autism Res 2017, 10: 1221-1238. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. © 2017 International Society for Autism

Low-frequency oscillations and vasoreactivity of cortical vessels in obstructive sleep apnea during wakefulness

DEFF Research Database (Denmark)

Schytz, Henrik Winther; Jensen, Benedicte Ersted; Jennum, Poul

2013-01-01

Effective nasal continuous positive airway pressure (CPAP) therapy reduces the cardiovascular outcomes associated with obstructive sleep apnea (OSA), but the mechanism behind this effect is unclear. We investigated if OSA patients during wakefulness showed signs of increased sympathetic activity...... and decreased vasoreactivity in cerebral cortical vessels as measured with near-infrared spectroscopy (NIRS), and if this may be reversed by CPAP treatment....

Perceived stress, disturbed sleep, and cognitive impairments in patients with work-related stress complaints: a longitudinal study.

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Eskildsen, Anita; Fentz, Hanne Nørr; Andersen, Lars Peter; Pedersen, Anders Degn; Kristensen, Simon Bang; Andersen, Johan Hviid

2017-07-01

Patients on sick leave due to work-related stress often present with cognitive impairments as well as sleep disturbances. The aim of this longitudinal study was to examine the role of perceived stress and sleep disturbances in the longitudinal development in cognitive impairments in a group of patients with prolonged work-related stress (N = 60) during a period of 12 months following initial professional care-seeking. Objective cognitive impairments (neuropsychological tests) were measured on two occasions - at initial professional care-seeking and at 12-month follow-up. Questionnaires on perceived stress, sleep disturbances, and cognitive complaints were completed seven times during the 12 months which facilitated multilevel analysis with segregation of within-person (change) and between-person (baseline level) components of the time-varying predictors (perceived stress and sleep disturbances). Change in perceived stress was associated with concurrent and subsequent change in self-reported cognitive complaints over the period of 12 months and to a lesser extent the change in performance on neuropsychological tests of processing speed from baseline to 12-month follow-up. Change in sleep disturbances was also associated with concurrent and subsequent change in self-reported cognitive complaints over the 12 months but not with change on neuropsychological test performance. Although the mechanism behind the improvement in cognitive impairments in patients with work-related stress should be further explored in future studies, the results could suggest that improvement in cognitive impairments is partly mediated by decreasing levels of perceived stress and, to a lesser extent, decreasing levels of sleep disturbances. Lay summary This study examines the role of perceived stress and sleep disturbances in respect to the development of cognitive impairments (e.g. memory and concentration) in a group of patients with work-related stress. We found that change in

The 2007 AASM recommendations for EEG electrode placement in polysomnography: impact on sleep and cortical arousal scoring.

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Ruehland, Warren R; O'Donoghue, Fergal J; Pierce, Robert J; Thornton, Andrew T; Singh, Parmjit; Copland, Janet M; Stevens, Bronwyn; Rochford, Peter D

2011-01-01

To examine the impact of using American Academy of Sleep Medicine (AASM) recommended EEG derivations (F4/M1, C4/M1, O2/M1) vs. a single derivation (C4/M1) in polysomnography (PSG) on the measurement of sleep and cortical arousals, including inter- and intra-observer variability. Prospective, non-blinded, randomized comparison. Three Australian tertiary-care hospital clinical sleep laboratories. 30 PSGs from consecutive patients investigated for obstructive sleep apnea (OSA) during December 2007 and January 2008. N/A. To examine the impact of EEG derivations on PSG summary statistics, 3 scorers from different Australian clinical sleep laboratories each scored separate sets of 10 PSGs twice, once using 3 EEG derivations and once using 1 EEG derivation. To examine the impact on inter- and intra-scorer reliability, all 3 scorers scored a subset of 10 PSGs 4 times, twice using each method. All PSGs were de-identified and scored in random order according to the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Using 3 referential EEG derivations during PSG, as recommended in the AASM manual, instead of a single central EEG derivation, as originally suggested by Rechtschaffen and Kales (1968), resulted in a mean ± SE decrease in N1 sleep of 9.6 ± 3.9 min (P = 0.018) and an increase in N3 sleep of 10.6 ± 2.8 min (P = 0.001). No significant differences were observed for any other sleep or arousal scoring summary statistics; nor were any differences observed in inter-scorer or intra-scorer reliability for scoring sleep or cortical arousals. This study provides information for those changing practice to comply with the 2007 AASM recommendations for EEG placement in PSG, for those using portable devices that are unable to comply with the recommendations due to limited channel options, and for the development of future standards for PSG scoring and recording. As the use of multiple EEG derivations only led to small changes in the distribution of derived sleep

Sleep problems and daily functioning in children with ADHD: An investigation of the role of impairment, ADHD presentations, and psychiatric comorbidity

DEFF Research Database (Denmark)

Virring, Anne; Lambek, Rikke; Jennum, Poul Jørgen

2017-01-01

, the Weiss Functional Impairment Rating Scale, and the ADHD Rating Scale. RESULTS: We found a moderate, positive correlation between sleep problems and impaired functioning in both children with ADHD and in typically developed children. ADHD presentations did not differ significantly with respect to sleep......OBJECTIVE: Little systematic information is available regarding how sleep problems influence daytime functioning in children with ADHD, as the role of ADHD presentations and comorbidity is unclear. METHOD: In total, 397 children were assessed with the Children's Sleep Habits Questionnaire...... problem profile, but having a comorbid internalizing or autistic disorder lead to higher sleep problem score. CONCLUSION: Sleep problems and impaired daily functioning were more common in children with ADHD, but the overall association between sleep problems and impaired daily functioning was similar...

Sleep Deprivation Impairs and Caffeine Enhances My Performance, but Not Always Our Performance.

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Faber, Nadira S; Häusser, Jan A; Kerr, Norbert L

2017-02-01

What effects do factors that impair or enhance performance in individuals have when these individuals act in groups? We provide a framework, called the GIE ("Effects of Grouping on Impairments and Enhancements") framework, for investigating this question. As prominent examples for individual-level impairments and enhancements, we discuss sleep deprivation and caffeine. Based on previous research, we derive hypotheses on how they influence performance in groups, specifically process gains and losses in motivation, individual capability, and coordination. We conclude that the effect an impairment or enhancement has on individual-level performance is not necessarily mirrored in group performance: grouping can help or hurt. We provide recommendations on how to estimate empirically the effects individual-level performance impairments and enhancements have in groups. By comparing sleep deprivation to stress and caffeine to pharmacological cognitive enhancement, we illustrate that we cannot readily generalize from group results on one impairment or enhancement to another, even if they have similar effects on individual-level performance.

CARDIOVASCULAR AND METABOLIC IMPAIRMENT IN PATIENTS WITH OBSTRUCTIVE SLEEP APNEA

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M. V. Gorbunova

2018-01-01

Full Text Available Since the moment when the obstructive nature of sleep apnea was first revealed, many new in-formation on this disease have been obtained. Now obstructive sleep apnea (OSA recognized as an  independent predictor of the development of impaired glucose  tolerance (insulin resistance, fasting hyperglycaemia, type 2  diabetes mellitus (DM2, resistant arterial hypertension, cardio- vascular death. The problem of identifying and treating patients with OSA is still actual. In real clinical practice, there is a need for an integrated approach to the diagnosis and therapy of comorbid OSA patients with metabolic impairment and cardiovascular  diseases.The aim of this review is to assess the clinical and  pathogenesis features of metabolic impaired, carbohydrate metabolism, basic metabolism, eating behavior, body weight fluctuations in patients with ob-structive sleep apnea syndrome. Methods. In our work, we used a retrospective analysis of pub-lished clinical research data of domestic and foreign authors  over the past 20 years. The review included studies with adequate  design from the standpoint of «good clinical practice» (GCP and  evidence-based medicine.The conclusion. According to modern  interpretation, obstructive sleep apnea is considered as an  independent disease that has its pathogenic mechanisms, clinical  and functional manifestations. There are several main causes of the effect of OSA on the metabolic component and the work of the cardiovascular system. Among them, intermittent hypoxemia,  endothelial dysfunction, fluctuations in intrathoracic pressure,  increased activity of the sympathetic nervous system, disturbance of the structure of sleep are leading. OSA is considered as a disease capable of disabling patients of working age, dramatically changing  the quality of life, leading to early mortality due to cardiovascular  disasters. Timely detection of clinical symptoms of OSA and the  strategy of early

Losing Neutrality: The Neural Basis of Impaired Emotional Control without Sleep.

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Simon, Eti Ben; Oren, Noga; Sharon, Haggai; Kirschner, Adi; Goldway, Noam; Okon-Singer, Hadas; Tauman, Rivi; Deweese, Menton M; Keil, Andreas; Hendler, Talma

2015-09-23

Sleep deprivation has been shown recently to alter emotional processing possibly associated with reduced frontal regulation. Such impairments can ultimately fail adaptive attempts to regulate emotional processing (also known as cognitive control of emotion), although this hypothesis has not been examined directly. Therefore, we explored the influence of sleep deprivation on the human brain using two different cognitive-emotional tasks, recorded using fMRI and EEG. Both tasks involved irrelevant emotional and neutral distractors presented during a competing cognitive challenge, thus creating a continuous demand for regulating emotional processing. Results reveal that, although participants showed enhanced limbic and electrophysiological reactions to emotional distractors regardless of their sleep state, they were specifically unable to ignore neutral distracting information after sleep deprivation. As a consequence, sleep deprivation resulted in similar processing of neutral and negative distractors, thus disabling accurate emotional discrimination. As expected, these findings were further associated with a decrease in prefrontal connectivity patterns in both EEG and fMRI signals, reflecting a profound decline in cognitive control of emotion. Notably, such a decline was associated with lower REM sleep amounts, supporting a role for REM sleep in overnight emotional processing. Altogether, our findings suggest that losing sleep alters emotional reactivity by lowering the threshold for emotional activation, leading to a maladaptive loss of emotional neutrality. Significance statement: Sleep loss is known as a robust modulator of emotional reactivity, leading to increased anxiety and stress elicited by seemingly minor triggers. In this work, we aimed to portray the neural basis of these emotional impairments and their possible association with frontal regulation of emotional processing, also known as cognitive control of emotion. Using specifically suited EEG and f

Sleep in the human hippocampus: a stereo-EEG study.

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Fabio Moroni

Full Text Available BACKGROUND: There is compelling evidence indicating that sleep plays a crucial role in the consolidation of new declarative, hippocampus-dependent memories. Given the increasing interest in the spatiotemporal relationships between cortical and hippocampal activity during sleep, this study aimed to shed more light on the basic features of human sleep in the hippocampus. METHODOLOGY/PRINCIPAL FINDINGS: We recorded intracerebral stereo-EEG directly from the hippocampus and neocortical sites in five epileptic patients undergoing presurgical evaluations. The time course of classical EEG frequency bands during the first three NREM-REM sleep cycles of the night was evaluated. We found that delta power shows, also in the hippocampus, the progressive decrease across sleep cycles, indicating that a form of homeostatic regulation of delta activity is present also in this subcortical structure. Hippocampal sleep was also characterized by: i a lower relative power in the slow oscillation range during NREM sleep compared to the scalp EEG; ii a flattening of the time course of the very low frequencies (up to 1 Hz across sleep cycles, with relatively high levels of power even during REM sleep; iii a decrease of power in the beta band during REM sleep, at odds with the typical increase of power in the cortical recordings. CONCLUSIONS/SIGNIFICANCE: Our data imply that cortical slow oscillation is attenuated in the hippocampal structures during NREM sleep. The most peculiar feature of hippocampal sleep is the increased synchronization of the EEG rhythms during REM periods. This state of resonance may have a supportive role for the processing/consolidation of memory.

Different Functional and Microstructural Changes Depending on Duration of Mild Cognitive Impairment in Parkinson Disease.

Science.gov (United States)

Shin, N-Y; Shin, Y S; Lee, P H; Yoon, U; Han, S; Kim, D J; Lee, S-K

2016-05-01

The higher cortical burden of Lewy body and Alzheimer disease-type pathology has been reported to be associated with a faster onset of cognitive impairment of Parkinson disease. So far, there has been a few studies only about the changes of gray matter volume depending on duration of cognitive impairment in Parkinson disease. Therefore, our aim was to evaluate the different patterns of structural and functional changes in Parkinson disease with mild cognitive impairment according to the duration of parkinsonism before mild cognitive impairment. Fifty-nine patients with Parkinson disease with mild cognitive impairment were classified into 2 groups on the basis of shorter (parkinsonism before mild cognitive impairment. Fifteen drug-naïve patients with de novo Parkinson disease with intact cognition were included for comparison. Cortical thickness, Tract-Based Spatial Statistics, and seed-based resting-state functional connectivity analyses were performed. Age, sex, years of education, age at onset of parkinsonism, and levodopa-equivalent dose were included as covariates. The group with shorter duration of parkinsonism before mild cognitive impairment showed decreased fractional anisotropy and increased mean and radial diffusivity values in the frontal areas compared with the group with longer duration of parkinsonism before mild cognitive impairment (corrected P parkinsonism before mild cognitive impairment showed decreased resting-state functional connectivity in the default mode network area when the left or right posterior cingulate was used as a seed, and in the dorsolateral prefrontal areas when the left or right caudate was used as a seed (corrected P parkinsonism before mild cognitive impairment showed decreased resting-state functional connectivity mainly in the medial prefrontal cortex when the left or right posterior cingulate was used as a seed, and in the parieto-occipital areas when the left or right caudate was used as a seed (corrected P Parkinson

Obstructive sleep apnea syndrome and cognitive impairment: effects of CPAP

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Alessandra Giordano

2011-10-01

Full Text Available Obstructive Sleep Apnea Syndrome (OSAS is a sleep disorder characterised by repetitive episodes of upper airway obstruction (apnea or reduced airflow (hypopnoea despite persistent respiratory effort. Apnea is defined as the cessation of breathing for at least 10 seconds during sleep, while hypopnoea is defined as at least 30% reduction in airflow for 10 seconds associated with oxygen desaturation and sleep fragmentation. The presence in the general population is about 4%. The principal symptoms are: excessive daytime sleepiness (EDS, snoring, dry throat, morning headache, night sweats, gastro-esophageal reflux, and increased blood pressure.Long term complications can be: increased cardio-cerebrovascular risk and cognitive impairment such as deficiency in attention, vigilance, visual abilities, thought, speech, perception and short term memory.Continuous Positive Airway Pressure (CPAP is currently the best non-invasive therapy for OSAS.CPAP guarantees the opening of upper airways using pulmonary reflexive mechanisms increasing lung volume during exhalation and resistance reduction, decreasing electromyografical muscular activity around airways.The causes of cognitive impairments and their possible reversibility after CPAP treatment have been analysed in numerous studies. The findings, albeit controversial, show that memory, attention and executive functions are the most compromised cognitive functions.The necessity of increasing the patient compliance with ventilotherapy is evident, in order to prevent cognitive deterioration and, when possible, rehabilitate the compromised functions, a difficult task for executive functions.

Slow oscillating transcranial direct current stimulation during non-rapid eye movement sleep improves behavioral inhibition in attention-deficit/ hyperactivity disorder

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Manuel Tobias Munz

2015-08-01

Full Text Available Background: Behavioral inhibition, which is a later-developing executive function (EF and anatomically located in prefrontal areas, is impaired in attention-deficit and hyperactivity disorder (ADHD. While optimal EFs have been shown to depend on efficient sleep in healthy subjects, the impact of sleep problems, frequently reported in ADHD, remains elusive. Findings of macroscopic sleep changes in ADHD are inconsistent, but there is emerging evidence for distinct microscopic changes with a focus on prefrontal cortical regions and non-rapid eye movement (non-REM slow-wave sleep. Recently, slow oscillations (SO during non-REM sleep were found to be less functional and, as such, may be involved in sleep-dependent memory impairments in ADHD. Objective: By augmenting slow-wave power through bilateral, slow oscillating transcranial direct current stimulation (so-tDCS, frequency = 0.75 Hz during non-REM sleep, we aimed to improve daytime behavioral inhibition in children with ADHD. Methods: 14 boys (10-14 yrs diagnosed with ADHD were included. In a randomized, double-blind, cross-over design, patients received so-tDCS either in the first or in the second experimental sleep night. Inhibition control was assessed with a visuomotor go/no-go task. Intrinsic alertness was assessed with a simple stimulus response task. To control for visuomotor performance, motor memory was assessed with a finger sequence tapping task. Results: SO-power was enhanced during early non-REM sleep, accompanied by slowed reaction times and decreased standard deviations of reaction times, in the go/no-go task after so-tDCS. In contrast, intrinsic alertness and motor memory performance were not improved by so-tDCS. Conclusion: Since behavioral inhibition but not intrinsic alertness or motor memory was improved by so-tDCS, our results suggest that lateral prefrontal slow oscillations during sleep might play a specific role for executive functioning in ADHD.

Sleep-Dependent Modulation of Metabolic Rate in Drosophila.

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Stahl, Bethany A; Slocumb, Melissa E; Chaitin, Hersh; DiAngelo, Justin R; Keene, Alex C

2017-08-01

Dysregulation of sleep is associated with metabolic diseases, and metabolic rate (MR) is acutely regulated by sleep-wake behavior. In humans and rodent models, sleep loss is associated with obesity, reduced metabolic rate, and negative energy balance, yet little is known about the neural mechanisms governing interactions between sleep and metabolism. We have developed a system to simultaneously measure sleep and MR in individual Drosophila, allowing for interrogation of neural systems governing interactions between sleep and metabolic rate. Like mammals, MR in flies is reduced during sleep and increased during sleep deprivation suggesting sleep-dependent regulation of MR is conserved across phyla. The reduction of MR during sleep is not simply a consequence of inactivity because MR is reduced ~30 minutes following the onset of sleep, raising the possibility that CO2 production provides a metric to distinguish different sleep states in the fruit fly. To examine the relationship between sleep and metabolism, we determined basal and sleep-dependent changes in MR is reduced in starved flies, suggesting that starvation inhibits normal sleep-associated effects on metabolic rate. Further, translin mutant flies that fail to suppress sleep during starvation demonstrate a lower basal metabolic rate, but this rate was further reduced in response to starvation, revealing that regulation of starvation-induced changes in MR and sleep duration are genetically distinct. Therefore, this system provides the unique ability to simultaneously measure sleep and oxidative metabolism, providing novel insight into the physiological changes associated with sleep and wakefulness in the fruit fly. © Sleep Research Society 2017. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.

Neurobehavioral Performance Impairment in Insomnia: Relationships with Self-Reported Sleep and Daytime Functioning

Science.gov (United States)

Shekleton, Julia A.; Flynn-Evans, Erin E.; Miller, Belinda; Epstein, Lawrence J.; Kirsch, Douglas; Brogna, Lauren A.; Burke, Liza M.; Bremer, Erin; Murray, Jade M.; Gehrman, Philip; Lockley, Steven W.; Rajaratnam, Shantha M. W.

2014-01-01

Study Objectives: Despite the high prevalence of insomnia, daytime consequences of the disorder are poorly characterized. This study aimed to identify neurobehavioral impairments associated with insomnia, and to investigate relationships between these impairments and subjective ratings of sleep and daytime dysfunction. Design: Cross-sectional, multicenter study. Setting: Three sleep laboratories in the USA and Australia. Patients: Seventy-six individuals who met the Research Diagnostic Criteria (RDC) for Primary Insomnia, Psychophysiological Insomnia, Paradoxical Insomnia, and/or Idiopathic Childhood Insomnia (44F, 35.8 ± 12.0 years [mean ± SD]) and 20 healthy controls (14F, 34.8 ± 12.1 years). Interventions: N/A. Measurements and Results: Participants completed a 7-day sleep-wake diary, questionnaires assessing daytime dysfunction, and a neurobehavioral test battery every 60-180 minutes during an afternoon/evening sleep laboratory visit. Included were tasks assessing sustained and switching attention, working memory, subjective sleepiness, and effort. Switching attention and working memory were significantly worse in insomnia patients than controls, while no differences were found for simple or complex sustained attention tasks. Poorer sustained attention in the control, but not the insomnia group, was significantly associated with increased subjective sleepiness. In insomnia patients, poorer sustained attention performance was associated with reduced health-related quality of life and increased insomnia severity. Conclusions: We found that insomnia patients exhibit deficits in higher level neurobehavioral functioning, but not in basic attention. The findings indicate that neurobehavioral deficits in insomnia are due to neurobiological alterations, rather than sleepiness resulting from chronic sleep deficiency. Citation: Shekleton JA; Flynn-Evans EE; Miller B; Epstein LJ; Kirsch D; Brogna LA; Burke LM; Cremer E; Murray JM; Gehrman P; Lockley SW; Rajaratnam SMW

What are the causes and consequences of impaired sleep quality during and following extended hospitalisation amongst older adults?

OpenAIRE

AISLINN FELICITY LALOR

2017-01-01

Sleep is essential to everyone's health and wellbeing. Between 30-40% of people experience impaired sleep and is most common in older adults. Older adults also experience a higher number of hospitalisations in comparison to any other age group. This thesis aimed to investigate the causes and consequences of impaired sleep quality for older adults during and following hospital admission. Over 80% of older adults with self-reported poor sleep do not discuss it with any health professionals. Thi...

EEG transients in the sigma range during non-REM sleep predict learning in dogs

NARCIS (Netherlands)

Iotchev, I.B.; Kis, A.; Bodizs, R.; Luijtelaar, E.L.J.M. van; Kubinyi, E.

2017-01-01

Sleep spindles are phasic bursts of thalamo-cortical activity, visible in the cortex as transient oscillations in the sigma range (usually defined in humans as 12-14 or 9-16 Hz). They have been associated with sleep-dependent memory consolidation and sleep stability in humans and rodents.

The Reliability of the CVI Range: A Functional Vision Assessment for Children with Cortical Visual Impairment

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Newcomb, Sandra

2010-01-01

Children who are identified as visually impaired frequently have a functional vision assessment as one way to determine how their visual impairment affects their educational performance. The CVI Range is a functional vision assessment for children with cortical visual impairment. The purpose of the study presented here was to examine the…

Sleep deprivation during a specific 3-hour time window post-training impairs hippocampal synaptic plasticity and memory

NARCIS (Netherlands)

Prince, Toni-Moi; Wimmer, Mathieu; Choi, Jennifer; Havekes, Robbert; Aton, Sara; Abel, Ted

2014-01-01

Sleep deprivation disrupts hippocampal function and plasticity. In particular, long-term memory consolidation is impaired by sleep deprivation, suggesting that a specific critical period exists following learning during which sleep is necessary. To elucidate the impact of sleep deprivation on

Decreased prefrontal cortical dopamine transmission in alcoholism.

Science.gov (United States)

Narendran, Rajesh; Mason, Neale Scott; Paris, Jennifer; Himes, Michael L; Douaihy, Antoine B; Frankle, W Gordon

2014-08-01

Basic studies have demonstrated that optimal levels of prefrontal cortical dopamine are critical to various executive functions such as working memory, attention, inhibitory control, and risk/reward decisions, all of which are impaired in addictive disorders such as alcoholism. Based on this and imaging studies of alcoholism that have demonstrated less dopamine in the striatum, the authors hypothesized decreased dopamine transmission in the prefrontal cortex in persons with alcohol dependence. To test this hypothesis, amphetamine and [11C]FLB 457 positron emission tomography were used to measure cortical dopamine transmission in 21 recently abstinent persons with alcohol dependence and 21 matched healthy comparison subjects. [11C]FLB 457 binding potential, specific compared to nondisplaceable uptake (BPND), was measured in subjects with kinetic analysis using the arterial input function both before and after 0.5 mg kg-1 of d-amphetamine. Amphetamine-induced displacement of [11C]FLB 457 binding potential (ΔBPND) was significantly smaller in the cortical regions in the alcohol-dependent group compared with the healthy comparison group. Cortical regions that demonstrated lower dopamine transmission in the alcohol-dependent group included the dorsolateral prefrontal cortex, medial prefrontal cortex, orbital frontal cortex, temporal cortex, and medial temporal lobe. The results of this study, for the first time, unambiguously demonstrate decreased dopamine transmission in the cortex in alcoholism. Further research is necessary to understand the clinical relevance of decreased cortical dopamine as to whether it is related to impaired executive function, relapse, and outcome in alcoholism.

Sleep-dependent facilitation of episodic memory details.

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van der Helm, Els; Gujar, Ninad; Nishida, Masaki; Walker, Matthew P

2011-01-01

While a role for sleep in declarative memory processing is established, the qualitative nature of this consolidation benefit, and the physiological mechanisms mediating it, remain debated. Here, we investigate the impact of sleep physiology on characteristics of episodic memory using an item- (memory elements) and context- (contextual details associated with those elements) learning paradigm; the latter being especially dependent on the hippocampus. Following back-to-back encoding of two word lists, each associated with a different context, participants were assigned to either a Nap-group, who obtained a 120-min nap, or a No Nap-group. Six hours post-encoding, participants performed a recognition test involving item-memory and context-memory judgments. In contrast to item-memory, which demonstrated no between-group differences, a significant benefit in context-memory developed in the Nap-group, the extent of which correlated both with the amount of stage-2 NREM sleep and frontal fast sleep-spindles. Furthermore, a difference was observed on the basis of word-list order, with the sleep benefit and associated physiological correlations being selective for the second word-list, learned last (most proximal to sleep). These findings suggest that sleep may preferentially benefit contextual (hippocampal-dependent) aspects of memory, supported by sleep-spindle oscillations, and that the temporal order of initial learning differentially determines subsequent offline consolidation.

Sleep-dependent facilitation of episodic memory details.

Directory of Open Access Journals (Sweden)

Els van der Helm

Full Text Available While a role for sleep in declarative memory processing is established, the qualitative nature of this consolidation benefit, and the physiological mechanisms mediating it, remain debated. Here, we investigate the impact of sleep physiology on characteristics of episodic memory using an item- (memory elements and context- (contextual details associated with those elements learning paradigm; the latter being especially dependent on the hippocampus. Following back-to-back encoding of two word lists, each associated with a different context, participants were assigned to either a Nap-group, who obtained a 120-min nap, or a No Nap-group. Six hours post-encoding, participants performed a recognition test involving item-memory and context-memory judgments. In contrast to item-memory, which demonstrated no between-group differences, a significant benefit in context-memory developed in the Nap-group, the extent of which correlated both with the amount of stage-2 NREM sleep and frontal fast sleep-spindles. Furthermore, a difference was observed on the basis of word-list order, with the sleep benefit and associated physiological correlations being selective for the second word-list, learned last (most proximal to sleep. These findings suggest that sleep may preferentially benefit contextual (hippocampal-dependent aspects of memory, supported by sleep-spindle oscillations, and that the temporal order of initial learning differentially determines subsequent offline consolidation.

The association between poor sleep quality and global cortical atrophy is related to age. Results from the Atahualpa Project

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Oscar H. Del Brutto

2016-07-01

Full Text Available Community-dwellers aged ≥60 years enrolled in the Atahualpa Project underwent brain MRI and were interviewed with the Pittsburgh Sleep Quality Index. Of 290 participants, 94 (32% had poor sleep quality and 143 (49% had global cortical atrophy (GCA. In a logistic regression model (adjusted for demographics, cardiovascular risk factor, severe edentulism, symptoms of depression, the MoCA score, and neuroimaging signatures of cerebrovascular damage, poor sleep quality was associated with GCA (p=0.004. A multivariate probability model showed that the probability of moderate-to-severe GCA significantly increased in individuals with poor sleep quality aged ≥67 years. This study provides evidence for an association between poor sleep quality and GCA in older adults and the important interaction of age in this association.

Association between cortical thickness and CSF biomarkers in mild cognitive impairment and Alzheimer’s disease

DEFF Research Database (Denmark)

Mohades, Sara; Dubois, Jonathan; Parent, Maxime

regional cortical thinning (CT) measured by Magnetic Resonance Imaging (MRI) and brain amyloidosis (measured by CSF Ab 1-42 concentrations), or tau hyperphosphorylation (tau 181; p-tau) in Alzheimer’s Disease (AD) and Mild Cognitive Impairment (MCI) patients. We test the hypothesis that the association...... (CN; n¼8) were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. Cortical surface reconstruction and group registration were generated using Freesurfer. A general linear model was used to conduct regressions between CSF markers and cortical thickness. Results: Correlation...

Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation.

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Kim, Bowon; Kocsis, Bernat; Hwang, Eunjin; Kim, Youngsoo; Strecker, Robert E; McCarley, Robert W; Choi, Jee Hyun

2017-02-28

Homeostatic rebound in rapid eye movement (REM) sleep normally occurs after acute sleep deprivation, but REM sleep rebound settles on a persistently elevated level despite continued accumulation of REM sleep debt during chronic sleep restriction (CSR). Using high-density EEG in mice, we studied how this pattern of global regulation is implemented in cortical regions with different functions and network architectures. We found that across all areas, slow oscillations repeated the behavioral pattern of persistent enhancement during CSR, whereas high-frequency oscillations showed progressive increases. This pattern followed a common rule despite marked topographic differences. The findings suggest that REM sleep slow oscillations may translate top-down homeostatic control to widely separated brain regions whereas fast oscillations synchronizing local neuronal ensembles escape this global command. These patterns of EEG oscillation changes are interpreted to reconcile two prevailing theories of the function of sleep, synaptic homeostasis and sleep dependent memory consolidation.

Sleep Deprivation Impairs the Human Central and Peripheral Nervous System Discrimination of Social Threat.

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Goldstein-Piekarski, Andrea N; Greer, Stephanie M; Saletin, Jared M; Walker, Matthew P

2015-07-15

Facial expressions represent one of the most salient cues in our environment. They communicate the affective state and intent of an individual and, if interpreted correctly, adaptively influence the behavior of others in return. Processing of such affective stimuli is known to require reciprocal signaling between central viscerosensory brain regions and peripheral-autonomic body systems, culminating in accurate emotion discrimination. Despite emerging links between sleep and affective regulation, the impact of sleep loss on the discrimination of complex social emotions within and between the CNS and PNS remains unknown. Here, we demonstrate in humans that sleep deprivation impairs both viscerosensory brain (anterior insula, anterior cingulate cortex, amygdala) and autonomic-cardiac discrimination of threatening from affiliative facial cues. Moreover, sleep deprivation significantly degrades the normally reciprocal associations between these central and peripheral emotion-signaling systems, most prominent at the level of cardiac-amygdala coupling. In addition, REM sleep physiology across the sleep-rested night significantly predicts the next-day success of emotional discrimination within this viscerosensory network across individuals, suggesting a role for REM sleep in affective brain recalibration. Together, these findings establish that sleep deprivation compromises the faithful signaling of, and the "embodied" reciprocity between, viscerosensory brain and peripheral autonomic body processing of complex social signals. Such impairments hold ecological relevance in professional contexts in which the need for accurate interpretation of social cues is paramount yet insufficient sleep is pervasive. Copyright © 2015 the authors 0270-6474/15/3510135-11$15.00/0.

Sleep-Dependent Reactivation of Ensembles in Motor Cortex Promotes Skill Consolidation.

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Dhakshin S Ramanathan

Full Text Available Despite many prior studies demonstrating offline behavioral gains in motor skills after sleep, the underlying neural mechanisms remain poorly understood. To investigate the neurophysiological basis for offline gains, we performed single-unit recordings in motor cortex as rats learned a skilled upper-limb task. We found that sleep improved movement speed with preservation of accuracy. These offline improvements were linked to both replay of task-related ensembles during non-rapid eye movement (NREM sleep and temporal shifts that more tightly bound motor cortical ensembles to movements; such offline gains and temporal shifts were not evident with sleep restriction. Interestingly, replay was linked to the coincidence of slow-wave events and bursts of spindle activity. Neurons that experienced the most consistent replay also underwent the most significant temporal shift and binding to the motor task. Significantly, replay and the associated performance gains after sleep only occurred when animals first learned the skill; continued practice during later stages of learning (i.e., after motor kinematics had stabilized did not show evidence of replay. Our results highlight how replay of synchronous neural activity during sleep mediates large-scale neural plasticity and stabilizes kinematics during early motor learning.

Zeigarnik's sleepless nights: How unfinished tasks at the end of the week impair employee sleep on the weekend through rumination.

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Syrek, Christine J; Weigelt, Oliver; Peifer, Corinna; Antoni, Conny H

2017-04-01

It is almost common sense that work stress leads to sleep impairment, but the question of how work-related stressors impair employee sleep remains open. This study focuses on the role of rumination as the underlying mechanism for sleep impairment. Specifically, the authors contribute to recent research differentiating affective rumination from problem-solving pondering and examine the impact of both forms of rumination on the stressor-sleep relationship. Following theories of rumination and the Zeigarnik effect, they focus on unfinished tasks as a key onset for rumination. Unfinished tasks have received much research attention in the memory context but have been neglected as a stressor that can impact recovery. Drawing on theory, differential indirect links between unfinished tasks and sleep through affective rumination versus problem-solving pondering are examined. Further, the number of unfinished tasks extending over a 3-month period may impair employee sleep more than unfinished tasks within the acute phase. In this study, intraindividual links in a diary study supplemented by depicting between-person effects of unfinished tasks over a period of 3 months are examined. The authors matched 357 Friday and Monday observations over a 12-week interval for 59 employees. The results of the multilevel analysis suggest that the within-person relationship between unfinished tasks and sleep is mediated by affective rumination. Although problem-solving pondering was negatively related to sleep impairment, the indirect effect was not significant. Finally, beyond the acute effect, the authors found higher levels of unfinished tasks over 3 months are related to increased sleep impairment on the weekend. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

Unfinished tasks foster rumination and impair sleeping - particularly if leaders have high performance expectations.

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Syrek, Christine J; Antoni, Conny H

2014-10-01

This study examines the relationship between time pressure and unfinished tasks as work stressors on employee well-being. Relatively little is known about the effect of unfinished tasks on well-being. Specifically, excluding the impact of time pressure, we examined whether the feeling of not having finished the week's tasks fosters perseverative cognitions and impairs sleep. Additionally, we proposed that leader performance expectations moderate these relationships. In more detail, we expected the detrimental effect of unfinished tasks on both rumination and sleep would be enhanced if leader expectations were perceived to be high. In total, 89 employees filled out online diary surveys both before and after the weekend over a 5-week period. Multilevel growth modeling revealed that time pressure and unfinished tasks impacted rumination and sleep on the weekend. Further, our results supported our hypothesis that unfinished tasks explain unique variance in the dependent variables above and beyond the influence of time pressure. Moreover, we found the relationship between unfinished tasks and both rumination and sleep was moderated by leader performance expectations. Our results emphasize the importance of unfinished tasks as a stressor and highlight that leadership, specifically in the form of performance expectations, contributes significantly to the strength of this relationship.

Cortical Visual Impairment in Children: Presentation Intervention, and Prognosis in Educational Settings

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Swift, Suzanne H.; Davidson, Roseanna C.; Weems, Linda J.

2008-01-01

Children with cortical visual impairment (CVI) exhibit distinct visual behaviors which are often misinterpreted. As the incidence of CVI is on the rise, this has subsequently caused an increased need for identification and intervention with these children from teaching and therapy service providers. Distinguishing children with CVI from children…

TNFα G308A polymorphism is associated with resilience to sleep deprivation-induced psychomotor vigilance performance impairment in healthy young adults.

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Satterfield, Brieann C; Wisor, Jonathan P; Field, Stephanie A; Schmidt, Michelle A; Van Dongen, Hans P A

2015-07-01

Cytokines such as TNFα play an integral role in sleep/wake regulation and have recently been hypothesized to be involved in cognitive impairment due to sleep deprivation. We examined the effect of a guanine to adenine substitution at position 308 in the TNFα gene (TNFα G308A) on psychomotor vigilance performance impairment during total sleep deprivation. A total of 88 healthy women and men (ages 22-40) participated in one of five laboratory total sleep deprivation experiments. Performance on a psychomotor vigilance test (PVT) was measured every 2-3h. The TNFα 308A allele, which is less common than the 308G allele, was associated with greater resilience to psychomotor vigilance performance impairment during total sleep deprivation (regardless of time of day), and also provided a small performance benefit at baseline. The effect of genotype on resilience persisted when controlling for between-subjects differences in age, gender, race/ethnicity, and baseline sleep duration. The TNFα G308A polymorphism predicted less than 10% of the overall between-subjects variance in performance impairment during sleep deprivation. Nonetheless, the differential effect of the polymorphism at the peak of performance impairment was more than 50% of median performance impairment at that time, which is sizeable compared to the effects of other genotypes reported in the literature. Our findings provided evidence for a role of TNFα in the effects of sleep deprivation on psychomotor vigilance performance. Furthermore, the TNFα G308A polymorphism may have predictive potential in a biomarker panel for the assessment of resilience to psychomotor vigilance performance impairment due to sleep deprivation. Copyright © 2014 Elsevier Inc. All rights reserved.

Nicotine dependence and sleep quality in young adults.

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Dugas, E N; Sylvestre, M P; O'Loughlin, E K; Brunet, J; Kakinami, L; Constantin, E; O'Loughlin, J

2017-02-01

More cigarette smokers report poor sleep quality than non-smokers, but the association between nicotine dependence (ND) and sleep quality has not been well-characterized. The objective of this study was to describe the associations among frequency and intensity of cigarette smoking, ND symptoms, and sleep quality in young adults. Data on past-year smoking frequency, number of cigarettes smoked in the past month, five ND indicators (i.e., withdrawal, craving, self-medication symptoms, mFTQ, ICD-10 criteria for tobacco dependence), and sleep quality (measured with the Pittsburgh Sleep Quality Index (PSQI)) were collected in 2011-12 in self-report questionnaires completed by 405 young adult smokers (mean age 24 (0.6) years; 45% male; 45% daily smokers) participating in a longitudinal investigation of the natural course of ND. Associations between indicators of cigarette smoking, ND symptoms, and sleep quality were examined in multivariable logistic regression analyses controlling for age, sex, mother's education, and alcohol use. Thirty-six percent of participants reported poor sleep quality (PSQI>5). Higher cigarette consumption (OR(95% CI), 1.03(1.001-1.05)) but not frequency of past-year smoking, more frequent withdrawal symptoms (1.05(1.004-1.10)), more frequent cravings (1.05(1.004-1.10)), higher mFTQ scores (1.14(1.02-1.27)), and endorsing more ICD-10 criteria for tobacco dependence (1.19(1.04-1.36)) were also associated with poor sleep quality. Cigarette smoking and ND symptoms are associated with poor sleep quality in young adult smokers. Advice from practitioners to cut back on number of cigarettes smoked per day and treatment of ND symptoms may improve sleep quality in young adult smokers. Copyright © 2016 Elsevier Ltd. All rights reserved.

Memory consolidation in human sleep depends on inhibition of glucocorticoid release.

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Plihal, W; Born, J

1999-09-09

Early sleep dominated by slow-wave sleep has been found to be particularly relevant for declarative memory formation via hippocampo-neocortical networks. Concurrently, early nocturnal sleep is characterized by an inhibition of glucocorticoid release from the adrenals. Here, we show in healthy humans that this inhibition serves to support declarative memory consolidation during sleep. Elevating plasma glucocorticoid concentration during early sleep by administration of cortisol impaired consolidation of paired associate words, but not of non-declarative memory of visuomotor skills. Since glucocorticoid concentration was enhanced only during retention sleep, but not during acquisition or retrieval, a specific effect on the consolidation process is indicated. Blocking mineralocorticoid receptors by canrenoate did not affect memory, suggesting inactivation of glucocorticoid receptors to be the essential prerequisite for memory consolidation during early sleep.

An examination of the association between chronic sleep restriction and electrocortical arousal in college students.

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Witkowski, Sarah; Trujillo, Logan T; Sherman, Stephanie M; Carter, Patricia; Matthews, Michael D; Schnyer, David M

2015-03-01

The deleterious neurocognitive effects of laboratory-controlled short-term sleep deprivation are well-known. The present study investigated neurocognitive changes arising from chronic sleep restriction outside the laboratory. Sleep patterns of 24 undergraduates were tracked via actigraphy across a 15-week semester. At the semester beginning, at a midpoint, and a week before finals, students performed the Psychomotor Vigilance Test (PVT) and cortical arousal was measured via event-related potentials (ERP) and resting state electroencephalography (EEG). Average daily sleep decreased between Session 1 and Sessions 2 and 3. Calculated circadian rhythm measures indicated nighttime movement increased and sleep quality decreased from Sessions 1 and 2 to Session 3. Parallel to the sleep/activity measures, PVT reaction time increased between Session 1 and Sessions 2 and 3 and resting state alpha EEG reactivity magnitude and PVT-evoked P3 ERP amplitude decreased between Session 1 and Sessions 2 and 3. Cross-sectional regressions showed PVT reaction time was negatively associated with average daily sleep, alpha reactivity, and P3 changes; sleep/circadian measures were associated with alpha reactivity and/or P3 changes. Small, but persistent sleep deficits reduced cortical arousal and impaired vigilant attention. Chronic sleep restriction impacts neurocognition in a manner similar to laboratory controlled sleep deprivation. Copyright © 2014 International Federation of Clinical Neurophysiology. All rights reserved.

Brain Networks are Independently Modulated by Donepezil, Sleep, and Sleep Deprivation.

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Wirsich, Jonathan; Rey, Marc; Guye, Maxime; Bénar, Christian; Lanteaume, Laura; Ridley, Ben; Confort-Gouny, Sylviane; Cassé-Perrot, Catherine; Soulier, Elisabeth; Viout, Patrick; Rouby, Franck; Lefebvre, Marie-Noëlle; Audebert, Christine; Truillet, Romain; Jouve, Elisabeth; Payoux, Pierre; Bartrés-Faz, David; Bordet, Régis; Richardson, Jill C; Babiloni, Claudio; Rossini, Paolo Maria; Micallef, Joelle; Blin, Olivier; Ranjeva, Jean-Philippe

2018-05-01

Resting-state connectivity has been widely studied in the healthy and pathological brain. Less well-characterized are the brain networks altered during pharmacological interventions and their possible interaction with vigilance. In the hopes of finding new biomarkers which can be used to identify cortical activity and cognitive processes linked to the effects of drugs to treat neurodegenerative diseases such as Alzheimer's disease, the analysis of networks altered by medication would be particularly interesting. Eleven healthy subjects were recruited in the context of the European Innovative Medicines Initiative 'PharmaCog'. Each underwent five sessions of simultaneous EEG-fMRI in order to investigate the effects of donepezil and memantine before and after sleep deprivation (SD). The SD approach has been previously proposed as a model for cognitive impairment in healthy subjects. By applying network based statistics (NBS), we observed altered brain networks significantly linked to donepezil intake and sleep deprivation. Taking into account the sleep stages extracted from the EEG data we revealed that a network linked to sleep is interacting with sleep deprivation but not with medication intake. We successfully extracted the functional resting-state networks modified by donepezil intake, sleep and SD. We observed donepezil induced whole brain connectivity alterations forming a network separated from the changes induced by sleep and SD, a result which shows the utility of this approach to check for the validity of pharmacological resting-state analysis of the tested medications without the need of taking into account the subject specific vigilance.

Visual Attention to Movement and Color in Children with Cortical Visual Impairment

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Cohen-Maitre, Stacey Ann; Haerich, Paul

2005-01-01

This study investigated the ability of color and motion to elicit and maintain visual attention in a sample of children with cortical visual impairment (CVI). It found that colorful and moving objects may be used to engage children with CVI, increase their motivation to use their residual vision, and promote visual learning.

Sleep enhances false memories depending on general memory performance.

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Diekelmann, Susanne; Born, Jan; Wagner, Ullrich

2010-04-02

Memory is subject to dynamic changes, sometimes giving rise to the formation of false memories due to biased processes of consolidation or retrieval. Sleep is known to benefit memory consolidation through an active reorganization of representations whereas acute sleep deprivation impairs retrieval functions. Here, we investigated whether sleep after learning and sleep deprivation at retrieval enhance the generation of false memories in a free recall test. According to the Deese, Roediger, McDermott (DRM) false memory paradigm, subjects learned lists of semantically associated words (e.g., "night", "dark", "coal", etc.), lacking the strongest common associate or theme word (here: "black"). Free recall was tested after 9h following a night of sleep, a night of wakefulness (sleep deprivation) or daytime wakefulness. Compared with memory performance after a retention period of daytime wakefulness, both post-learning nocturnal sleep as well as acute sleep deprivation at retrieval significantly enhanced false recall of theme words. However, these effects were only observed in subjects with low general memory performance. These data point to two different ways in which sleep affects false memory generation through semantic generalization: one acts during consolidation on the memory trace per se, presumably by active reorganization of the trace in the post-learning sleep period. The other is related to the recovery function of sleep and affects cognitive control processes of retrieval. Both effects are unmasked when the material is relatively weakly encoded. Crown Copyright 2009. Published by Elsevier B.V. All rights reserved.

Altered sleep composition after traumatic brain injury does not affect declarative sleep-dependent memory consolidation

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Janna eMantua

2015-06-01

Full Text Available Individuals with a history of traumatic brain injury (TBI often report sleep disturbances, which may be caused by changes in sleep architecture or reduced sleep quality (greater time awake after sleep onset, poorer sleep efficiency, and sleep stage proportion alterations. Sleep is beneficial for memory formation, and herein we examine whether altered sleep physiology following TBI has deleterious effects on sleep-dependent declarative memory consolidation. Participants learned a list of word pairs in the morning or evening, and recall was assessed 12-hrs later, following an interval awake or with overnight sleep. Young adult participants (18-22 yrs were assigned to one of four experimental groups: TBI Sleep (n=14, TBI Wake (n=12, non-TBI Sleep (n=15, non-TBI Wake (n=15. Each TBI participant was >1 yr post-injury. Sleep physiology was measured with polysomnography. Memory consolidation was assessed by comparing change in word-pair recall over 12-hr intersession intervals. The TBI group spent a significantly greater proportion of the night in SWS than the non-TBI group at the expense of NREM1. The TBI group also had marginally lower EEG delta power during SWS in the central region. Intersession changes in recall were greater for intervals with sleep than without sleep in both groups. However, despite abnormal sleep stage proportions for individuals with a TBI history, there was no difference in the intersession change in recall following sleep for the TBI and non-TBI groups. In both Sleep groups combined, there was a positive correlation between Intersession Change and the proportion of the night in NREM2 + SWS. Overall, sleep composition is altered following TBI but such deficits do not yield insufficiencies in sleep-dependent memory consolidation.

Chronopathological aspects of sleep disorders and cognitive dysfunctions in children with visual impairments

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I. A. Kelmanson

2015-01-01

Full Text Available The most important and noticeable rhythmical phenomenon observed in the human body is a sleep-wake rhythm and related physical and mental changes. The so-called circadian rhythms that vary over a period of approximately 24 hours are most important. The suprachi-asmatic nucleus of the hypothalamus is a primary circadian pacemaker in mammals; and light pulses out of all stimuli obtained by this structure have been mostly studied. The light pulses unrelated to visual perception serve as the most important synchronizers of circadian rhythms. Children with visual impairments lack adequate photic stimulation and hence circadian rhythm disorders develop and cognitive impairments worsen with a high probability. The most important types of sleep disorders in children with visual impairments are considered; their negative impact on a child's cognitive functions is discussed; possible correction approaches are laid down.

Prenatal exposure to arsenic impairs behavioral flexibility and cortical structure in mice

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Kyaw Htet eAung

2016-03-01

Full Text Available Exposure to arsenic from well water in developing countries is suspected to cause developmental neurotoxicity. Although it has been demonstrated that exposure to sodium arsenite (NaAsO2 suppresses neurite outgrowth of cortical neurons in vitro, it is largely unknown how developmental exposure to NaAsO2 impairs higher brain function and affects cortical histology. Here, we investigated the effect of prenatal NaAsO2 exposure on the behavior of mice in adulthood, and evaluated histological changes in the prelimbic cortex (PrL, which is a part of the medial prefrontal cortex that is critically involved in cognition. Drinking water with or without NaAsO2 (85 ppm was provided to pregnant C3H mice from gestational days 8 to 18, and offspring of both sexes were subjected to cognitive behavioral analyses at 60 weeks of age. The brains of female offspring were subsequently harvested and used for morphometrical analyses. We found that both male and female mice prenatally exposed to NaAsO2 displayed an impaired adaptation to repetitive reversal tasks. In morphometrical analyses of Nissl- or Golgi-stained tissue sections, we found that NaAsO2 exposure was associated with a significant increase in the number of pyramidal neurons in layers V and VI of the PrL, but not other layers of the PrL. More strikingly, prenatal NaAsO2 exposure was associated with a significant decrease in neurite length but not dendrite spine density in all layers of the PrL. Taken together, our results indicate that prenatal exposure to NaAsO2 leads to behavioral inflexibility in adulthood and cortical disarrangement in the PrL might contribute to this behavioral impairment.

Insomnia is Associated with Cortical Hyperarousal as Early as Adolescence

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Fernandez-Mendoza, Julio; Li, Yun; Vgontzas, Alexandros N.; Fang, Jidong; Gaines, Jordan; Calhoun, Susan L.; Liao, Duanping; Bixler, Edward O.

2016-01-01

Study Objectives: To examine whether insomnia is associated with spectral electroencephalographic (EEG) dynamics in the beta (15–35Hz) range during sleep in an adolescent general population sample. Methods: A case-control sample of 44 adolescents from the Penn State Child Cohort underwent a 9-h polysomnography, clinical history and physical examination. We examined low-beta (15–25 Hz) and high-beta (25–35 Hz) relative power at central EEG derivations during sleep onset latency (SOL), sleep onset (SO), non-rapid eye movement (NREM) sleep, and wake after sleep onset (WASO). Results: Compared to controls (n = 21), individuals with insomnia (n = 23) showed increased SOL and WASO and decreased sleep duration and efficiency, while no differences in sleep architecture were found. Insomniacs showed increased low-beta and high-beta relative power during SOL, SO, and NREM sleep as compared to controls. High-beta relative power was greater during all sleep and wake states in insomniacs with short sleep duration as compared to individuals with insomnia with normal sleep duration. Conclusions: Adolescent insomnia is associated with increased beta EEG power during sleep, which suggests that cortical hyperarousal is present in individuals with insomnia as early as adolescence. Interestingly, cortical hyperarousal is greatest in individuals with insomnia with short sleep duration and may explain the sleep complaints of those with normal sleep duration. Disturbed cortical networks may be a shared mechanism putting individuals with insomnia at risk of psychiatric disorders. Citation: Fernandez-Mendoza J, Li Y, Vgontzas AN, Fang J, Gaines J, Calhoun SL, Liao D, Bixler EO. Insomnia is associated with cortical hyperarousal as early as adolescence. SLEEP 2016;39(5):1029–1036. PMID:26951400

Chronic Underactivity of Medial Frontal Cortical β2-Containing Nicotinic Receptors Increases Clozapine-Induced Working Memory Impairment in Female Rats

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Levin, Edward D.; Perkins, Abigail; Brotherton, Terrell; Qazi, Melissa; Berez, Chantal; Montalvo-Ortiz, Janitza; Davis, Kasey; Williams, Paul; Christopher, N. Channelle

2009-01-01

Nicotinic receptor decreases in the frontal cortex and hippocampus are important mediators of cognitive impairment in both schizophrenia and Alzheimer's disease. Drug treatments for these diseases should take into account the impacts of compromised brain function on drug response. This study investigated the impact of compromised nicotinic receptor activity in the frontal cortex in rats on memory function. Since both Alzheimer's disease and schizophrenia can involve psychosis, antipsychotic drugs are often given. The impacts of antipsychotic drugs on cognitive function have been found to be quite variable. It is the hypothesis of this and previous studies that the cognitive effects of antispychotic drugs on cognitive function depend on the integrity of brain systems involved in cognition. Previously in studies of the hippocampus, we found that chronic inhibition of β2-containing nicotinic receptors with dihydro-β-erythrodine (DHβE) impaired working memory and that this effect was attenuated by the antipsychotic drug clozapine. In contrast, chronic hippocampal α7 nicotinic receptor blockade with methyllycaconitine (MLA) potentiated the clozapine-induced memory impairment which is seen in rats without compromised nicotinic receptor activity. The current study determined medial frontal cortical α7 and β2-containing nicotinic receptor involvement in memory and the interactions with antipsychotic drug therapy with clozapine. Chronic DHβE and MLA infusion effects and interactions with systemic clozapine were assessed in female rats tested for memory on the radial-arm maze. Antipsychotic drug interactions with chronic systemic nicotine were investigated because nicotinic procognitive treatment has been proposed. The same local infusion DHβE dose that impaired memory with hippocampal infusion did not impair memory when infused in the medial frontal cortex. Frontal DHβE infusion potentiated clozapine-induced memory impairment, whereas previously the memory

Chronic underactivity of medial frontal cortical beta2-containing nicotinic receptors increases clozapine-induced working memory impairment in female rats.

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Levin, Edward D; Perkins, Abigail; Brotherton, Terrell; Qazi, Melissa; Berez, Chantal; Montalvo-Ortiz, Janitza; Davis, Kasey; Williams, Paul; Christopher, N Channelle

2009-03-17

Nicotinic receptor decreases in the frontal cortex and hippocampus are important mediators of cognitive impairment in both schizophrenia and Alzheimer's disease. Drug treatments for these diseases should take into account the impacts of compromised brain function on drug response. This study investigated the impact of compromised nicotinic receptor activity in the frontal cortex in rats on memory function. Since both Alzheimer's disease and schizophrenia can involve psychosis, antipsychotic drugs are often given. The impacts of antipsychotic drugs on cognitive function have been found to be quite variable. It is the hypothesis of this and previous studies that the cognitive effects of antispychotic drugs on cognitive function depend on the integrity of brain systems involved in cognition. Previously in studies of the hippocampus, we found that chronic inhibition of beta2-containing nicotinic receptors with dihydro-beta-erythrodine (DHbetaE) impaired working memory and that this effect was attenuated by the antipsychotic drug clozapine. In contrast, chronic hippocampal alpha7 nicotinic receptor blockade with methyllycaconitine (MLA) potentiated the clozapine-induced memory impairment which is seen in rats without compromised nicotinic receptor activity. The current study determined medial frontal cortical alpha7 and beta2-containing nicotinic receptor involvement in memory and the interactions with antipsychotic drug therapy with clozapine. Chronic DHbetaE and MLA infusion effects and interactions with systemic clozapine were assessed in female rats tested for memory on the radial-arm maze. Antipsychotic drug interactions with chronic systemic nicotine were investigated because nicotinic procognitive treatment has been proposed. The same local infusion DHbetaE dose that impaired memory with hippocampal infusion did not impair memory when infused in the medial frontal cortex. Frontal DHbetaE infusion potentiated clozapine-induced memory impairment, whereas previously

Reversible cortical blindness in a case of hepatic encephalopathy

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Amlan Kanti Biswas

2016-01-01

Full Text Available Hepatic encephalopathy is a frequent and often fatal manifestation of chronic liver disease. The pathogenesis of hepatic encephalopathy is believed to be multifactorial including impaired blood-brain barrier function, imbalance between the excitatory and inhibitory neurotransmitters in cortex, accumulation of various toxic and false neurotransmitters, and lack of nutrients like oxygen and glucose. Signs and symptoms of hepatic encephalopathy varies and commonly ranges from personality changes, disturbed consciousness, sleep pattern alternation, intellectual deterioration, speech disturbances, asterixis to frank coma and even death. Reversible or transient cortical blindness is rare manifestation of hepatic encephalopathy. It may even precede the phase of altered consciousness in such patients. Very few similar cases have been reported worldwide. Hence, we would like to report a case of transient cortical blindness in a patient of hepatic encephalopathy.

Association between sleep-disordered breathing, sleep-wake pattern, and cognitive impairment among patients with chronic heart failure.

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Hjelm, Carina; Strömberg, Anna; Arestedt, Kristofer; Broström, Anders

2013-05-01

Chronic heart failure (CHF) and sleep-disordered breathing (SDB) are often co-existing problems among the elderly. Apnoeic events may cause cognitive impairment. The aim of the study was to compare sleep and wake patterns, insomnia, daytime sleepiness, and cognitive function in community-dwelling CHF patients, with and without SDB, and to investigate the association between sleep-related factors and cognitive dysfunction. In this cross-sectional observational study, SDB was measured with an ApneaLink device and defined as an apnoea-hypopnoea index (AHI) ≥15/h of sleep. Sleep and wake patterns were measured with actigraphy for 1 week. Insomnia was measured with the Minimal Insomnia Symptom Scale, daytime sleepiness with the Epworth Sleepiness Scale, and cognitive function with a neuropsychological test battery. A total of 137 patients (68% male, median age 72 years, 58% NYHA functional class II) were consecutively included. Forty-four per cent had SDB (AHI ≥15). The SDB group had significantly higher saturation time below 90%, more difficulties maintaining sleep, and lower levels of daytime sleepiness compared with the non-SDB group. Cognitive function and sleep and wake patterns did not differ between the SDB and the non-SDB group. Insomnia was associated with decreased global cognition. The prevalence of cognitive dysfunction was low in this population with predominantly mild to moderate CHF. This might have influenced the lack of associations between cognitive function and SDB. Insomnia was the only sleep-related factor significantly influencing cognition.

Conversion Discriminative Analysis on Mild Cognitive Impairment Using Multiple Cortical Features from MR Images

NARCIS (Netherlands)

Guo, Shengwen; Lai, Chunren; Wu, Congling; Cen, Guiyin; Hariharan, A.; Vijayakumari, Anupa A.; Aarabi, Mohammad Hadi; Aballi, John; Nour, Abd Elazeim Abd Alla Mohamed; Abdelaziz, Mohammed; Abdolalizadeh, AmirHussein; Abdollahi, Mahsa; Abdul Aziz, Siti Aishah; Salam, Amritha Abdul; Abdulaziz, Nidhal; Abdulkadir, Ahmed; Abdullah, Sachal; Abdullah, Osama; Abrigo, Jill; Adachi, Noriaki; Adamson, Christopher; Adduru, Viraj; Adel, Tameem; Aderghal, Karim; Ades-Aron, Benjamin; Adeyosoye, Michael; Adlard, Paul; Srinivasa, Ag; Aganj, Iman; Agarwal, Ayush; Agarwal, Anupam; Agarwal, Anchit; Aguero, Cinthya; Aguiar, Pablo; Ahdidan, Jamila; Ahmad, Fayyaz; Ahmad, Rziwan; Ahmadi, Hessam; Ahmed, Nisar; Sid, Farid Ahmed; Ai, Edward; Ai, Qing; Aicha, Benyahia; Aitharaju, Sai; Aiyer, Aditya; Akkus, Zeynettin; Akodad, Sanae; Akramifard, Hamid; Aksman, Leon; Aktas, Said; Al-Janabi, Omar; Al-Nuaimi, Ali; AlAila, BahaaEddin; Alakwaa, Fadhl; Alam, Saruar; Alam, Fakhre; Alam Zaidi, Syed Farhan; Alan, Wiener; Alansari, Mukhtar; Alareqi, Ebrahim; Alberdi, Ane; Albsoul, Mohammad; Alderson, Thomas; Aleem, Hassan; Alex, Aishwarya; Alexander, Jacob; Alexopoulos, Panagiotis; Alfoldi, Jessica; Ali, Ayesha; Ali, Imdad; Alimoradian, Shirin; Aljabar, Paul; Aljabbouli, Hasan; Aljovic, Almir; Allen, Genevera; Alliende, Luz Maria; Almaguel, Frankis; Almgren, Hannes; Montes, Carmen Alonso; Alowaisheq, Tasneem; Alryalat, Saif Aldeen; Alsado, Majd; Alsaedi, Abdalrahman; Alshehri, Haifa; Altaf, Tooba; Altendahl, Marie; Altmann, Andre; Alvand, Ashkan; Filho, Manoel Alves; Alzubi, Raid; Amaral, Robert; Ambatipudi, Mythri; Amernath, Remya; Amlien, Inge; Amoroso, Nicola; Amri, Hakima; Anastasiou, Athanasios; Anbarasi, Jani; Anbarjafari, Gholamreza; Anderson, Wes; Anderson, Jeff; Anderson, Valerie; Anderson, Loretta; Andonov, Jovan; Andova, Vesna; Andreopoulou, Irene; Andrews, K. Abigail; Andrews, Cameron; Angeles, Michel; Anne-Laure, Aziz; Ansari, Ghulam Jillani; Ansari, Sharaf; Anstey, Kaarin; Antunes, Augusto; Aoshuang, Zhang; Aouf, Mazin; Aow Yong, Li Yew; Aporntewan, Chatchawit; Apostolova, Liana; Appiah, Frank; Apsvalka, Dace; Arab, Abazar; Araque Caballero, Miguel Ángel; Arbabyazd, Mohammad; Arbelaez, Pablo; Archer, Kellie; Ardekani, Babak; Aretouli, Eleni; Arfanakis, Konstantinos; Arisi, Ivan; Armentrout, Steven; Arnold, Matthias; Arnold, Steven; Arslan, Salim; Artacho-Perula, Emilio; Arthofer, Christoph; Aruchamy, Srinivasan; Arya, Zobair; Pizarro, Carlos Asensio; Ashford, Wes; Ashraf, Azhaar; Askland, Kathleen; Aslaksen, Per; Aslakson, Eric; Aso, Toshihiko; Astphan, Michele; Ataloglou, Dimitrios; Atay, Meltem; Athanas, Argus; Atri, Roozbeh; Au, April; Aurich, Maike; Avants, Brian; Awasthi, Niharika; Awate, Suyash; Ayaz, Aymen; Son, Yesim Aydin; Aydogan, Dogu Baran; Ayhan, Murat; Ayton, Scott; Aziz, Adel; Azmi, Mohd Hafrizal; Ba, Maowen; Bach, Kevin; Badea, Alexandra; Bag, Asim; Bagewadi, Shweta; Bai, Xiangqi; Bai, Zilong; Bai, Haoli; Baird, Geoffrey; Baiwen, Zhang; Baker, Elizabeth; Baker, John; Bakker, Arnold; Ball, Erika; Ballén Galindo, Miguel Ángel; Banaei, Amin; Bandyopadhyay, Dipankar; Bang, Ki Hun; Bangen, Katherine; Banks, Sarah; Banning, Leonie; Bao, Wan Yun; Barakat, Rita; Barbará, Eduardo; Barber, Philip; Barber, Robert; de Araujo, Flavia Roberta Barbosa; Barnes, Josephine; Barredo, Jennifer; Barret, Olivier; Barrett, Matthew; Barsamian, Barsam; Barsky, Andrey; Bartel, Fabian; Bartoszewicz, Jakub; Bartram-Shaw, David; Barwood, Caroline; Basavaraj, Suryakanth; Basavaraj, Arshitha; Basiouny, Ahmed; Baskaran, Bhuvaneshwari; Basu, Arindam; Baths, Veeky; Bathula, Deepti; Batmanghelich, Nematollah Kayhan; Bauer, Roman; Bauer, Corinna; Bawa, Vanshika; Bayley, Peter; Bayram, Ali; Bazi, Yakoub; Beach, Thomas; Beaudoin, Kristin; Beaulieu, Christian; Becker, Cassiano; Beckett, Laurel; Bedding, Alun; Beer, Simone; Beer, Joanne; Beg, Mirza Faisal; Behfar, Qumars; Behjat, Hamed; Behjat, Hamid; Behseta, Sam; Bekris, Lynn; Suresh, Mahanand Belathur; Belichenko, Nadia; Bellio, Maura; Belyaev, Mikhail; Bemiller, Shane; Ahmed, Olfa Ben; Ben Bouallègue, Fayçal; Benedikt, Michael; Benge, Jared; Benitez, Andreana; Benlloch, Jose María; Benn, Marianne; Benyoussef, El Mehdi; Bergeron, David; Bermudez, Elaine; Bessadok, Alaa; Betzel, Richard; Bezuidenhoudt, Mauritz; Bhagwat, Nikhil; Bhalerao, Shailesh; Bhandari, Anindya; Bhasin, Harsh; Bhati, Radhika; Bhatkoti, Pushkar; Bhatt, Priya; Bhattacharjee, Debotosh; Bhattacharyya, Sudeepa; Bi, Rui; Bi, Jinbo; Bi, Harvy; Biancardi, Alberto; Bidart, Rene; Bilgel, Murat; Billiet, Thibo; Binczyk, Franciszek; Bingsheng, Huang; Bird, Christopher; Bischof, Gérard; Bishnoi, Ram; Biswas, Shameek; Bjelke, David; Black, Sandra; Blackwood, Jennifer; Blaese, Elise; Blair, James; Blanchard, Gilles; Bloom, Toby; Blujus, Jenna; Blusztajn, Jan Krzysztof; Bo, Wu; Bo, Jun; Boda, Ravi; Boellaard, Ronald; Bogorodzki, Piotr; Bokde, Arun; Bolhasani, Ehsan; Bonakdarpour, Borna; Bonazzoli, Matthew; Bône, Alexandre; Borkowsky, Jennifer; Borrajo, Danielle; Bos, Isabelle; Bosco, Paolo; Bott, Nicholas; Rodrigues, Renato Botter Maio Lopes; Boughanmi, Amani; Bougias, Haralabos; Boulier, Thomas; Bourgeat, Pierrick; Bouyagoub, Samira; Bowes, Mike; Boyes, Richard; Bozoki, Andrea; Bradshaw, Tyler; Pereira, Joana Braga; Brahami, Yoann; Brambati, Simona Maria; Bras, Jose; Braskie, Meredith; Brecheisen, Ralph; Bregman, Noa; Brewer, James; Briassouli, Alexia; Brickman, Adam; Bridges, Robert; Brihmat, Nabila; Brinkmann, Benjamin; Britschgi, Markus; Broers, Thomas; Bron, Esther; Brown, Jesse; Brown, Matthew; Brown, Abel; Brown, Maria; Brunberg, James; Bu, Tao; Bubbico, Giovanna; Bubenik, Peter; Bubu, Omonigho; Buchanan, Daniel; Buchholz, Hans-Georg; Buchsbaum, Bradley; Buck, Katharina; Buckley, Rachel; Budgeon, Charley; Buhl, Derek; Sánchez, Manuel Buitrago; Bundela, Saurabh; Burciu, Irina; Burgos, Ninon; Burke, Shanna; Burn, Katherine; Burns, Jeffrey; Burns, Gully; Burzykowski, Tomasz; Bush, Sammie; Buss, Stephanie; Butcher, Bradley; Butt, Victoria; Buxbaum, Joseph; Sandeep, C. S.; Cabrera, Cristóbal; Cahyaningrum, Winda; Cai, Zhen-Nao; Cai, Siqi; Cai, Erik; Cajka, Tomas; Calamia, Matthew; Caligiuri, Maria Eugenia; Calixte, Christopher; Calon, Frederic; Cameron, Briana; Campbell, Roy; Lopez, Jose Antonio Campos; Cao, Hongliu; Cao, Jiguo; Cao, Guanqun; Cao, Bo; Capizzano, Aristides; Capon, Daniel; Carmasin, Jeremy; Carmichael, Owen; Carr, Sarah; Carrier, Jason; Carter, Greg; Carvalho, Luis; Carvalho, Janessa; Carvalho, Carolina; Casamitjana, Adrià; Casanova, Ramon; Casas, Josep R.; Cash, David; Castelluccio, Pete; Castiglioni, Isabella; Caswell, Carrie; Cattell, Liam; Cauda, Franco; Cepeda, Ileana; Çevik, Alper; Cha, Jungho; Chakrabarti, Shreya; Chakraborty, Shouvik; Chammam, Takwa; Chan, Christina; Chand, Ganesh; Chang, Catie; Chang, Yu-Ming; Chang, Rui; Chang, Hyunggi; Chang, Yu-Chuan; Chang, Ki Jung; Chang, Che-Wei; Chantrel, Steeve; Chao, Justin; Chao, Linda; Chapleau, Marianne; Charil, Arnaud; Chatterjee, Pratishtha; Chatterjee, Sambit; Chaudhry, Zainab; Chauhan, Harmanpreet; Chehade, Abdallah; Chekuri, Omkar; Cheloshkina, Kseniia; Chen, Jianhong; Chen, Gang; Chen, Geng; Chen, Ting-Huei; Chen, Yin Jie; Chen, Xi; Chen, Tzu-Chieh; Chen, Guojun; Chen, Shuzhong; Chen, Jerome; Chen, Fang; Chen, Kaifeng; Chen, Gennan; Chen, Jason; Chen, Guanhua; Chen, Ying-Hsiang; Chen, Ming-Hui; Chen, Chenbingyao; Chen, S. Y.; Chen, Hsu-Hsin; Chen, Xing; Chen, Kewei; Chen, Yuhan; Chen, Hugo; Chen, Rong; Chen, Ing-jou; Chen, Jun; Chen, Jean; Chen, Bo; Cheng, Danni; Cheng, Hewei; Cheng, Yong; Cheng, Yang; Cheng, Zhang; Cheng, Wai Ho; Chenhall, Tanya; Chepkoech, Joy-Loi; Cherukuri, Venkateswararao; Chhibber, Aparna; Chi, Haoyuan; Chi, Chih-Lin; Chiang, Gloria; Chiesa, Patrizia; Childress, Daniel Micah; Chilukuri, Yogitha; Fatt, Cherise Chin; Chincarini, Andrea; Ching, Christopher; Chiotis, Konstantinos; Cho, Soo Hyun; Cho, Yongrae; Cho, Sooyun; Choi, Jun-Sik; Choi, Hongyoon; Choi, Yeoreum; Choi, Sophia; Choi, Jaesik; Choi, Euna; Choo, I. L. Han; Chopra, Vishal; Chougrad, Hiba; Chouraki, Vincent; Christini, Amanda; Chu, Yufang; Chuang, Tzu-Chao; Chuanji, Luo; Chuanjian, Yu; Chun, Marvin; Chun, Sung; Chung, Ai; Chung, Yu-Min; Chung, Jung-Che; Chung, Ai Wern; Chung, Jaeeun; Chyzhyk, Darya; Ciarleglio, Adam; Cioli, Claudia; Cittanti, Corrado; Cives, Ana; Clark, Marissa; Clayton, David; Clement, Mark; Clifft, Daniel; Climer, Sharlee; Clouston, Sean; Clunie, David; Cohen, Phoebe; Cohen, Taco; Cole, Michael; Cole, James; Colletti, Patrick; Collingwood, Joanna; Comley, Robert; Conklin, Bryan; Conner, Lindsay; Conover, Joanne; Contardo-Berning, Ivona; Conway, Ronan; Copani, Agata; Coppola, Giovanni; Corbett, Syl; Corlier, Fabian; Correia, Rui; Cosman, Joshua; Costantino, Sebastian; Coubard, Olivier; Coulson, Elizabeth; Couser, Elizabeth; Cox, Kris; Coyle, Patrick; Cozzi, Brian; Craddock, Cameron; Crawford, Karen; Creese, Byron; Cribben, Ivor; Crisostomo-Wynne, Theodore; Crossley, Nicolas; Croteau, Etienne; Cruchaga, Carlos; Cuajungco, Math; Cui, Jing; Cui, Sue; Cullen, Nicholas; Cuneo, Daniel; Cutanda, Vicente; Cynader, Max; Binu, D.; D'Avossa, Giovanni; Dai, Tian; Dai, Peng; Dai, Hui; Davied Hong, Daivied Hong; Dakovic, Marko; Dalca, Adrian; Damiani, Stefano; Dammak, Mouna; Damoiseaux, Jessica; Dan, Zou; Dang, Xuan Hong; Dang, Shilpa; Daniel, Zinkert; Danjou, Fabrice; Darby, Eveleen; Darby, Ryan; Dardzinska, Agnieszka; Darst, Burcu; Darvesh, Sultan; Das, Kalyan; Das, Devsmita; Das, Sandhitsu; Das, Dulumani; Datta, Shounak; Dauvillier, Jérôme; Davatzikos, Christos; Davidson, Ian; de Boer, Renske; de Bruijne, Marleen; de Buhan, Maya; de Jager, Philip; de La Concha Vega, Nuño; de Lange, Siemon; de Luis Garcia, Rodrigo; de Marco, Matteo; de Sitter, Alexandra; Dean, Scott; Decarli, Charles; Decker, Summer; del Gaizo, John; Demir, Zeynep; Denby, Charles; Deng, Yanjia; Deng, Wanyu; Denisova, Kristina; Denney, William; Depue, Brendan; DeRamus, Thomas; Desikan, Rahul; Desplats, Paula; Desrosiers, Christian; Devadas, Vivek; Devanarayan, Viswanath; Devarajan, Sridharan; Devenyi, Gabriel; Dezhina, Zalina; Dhami, Devendra; Dharsee, Moyez; Dhillon, Permesh; Di, Xin; Di Mauro, Nicola; Diah, Kimberly; Diamond, Sara; Diaz-Asper, Catherine; Diciotti, Stefano; Dickerson, Bradford; Dickie, David Alexander; Dickinson, Philip; Dicks, Ellen; Diedrich, Karl; Dieumegarde, Louis; Dill, Vanderson; Dilliott, Allison; Ding, Zhaohua; Ding, Shanshan; Ding, Yanhui; Ding, Xiuhua; Ding, Xuemei; Dinov, Ivo; Dinu, Valentin; Diouf, Ibrahima; Dmitriev, Phillip; Dobromyslin, Vitaly; Dodge, Hiroko; Dolui, Sudipto; Dona, Olga; Dondelinger, Frank; Dong, Wen; Dong, Hao-Ming; Kehoe, Patricio Donnelly; Donohue, Michael; Dore, Vincent; Dougherty, Chase; Doughty, Mitchell; Dowling, N. Maritza; Doyle, Senan; Doyle, Andrew; Dragan, Matthew; Draganski, Bogdan; Draghici, Sorin; Dragomir, Andrei; Drake, Derek; Drake, Erin; Drd, Shilpa; Dronkers, Nina; Drozdowski, Madelyn; Du, Changde; Du, Yuhui; Du, Lei; Du, Guangwei; Du, Xingqi; Duan, Fang; Duan, Yuzhuo; Duan, Kuaikuai; Duchesne, Simon; Duggento, Andrea; Dukart, Juergen; Dumont, Matthieu; Dunn, Ruth; Duong, Vu; Duraisamy, Baskar; Duran, Tugce; Durrleman, Stanley; Dutta, Joyita; Dyrba, Martin; Dyvorne, Hadrien; R, Amulya E.; Eads, Jennifer; Eastman, Jennifer; Eaton, Susan; Edlund, Christopher; Edmonds, Emily; Edmondson, Mackenzie; Ehsan, Fatima; El-Gabalawy, Fady; Elander, Annie; Elango, Vidhya E.; Eldeeb, Ghaidaa; Elgamal, Fatmaelzahraa; Rodrigues, Yuri Elias; Elman, Jeremy; Elrakaiby, Nada; Emahazion, Tesfai; Emami, Behnaz; Embrechts, Jurriën; Emran Khan Emon, Mohammad Asif; Emrani, Saba; Emrani, Asieh; Emri, Miklós; Engelhardt, Barbara; Engle, Bob; Epstein, Noam; Er, Fusun; Erhardt, Erik; Eriksson, Oscar; Omay, Zeynep Erson; Escudero, Javier; Eshleman, Jason; Eskildsen, Simon; Espinosa, Luis; Essex, Ryan; Esteban, Oscar; Estrada, Karol; Ethell, Douglas; Ethridge, Kimberly; Ettehadi, Seyedrohollah; Eva, Bouguen; Evenden, Dave; Evtikheeve, Rina; Ewert, Siobhan; Fague, Scot; Fahmi, Rachid; Faizal, Sherin; Falahati, Farshad; Fan, Li; Fan, Zhen; Fan, Yong; Fan, Maohua; Fan, Yonghui; Fan, Sili; Fan, Ruzong; Fang, Chen; Fang, Xiaoling; Fanjul-Vélez, Félix; Fanti, Alessandro; Far, Bab; Farah, Martha; Farahani, Naemeh; Farahibozorg, Seyedehrezvan; Farahnak, Farhood; Farajpour, Maryam; Fardo, David; Farkhani, Sadaf; Farnsworth, Bryn; Farooq, Hamza; Farooq, Ammarah; Farouk, Yasmeen; Farrar, Danielle; Farrer, Lindsay; Fatemehh, Fatemeh; Fatemizadeh, Emad; Fatfat, Kim; Fatima, Shizza; Faux, Noel; Favan-Niven, Anne; Favary, Clélia; Fazlollahi, Amir; Fei, Gao; Feingold, Franklin; Feizi, Soheil; Félix, Eloy; Femminella, Grazia Daniela; Feng, Zijun; Feng, Ao; Feng, Brad; Feng, Xinyang; Feragen, Aasa; Fereidouni, Marzieh; Fernandes, Miguel; Fernández, Víctor; Ferrari, Ricardo; Ferraris, Sebastiano; Ferreira, Francisco; Ferreira, Luiz Kobuti; Ferreira, Hugo; Fiecas, Mark; Fieremans, Els; Fiford, Cassidy; Figurski, Michal; Filippi, Massimo; Filshtein, Teresa; Findley, Caleigh; Finger, Elizabeth; Firth, Nicholas; Fischer, Christopher; Fischer, Florian; Fitall, Simon; Fleet, Blair; Fleishman, Greg; Flokas, Lambros; Flores, Alberto; Focke, Niels; Fok, Wai Yan; Foldi, Nancy; Fôlego, Guilherme; Forero, Aura; Fornage, Myriam; Fos Guarinos, Belén; Founshtein, Gregory; Franc, Benjamin; Francois, Clement; Franke, Katja; Fraser, Mark; Frasier, Mark; Frederick, Blaise; Freitas, Fernandho; Escalin, Frency Jj; Freudenberg-Hua, Yun; Friedman, Brad; Friedmann, Theodore; Friedrich, Christoph M.; Frings, Lars; Frisoni, Giovanni; Fritzsche, Klaus; Frolov, Alexander; Frost, Robert; Fu, Ling; Fu, Zening; Fudao, Ke; Fuentes, Emmanuel; Fujishima, Motonobu; Fujiwara, Ken; Fukami, Tadanori; Funk, Cory; Furcila, Diana; Fuselier, Jessica; Nagarjuna Reddy, G.; Gaasterland, Terry; Gabelle, Audrey; Gahm, Jin; Gaiteri, Chris; Gajawelli, Niharika; Galantino, Alexis; Galarza Hernández, Javier; Galasko, Douglas; Galea, Liisa; Galisot, Gaetan; Sánchez, Antonio Javier Gallego; Gallins, Paul; Gamberger, Dragan; Gan, Hong Seng; Gan, Gavin; Ganapathi, Subha; Gancayco, Christina; Gangishetti, Umesh; Ganzetti, Marco; Gao, Fei; Gao, Jingjing; Gao, Linlin; Gao, Tianxiang; Gao, Yuanyuan; Gao, Xiaohong; Garani, Ranjini; Garbarino, Sara; Garcia, Ivan; Garcia, Xiadnai; Garcia, Jorge; Garcia, Tanya; Garcia Arias, Hernan Felipe; de La Garza, Angel Garcia; Gaig, Mireia Garcia; Novoa, Jorge Garcia; Valero, Mar Garcia; Garcia-Ojalvo, Jord; García-Polo, Pablo; Garg, Rahul; Garg, Gaurav; Garg, Divya; Garibotto, Valentina; Garvey, Matthew; Garza-Villarreal, Eduardo; Gaubert, Malo; Gauthier, Serge; Gavett, Brandon; Gavidia, Giovana; Gavtash, Barzin; Gawryluk, Jodie; Gbah, Messon; Ge, Tian; Geerts, Hugo; Geisser, Niklaus; Geng, Junxian; Gentili, Claudio; Gess, Felix; Ghaderi, Halleh; Ghahari, Shabnam; Ghanbari, Yaghoob; Ghazi-Saidi, Ladan; Ghodrati, Mojgan; Ghorbani, Behnaz; Ghoreishiamiri, Reyhaneh; Ghosal, Sayan; Ghosh, Sukanta; Ghosh, Saheb; Ghosh, Sreya; Ghoshal, Ankur; Giannicola, Galetta; Gibert, Karina; Gibson, Gary; Gieschke, Ronald; Gil Valencia, Jorge Mario; Gillen, Daniel; Giordani, Alessandro; Giraldo, Diana; Gispert, Juan D.; Gitelman, Darren; Giuffrida, Mario Valerio; Madhu, G. K.; Glass, Jesse; Glazier, Brad; Gleason, Carey; Glerean, Enrico; Glozman, Tanya; Godbey, Michael; Goettlich, Martin; Gogoi, Minakshi; Gola, Kelly; Golbabaei, Soroosh; Golden, Daniel; Goldstein, Felicia; Gomes, Carlos; de Olivera, Ramon Gomes Durães; Gomez, Isabel; Gomez Gonzalez, Juan Pablo; Gomez-Verdejo, Vanessa; Gong, Weikang; Gong, Enhao; Gong, Kuang; Gonneaud, Julie; Gonzalez, Clio; Gonzalez, Evelio; Gonzalez, Gerardo; Moreira, Eduardo Gonzalez; Goodman, James; Gopinath, Srinath; Gopu, Anusharani; Gordon, Brian; Gordon, David; Gordon, Mark; Gorriz, Juan Manuel; Gors, Dorothy; Göttler, Jens; Gounari, Xanthippi; Goyal, Devendra; Graf, John; Graff, Ariel; Graham, Leah; Graham, Jinko; Grajski, Kamil; Grami, Maziyar; Grand'Maison, Marilyn; Grant, Kiran; Grassi, Elena; Gray, Katherine; Grecchi, Elisabetta; Green, Robert; Green, Elaine; Greenberg, Jonathan; Greening, Steven; Greenwood, Bryson; Gregori, Johannes; Gregory, Michael; Greicius, Michael; Greve, Douglas; Griffin, Jason; Grill, Joshua; Grodner, Kelsey; Grolmusz, Vince; Groot, Perry; Groothuis, Irme; Gross, Alden; Grundstad, Arne; Grundy, Edward; Grzegorczyk, Tomasz; Nandith, G. S.; Gu, David; Gu, Jiena; Gu, Yun; Gu, Ginam; Guan, Sheng; Guan, Yuanfang; Guennel, Tobias; Guerin, Laurent; Guerrero, Ricardo; Guerrier, Laura; Guevara, Pamela; Guggari, Shankru; Roy, Abhijit Guha; Guidotti, Roberto; Guillon, Jérémy; Gulcher, Jeff; Gulia, Sarita; Gumedze, Freedom; Gunawardena, Nishan; Gunn, Roger; Guo, Michael; Guo, Xiao; Guo, Xingzhi; Guo, Yi; Kai, Zhang Guo; Zhao, Ma Guo; Gupta, Navin; Gupta, Anubha; Gupta, Ishaan; Guren, Onan; Gurnani, Ashita; Gurol, Mahmut Edip; Guzman, Gloria; Gyy, Gyy; Rajanna, Vanamala H.; Ha, Seongwook; Haacke, Ewart; Haaksma, Miriam; Habadi, Maryam; Habeck, Christian; Habes, Mohamad; Hackspiel Zarate, Maria Mercedes; Hadimani, Ravi; Hahn, William; Hahn, Tim; Haight, Thaddeus; Hair, Nicole; Haixing, Wang; Hajarolasvadi, Noushin; Hajjar, Ihab; Hajjo, Rima; Halchenko, Yaroslav; Hall, Anette; Hallock, Kevin; Hamdi, Shah Muhammad; Hameed, Farhan; Hamidian, Hajar; Han, Dong; Han, Yang; Han, Hio-Been; Han, Qingchang; Han, Beomsoo; Han, Duke; Han, Shizhong; Han, Xiaoxia; Han, Peipei; Han, Joo Yoon; Han, Dong-Sig; Handsaker, Robert; Hanna-Pladdy, Brenda; Hanseeuw, Bernard; Hansson, Björn; Hao, Yang; Hao, Jhon; Happ, Clara; Harischandra, Dilshan; Haritaoglu, Esin; Harris, Richard; Harris, Breanna; Hart, Brian; Hartzell, James; Harvey, Danielle; Hashimoto, Tsuyoshi; Hasooni, Hossein; Hassan, Moaied; Hassan, Mehdi; Hassanzadeh, Hamid Reza; Hassanzadeh, Oktie; Hatton, Sean; Hawchar, Jinan; Hayashi, Toshihiro; Hayashi, Norio; Hayes, Jasmeet; Hayete, Boris; Haynor, David; He, Linchen; He, Yan; He, Yao; He, Huiguang; Heegaard, Niels; Hefny, Mohamed; Heil, Julius; Heindel, William; Henderson, Samuel; Henf, Judith; Henriquez, Claudio; Herholz, Karl; Hermessi, Haithem; Hernandez, Monica; Herrera, Luis; Hibar, Derrek; Hidane, Moncef; Higuchi, Satomi; Hind, Jade; Hives, Florent; Hoang, Mimi; Hobel, Zachary; Hoffman, John; Hofmeister, Jeremy; Hohman, Timothy; Holder, Daniel; Holguin, Jess; Holmes, Robin; Hong, John; Hongliang, Zou; Hongyu, Guo; Hopkins, Paul; Hor, Soheil; Hornbeck, Russ; Horng, Andy; Horton, Wesley; Hosny, Khalid; Hosseini, Eghbal; Hosseini, Hadi; Hosseini, Zahra; Asl, Ehsan Hosseini; Hou, Beibei; Houghton, Richard; Houghton, Katherine; Householder, Erin; Howlett, James; Hsiao, John; Hsiao, Ing-Tsung; Hsu, Chih-Chin; Hu, Xixi; Hu, Lingjing; Hu, Nan; Hu, Kun; Hu, Tao; Hu, Li; Hu, Xiaolan; Hua, Fei; Huang, Marissa; Huang, Qi; Huang, Michelle; Huang, Chao; Huang, JunMing; Huang, Xingyuan; Huang, Yuhan; Huang, Sing-Hang; Huang, Shuai; Huang, Peiyu; Huang, Chun-Chao; Huang, Zhiyue; Huang, Meiyan; Huang, Zhiwen; Hubrich, Markus; Huestis, Michael; Huey, Edward; Hufton, Andrew; Huijbers, Willem; Huisman, Sjoerd; Hung, Joe; Hunsaker, Naomi; Hunt, Fostor; Huppertz, Hans-Jürgen; Huser, Vojtech; Hussain, Lal; Hutchison, R. Matthew; Hutton, Alexandre; Huyck, Els; Hwang, Jihye; Hyun, JungMoon; Iakovakis, Dimitris; Ibañez, Victoria; Ide, Kayoko; Igarashi, Takuma; Iglesias, Juan Eugenio; Muñoz, Laura Igual; Iidaka, Tetsuya; Ikeuchi, Takeshi; Ikhena, John; Ikuta, Toshikazu; Im, Hyung-Jun; Insausti, Ana; Insel, Philip; Invernizzi, Azzurra; Iosif, Ana-Maria; Ip, Nancy; Irizarry, Sierra; Irmak, Emrah; Irwin, David; Isaza, Mariano; Ishii, Makoto; Ishii, Kenji; Islam, Jyoti; Israel, Ariel; Isufi, Elvin; Ito, Kaori; Ito, Masato; Izquierdo, Walter; Alphin, J.; Akhila, J. A.; Jaberzadeh, Amir; Jackowiak, Edward; Jackson, Eric; Jackson, Chris; Jackson, Jonathan; Jacob, Samson; Jacobsen, Nina; Jacobsen, Jörn; Jacquemont, Thomas; Jacques, Nerline; Jaeger, Ralf; Jafari, Tahere; Jafari-Khouzani, Kourosh; Jagadish, Akshay Kumar; Jagtap, Priti; Jagust, William; Jahr, Joseph; Jain, Shubhankar; Jain, Shubham; Jaiswal, Ayush; Jaiswal, Akshay; Jait, Amine; Jakkoju, Chetan; Jakobsson, Andreas; James, Olga; James, Oliver; Jamlai, Maedeh; Jammeh, Emmanuel; Janardhana, Lajavanthi; Jang, Jinseong; Jang, Jae-Won; Jang, Jinhee; Jang, Hyesue; Janghel, Rekh Ram; Jawahar, Shasvat; Jean, Kharne; Jean-Baptiste, Schiratti; Jedynak, Bruno; Jefferson, Angela; Jennings, Danna; Jennings, Dominique; Jeon, Seun; Jeong, Yong; Jester, Charles; Jethwa, Ketan; Jha, Debesh; Ji, Gong-Jun; Ji, Chong; Ji, Jin; Jia, Bowen; Jiacheng, Lee; Jiajia, Guo; Jian, Weijian; Jiang, Shan; Jiang, Chunxiang; Jianhua, Gao; Jiao, Zhuqing; Jiao, Zeyu; Jiao, Du; Jimenez Alaniz, Juan Ramon; Gomez, Carolina Jimenez; Jiménez-Huete, Adolfo; Jimura, Koji; Jin, Yan; Jin, Zhu; Jogia, Jigar; Johansson, Per; John, Kimberley; Johnsen, Stian; Johnson, Leonard; Johnson, Sterling; Johnson, Kent; Johnston, Jane; Johnston, Stephen; Jomeiri, Alireza; Jonas, Katherine; Jones, Richard; Jones-Davis, Dorothy; Jönsson, Linus; Joseph, Jane; Joshi, Himanshu; Joshi, Shantanu; Joshi, Abhinay; Joyce, Katherine; Juengling, Freimut; Jung, Youngjin; Junker, Viv; Junwei, Ding; Jyothi, Singaraju; Jyotiyana, Monika; Sarthaj, K.; Kachouane, Mouloud; Kadian, Amit; Kaewaramsri, Yothin; Kaicheng, Li; Kaiser, Marcus; Kakinami, Lisa; Kalra, Sanjay; Kam, Hye Jin; Kamarudin, Nur Shazwani; Kaminker, Josh; Kandel, Benjamin; Kandiah, Nagaendran; Kaneko, Tomoki; Kang, Yun Seok; Kang, Ju Hee; Kang, Hakmook; Kang, Jian; Kansal, Anuraag; Kaouache, Mohammed; Kaplan, Adam; Kottaram, Akhil Karazhma; Karim, Faizan; Karimi-Mostowfi, Nicki; Karjoo, Mahboobe; Karlin, Daniel; Karp, Juliana; Karray, Chiheb; Kartsonis, Nick; Karu, Naama; Kasa, Jaya; Kasiri, Keyvan; Katako, Audrey; Kato, Ryo; Katsonis, Panagiotis; Katti, Hkkatti; Kaur, Prabhjot; Kauwe, John; Kawaguchi, Atsushi; Kazemi, Samaneh; Kazemi, Yosra; Rijan, K. C.; Kechin, Andrey; Kelkhoff, Douglas; Kelleher, Thomas; Kellner-Weldon, Frauke; Kennion, Oliver; Kerr, Daniel; Kesler, Shelli; Kesselman, Carl; Kessler, Daniel; Keuken, Max; Keyvanfard, Farzaneh; Khademi, April; Khajehnejad, Moein; Khan, Wasim; Khan, Tabrej; Khan, Hikmat; Khan, Anzalee; Khan, Samreen; Khanmohammadi, Sina; Khasanova, Tatiana; Khazaee, Ali; Khazan, Lenny; Kherif, Ferath; Khl, Aym; KHlif, Mohamed Salah; Khondoker, Mizanur; Khoo, Sok Kean; Khosrowabadi, Reza; Khurshid, Kiran; Kianfard, Reihaneh; Kida, Satoshi; Kiddle, Steven; Kikuchi, Masashi; Killiany, Ron; Kim, Jeongchul; Kim, Jong Hun; Kim, Hyunwoo; Kim, Jongin; Kim, Yeo Jin; Kim, Jung-Jae; Kim, Hang-Rai; Kim, Jaeyeol; Kim, Ki Hwan; Kim, Joseph; Kim, Younghoon; Kim, Mijung; Kim, Jeongsik; Kim, Bohyun; Kim, Taehyun; Kim, Heeyoung; Kim, Seonjik; Kim, Nakyoung; Kim, Byeongnam; Kim, ChanMi; Kim, Jeonghun; Kim, Seong Yoon; Kim, Sunhee; Kingery, Lisle; Kinnunen, Kirsi; Kinomes, Marie; Kirchner, Jan Hendrik; Caldwell, Jessica Kirkland; Kirwan, Brock; Kitamura, Chiemi; Kitty, Kitty; Kiviat, David; Kiyasova, Vera; Klein, Richard; Klein, Alison; Klein, Gregory; Klein, Jan; Kleinman, Aaron; Kling, Mitchel; Klinger, Joern; Klinger, Rebecca; Klink, Katharina; Kocaturk, Mustafa; Koch, Philipp Johannes; Kochova, Elena; Koenig, Loren; Koh, Natalie; Köhler, Jens Erik; Koikkalainen, Juha; Koini, Marisa; Kolachalama, Vijaya; Koncz, Rebecca; Kong, Xiang-Zhen; Kong, Vincent; Kong, Xiangzhen; Kong, Dehan; Kong, Linglong; Konukoglu, Ender; Kopeinigg, Daniel; Kopera, Krzysztof; Koppers, Simon; Korb, Matheus; Korfiatis, Panagiotis; Korolev, Igor; Korolev, Sergey; Korostyshevskiy, Valeriy; Koshiya, Heena; Kost, James; Kotari, Vikas; Koutra, Danai; Koychev, Ivan; Kruthika, K. R.; Krahnke, Tillmann; Krause, Matthew; Kraybill, Matt; Kriebel, Martin; Hari Krishna, M.; Krohn, Stephan; Kruggel, Frithjof; Kuceyeski, Amy; Kuhl, Donald; Kulshreshtha, Devang; Kumar, Santosh; Kumar, Sambath; Kumar, Kuldeep; Kumar, Anil; Kumar, Abhishek; Kumar, A.; Kumar, Saurabh; Kumar, Ashwani; Kumar, Ambar; Kumar, Dinesh; Kumar, Rishab; Kumarasinghe, Janaka; Kundu, Suprateek; Kung, Te-Han; Kuo, Li-Wei; Kuo, Phillip; Channappa, Usha Kuppe; Kuriakose, Elmy; Kurian, P.; Kwan, Kenneth; Kwasigroch, Arkadiusz; Kwon, Young Hye; Kyeong, Sunghyon; Fleur, Claire La; Wungo, Supriyadi La; Labbe, Tomas; Lacombe, Daniel; Lad, Meher; Lahoti, Geet; Lai, Ying Liang; Lai, Catherine; Lai, Dongbing; Laird, Dillon; Lakatos, Anita; Lam, Alice; Lama, Ramesh; Lambert, Christian; Landau, Susan; Landman, Bennett; Landre, Victor; Lane, Elizabeth; Lange, Catharina; Langenieux, Alexandre; Lareau, Caleb; Larson, Katelyn; Latif, Ghazanfar; Lauber, Ross; Lawliet, Z. H.; Lawrence, Emma; Lazar, Anca; Le, Ngan; Le, Thi Khuyen; Le, Matthieu; Guen, Yann Le; Scouiller, Stephanie Le; Leandrou, Stephanos; Leatherday, Christopher; Leavitt, Mackenzie; Ledbetter, Christina; Lee, Hyekyoung; Lee, Wook; Lee, Annie; Lee, Jaehong; Lee, Dongyoung; Lee, Joel; Lee, Song-Ting; Lee, Kuo-Jung; Lee, Subin; Lee, Jaeho; Lee, Catherine; Lee, Gyungtae; Lee, Suzee; Lee, Erik; Lee, Yunseong; Lee, Sang-Gil; Lee, Seonjoo; Lee, Peng Jung; Lee, Hyunna; Lee, Cheng-Hsien; Lee, Hengtong; Lee, Mi Ri; Lee, Ilgu; Lee, Qixiang; Lefterov, Iliya; Leger, Charlie; Lehallier, Benoit; Lei, B.; Lei, Shi; Lei, Hongxing; Lei, Haoyun; Leong, Tze Yun; Leong, Sharlene; Leoutsakos, Jeannie-Marie; Lepore, Natasha; Lerch, Ondrej; Leung, Yip Sang; Leung, Yuk Yee; Leung, Shuyu; Leung, Hoi-Chung; Leung, Ming-Ying; Levakov, Gidon; Levine, Abraham; Li, Chawn; Li, Miranda; Li, Huijie; Li, Junning; Li, Xiaofeng; Li, Yi; Li, Jinchao; Li, Tianhong; Li, Yongming; Li, Xiangrui; Li, Tieqiang; Li, Yan; Li, Fuhai; Li, Feijiang; Li, Shuyang; Li, Zhi; Li, Xing; Li, Rongjian; Li, Rui; Li, Y. U.; Li, Kang; Li, Zhenzhen; Li, Qingqin; Li, Wenjun; Li, Yang; Li, Jialu; Li, Guangyu; Li, Michelle; Li, Yibai; Li, Yupeng; Li, Tao; Li, Zhujun; Li, Yafen; Li, Muwei; Li, Xuan; Li, Yi-Ju; Li, Cen Sing; Li, X. W.; Li, Yingjie; Li, Lin; Li, Yihan Jessie; Li, Yaqing; Li, Xiantao; Li, Xingfeng; Li, Chenxi; Li, Chao; Li, Jicong; Li, Jiewei; Li, Tengfei; Li, Wei; Li, Xinzhong; Li, Nannan; Li, Chunfei; Li, Yeshu; Liang, Chen; Liang, Nanying; Liang, Jingjing; Liang, Shengxiang; Liang, Xiaoyun; Liang, Xia; Liang, Ying; Liberman, Sofia; Libon, David; Liébana, Sergio; Liedes, Hilkka; Lim, Wee Keong; Lim, Yen Ying; Lin, Yenching; Lin, Katherine; Lin, Ming; Lin, Ai-Ling; Lin, Ching-Heng; Lin, Bing; Lin, Lin; Lin, Jyh-Miin; Lin, W. M.; Lin, Chien-Tong; Lin, Liyan; Lin, Jing; Lindberg, Olof; Linesch, Paul; Linn, Kristin; Lippert, Christoph; Litovka, Nikita; Little, Graham; Liu, Man-Yun; Liu, Jin; Liu, Chin-Fu; Liu, Zhaowen; Liu, Eulanca; Liu, Weixiang; Liu, K. E.; Liu, Hao Chen; Liu, Jia; Liu, Richann; Liu, Dongbo; Liu, Victor; Liu, Wenjie; Liu, Tao; Liu, Xiaoli; Liu, Yong; Liu, Lin; Liu, Dan; Liu, Xiuwen; Liu, Mengmeng; Liu, Chia-Shang; Liu, Ying; Liu, Yan; Liu, Xueqing; Liu, Han; Liu, Chien-Liang; Liu, Sidong; Liu, Jundong; Liu, Yang; Liu, Tianming; Liu, Tingshan; Liu, Ning; Liu, Lan; Liuyu, Liuyu; Lizarraga, Gabriel; Llido, Jerome; Lobach, Iryna; Lockhart, Samuel; Loft, Henrik; Lohr, Kelly; Lon, Hoi Kei; Lone, Kashif Javed; Long, Ziyi; Long, Xiaojing; Longo, Frank; Alves, Isadora Lopes; Lopez, Guadalupe; Lorenzi, Marco; Lotan, Eyal; Louie, Gregory; Louis, Maxime; Loukas, Andreas; Love, Seth; Lowe, Deborah; Lu, Bin; Lu, Chia-Feng; Lu, Zixiang; Lu, Lijun; Lu, Pascal; Lu, Shen; Lu, Qing; Lu, Zheshen; Lu, Chuan; Lu, Patty; Lu, Hangquan; Lu, Bo; Luktuke, Yadnyesh; Luo, Wei; Luo, Suhuai; Luo, Sheng; Luo, Shaojun; Luo, Peggy; Luo, Shan; Luo, Weidong; Luo, Liao; Luo, Xiao; Lupton, Michelle; Lutz, Michael; Lv, Eric; Lyu, Juan; Angshul, M.; Radha, M. R.; Dinesh, M. S.; Ma, Xiangyu; Ma, Chao; Ma, Li; Ma, Yu; Ma, Qianli; MacArthur, Daniel; Macey, Paul; Mach, Eric; MacPhee, Imola; Madadi, Mahboubeh; Madan, Christopher; Madan, Bharat; Madero, Giovanny; Madhavan, Radhika; Madhyastha, Tara; Maeno, Nobuhisa; Magsood, Hamzah; Mah, Linda; Mahdavi, Shirin; Mahdavi, Asef; Mahmoud, Abeer; Mahmoud, Hentati; Mahmoud, Kariman; Mahmoudi, Ahmad; Dehkordi, Siamak Mahmoudian; Mahor, Monika; Mahseredjian, Taleen; Mai, Cha; Maia, Rui; Maiti, Taps; Maj, Carlo; Maji, Pradipta; Majidpour, Jafar; Makhlouf, Laouchedi; Makino, Satoshi; Makrievski, Stefan; Makse, Hernan; Malagi, Archana; Malakhova, Katerina; Malamon, John; Malashenkova, Irina; Malchano, Zach; Maleki-Balajoo, Somayeh; Malik, Sadia; Malik, Tamoor; Mallik, Abhirup; Malm, Tarja; Malpas, Charles; Malpica, Norberto; Malviya, Meenakshi; Mamandi, A.; Manandhar, Abinash; Mandal, Pravat; Mandali, Alekhya; Mane, Prajakta; Manning, Emily; Manoufali, Mohamed; Manser, Paul; Mantini, Dante; Mantri, Ninad; Manyakov, Nikolay; Manzak, Dİlek; Mao, Shuai; Maoyu, Tian; Maple Grødem, Jodi; Maravilla, Kenneth; Marco, Simonetti; Marcus, Daniel; Margetis, John; Margolin, Richard; Mariano, Laura; Marinescu, Razvan Valentin; Markett, Sebastian; Markiewicz, Pawel; Marnane, Michael; Maroof, Asif; Marple, Laura; Marques, Cristiane; Marrakchi, Linda; Marshall, Gad; Märtens, Kaspar; Mårtensson, Gustav; Marti, Cristian; Martin, Harold; Martinaud, Olivier; Martinez, Victor; Martinez, Oliver; Martinez, Jesus; Martinez, Carlos; Abadías, Neus Martinez; Torteya, Antonio Martinez; Martini, Jean-Baptiste; Martins, Samuel; Masciotra, Viviane; Masmoudi, Ahmed; Masny, Aliaksandr; Shah, Pir Masoom; Massaro, Tyler; Masumoto, Jun; Matan, Cristy; Mate, Karen; Mateus, Pedro; Mather, Mara; Mather, Karen; Mathew, Jesia; Mathias, Samuel; Mathiyalagan, Tamilalaghan; Matloff, Will; Matsubara, Keisuke; Matsubara, Takashi; Matsuda, Yukihisa; Matthews, Dawn; Mattis, Paul; May, Patrick; Mayburd, Anatoly; Mayo, Chantel; Mayordomo, Elvira; Mbuyi, Gaylord; McCallum, Colleen; McCann, Bryony; McCollough, Todd; McCormick, Shannon; McCurdy, Sean; McDonald, Carrie; McEligot, Archana; McEvoy, Linda; McGeown, William; McGinnis, Scott; McHugh, Thomas; McIntosh, Elissa; McIntosh, Randy; McKenzie, Andrew; McLaren, Donald; McMillan, Corey; McMillan, Alan; McPherson, Brent; McRae-McKee, Kevin; Zaini, Muhammad Hafiz Md; Meadowcroft, Mark; Mecca, Adam; Meda, Shashwath; Medikonda, Venkata Srinu; Meeker, Karin; Megherbi, Thinhinane; Mehmood, Anum; Mehrtash, Alireza; Meiberth, Dix; Meier, Dominik; Meijerman, Antoine; Mejia, Jose; Mekkayil, Lasitha; Meles, Sanne; Melie-Garcia, Lester; Melo, Hans; Melrose, Rebecca; Melzer, Corina; Mendes, Aline; Leon, Ricardo Antonio Mendoza; Gonzalez, Manuel Menendez; Meng, Dewen; Meng, Xianglai; Meng, Guilin; Mengel, David; Menon, Ramesh; Menon, Ravi; Mercado, Flavio; Messick, Viviana; Meyer, Pierre-Francois; Meyer, Carsten; Mezher, Adam; Mi, Liang; Miao, Hongyu; Michailovich, Oleg; Michels, Lars; Mickael, Guedj; Mikhail, Mark; Mikhno, Arthur; Milana, Diletta; Miller, Rachel; Miller, Brendan; Millikin, Colleen; Min, Byung Wook; Minadakis, George; Minghui, Hu; Chinh, Truong Minh; Minkova, Lora; Miranda, Michelle; Misevic, Dusan; Mishra, Amit; Mishra, Chetan; Mishra, Shiwangi; Mishra, Ashutosh; Mishra, Krishna; Misquitta, Karen; Mitchell, Brian; Mithawala, Keyur; Mitnitski, Arnold; Mitra, Sinjini; Mittal, Gaurav; Mittner, Matthias; Miyapuram, Krishna Prasad; Mlalazi, Rebaone; Mo, Daojun; Moghekar, Abhay; Moguilner, Sebastian; Moh, Heba; Mohabir, Mark; Mohajer, Bahram; Mohamed, Moataz; Mohammadi, Sadeq; Mohammadi-Nejad, Ali-Reza; Mohammady, Saed; Taqi, Arwa Mohammed; Mohan, Kishore Kumar; Mohy-Ud-Din, Hassan; Moitra, Dipanjan; Mojaradi, Mehdi; Mojtabavi, Alireza; Molina, Helena; Mollon, Jennifer; Molteni, Erika; Montajabi, Mohaddeseh; Montal, Victor; Montazami, Aram; Monté-Rubio, Gemma; Montembeault, Maxime; Montero-Odasso, Manuel; Montillo, Albert; Moon, Byung-Seung; Moon, Chan; Moon, Chooza; Moore, Archer; Morabito, Francesco C.; Moradi, Masoud; Moraes, Renato; Ballesteros, Orlando Morales; Morales-Henriquez, Daniela; Moratal, David; Moreno, Herman; Morihara, Ryuta; Mormino, Elizabeth; Morris, Jeffrey; Mortamet, Bénédicte; Morton, John; Moscato, Pablo; Rial, Alexis Moscoso; Mossa, Abdela Ahmed; Mottaghi, Setare; Mouelhi, Aymen; Moussavi, Arezou; Moustafa, Ahmed; Mowrey, Wenzhu; Mtetwa, Lungile; Muehlboeck, Sebastian; Mueller, Susanne; Mueller-Sarnowski, Felix; Mufidah, Ratna; Mukherjee, Rik; Mukherjee, Shubhabrata; Müller, Christian; Müller, Hans-Peter; Mullins, Paul; Mullins, Roger; Muncy, Nathan; Munir, Akhtar; Munirathinam, Ramesh; Munoz, David; Munro, Catherine; Muranevici, Gabriela; Rendon, Santiago Murillo; Murilo, Robson; Murphy, Sonya; Muscio, Cristina; Musso, Gabriel; Mustafa, Yasser; Myall, Daniel; Gayathri, N.; Nabavi, Shahab; Nabeel, Eman; Nagele, Robert; Naghshbandi, Hane; Naik, Shruti; Najmitabrizi, Neda; Nakawah, Mohammad Obadah; Nalls, Mike; Namboori, Krishnan; Nancy, Annie; Napolitano, Giulio; Narayan, Manjari; Narkhede, Atul; Naseri, Mahsa; Nasrallah, Ilya; Nasrallah, Fatima; Nassif, Rana; Nath, Sruthi R.; Nathoo, Farouk; Nation, Daniel; Naughton, Brian; Nault, Larry; Nautiyal, Deeksha; Nayak, Deepak Ranjan; Naz, Mufassra; Nazemian, Shayan; Nazeri, Arash; Neckoska, Emilija; Neelamegam, Malinee; Nehary, Ebrahim; Nelson, Peter; Nelson, Linda; Nematzadeh, Hosein; Nerur, Shubha; Nesteruk, Thomas; Neu, Scott; Ng, Yen-Bee; Nguyen, Tin; Nguyen, Thanh; Nguyen, Harrison; Nguyen, Nghi; Trung, Hieu Nguyen; Ni, Lucy; Nian, Yongjian; Nichols, Thomas; Nicodemus, Kristin; Nie, Yunlong; Nielsen, Casper; Nikolov, Robert; Nila, Jessica; Nishioka, Christopher; Njeh, Ines; Njie, Emalick; Nobakht, Samaneh; Noble, Andrew; Noda, Art; Noroozi, Ali; Norton, Derek; Nosarti, Chiara; Nosheny, Rachel; Notsu, Akifumi; Novak, Gerald; Nozadi, Seyed Hossein; Nu, Fen; Nudelman, Kelly; Nunes, Adonay; Nunes, Ana; Núñez, Christian; Nuno, Michelle; Nuriel, Tal; Nygaard, Haakon; Nyquist, Paul; O'Bott, Jacob; O'Charoen, Sirimon; O'Neill, William; O'Rawe, Jonathan; Obrzut, Grzegorz; Och, Ganzorig; Odaibo, David; Odry, Benjamin; Oehmichen, Axel; Ofori, Edward; Ogunsanmi, Abdulfatai; Oguz, Kaya; Oh, Jungsu; Oh, Minyoung; Oh, Hwamee; Ohigashi, Hironori; Oishi, Kenichi; Oishi, Naoya; Okhravi, Hamid; Okonkwo, Ozioma; Okyay, Savaş; Oliveira, Cyrill; Oliveira, João; Oliveira, Francisco; Oliver, Ruth; Olmos, Salvador; Olszowy, Wiktor; Oltra-Cucarella, Javier; Önen, Zehra; Ong, Rowena; Onoda, Keiichi; Onyike, Chiadi; Operto, Grégory; Oppedal, Ketil; Orejuela, Juan; Orhon, Atila; Orozco, Max; Ortuño, Juan; Osadebey, Michael; Osborn, Joseph; Osoba, Osonde; Ostadrahimi, Hamid; Ostovari, Parisa; Otis, Sarah; Overgaard, Shauna; Owen, Catrin Elin; Oxtoby, Neil; Öziç, Muhammet Üsame; Ozkaya, Gorkem; Okur, Ozlem Ozmen; Ozsolak, Fatih; Ozyildirim, Melis; Pa, Judy; Pacheco, Joe; Pack, Gary; Padilla, Daniel; Cerezo, Berizohar Padilla; Padovese, Bruno; Pae, Chongwon; Pagano, Gennaro; Pahuja, Gunjan; Pai, Shraddha; Pajavand, Shahryar; Pajula, Juha; Pak, Kyoungjune; Pakzad, Ashkan; Palaniappan, Mathiyalagan; Palanisamy, Sindhu; Palmqvist, Sebastian; Palsson, Frosti; Pan, Dan; Pan, Tiffany; Pan, Yuqing; Pan, Wei; Pan, Sun; Pan, Hongliang; Pan, Xiaoxi; Pandey, Lokesh; Pang, Qiaoyu; Pangilinan, Erin; Pannetier, Nicolas; Panpan, Xu; Panyavaraporn, Jantana; Pardini, Matteo; Paredes, José; Parikh, Jignesh; Park, Seongbeom; Park, Young Ho; Park, Min Tae; Park, Hyunjin; Park, Sejin; Park, JongSeong; Park, DooHyun; Park, Ji Eun; Park, Yuhyun; Park, Jiyong; Parker, Jason; Parker, Richard; Parodi, Alice; Bautista, Yohn Jairo Parra; Parrish, Marcus; Parthiban, Preethy; Pascariello, Guido; Pascual, Belen; Paskov, Hristo; Pasquini, Lorenzo; Tantaleán, Julio Sergio Eduardo Pastor; Pastur, Lucas; Patel, Raihaan; Patel, Sejal; Paterson, Ross; Paton, Bryan; Patriarche, Julia; Patriat, Rémi; Pattichis, Constantinos; Paul, Debashis; Pawar, Kuldeep; Pawlak, Mikolaj; Paz, Rotem; Pedroto, Maria; Pelekanos, Matthew; Péléraux, Annick; Peng, Dan; Peng, Jing; Pengfei, Tian; Perani, Daniela; Peraza, Luis; Pereira, Fabricio; Pereira, Francisco; Perkins, Diana; Perneczky, Robert; Persad, Umesh; Peter, Jessica; Peters, Mette; Peters, Ruth; Pether, Mark; Petrella, Jeffrey; Petrenko, Roman; Petrone, Paula; Petrov, Dmitry; Pezzatini, Daniele; Pfenning, Andreas; Pham, Chi-Tuan; Philipson, Pete; Phillips, Jeffrey; Phillips, Nicole; Phophalia, Ashish; Phuah, Chia-Ling; Pichai, Shanthi; Pichardo, Cesar; Binette, Alexa Pichet; Pietras, Olga; Pietrzyk, Mariusz; Pike, Kerryn; Pillai, Jagan; Piludu, Francesca; Pineda, Joanna; Ping, He; Pirraglia, Elizabeth; Pither, Richard; Piyush, Ranjan; Pizzi, Nick; Gonzalez, Luis Fernando Planella; Plassard, Andrew; Platero, Carlos; Plocharski, Maciej; Podhorski, Adam; Poggiali, Davide; Poghosyan, Mher; Pohl, Kilian; Poirier, Judes; Polakow, Jean Jacques; Politis, Marios; Poljak, Anne; Poloni, Katia Maria; Poole, Victoria; Poppenk, Jordan; Porsteinsson, Anton; Portelius, Erik; Posta, Filippo; Posthuma, Danielle; 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Nunes; Urrutia, Leandro; Usama, Ahmed; Ustun, Ali Alp; Uus, Alena; Uyar, Muharrem Umit; Visalatchi, V.; Rajinikanth, V.; Vafaei, Amin; Vairre, Darlene; Vaishnavi, Sanjeev; Vaithinathan, Krishnakumar; Vakorin, Vasily; Hernández, Maria Valdés; van Bokhoven, Pieter; Deerlin, Vivianna Van; van der Brug, Marcel; Dijk, Koene Van; van Duijn, Cornelia; van Erp, Theo; van Hooren, Roy; Leemput, Koen Van; van Loenhoud, Anita; Schependom, Jeroen Van; van Velden, Floris; van Westen, Danielle; Vandekar, Simon; Vandijck, Manu; Vanhoutte, Matthieu; Vannini, Patrizia; Vansteenkiste, Elias; Varatharajah, Yogatheesan; Vardarajan, Badri; Varey, Stephen; Vargas, Hernan; Varkey, Julia; Varma, Susheel; Varma, Vijay; Varma, Sudhr; Vasanthakumar, Aparna; Vashi, Tejal; Vasilchuk, Kseniia; Vassileva, Albena; Vatsalan, Dinusha; Vb, Nastaran; Veeramacheneni, Teja; Veeranah, Darvesh; Vejdani, Kaveh; Veldsman, Michele; Velgos, Stefanie; Veloso, Adriano; Vemuri, Prashanthi; Venero, Cesar; Venkataraman, Ashwin; Venkatasubramanian, Palamadai; Venkatraghavan, Vikram; Venugopal, Vinisha; Venugopalan, Janani; Verbeeck, Rudi; Verbel, David; Verbist, Bie; Verdoliva, Luisa; Verma, Ajay Kumar; Verma, Tarun; Verma, Ishan; Veronese, Mattia; Grabovetsky, Alejandro Vicente; Victor, Jonathan; Vieira, Domingos; Vijayaraj, Vinesh Raja; Vikas, Vinutha; Vilaplana, Veronica; Vilaplana, Eduard; Villar, José Ramón; Vincent, Fabrice; Vinkler, Mojmir; Viswanath, Satish; Viswanathan, Srikrishnan; Vitek, Michael; Viti, Mario; Vladutu, Liviu; Vlock, Daniel; Voineskos, Aristotle; Vora, Anvi; Vos, Stephanie; Voyle, Nicola; Vrenken, Hugo; Vu, Tien Duong; Vucetic, Zivjena; Vuksanovic, Vesna; Wachinger, Christian; Wada, Masataka; Wade, Sara; Wagstyl, Konrad; Wahba, Grace; Waldorf, Johannes; Walker, Douglas; Moore, Kim Poki Walker; Walsh, Dominic; Wan, Lin; Wang, Di; Wang, Jane-Ling; Wang, Yongmao; Wang, Huaming; Wang, Miao; Wang, Zi-Rui; Wang, Zheyu; Wang, Z. 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2017-01-01

Neuroimaging measurements derived from magnetic resonance imaging provide important information required for detecting changes related to the progression of mild cognitive impairment (MCI). Cortical features and changes play a crucial role in revealing unique anatomical patterns of brain regions,

One night of sleep loss impairs innovative thinking and flexible decision making.

Science.gov (United States)

Harrison, Y; Horne, J A

1999-05-01

Recent findings with clinically oriented neuropsychological tests suggest that one night without sleep causes particular impairment to tasks requiring flexible thinking and the updating of plans in the light of new information. This relatively little investigated field of sleep deprivation research has real-world implications for decision makers having lost a night's sleep. To explore this latter perspective further, we adapted a dynamic and realistic marketing decision making "game" embodying the need for these skills, and whereby such performance could be measured. As the task relied on the comprehension of a large amount of written information, a critical reasoning test was also administered to ascertain whether any failure at the marketing game might lie with information acquisition rather than with failures in decision making. Ten healthy highly motivated and trained participants underwent two counterbalanced 36 h trials, sleep vs no sleep. The critical reasoning task was unaffected by sleep loss, whereas performance at the game significantly deteri orated after 32-36 h of sleep loss, when sleep deprivation led to more rigid thinking, increased perseverative errors, and marked difficulty in appreciating an updated situation. At this point, and despite the sleep-deprived participants' best efforts to do well, their play collapsed, unlike that of the nonsleep-deprived participants. Copyright 1999 Academic Press.

Cortical deactivation induced by visual stimulation in human slow-wave sleep

DEFF Research Database (Denmark)

Born, Alfred Peter; Law, Ian; Lund, Torben E

2002-01-01

. It is unresolved whether this negative BOLD response pattern is of developmental neurobiological origin particular to a given age or to a general effect of sleep or sedative drugs. To further elucidate this issue, we used fMRI and positron emission tomography (PET) to study the brain activation pattern during......It has previously been demonstrated that sleeping and sedated young children respond with a paradoxical decrease in the blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signal in the rostro-medial occipital visual cortex during visual stimulation...... visual stimulation in spontaneously sleeping adult volunteers. In five sleeping volunteers fMRI studies confirmed a robust signal decrease during stimulation in the rostro-medial occipital cortex. A similar relative decrease at the same location was found during visual stimulation...

Short-term sleep deprivation impairs spatial working memory and modulates expression levels of ionotropic glutamate receptor subunits in hippocampus.

Science.gov (United States)

Xie, Meilan; Yan, Jie; He, Chao; Yang, Li; Tan, Gang; Li, Chao; Hu, Zhian; Wang, Jiali

2015-06-01

Hippocampus-dependent learning memory is sensitive to sleep deprivation (SD). Although the ionotropic glutamate receptors play a vital role in synaptic plasticity and learning and memory, however, whether the expression of these receptor subunits is modulated by sleep loss remains unclear. In the present study, western blotting was performed by probing with specific antibodies against the ionotropic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits GluA1, GluA2, GluA3, and against the N-methyl-d-aspartate (NMDA) glutamate receptor subunits GluN1, GluN2A, GluN2B. In hippocampus, down regulation of surface GluA1 and GluN2A surface expression were observed in both SD groups. However, surface expression level of GluA2, GluA3, GluN1 and GluN2B was significantly up-regulated in 8h-SD rats when compared to the 4h-SD rats. In parallel with the complex changes in AMPA and NMDA receptor subunit expressions, we found the 8h-SD impaired rat spatial working memory in 30-s-delay T-maze task, whereas no impairment of spatial learning was observed in 4h-SD rats. These results indicate that sleep loss alters the relative expression levels of the AMPA and NMDA receptors, thus affects the synaptic strength and capacity for plasticity and partially contributes to spatial memory impairment. Copyright © 2015. Published by Elsevier B.V.

Implications of the bedform phase diagram for size-dependent changes of ooid cortical fabric

Science.gov (United States)

Anderson, N. T.; Cowan, C. A.

2017-12-01

Preliminary petrographic and electron microprobe analyses of well-preserved concentric and radial-concentric ooids in Late Cambrian carbonates of the Port au Port Group, western Newfoundland, Canada, show no Sr enrichment indicative of an aragonite precursor for ooid cortices. Dissolution features such as elephantine ooids, spalled cortices, and dropped nuclei reported by other authors in these and equivalent carbonates elsewhere were not analyzed in this study. It is likely that the pristine concentric and radial-concentric ooids studied here were originally calcite and may exhibit a "banded-radial" fabric (sensu Medwedeff and Wilkinson 1983). Thus, the change in petrographic fabric does not correspond to a change in mineralogy in these ooids. Furthermore, ooids in these rocks and in previous studies of similar rocks exhibit a change from radial to concentric fabric at locally consistent diameters. These two observations suggest that hydrodynamic conditions are the causal mechanism for shifts in ooid cortical fabric. Previous workers have taken this size-dependent shift in cortical fabric to represent increased abrasion that occurs with the transition from suspended load to bedload transport, but disregard bedform stability. We note that at a given flow velocity and depth, ooid growth can trigger a shift from the ripple stability field to the dune stability field. Observations of the rate of migration of modern meter-scale ooid tidal dunes in the Bahamas can be used to constrain ooid transport, and suggest that ooids in these settings may be transported for only minutes to hours twice per year. Therefore, the duration of ooid "sleep" (the time spent buried within the dune) may be 105 greater in dunes compared to ripples. This prolonged subsurface residence time may be a heretofore unconsidered control on the development of ooid cortices. It may dictate radial vs. concentric fabric; drastically diminish abrasion; sequester ooids chemically (and biochemically) from

Sleep disturbances and memory impairment among pregnant women consuming khat: An under-recognized problem

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Md. Dilshad Manzar

2017-01-01

Full Text Available Khat (Catha edulis is a evergreen flowering shrub that is cultivated at high altitudes, especially in East Africa and the southwest of the Arabian Peninsula. The plant contains alkaloids, of which cathinone and cathine have structural similarity and pharmacological action similar to amphetamines. The leaves are, therefore, consumed in some regions as a psychoactive stimulant due to cultural beliefs and misperceptions on the health benefits of khat consumption. This resulted in a growing prevalence of khat consumption among pregnant women. The myriad of physiological changes associated with pregnancy impairs sleep and memory. Moreover, khat has also been shown to have adverse effects on memory and sleep. Therefore, its use during pregnancy may further aggravate those impairments. The purpose of this mini-review is to summarize the changes in sleep and memory during pregnancy and the evidence supporting a relationship between khat consumption and neurocognitive deficits and sleep dysfunctions. The misperceptions of beneficial effects of khat, the high prevalence of consumption among pregnant women, and the possibility of under-reporting of khat abuse do necessitate the development of alternative methodologies to identify cases of unreported khat abuse in pregnant women. It is proposed that screening for sleep problems and memory deficits may help identify under-reported cases of khat abuse in pregnant women.

Brain Phosphorus Magnetic Resonance Spectroscopy Imaging of Sleep Homeostasis and Restoration in Drug Dependence

Directory of Open Access Journals (Sweden)

George H. Trksak

2007-01-01

Full Text Available Numerous reports have documented a high occurrence of sleep difficulties in drug-dependent populations, prompting researchers to characterize sleep profiles and physiology in drug abusing populations. This mini-review examines studies indicating that drug-dependent populations exhibit alterations in sleep homeostatic and restoration processes in response to sleep deprivation. Sleep deprivation is a principal sleep research tool that results in marked physiological challenge, which provides a means to examine sleep homeostatic processes in response to extended wakefulness. A report from our laboratory demonstrated that following recovery sleep from sleep deprivation, brain high-energy phosphates particularly beta–nucleoside triphosphate (beta-NTP are markedly increased as measured with phosphorus magnetic resonance spectroscopy (MRS. A more recent study examined the effects of sleep deprivation in opiate-dependent methadone-maintained (MM subjects. The study demonstrated increases in brain beta-NTP following recovery sleep. Interestingly, these increases were of a markedly greater magnitude in MM subjects compared to control subjects. A similar study examined sleep deprivation in cocaine-dependent subjects demonstrating that cocaine-dependent subjects exhibit greater increases in brain beta-NTP following recovery sleep when compared to control subjects. The studies suggest that sleep deprivation in both MM subjects and cocaine-dependent subjects is characterized by greater changes in brain ATP levels than control subjects. Greater enhancements in brain ATP following recovery sleep may reflect a greater disruption to or impact of sleep deprivation in drug dependent subjects, whereby sleep restoration processes may be unable to properly regulate brain ATP and maintain brain high-energy equilibrium. These studies support the notion of a greater susceptibility to sleep loss in drug dependent populations. Additional sleep studies in drug abusing

Inter-Individual Differences in Neurobehavioural Impairment following Sleep Restriction Are Associated with Circadian Rhythm Phase

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Sletten, Tracey L.; Segal, Ahuva Y.; Flynn-Evans, Erin E.; Lockley, Steven W.; Rajaratnam, Shantha M. W.

2015-01-01

Although sleep restriction is associated with decrements in daytime alertness and neurobehavioural performance, there are considerable inter-individual differences in the degree of impairment. This study examined the effects of short-term sleep restriction on neurobehavioural performance and sleepiness, and the associations between individual differences in impairments and circadian rhythm phase. Healthy adults (n = 43; 22 M) aged 22.5 ± 3.1 (mean ± SD) years maintained a regular 8:16 h sleep:wake routine for at least three weeks prior to laboratory admission. Sleep opportunity was restricted to 5 hours time-in-bed at home the night before admission and 3 hours time-in-bed in the laboratory, aligned by wake time. Hourly saliva samples were collected from 5.5 h before until 5 h after the pre-laboratory scheduled bedtime to assess dim light melatonin onset (DLMO) as a marker of circadian phase. Participants completed a 10-min auditory Psychomotor Vigilance Task (PVT), the Karolinska Sleepiness Scale (KSS) and had slow eye movements (SEM) measured by electrooculography two hours after waking. We observed substantial inter-individual variability in neurobehavioural performance, particularly in the number of PVT lapses. Increased PVT lapses (r = -0.468, p circadian phase. When the difference between DLMO and sleep onset was less than 2 hours, individuals were significantly more likely to have at least three attentional lapses the following morning. This study demonstrates that the phase of an individual’s circadian system is an important variable in predicting the degree of neurobehavioural performance impairment in the hours after waking following sleep restriction, and confirms that other factors influencing performance decrements require further investigation. PMID:26043207

Alterations of whole-brain cortical area and thickness in mild cognitive impairment and Alzheimer's disease.

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Li, Chuanming; Wang, Jian; Gui, Li; Zheng, Jian; Liu, Chen; Du, Hanjian

2011-01-01

Gray matter volume and density of several brain regions, determined by magnetic resonance imaging (MRI), are decreased in Alzheimer's disease (AD). Animal studies have indicated that changes in cortical area size is relevant to thinking and behavior, but alterations of cortical area and thickness in the brains of individuals with AD or its likely precursor, mild cognitive impairment (MCI), have not been reported. In this study, 25 MCI subjects, 30 AD subjects, and 30 age-matched normal controls were recruited for brain MRI scans and Functional Activities Questionnaire (FAQ) assessments. Based on the model using FreeSurfer software, two brain lobes were divided into various regions according to the Desikan-Killiany atlas and the cortical area and thickness of every region was compared and analyzed. We found a significant increase in cortical area of several regions in the frontal and temporal cortices, which correlated negatively with MMSE scores, and a significant decrease in cortical area of several regions in the parietal cortex and the cingulate gyrus in AD subjects. Increased cortical area was also seen in some regions of the frontal and temporal cortices in MCI subjects, whereas the cortical thickness of the same regions was decreased. Our observations suggest characteristic differences of the cortical area and thickness in MCI, AD, and normal control subjects, and these changes may help diagnose both MCI and AD.

Impaired cognitive control mediates the relationship between cortical thickness of the superior frontal gyrus and role functioning in schizophrenia.

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Tully, Laura M; Lincoln, Sarah Hope; Liyanage-Don, Nadia; Hooker, Christine I

2014-02-01

Structural abnormalities in the lateral prefrontal cortex (LPFC) are well-documented in schizophrenia and recent evidence suggests that these abnormalities relate to functional outcome. Cognitive control mechanisms, reliant on the LPFC, are impaired in schizophrenia and predict functional outcome, thus impaired cognitive control could mediate the relationship between neuroanatomical abnormalities in the LPFC and functional outcome. We used surface-based morphometry to investigate relationships between cortical surface characteristics, cognitive control, and measures of social and role functioning in 26 individuals with schizophrenia and 29 healthy controls. Results demonstrate that schizophrenia participants had thinner cortex in a region of the superior frontal gyrus (BA10). Across all participants, decreased cortical thickness in this region related to decreased cognitive control and decreased role functioning. Moreover, cognitive control fully mediated the relationship between cortical thickness in the superior frontal gyrus and role functioning, indicating that neuroanatomical abnormalities in the LPFC adversely impact role functioning via impaired cognitive control processes. Copyright © 2013 Elsevier B.V. All rights reserved.

Interaction of sleep quality and sleep duration on impaired fasting glucose: a population-based cross-sectional survey in China.

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Lou, Peian; Chen, Peipei; Zhang, Lei; Zhang, Pan; Chang, Guiqiu; Zhang, Ning; Li, Ting; Qiao, Cheng

2014-03-13

To explore the interactions of sleep quality and sleep duration and their effects on impaired fasting glucose (IFG) in Chinese adults. Cross-sectional survey. Community-based investigation in Xuzhou, China. 15 145 Chinese men and women aged 18-75 years old who fulfilled the inclusion criteria. The Pittsburgh Sleep Quality Index was used to produce sleep quality categories of good, common and poor. Fasting blood glucose levels were assessed for IFG. Sleep duration was measured by average hours of sleep per night, with categories of 8 h. The products of sleep and family history of diabetes, obesity and age were added to the logistic regression model to evaluate the addictive interaction and relative excess risk of interaction (RERI) on IFG. The attributable proportion (AP) of the interaction and the synergy index (S) were applied to evaluate the additive interaction of two factors. Bootstrap measures were used to calculate 95% CI of RERI, AP and S. The prevalence of IFG was greatest in those with poor sleep quality and short sleep duration (OR 6.37, 95% CI 4.66 to 8.67; pquality and 6-8 h sleep duration, after adjusting for confounders. After adjusting for potential confounders RERI, AP and S values (and their 95% CI) were 1.69 (0.31 to 3.76), 0.42 (0.15 to 0.61) and 2.85 (2.14 to 3.92), respectively, for the interaction between poor sleep quality and short sleep duration, and 0.78 (0.12 to 1.43), 0.61 (0.26 to 0.87) and -65 (-0.94 to -0.27) for the interaction between good sleep quality and long sleep duration. The results suggest that there are additive interactions between poor sleep quality and short sleep duration.

Sleep loss disrupts Arc expression in dentate gyrus neurons.

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Delorme, James E; Kodoth, Varna; Aton, Sara J

2018-04-07

Sleep loss affects many aspects of cognition, and memory consolidation processes occurring in the hippocampus seem particularly vulnerable to sleep loss. The immediate-early gene Arc plays an essential role in both synaptic plasticity and memory formation, and its expression is altered by sleep. Here, using a variety of techniques, we have characterized the effects of brief (3-h) periods of sleep vs. sleep deprivation (SD) on the expression of Arc mRNA and Arc protein in the mouse hippocampus and cortex. By comparing the relative abundance of mature Arc mRNA with unspliced pre-mRNA, we see evidence that during SD, increases in Arc across the cortex, but not hippocampus, reflect de novo transcription. Arc increases in the hippocampus during SD are not accompanied by changes in pre-mRNA levels, suggesting that increases in mRNA stability, not transcription, drives this change. Using in situ hybridization (together with behavioral observation to quantify sleep amounts), we find that in the dorsal hippocampus, SD minimally affects Arc mRNA expression, and decreases the number of dentate gyrus (DG) granule cells expressing Arc. This is in contrast to neighboring cortical areas, which show large increases in neuronal Arc expression after SD. Using immunohistochemistry, we find that Arc protein expression is also differentially affected in the cortex and DG with SD - while larger numbers of cortical neurons are Arc+, fewer DG granule cells are Arc+, relative to the same regions in sleeping mice. These data suggest that with regard to expression of plasticity-regulating genes, sleep (and SD) can have differential effects in hippocampal and cortical areas. This may provide a clue regarding the susceptibility of performance on hippocampus-dependent tasks to deficits following even brief periods of sleep loss. Copyright © 2018. Published by Elsevier Inc.

Sleep inertia, sleep homeostatic and circadian influences on higher-order cognitive functions.

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Burke, Tina M; Scheer, Frank A J L; Ronda, Joseph M; Czeisler, Charles A; Wright, Kenneth P

2015-08-01

Sleep inertia, sleep homeostatic and circadian processes modulate cognition, including reaction time, memory, mood and alertness. How these processes influence higher-order cognitive functions is not well known. Six participants completed a 73-day-long study that included two 14-day-long 28-h forced desynchrony protocols to examine separate and interacting influences of sleep inertia, sleep homeostasis and circadian phase on higher-order cognitive functions of inhibitory control and selective visual attention. Cognitive performance for most measures was impaired immediately after scheduled awakening and improved during the first ~2-4 h of wakefulness (decreasing sleep inertia); worsened thereafter until scheduled bedtime (increasing sleep homeostasis); and was worst at ~60° and best at ~240° (circadian modulation, with worst and best phases corresponding to ~09:00 and ~21:00 hours, respectively, in individuals with a habitual wake time of 07:00 hours). The relative influences of sleep inertia, sleep homeostasis and circadian phase depended on the specific higher-order cognitive function task examined. Inhibitory control appeared to be modulated most strongly by circadian phase, whereas selective visual attention for a spatial-configuration search task was modulated most strongly by sleep inertia. These findings demonstrate that some higher-order cognitive processes are differentially sensitive to different sleep-wake regulatory processes. Differential modulation of cognitive functions by different sleep-wake regulatory processes has important implications for understanding mechanisms contributing to performance impairments during adverse circadian phases, sleep deprivation and/or upon awakening from sleep. © 2015 European Sleep Research Society.

Neurobehavioral performance impairment in insomnia: relationships with self-reported sleep and daytime functioning.

Science.gov (United States)

Shekleton, Julia A; Flynn-Evans, Erin E; Miller, Belinda; Epstein, Lawrence J; Kirsch, Douglas; Brogna, Lauren A; Burke, Liza M; Bremer, Erin; Murray, Jade M; Gehrman, Philip; Lockley, Steven W; Rajaratnam, Shantha M W

2014-01-01

Despite the high prevalence of insomnia, daytime consequences of the disorder are poorly characterized. This study aimed to identify neurobehavioral impairments associated with insomnia, and to investigate relationships between these impairments and subjective ratings of sleep and daytime dysfunction. Cross-sectional, multicenter study. Three sleep laboratories in the USA and Australia. Seventy-six individuals who met the Research Diagnostic Criteria (RDC) for Primary Insomnia, Psychophysiological Insomnia, Paradoxical Insomnia, and/or Idiopathic Childhood Insomnia (44F, 35.8 ± 12.0 years [mean ± SD]) and 20 healthy controls (14F, 34.8 ± 12.1 years). N/A. Participants completed a 7-day sleep-wake diary, questionnaires assessing daytime dysfunction, and a neurobehavioral test battery every 60-180 minutes during an afternoon/evening sleep laboratory visit. Included were tasks assessing sustained and switching attention, working memory, subjective sleepiness, and effort. Switching attention and working memory were significantly worse in insomnia patients than controls, while no differences were found for simple or complex sustained attention tasks. Poorer sustained attention in the control, but not the insomnia group, was significantly associated with increased subjective sleepiness. In insomnia patients, poorer sustained attention performance was associated with reduced health-related quality of life and increased insomnia severity. We found that insomnia patients exhibit deficits in higher level neurobehavioral functioning, but not in basic attention. The findings indicate that neurobehavioral deficits in insomnia are due to neurobiological alterations, rather than sleepiness resulting from chronic sleep deficiency.

Subjective sleep impairment in adults with type 1 or type 2 diabetes: Results from Diabetes MILES-The Netherlands

NARCIS (Netherlands)

Nefs, G.; Donga, E.; van Someren, E.J.W.; Bot, M.; Speight, J.; Pouwer, F.

2015-01-01

Aims: Despite growing recognition of the impact of sleep on diabetes, a clear profile of people with diabetes regarding subjective sleep impairment has yet to be established. This study examines: (1) subjective sleep characteristics in adults with type 1 and type 2 diabetes; (2) the relationship of

Subjective sleep impairment in adults with type 1 or type 2 diabetes : Results from Diabetes MILES-The Netherlands

NARCIS (Netherlands)

Nefs, Giesje; Donga, Esther; van Someren, Eus; Bot, Mariska; Speight, Jane; Pouwer, François

AIMS: Despite growing recognition of the impact of sleep on diabetes, a clear profile of people with diabetes regarding subjective sleep impairment has yet to be established. This study examines: (1) subjective sleep characteristics in adults with type 1 and type 2 diabetes; (2) the relationship of

Pronounced impairment of everyday skills and self-care in posterior cortical atrophy.

Science.gov (United States)

Shakespeare, Timothy J; Yong, Keir X X; Foxe, David; Hodges, John; Crutch, Sebastian J

2015-01-01

Posterior cortical atrophy (PCA) is a neurodegenerative syndrome characterized by progressive visual dysfunction and parietal, occipital, and occipitotemporal atrophy. The aim of this study was to compare the impact of PCA and typical Alzheimer's disease (tAD) on everyday functional abilities and neuropsychiatric status. The Cambridge Behavioural Inventory-Revised was given to carers of 32 PCA and 71 tAD patients. PCA patients showed significantly greater impairment in everyday skills and self-care while the tAD group showed greater impairment in aspects of memory and orientation, and motivation. We suggest that PCA poses specific challenges for those caring for people affected by the condition.

Sleep-dependent directional coupling between human neocortex and hippocampus.

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Wagner, Tobias; Axmacher, Nikolai; Lehnertz, Klaus; Elger, Christian E; Fell, Jürgen

2010-02-01

Complex interactions between neocortex and hippocampus are the neural basis of memory formation. Two-step theories of memory formation suggest that initial encoding of novel information depends on the induction of rapid plasticity within the hippocampus, and is followed by a second sleep-dependent step of memory consolidation. These theories predict information flow from the neocortex into the hippocampus during waking state and in the reverse direction during sleep. However, experimental evidence that interactions between hippocampus and neocortex have a predominant direction which reverses during sleep rely on cross-correlation analysis of data from animal experiments and yielded inconsistent results. Here, we investigated directional coupling in intracranial EEG data from human subjects using a phase-modeling approach which is well suited to reveal functional interdependencies in oscillatory data. In general, we observed that the anterior hippocampus predominantly drives nearby and remote brain regions. Surprisingly, however, the influence of neocortical regions on the hippocampus significantly increased during sleep as compared to waking state. These results question the standard model of hippocampal-neocortical interactions and suggest that sleep-dependent consolidation is accomplished by an active retrieval of hippocampal information by the neocortex. Copyright 2009 Elsevier Srl. All rights reserved.

Functional imaging correlates of impaired distractor suppression following sleep deprivation.

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Kong, Danyang; Soon, Chun Siong; Chee, Michael W L

2012-05-15

Sleep deprivation (SD) has been shown to affect selective attention but it is not known how two of its component processes: target enhancement and distractor suppression, are affected. To investigate, young volunteers either attended to houses or were obliged to ignore them (when attending to faces) while viewing superimposed face-house pictures. MR signal enhancement and suppression in the parahippocampal place area (PPA) were determined relative to a passive viewing control condition. Sleep deprivation was associated with lower PPA activation across conditions. Critically SD specifically impaired distractor suppression in selective attention, leaving target enhancement relatively preserved. These findings parallel some observations in cognitive aging. Additionally, following SD, attended houses were not significantly better recognized than ignored houses in a post-experiment test of recognition memory contrasting with the finding of superior recognition of attended houses in the well-rested state. These results provide evidence for co-encoding of distracting information with targets into memory when one is sleep deprived. Copyright © 2012 Elsevier Inc. All rights reserved.

Insomnia is Associated with Cortical Hyperarousal as Early as Adolescence.

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Fernandez-Mendoza, Julio; Li, Yun; Vgontzas, Alexandros N; Fang, Jidong; Gaines, Jordan; Calhoun, Susan L; Liao, Duanping; Bixler, Edward O

2016-05-01

To examine whether insomnia is associated with spectral electroencephalographic (EEG) dynamics in the beta (15-35Hz) range during sleep in an adolescent general population sample. A case-control sample of 44 adolescents from the Penn State Child Cohort underwent a 9-h polysomnography, clinical history and physical examination. We examined low-beta (15-25 Hz) and high-beta (25-35 Hz) relative power at central EEG derivations during sleep onset latency (SOL), sleep onset (SO), non-rapid eye movement (NREM) sleep, and wake after sleep onset (WASO). Compared to controls (n = 21), individuals with insomnia (n = 23) showed increased SOL and WASO and decreased sleep duration and efficiency, while no differences in sleep architecture were found. Insomniacs showed increased low-beta and high-beta relative power during SOL, SO, and NREM sleep as compared to controls. High-beta relative power was greater during all sleep and wake states in insomniacs with short sleep duration as compared to individuals with insomnia with normal sleep duration. Adolescent insomnia is associated with increased beta EEG power during sleep, which suggests that cortical hyperarousal is present in individuals with insomnia as early as adolescence. Interestingly, cortical hyperarousal is greatest in individuals with insomnia with short sleep duration and may explain the sleep complaints of those with normal sleep duration. Disturbed cortical networks may be a shared mechanism putting individuals with insomnia at risk of psychiatric disorders. © 2016 Associated Professional Sleep Societies, LLC.

Network-dependent modulation of brain activity during sleep.

Science.gov (United States)

Watanabe, Takamitsu; Kan, Shigeyuki; Koike, Takahiko; Misaki, Masaya; Konishi, Seiki; Miyauchi, Satoru; Miyahsita, Yasushi; Masuda, Naoki

2014-09-01

Brain activity dynamically changes even during sleep. A line of neuroimaging studies has reported changes in functional connectivity and regional activity across different sleep stages such as slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep. However, it remains unclear whether and how the large-scale network activity of human brains changes within a given sleep stage. Here, we investigated modulation of network activity within sleep stages by applying the pairwise maximum entropy model to brain activity obtained by functional magnetic resonance imaging from sleeping healthy subjects. We found that the brain activity of individual brain regions and functional interactions between pairs of regions significantly increased in the default-mode network during SWS and decreased during REM sleep. In contrast, the network activity of the fronto-parietal and sensory-motor networks showed the opposite pattern. Furthermore, in the three networks, the amount of the activity changes throughout REM sleep was negatively correlated with that throughout SWS. The present findings suggest that the brain activity is dynamically modulated even in a sleep stage and that the pattern of modulation depends on the type of the large-scale brain networks. Copyright © 2014 Elsevier Inc. All rights reserved.

The effect of ice skating on psychological well-being and sleep quality of children with visual or hearing impairment.

Science.gov (United States)

Dursun, Onur Burak; Erhan, Süleyman Erim; Ibiş, Esra Özhan; Esin, Ibrahim Selcuk; Keleş, Sadullah; Şirinkan, Ahmet; Yörük, Özgür; Acar, Ethem; Beyhun, Nazim Ercument

2015-01-01

Physical exercise and sports have a key role in preventing physical and psychiatric problems in children. However, children with a disability often experience difficulty participating in physical activity due to a lack of suitable opportunities. Participation in an accessible sport is particularly important for these children, but studies examining which sports are beneficial for which disability groups are rare. In this study, we assessed the effects of ice skating on the psychological well-being, self-concept, and sleep quality of children with hearing or visual impairment. Forty students (20 visually impaired and 20 hearing impaired) aged 8-16 were included in a regular ice skating programme for three months. We examined the sleep quality, self-concept, and behavioural and emotional states of the children before and after participating in the programme. There was a significant improvement in self-concept, behavioural and emotional problems, and sleep quality (p sleep quality (p = 0.019) and emotional problem scores (p = 0.000) of the visually impaired children improved; self-concept, peer relations and hyperactivity scores of these children worsened (p sport alternatives that gives children the opportunity to exercise and have fun together. The results of this study revealed that regular ice skating programmes may have positive effects on the psychological well-being of children with hearing impairment. Despite some positive effects, caution must be use when including visually impaired children in ice skating programmes. Generalization of the study's outcomes is limited as the study group were residential students enrolled in special education institutions for children who are blind or deaf. Ice skating is a community-based sport and a popular leisure activity that can also have benefits for people with disabilities. Ice skating and children with hearing impairment: Self-concept, behavioural and emotional problems, and sleep quality of the children

Cortical deactivation induced by visual stimulation in human slow-wave sleep

DEFF Research Database (Denmark)

Born, Alfred Peter; Law, Ian; Lund, Torben E

2002-01-01

It has previously been demonstrated that sleeping and sedated young children respond with a paradoxical decrease in the blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) signal in the rostro-medial occipital visual cortex during visual stimulation. It is unreso...... that this decrease was secondary to a relative rCBF decrease. Possible mechanisms for the paradoxical response pattern during sleep include an active inhibition of the visual cortex or a disruption of an energy-consuming process...

Impaired fear memory specificity associated with deficient endocannabinoid-dependent long-term plasticity.

Science.gov (United States)

Lovelace, Jonathan W; Vieira, Philip A; Corches, Alex; Mackie, Ken; Korzus, Edward

2014-06-01

In addition to its central role in learning and memory, N-methyl D-aspartate receptor (NMDAR)-dependent signaling regulates central glutamatergic synapse maturation and has been implicated in schizophrenia. We have transiently induced NMDAR hypofunction in infant mice during postnatal days 7-11, followed by testing fear memory specificity and presynaptic plasticity in the prefrontal cortex (PFC) in adult mice. We show that transient NMDAR hypofunction during early brain development, coinciding with the maturation of cortical plasticity results in a loss of an endocannabinoid (eCB)-mediated form of long-term depression (eCB-LTD) at adult central glutamatergic synapses, while another form of presynaptic long-term depression mediated by the metabotropic glutamate receptor 2/3 (mGluR2/3-LTD) remains intact. Mice with this selective impairment of presynaptic plasticity also showed deficits in fear memory specificity. The observed deficit in cortical presynaptic plasticity may represent a neural maladaptation contributing to network instability and abnormal cognitive functioning.

Inter-Individual Differences in Neurobehavioural Impairment following Sleep Restriction Are Associated with Circadian Rhythm Phase.

Directory of Open Access Journals (Sweden)

Tracey L Sletten

Full Text Available Although sleep restriction is associated with decrements in daytime alertness and neurobehavioural performance, there are considerable inter-individual differences in the degree of impairment. This study examined the effects of short-term sleep restriction on neurobehavioural performance and sleepiness, and the associations between individual differences in impairments and circadian rhythm phase. Healthy adults (n = 43; 22 M aged 22.5 ± 3.1 (mean ± SD years maintained a regular 8:16 h sleep:wake routine for at least three weeks prior to laboratory admission. Sleep opportunity was restricted to 5 hours time-in-bed at home the night before admission and 3 hours time-in-bed in the laboratory, aligned by wake time. Hourly saliva samples were collected from 5.5 h before until 5 h after the pre-laboratory scheduled bedtime to assess dim light melatonin onset (DLMO as a marker of circadian phase. Participants completed a 10-min auditory Psychomotor Vigilance Task (PVT, the Karolinska Sleepiness Scale (KSS and had slow eye movements (SEM measured by electrooculography two hours after waking. We observed substantial inter-individual variability in neurobehavioural performance, particularly in the number of PVT lapses. Increased PVT lapses (r = -0.468, p < 0.01, greater sleepiness (r = 0.510, p < 0.0001, and more slow eye movements (r = 0.375, p = 0.022 were significantly associated with later DLMO, consistent with participants waking at an earlier circadian phase. When the difference between DLMO and sleep onset was less than 2 hours, individuals were significantly more likely to have at least three attentional lapses the following morning. This study demonstrates that the phase of an individual's circadian system is an important variable in predicting the degree of neurobehavioural performance impairment in the hours after waking following sleep restriction, and confirms that other factors influencing performance decrements require further

The Limited Capacity of Sleep-Dependent Memory Consolidation

Directory of Open Access Journals (Sweden)

Gordon B Feld

2016-09-01

Full Text Available Sleep supports memory consolidation. However, the conceptually important influence of the amount of items encoded in a memory test on this effect has not been investigated. In two experiments, participants (n=101 learned lists of word-pairs varying in length (40, 160, 320 word-pairs in the evening before a night of sleep (sleep group or of sleep deprivation (wake group. After 36 h (including a night allowing recovery sleep retrieval was tested. Compared with wakefulness, post-learning sleep enhanced retention for the 160 word-pair condition (p < 0.01, importantly, this effect completely vanished for the 320 word-pair condition. This result indicates a limited capacity for sleep-dependent memory consolidation, which is consistent with an active system consolidation view on sleep’s role for memory, if it is complemented by processes of active forgetting and/or gist abstraction. Whereas the absolute benefit from sleep should have increased with increasing amounts of successfully encoded items, if sleep only passively protected memory from interference. Moreover, the finding that retention performance was significantly diminished for the 320 word-pair condition compared to the 160 word-pair condition in the sleep group, makes it tempting to speculate that with increasing loads of information encoded during wakefulness, sleep might favour processes of forgetting over consolidation.

Extracellular levels of lactate, but not oxygen, reflect sleep homeostasis in the rat cerebral cortex.

Science.gov (United States)

Dash, Michael B; Tononi, Giulio; Cirelli, Chiara

2012-07-01

It is well established that brain metabolism is higher during wake and rapid eye movement (REM) sleep than in nonrapid eye movement (NREM) sleep. Most of the brain's energy is used to maintain neuronal firing and glutamatergic transmission. Recent evidence shows that cortical firing rates, extracellular glutamate levels, and markers of excitatory synaptic strength increase with time spent awake and decline throughout NREM sleep. These data imply that the metabolic cost of each behavioral state is not fixed but may reflect sleep-wake history, a possibility that is investigated in the current report. Chronic (4d) electroencephalographic (EEG) recordings in the rat cerebral cortex were coupled with fixed-potential amperometry to monitor the extracellular concentration of oxygen ([oxy]) and lactate ([lac]) on a second-by-second basis across the spontaneous sleep-wake cycle and in response to sleep deprivation. Basic sleep research laboratory. Wistar Kyoto (WKY) adult male rats. N/A. Within 30-60 sec [lac] and [oxy] progressively increased during wake and REM sleep and declined during NREM sleep (n = 10 rats/metabolite), but with several differences. [Oxy], but not [lac], increased more during wake with high motor activity and/or elevated EEG high-frequency power. Meanwhile, only the NREM decline of [lac] reflected sleep pressure as measured by slow-wave activity, mirroring previous results for cortical glutamate. The observed state-dependent changes in cortical [lac] and [oxy] are consistent with higher brain metabolism during waking and REM sleep in comparison with NREM sleep. Moreover, these data suggest that glycolytic activity, most likely through its link with glutamatergic transmission, reflects sleep homeostasis.

Brain state-dependence of electrically evoked potentials monitored with head-mounted electronics.

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Richardson, Andrew G; Fetz, Eberhard E

2012-11-01

Inferring changes in brain connectivity is critical to studies of learning-related plasticity and stimulus-induced conditioning of neural circuits. In addition, monitoring spontaneous fluctuations in connectivity can provide insight into information processing during different brain states. Here, we quantified state-dependent connectivity changes throughout the 24-h sleep-wake cycle in freely behaving monkeys. A novel, head-mounted electronic device was used to electrically stimulate at one site and record evoked potentials at other sites. Electrically evoked potentials (EEPs) revealed the connectivity pattern between several cortical sites and the basal forebrain. We quantified state-dependent changes in the EEPs. Cortico-cortical EEP amplitude increased during slow-wave sleep, compared to wakefulness, while basal-cortical EEP amplitude decreased. The results demonstrate the utility of using portable electronics to document state-dependent connectivity changes in freely behaving primates.

Abnormal cortical development after premature birth shown by altered allometric scaling of brain growth.

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Olga Kapellou

2006-08-01

Full Text Available We postulated that during ontogenesis cortical surface area and cerebral volume are related by a scaling law whose exponent gives a quantitative measure of cortical development. We used this approach to investigate the hypothesis that premature termination of the intrauterine environment by preterm birth reduces cortical development in a dose-dependent manner, providing a neural substrate for functional impairment.We analyzed 274 magnetic resonance images that recorded brain growth from 23 to 48 wk of gestation in 113 extremely preterm infants born at 22 to 29 wk of gestation, 63 of whom underwent neurodevelopmental assessment at a median age of 2 y. Cortical surface area was related to cerebral volume by a scaling law with an exponent of 1.29 (95% confidence interval, 1.25-1.33, which was proportional to later neurodevelopmental impairment. Increasing prematurity and male gender were associated with a lower scaling exponent (p < 0.0001 independent of intrauterine or postnatal somatic growth.Human brain growth obeys an allometric scaling relation that is disrupted by preterm birth in a dose-dependent, sexually dimorphic fashion that directly parallels the incidence of neurodevelopmental impairments in preterm infants. This result focuses attention on brain growth and cortical development during the weeks following preterm delivery as a neural substrate for neurodevelopmental impairment after premature delivery.

Sleeping of a Complex Brain Networks with Hierarchical Organization

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Zhang, Ying-Yue; Yang, Qiu-Ying; Chen, Tian-Lun

2009-01-01

The dynamical behavior in the cortical brain network of macaque is studied by modeling each cortical area with a subnetwork of interacting excitable neurons. We characterize the system by studying how to perform the transition, which is now topology-dependent, from the active state to that with no activity. This could be a naive model for the wakening and sleeping of a brain-like system, i.e., a multi-component system with two different dynamical behavior.

Impaired memory consolidation in children with obstructive sleep disordered breathing.

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Kiran Maski

.03, P = 0.04]. NREM slow oscillation power did not correlate with memory consolidation. All results retained significance after controlling for age and BMI. In sum, participants with mild OSA had impaired memory consolidation and results were mediated by N2 sigma power. These results suggest that N2 sigma power could serve as biomarker of risk for cognitive dysfunction in children with sleep disordered breathing.

Do Older Adults Need Sleep? A Review of Neuroimaging, Sleep, and Aging Studies.

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Scullin, Michael K

2017-09-01

Sleep habits, sleep physiology, and sleep disorders change with increasing age. However, there is a longstanding debate regarding whether older adults need sleep to maintain health and daily functioning (reduced-sleep-need view). An alternative possibility is that all older adults need sleep, but that many older adults have lost the ability to obtain restorative sleep (reduced-sleep-ability view). Prior research using behavioral and polysomnography outcomes has not definitively disentangled the reduced-sleep-need and reduced-sleep-ability views. Therefore, this review examines the neuroimaging literature to determine whether age-related changes in sleep cause-or are caused by-age-related changes in brain structure, function, and pathology. In middle-aged and older adults, poorer sleep quality, greater nighttime hypoxia, and shorter sleep duration related to cortical thinning in frontal regions implicated in slow wave generation, in frontoparietal networks implicated in cognitive control, and in hippocampal regions implicated in memory consolidation. Furthermore, poor sleep quality was associated with higher amyloid burden and decreased connectivity in the default mode network, a network that is disrupted in the pathway to Alzheimer's disease. All adults need sleep, but cortical thinning and amyloidal deposition with advancing age may weaken the brain's ability to produce restorative sleep. Therefore, sleep in older adults may not always support identical functions for physical, mental, and cognitive health as in young adults.

The tongue and its control by sleep state-dependent modulators.

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Horner, R L

2011-12-01

The neural networks controlling vital functions such as breathing are embedded in the brain, the neural and chemical environment of which changes with state, i.e., wakefulness, non-rapid eye movement (non-REM) sleep and REM sleep, and with commonly administered drugs such as anaesthetics, sedatives and ethanol. One particular output from the state-dependent chemical brain is the focus of attention in this paper; the motor output to the muscles of the tongue, specifically the actions of state-dependent modulators acting at the hypoglossal motor pool. Determining the mechanisms underlying the modulation of the hypoglossal motor output during sleep is relevant to understanding the spectrum of increased upper airway resistance, airflow limitation, hypoventilation and airway obstructions that occur during natural and drug-influenced sleep in humans. Understanding the mechanisms underlying upper airway dysfunction in sleep-disordered breathing is also important given the large and growing prevalence of obstructive sleep apnea syndrome which constitutes a major public health problem with serious clinical, social and economic consequences.

A Time for Learning and a Time for Sleep : The Effect of Sleep Deprivation on Contextual Fear Conditioning at Different Times of the Day

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Hagewoud, Roelina; Whitcomb, Shamiso N.; Heeringa, Amarins N.; Havekes, Robbert; Koolhaas, Jaap M.; Meerlo, Peter

2010-01-01

Study Objectives: Sleep deprivation negatively affects memory consolidation, especially in the case of hippocampus-dependent memories. Studies in rodents have shown that 5 hours of sleep deprivation immediately following footshock exposure selectively impairs the formation of a contextual fear

Sleep spindles are related to schizotypal personality traits and thalamic glutamine/glutamate in healthy subjects.

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Lustenberger, Caroline; O'Gorman, Ruth L; Pugin, Fiona; Tüshaus, Laura; Wehrle, Flavia; Achermann, Peter; Huber, Reto

2015-03-01

Schizophrenia is a severe mental disorder affecting approximately 1% of the worldwide population. Yet, schizophrenia-like experiences (schizotypy) are very common in the healthy population, indicating a continuum between normal mental functioning and the psychosis found in schizophrenic patients. A continuum between schizotypy and schizophrenia would be supported if they share the same neurobiological origin. Two such neurobiological markers of schizophrenia are: (1) a reduction of sleep spindles (12-15 Hz oscillations during nonrapid eye movement sleep), likely reflecting deficits in thalamo-cortical circuits and (2) increased glutamine and glutamate (Glx) levels in the thalamus. Thus, this study aimed to investigate whether sleep spindles and Glx levels are related to schizotypal personality traits in healthy subjects. Twenty young male subjects underwent 2 all-night sleep electroencephalography recordings (128 electrodes). Sleep spindles were detected automatically. After those 2 nights, thalamic Glx levels were measured by magnetic resonance spectroscopy. Subjects completed a magical ideation scale to assess schizotypy. Sleep spindle density was negatively correlated with magical ideation (r = -.64, P .1). The common relationship of sleep spindle density with schizotypy and thalamic Glx levels indicates a neurobiological overlap between nonclinical schizotypy and schizophrenia. Thus, sleep spindle density and magical ideation may reflect the anatomy and efficiency of the thalamo-cortical system that shows pronounced impairment in patients with schizophrenia. © The Author 2014. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.

Tumor Necrosis Factor Antagonism Normalizes Rapid Eye Movement Sleep in Alcohol Dependence

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Irwin, Michael R.; Olmstead, Richard; Valladares, Edwin M.; Breen, Elizabeth Crabb; Ehlers, Cindy L.

2009-01-01

Background In alcohol dependence, markers of inflammation are associated with increases in rapid eye movement (REM) sleep, which is thought to be a prognostic indicator of alcohol relapse. This study was undertaken to test whether blockade of biologically active tumor necrosis factor-α (TNF-α) normalizes REM sleep in alcohol-dependent adults. Methods In a randomized, placebo-controlled, double-blind, crossover trial, 18 abstinent alcohol-dependent male adults received a single dose of etanercept (25 mg) versus placebo in a counterbalanced order. Polysomnographic sleep was measured at baseline and for 3 nights after the acute dose of etanercept or placebo. Results Compared with placebo, administration of etanercept produced significant decreases in the amount and percentage of REM sleep. Decreases in REM sleep were robust and approached low levels typically found in age-comparable control subjects. Individual differences in biologically active drug as indexed by circulating levels of soluble tumor necrosis factor receptor II negatively correlated with the percentage of REM sleep. Conclusions Pharmacologic neutralization of TNF-α activity is associated with significant reductions in REM sleep in abstinent alcohol-dependent patients. These data suggest that circulating levels of TNF-α may have a physiologic role in the regulation of REM sleep in humans. PMID:19185287

Cognitive Impairment After Sleep Deprivation Rescued by Transcranial Magnetic Stimulation Application in Octodon degus.

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Estrada, C; López, D; Conesa, A; Fernández-Gómez, F J; Gonzalez-Cuello, A; Toledo, F; Tunez, I; Blin, O; Bordet, R; Richardson, J C; Fernandez-Villalba, E; Herrero, M T

2015-11-01

Sleep is indispensable for maintaining regular daily life activities and is of fundamental physiological importance for cognitive performance. Sleep deprivation (SD) may affect learning capacity and the ability to form new memories, particularly with regard to hippocampus-dependent tasks. Transcranial magnetic stimulation (TMS) is a non-invasive procedure of electromagnetic induction that generates electric currents, activating nearby nerve cells in the stimulated cortical area. Several studies have looked into the potential therapeutic use of TMS. The present study was designed to evaluate how TMS could improve learning and memory functions following SD in Octodon degus. Thirty juvenile (18 months old) females were divided into three groups (control, acute, and chronic TMS treatment-with and without SD). TMS-treated groups were placed in plastic cylindrical cages designed to keep them immobile, while receiving head magnetic stimulation. SD was achieved by gently handling the animals to keep them awake during the night. Behavioral tests included radial arm maze (RAM), Barnes maze (BM), and novel object recognition. When TMS treatment was applied over several days, there was significant improvement of cognitive performance after SD, with no side effects. A single TMS session reduced the number of errors for the RAM test and improved latency and reduced errors for the BM test, which both evaluate spatial memory. Moreover, chronic TMS treatment brings about a significant improvement in both spatial and working memories.

Cognitive flexibility: A distinct element of performance impairment due to sleep deprivation.

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Honn, K A; Hinson, J M; Whitney, P; Van Dongen, H P A

2018-03-14

In around-the-clock operations, reduced alertness due to circadian misalignment and sleep loss causes performance impairment, which can lead to catastrophic errors and accidents. There is mounting evidence that performance on different tasks is differentially affected, but the general principles underlying this differentiation are not well understood. One factor that may be particularly relevant is the degree to which tasks require executive control, that is, control over the initiation, monitoring, and termination of actions in order to achieve goals. A key aspect of this is cognitive flexibility, i.e., the deployment of cognitive control resources to adapt to changes in events. Loss of cognitive flexibility due to sleep deprivation has been attributed to "feedback blunting," meaning that feedback on behavioral outcomes has reduced salience - and that feedback is therefore less effective at driving behavior modification under changing circumstances. The cognitive mechanisms underlying feedback blunting are as yet unknown. Here we present data from an experiment that investigated the effects of sleep deprivation on performance after an unexpected reversal of stimulus-response mappings, requiring cognitive flexibility to maintain good performance. Nineteen healthy young adults completed a 4-day in-laboratory study. Subjects were randomized to either a total sleep deprivation condition (n = 11) or a control condition (n = 8). Athree-phase reversal learning decision task was administered at baseline, and again after 30.5 h of sleep deprivation, or matching well-rested control. The task was based on a go/no go task paradigm, in which stimuli were assigned to either a go (response) set or a no go (no response) set. Each phase of the task included four stimuli (two in the go set and two in the no go set). After each stimulus presentation, subjects could make a response within 750 ms or withhold their response. They were then shown feedback on the accuracy of

Self-reported nonrestorative sleep in fibromyalgia – relationship to impairments of body functions, personal function factors, and quality of life

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Liedberg GM

2015-08-01

Full Text Available Gunilla M Liedberg,1 Mathilda Björk,2 Björn Börsbo31Department of Social and Welfare Studies, Linköping University, Norrköping, 2Rehabilitation Centre and Department of Medical and Health Sciences, 3Rehabilitation Medicine, Department of Medicine and Health Sciences (IMH, Linköping University, Linköping, SwedenPurpose: The purpose of this study was: 1 to determine variables that might characterize good or bad sleep; and 2 to describe the relationship between sleep, impairment of body functions, personal function factors, and quality of life based on quality of sleep in women with fibromyalgia (FM. Methods: This cross-sectional descriptive study included 224 consecutive patients diagnosed at a specialist center. These patients were mailed a questionnaire concerning sleep, body functions, personal factors, and health-related quality of life. In total, 145 completed questionnaires were collected. Results: Using sleep variables (sleep quality, waking up unrefreshed, and tiredness when getting up, we identified two subgroups – the good sleep subgroup and the bad sleep subgroup – of women with FM. These subgroups exhibited significantly different characteristics concerning pain intensity, psychological variables (depressed mood, anxiety, catastrophizing, and self-efficacy, impairments of body functions, and generic and health-related quality of life. The good sleep subgroup reported a significantly better situation, including higher employment/study rate. The bad sleep subgroup reported a greater use of sleep medication. Five variables determined inclusion into either a good sleep or a bad sleep subgroup: pain in the evening, self-efficacy, anxiety, and according to the Short Form health survey role emotional and physical functioning. Conclusion: This study found that it was possible to identify two subgroups of women with FM based on quality of sleep variables. The two subgroups differed significantly with respect to pain, psychological

Short-Term Total Sleep-Deprivation Impairs Contextual Fear Memory, and Contextual Fear-Conditioning Reduces REM Sleep in Moderately Anxious Swiss Mice

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Munazah F. Qureshi

2017-11-01

Full Text Available The conditioning tasks have been widely used to model fear and anxiety and to study their association with sleep. Many reports suggest that sleep plays a vital role in the consolidation of fear memory. Studies have also demonstrated that fear-conditioning influences sleep differently in mice strains having a low or high anxiety level. It is, therefore, necessary to know, how sleep influences fear-conditioning and how fear-conditioning induces changes in sleep architecture in moderate anxious strains. We have used Swiss mice, a moderate anxious strain, to study the effects of: (i sleep deprivation on contextual fear conditioned memory, and also (ii contextual fear conditioning on sleep architecture. Animals were divided into three groups: (a non-sleep deprived (NSD; (b stress control (SC; and (c sleep-deprived (SD groups. The SD animals were SD for 5 h soon after training. We found that the NSD and SC animals showed 60.57% and 58.12% freezing on the testing day, while SD animals showed significantly less freezing (17.13% only; p < 0.001 on the testing day. Further, we observed that contextual fear-conditioning did not alter the total amount of wakefulness and non-rapid eye movement (NREM sleep. REM sleep, however, significantly decreased in NSD and SC animals on the training and testing days. Interestingly, REM sleep did not decrease in the SD animals on the testing day. Our results suggest that short-term sleep deprivation impairs fear memory in moderate anxious mice. It also suggests that NREM sleep, but not REM sleep, may have an obligatory role in memory consolidation.

The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T2* mapping at 7 T MRI.

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Louapre, Céline; Govindarajan, Sindhuja T; Giannì, Costanza; Madigan, Nancy; Nielsen, A Scott; Sloane, Jacob A; Kinkel, Revere P; Mainero, Caterina

2016-01-01

Using quantitative T 2 * at 7 Tesla (T) magnetic resonance imaging, we investigated whether impairment in selective cognitive functions in multiple sclerosis (MS) can be explained by pathology in specific areas and/or layers of the cortex. Thirty-one MS patients underwent neuropsychological evaluation, acquisition of 7 T multi-echo T 2 * gradient-echo sequences, and 3 T anatomical images for cortical surfaces reconstruction. Seventeen age-matched healthy subjects served as controls. Cortical T 2 * maps were sampled at various depths throughout the cortex and juxtacortex. Relation between T 2 *, neuropsychological scores and a cognitive index (CI), calculated from a principal component analysis on the whole battery, was tested by a general linear model. Cognitive impairment correlated with T 2 * increase, independently from white matter lesions and cortical thickness, in cortical areas highly relevant for cognition belonging to the default-mode network (p < 0.05 corrected). Dysfunction in different cognitive functions correlated with longer T 2 * in selective cortical regions, most of which showed longer T 2 * relative to controls. For most tests, this association was strongest in deeper cortical layers. Executive dysfunction, however, was mainly related with pathology in juxtameningeal cortex. T 2 * explained up to 20% of the variance of the CI, independently of conventional imaging metrics (adjusted-R 2 : 52-67%, p < 5.10 - 4 ). Location of pathology across the cortical width and mantle showed selective correlation with impairment in differing cognitive domains. These findings may guide studies at lower field strength designed to develop surrogate markers of cognitive impairment in MS.

A review of sleep disorders and melatonin.

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Xie, Zizhen; Chen, Fei; Li, William A; Geng, Xiaokun; Li, Changhong; Meng, Xiaomei; Feng, Yan; Liu, Wei; Yu, Fengchun

2017-06-01

Sleep disorders are a group of conditions that affect the ability to sleep well on a regular basis and cause significant impairments in social and occupational functions. Although currently approved medications are efficacious, they are far from satisfactory. Benzodiazepines, antidepressants, antihistamines and anxiolytics have the potential for dependence and addiction. Moreover, some of these medications can gradually impair cognition. Melatonin (N-acetyl-5-methoxytryptamine) is an endogenous hormone produced by the pineal gland and released exclusively at night. Exogenous melatonin supplementation is well tolerated and has no obvious short- or long-term adverse effects. Melatonin has been shown to synchronize the circadian rhythms, and improve the onset, duration and quality of sleep. It is centrally involved in anti-oxidation, circadian rhythmicity maintenance, sleep regulation and neuronal survival. This narrative review aims to provide a comprehensive overview of various therapeutic functions of melatonin in insomnia, sleep-related breathing disorders, hypersomnolence, circadian rhythm sleep-wake disorders and parasomnias. Melatonin offers an alternative treatment to the currently available pharmaceutical therapies for sleep disorders with significantly less side effects.

Accelerated Age-Dependent Hippocampal Volume Loss in Parkinson Disease With Mild Cognitive Impairment.

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Schneider, Christine B; Donix, Markus; Linse, Katharina; Werner, Annett; Fauser, Mareike; Klingelhoefer, Lisa; Löhle, Matthias; von Kummer, Rüdiger; Reichmann, Heinz; Storch, Alexander

2017-09-01

Patients with Parkinson disease are at high risk of developing dementia. During the course of the disease, a substantial number of patients will experience a cognitive decline, indicating the dynamics of the underlying neuropathology. Magnetic resonance imaging (MRI) has become increasingly useful for identifying structural characteristics in radiological brain anatomy existing prior to clinical symptoms. Whether these changes reflect pathology, whether they are aging related, or both often remains unclear. We hypothesized that aging-associated brain structural changes would be more pronounced in the hippocampal region among patients with Parkinson disease having mild cognitive deficits relative to cognitively unimpaired patients. Using MRI, we investigated 30 cognitively healthy patients with Parkinson disease and 33 patients with nondemented Parkinson disease having mild cognitive impairment. All participants underwent structural MRI scanning and extensive clinical and neuropsychological assessments. Irrespective of the study participants' cognitive status, older age was associated with reduced cortical thickness in various neocortical regions. Having mild cognitive impairment was not associated with an increased rate of cortical thinning or volume loss in these regions, except in the hippocampus bilaterally. Patients with Parkinson disease having mild cognitive impairment show an accelerated age-dependent hippocampal volume loss when compared with cognitively healthy patients with Parkinson disease. This may indicate pathological processes in a key region for memory functioning in patients with Parkinson disease at risk of developing dementia. Structural MRI of the hippocampal region could potentially contribute to identifying patients who should receive early treatment aimed at delaying the clinical onset of dementia.

Sleep and cognitive dysfunctions. Therapeutic approach

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M.G. Poluektov

2014-01-01

Full Text Available This review focuses on the possible mechanisms of sleep disorders in patients with cognitive impairment (CI of different severity. The interrelation between CI, emotional disorders and insomnia, as well as the dependence of CI severity on the degree of sleep disorders, are discussed. The issues related to treatment of sleep disorders in patients with CI, the advantages and disadvantages of modern somnogenic medications are studied. Recommendations on management of patients with a combination of sleep disorders and CI are provided. Data on the use of Egb 761 to treat CI no dementia and melatonin-based drugs to treat sleep disorders in patients with CI are presented. 

Sleep physiology and sleep disorders in childhood

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El Shakankiry HM

2011-09-01

Full Text Available Hanan M El ShakankiryKing Fahd University Hospital, Al Dammam University, Al Khobar, Kingdom of Saudi ArabiaAbstract: Sleep has long been considered as a passive phenomenon, but it is now clear that it is a period of intense brain activity involving higher cortical functions. Overall, sleep affects every aspect of a child's development, particularly higher cognitive functions. Sleep concerns are ranked as the fifth leading concern of parents. Close to one third of all children suffer from sleep disorders, the prevalence of which is increased in certain pediatric populations, such as children with special needs, children with psychiatric or medical diagnoses and children with autism or pervasive developmental disorders. The paper reviews sleep physiology and the impact, classification, and management of sleep disorders in the pediatric age group.Keywords: sleep physiology, sleep disorders, childhood, epilepsy

Assessment of Cortical Visual Impairment in Infants with Periventricular Leukomalacia: a Pilot Event-Related fMRI Study

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Yu, Bing; Guo, Qiyong [Shengjing Hospital of China Medical University, Shenyang (China); Fan, Guoguang [The First Hospital of China Medical University, Shenyang (China); Liu, Na [Greater China Region of Philips, Shanghai (China)

2011-08-15

We wanted to investigate the usefulness of event-related (ER) functional MRI (fMRI) for the assessment of cortical visual impairment in infants with periventricular leukomalacia (PVL). FMRI data were collected from 24 infants who suffered from PVL and from 12 age-matched normal controls. Slow ER fMRI was performed using a 3.0T MR scanner while visual stimuli were being presented. Data analysis was performed using Statistical Parametric Mapping software (SPM2), the SPM toolbox MarsBar was used to analyze the region of interest data, and the time to peak (TTP) of hemodynamic response functions (HRFs) was estimated for the surviving voxels. The number of activated voxels and the TTP values of HRFs were compared. Pearson correlation analysis was performed to compare visual impairment evaluated by using Teller Acuity Cards (TAC) with the number of activated voxels in the occipital lobes in all patients. In all 12 control infants, the blood oxygenation level-dependent (BOLD) signal was negative and the maximum response was located in the anterior and superior part of the calcarine fissure, and this might correspond to the anterior region of the primary visual cortex (PVC). In contrast, for the 24 cases of PVL, there were no activated pixels in the PVC in four subjects, small and weak activations in six subjects, deviated activations in seven subjects and both small and deviated activations in three subjects. The number of active voxels in the occipital lobe was significantly correlated with the TAC-evaluated visual impairment (p < 0.001). The mean TTP of the HRFs was significantly delayed in the cases of PVL as compared with that of the normal controls. Determining the characteristics of both the BOLD response and the ER fMRI activation may play an important role in the cortical visual assessment of infants with PVL.

Cortical gamma-aminobutyric acid and glutamate in posttraumatic stress disorder and their relationships to self-reported sleep quality.

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Meyerhoff, Dieter J; Mon, Anderson; Metzler, Thomas; Neylan, Thomas C

2014-05-01

To test if posttraumatic stress disorder (PTSD) is associated with low brain gamma-aminobutyric acid (GABA) levels and if reduced GABA is mediated by poor sleep quality. Laboratory study using in vivo proton magnetic resonance spectroscopy (1H MRS) and behavioral testing. VA Medical Center Research Service, Psychiatry and Radiology. Twenty-seven patients with PTSD (PTSD+) and 18 trauma-exposed controls without PTSD (PTSD-), recruited from United States Army reservists, Army National Guard, and mental health clinics. None. 1H MRS at 4 Tesla yielded spectra from three cortical brain regions. In parieto-occipital and temporal cortices, PTSD+ had lower GABA concentrations than PTSD-. As expected, PTSD+ had higher depressive and anxiety symptom scores and a higher Insomnia Severity Index (ISI) score. Higher ISI correlated with lower GABA and higher glutamate levels in parieto-occipital cortex and tended to correlate with lower GABA in the anterior cingulate. The relationship between parieto-occipital GABA and PTSD diagnosis was fully mediated through insomnia severity. Lower N-acetylaspartate and glutamate concentrations in the anterior cingulate cortex correlated with higher arousal scores, whereas depressive and anxiety symptoms did generally not influence metabolite concentrations. Low brain gamma-aminobutyric acid (GABA) concentration in posttraumatic stress disorder (PTSD) is consistent with most findings in panic and social anxiety disorders. Low GABA associated with poor sleep quality is consistent with the hyperarousal theory of both primary insomnia and PTSD. Our data demonstrate that poor sleep quality mediates low parieto-occipital GABA in PTSD. The findings have implications for PTSD treatment approaches.

Partial sleep in the context of augmentation of brain function.

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Ivan N. Pigarev

2014-05-01

Full Text Available Inability to solve complex problems or errors in decision making is often attributed to poor brain processing, and raises the issue of brain augmentation. Investigation of neuronal activity in the cerebral cortex in the sleep-wake cycle offers insights into the mechanisms underlying the reduction in mental abilities for complex problem solving. Some cortical areas may transit into a sleep state while an organism is still awake. Such local sleep would reduce behavioral ability in the tasks for which the sleeping areas are crucial. The studies of this phenomenon have indicated that local sleep develops in high order cortical areas. This is why complex problem solving is mostly affected by local sleep, and prevention of local sleep might be a potential way of augmentation of brain function. For this approach to brain augmentation not to entail negative consequences for the organism, it is necessary to understand the functional role of sleep. Our studies have given an unexpected answer to this question. It was shown that cortical areas that process signals from extero- and proprioreceptors during wakefulness, switch to the processing of interoceptive information during sleep. It became clear that during sleep all computational power of the brain is directed to the restoration of the vital functions of internal organs. These results explain the logic behind the initiation of total and local sleep. Indeed, a mismatch between the current parameters of any visceral system and the genetically determined normal range would provide the feeling of tiredness, or sleep pressure. If an environmental situation allows falling asleep, the organism would transit to a normal total sleep in all cortical areas. However, if it is impossible to go to sleep immediately, partial sleep may develop in some cortical areas in the still behaviorally awake organism. This local sleep may reduce both the intellectual power and the restorative function of sleep for visceral

Seizures and Sleep in the Thalamus: Focal Limbic Seizures Show Divergent Activity Patterns in Different Thalamic Nuclei.

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Feng, Li; Motelow, Joshua E; Ma, Chanthia; Biche, William; McCafferty, Cian; Smith, Nicholas; Liu, Mengran; Zhan, Qiong; Jia, Ruonan; Xiao, Bo; Duque, Alvaro; Blumenfeld, Hal

2017-11-22

The thalamus plays diverse roles in cortical-subcortical brain activity patterns. Recent work suggests that focal temporal lobe seizures depress subcortical arousal systems and convert cortical activity into a pattern resembling slow-wave sleep. The potential simultaneous and paradoxical role of the thalamus in both limbic seizure propagation, and in sleep-like cortical rhythms has not been investigated. We recorded neuronal activity from the central lateral (CL), anterior (ANT), and ventral posteromedial (VPM) nuclei of the thalamus in an established female rat model of focal limbic seizures. We found that population firing of neurons in CL decreased during seizures while the cortex exhibited slow waves. In contrast, ANT showed a trend toward increased neuronal firing compatible with polyspike seizure discharges seen in the hippocampus. Meanwhile, VPM exhibited a remarkable increase in sleep spindles during focal seizures. Single-unit juxtacellular recordings from CL demonstrated reduced overall firing rates, but a switch in firing pattern from single spikes to burst firing during seizures. These findings suggest that different thalamic nuclei play very different roles in focal limbic seizures. While limbic nuclei, such as ANT, appear to participate directly in seizure propagation, arousal nuclei, such as CL, may contribute to depressed cortical function, whereas sleep spindles in relay nuclei, such as VPM, may interrupt thalamocortical information flow. These combined effects could be critical for controlling both seizure severity and impairment of consciousness. Further understanding of differential effects of seizures on different thalamocortical networks may lead to improved treatments directly targeting these modes of impaired function. SIGNIFICANCE STATEMENT Temporal lobe epilepsy has a major negative impact on quality of life. Previous work suggests that the thalamus plays a critical role in thalamocortical network modulation and subcortical arousal

Sleep disorders and work performance: findings from the 2008 National Sleep Foundation Sleep in America poll.

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Swanson, Leslie M; Arnedt, J Todd; Rosekind, Mark R; Belenky, Gregory; Balkin, Thomas J; Drake, Christopher

2011-09-01

Chronic sleep deprivation is common among workers, and has been associated with negative work outcomes, including absenteeism and occupational accidents. The objective of the present study is to characterize reciprocal relationships between sleep and work. Specifically, we examined how sleep impacts work performance and how work affects sleep in individuals not at-risk for a sleep disorder; assessed work performance outcomes for individuals at-risk for sleep disorders, including insomnia, obstructive sleep apnea (OSA) and restless legs syndrome (RLS); and characterized work performance impairments in shift workers (SW) at-risk for shift work sleep disorders relative to SW and day workers. One-thousand Americans who work 30 h per week or more were asked questions about employment, work performance and sleep in the National Sleep Foundation's 2008 Sleep in America telephone poll. Long work hours were associated with shorter sleep times, and shorter sleep times were associated with more work impairments. Thirty-seven percent of respondents were classified as at-risk for any sleep disorder. These individuals had more negative work outcomes as compared with those not at-risk for a sleep disorder. Presenteeism was a significant problem for individuals with insomnia symptoms, OSA and RLS as compared with respondents not at-risk. These results suggest that long work hours may contribute to chronic sleep loss, which may in turn result in work impairment. Risk for sleep disorders substantially increases the likelihood of negative work outcomes, including occupational accidents, absenteeism and presenteeism. © 2010 European Sleep Research Society.

Chronic post-stroke oropharyngeal dysphagia is associated with impaired cortical activation to pharyngeal sensory inputs.

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Cabib, C; Ortega, O; Vilardell, N; Mundet, L; Clavé, P; Rofes, L

2017-11-01

The role of afferent sensory pathways in the pathophysiology of post-stroke oropharyngeal dysphagia is not known. We hypothesized that patients with chronic post-stroke dysphagia (PSD) would show impaired sensory cortical activation in the ipsilesional hemisphere. We studied 28 chronic unilateral post-stroke patients [17 PSD and 11 post-stroke non-dysphagic patients (PSnD)] and 11 age-matched healthy volunteers. Event-related sensory-evoked potentials to pharyngeal stimulation (pSEP) and sensory thresholds were assessed. We analyzed pSEP peak latency and amplitude (N1, P1, N2 and P2), and neurotopographic stroke characteristics from brain magnetic resonance imaging. Healthy volunteers presented a highly symmetric bihemispheric cortical pattern of brain activation at centroparietal areas (N1-P1 and N2-P2) to pharyngeal stimuli. In contrast, an asymmetric pattern of reduced ipsilesional activation was found in PSD (N2-P2; P = 0.026) but not in PSnD. PSD presented impaired safety of swallow (penetration-aspiration score: 4.3 ± 1.6), delayed laryngeal vestibule closure (360.0 ± 70.0 ms) and higher National Institute of Health Stroke Scale (7.0 ± 6.2 vs. 1.9 ± 1.4, P = 0.001) and Fazekas scores (3.0 ± 1.4 vs. 2.0 ± 1.1; P dysphagia is associated with stroke severity and degree of leukoaraoisis. Impaired conduction and cortical integration of pharyngeal sensory inputs at stroke site are key features of chronic PSD. These findings highlight the role of sensory pathways in the pathophysiology of post-stroke oropharyngeal dysphagia and offer a potential target for future treatments. © 2017 EAN.

THE NEUROBIOLOGY OF SLEEP AND WAKEFULNESS

Science.gov (United States)

Schwartz, Michael D.; Kilduff, Thomas S.

2015-01-01

SYNOPSIS Since the discovery of Rapid Eye Movement (REM) sleep in the late 1950s, identification of the neural circuitry underlying wakefulness, sleep onset and the alternation between REM and non-REM (NREM) sleep has been an active area of investigation. Synchronization and desynchronization of cortical activity as detected in the electroencephalogram (EEG) is due to a corticothalamocortical loop, intrinsic cortical oscillators, monoaminergic and cholinergic afferent input to the thalamus, and the basal forebrain cholinergic input directly to the cortex. The monoaminergic and cholinergic systems are largely wake-promoting; the brainstem cholinergic nuclei are also involved in REM sleep regulation. These wake-promoting systems receive excitatory input from the hypothalamic hypocretin/orexin system. Sleep-promoting nuclei are GABAergic in nature and found in the preoptic area, brainstem and lateral hypothalamus. Although the pons is critical for the expression of REM sleep, recent research has suggested that melanin-concentrating hormone/GABAergic cells in the lateral hypothalamus "gate" REM sleep. The temporal distribution of sleep and wakefulness is due to interaction between the circadian system and the sleep homeostatic system. Although the hypothalamic suprachiasmatic nuclei contain the circadian pacemaker, the neural circuitry underlying the sleep homeostat is less clear. Prolonged wakefulness results in the accumulation of extracellular adenosine, possibly from glial sources, which is an important feedback molecule for the sleep homeostatic system. Cortical neuronal nitric oxide (nNOS) neurons may also play a role in propagating slow waves through the cortex in NREM sleep. Several neuropeptides and other neurochemicals likely play important roles in sleep/wake control. Although the control of sleep and wakefulness seemingly involves multiple redundant systems, each of these systems provides a vulnerability that can result in sleep/wake dysfunction that may

Basic visual function and cortical thickness patterns in posterior cortical atrophy.

Science.gov (United States)

Lehmann, Manja; Barnes, Josephine; Ridgway, Gerard R; Wattam-Bell, John; Warrington, Elizabeth K; Fox, Nick C; Crutch, Sebastian J

2011-09-01

Posterior cortical atrophy (PCA) is characterized by a progressive decline in higher-visual object and space processing, but the extent to which these deficits are underpinned by basic visual impairments is unknown. This study aimed to assess basic and higher-order visual deficits in 21 PCA patients. Basic visual skills including form detection and discrimination, color discrimination, motion coherence, and point localization were measured, and associations and dissociations between specific basic visual functions and measures of higher-order object and space perception were identified. All participants showed impairment in at least one aspect of basic visual processing. However, a number of dissociations between basic visual skills indicated a heterogeneous pattern of visual impairment among the PCA patients. Furthermore, basic visual impairments were associated with particular higher-order object and space perception deficits, but not with nonvisual parietal tasks, suggesting the specific involvement of visual networks in PCA. Cortical thickness analysis revealed trends toward lower cortical thickness in occipitotemporal (ventral) and occipitoparietal (dorsal) regions in patients with visuoperceptual and visuospatial deficits, respectively. However, there was also a lot of overlap in their patterns of cortical thinning. These findings suggest that different presentations of PCA represent points in a continuum of phenotypical variation.

Cortical atrophy rates in Alzheimer's patients and subjects with mild cognitive impairment from the AddNeuroMed data collection

DEFF Research Database (Denmark)

Eskildsen, Simon Fristed; Westman, Eric; Gwadry-Sridhar, Femida

2010-01-01

Background: The AddNeuroMed project is a multi-centre European project which aims to identify biomarkers in Alzheimer's disease (AD). In this study we measured the rate of cortical atrophy in AD patients, subjects with mild cognitive impairment (MCI), and healthy controls (HC) using MRI. Methods...... quality control for both the acquisition and image processing were included in the study. Cortical thickness was measured using FACE (fast accurate cortex extraction) and averaged within main lobes using a stereotaxic atlas. Atrophy rates were calculated as percent decrease in cortical thickness and rate...

Impaired response inhibition and excess cortical thickness as candidate endophenotypes for trichotillomania

DEFF Research Database (Denmark)

Odlaug, Brian Lawrence; Chamberlain, Samuel R; Derbyshire, Katie L

2014-01-01

occupying an intermediate position. Permutation cluster analysis revealed significant excesses of cortical thickness in patients and their relatives compared to controls, in right inferior/middle frontal gyri (Brodmann Area, BA 47 & 11), right lingual gyrus (BA 18), left superior temporal cortex (BA 21......Trichotillomania is characterized by repetitive pulling out of one's own hair. Impaired response inhibition has been identified in patients with trichotillomania, along with gray matter density changes in distributed neural regions including frontal cortex. The objective of this study...

Sleep spindle activity in double cortex syndrome: a case report.

Science.gov (United States)

Sforza, Emilia; Marcoz, Jean-Pierre; Foletti, Giovanni

2010-09-01

Cortical dysgenesis is increasingly recognised as a cause of epilepsy. We report a case with double cortex heterotopia and secondarily generalized seizures with a generalised spike wave pattern. During the course of the disease, the child developed electrical status epilepticus in slow wave sleep. From the first examination, sleep pattern revealed increased frequency and amplitude of spindle activity, more evident in anterior areas. The role of the thalamocortical pathway in increased sleep spindle activity is discussed with emphasis on the possible role of altered thalamocortical pathways in abnormal cortical migration. A strong suspicion of cortical dysgenesis may therefore be based on specific EEG sleep patterns.

Sleep extension improves neurocognitive functions in chronically sleep-deprived obese individuals.

Science.gov (United States)

Lucassen, Eliane A; Piaggi, Paolo; Dsurney, John; de Jonge, Lilian; Zhao, Xiong-ce; Mattingly, Megan S; Ramer, Angela; Gershengorn, Janet; Csako, Gyorgy; Cizza, Giovanni

2014-01-01

Sleep deprivation and obesity, are associated with neurocognitive impairments. Effects of sleep deprivation and obesity on cognition are unknown, and the cognitive long-term effects of improvement of sleep have not been prospectively assessed in short sleeping, obese individuals. To characterize neurocognitive functions and assess its reversibility. Prospective cohort study. Tertiary Referral Research Clinical Center. A cohort of 121 short-sleeping (Sleep extension (468±88 days) with life-style modifications. Neurocognitive functions, sleep quality and sleep duration. At baseline, 44% of the individuals had an impaired global deficit score (t-score 0-39). Impaired global deficit score was associated with worse subjective sleep quality (p = 0.02), and lower urinary dopamine levels (p = 0.001). Memory was impaired in 33%; attention in 35%; motor skills in 42%; and executive function in 51% of individuals. At the final evaluation (N = 74), subjective sleep quality improved by 24% (psleep duration increased by 11% by questionnaires (pattention improved by 7% and 10%, respectively (both p = 0.001), and memory and executive functions tended to improve (p = 0.07 and p = 0.06). Serum cortisol increased by 17% (p = 0.02). In a multivariate mixed model, subjective sleep quality and sleep efficiency, urinary free cortisol and dopamine and plasma total ghrelin accounted for 1/5 of the variability in global cognitive function. Drop-out rate. Chronically sleep-deprived obese individuals exhibit substantial neurocognitive deficits that are partially reversible upon improvement of sleep in a non-pharmacological way. These findings have clinical implications for large segments of the US population. www.ClinicalTrials.gov NCT00261898. NIDDK protocol 06-DK-0036.

Title: Cytoskeletal proteins in cortical development and diseasesubtitle: Actin associated proteins in periventricular heterotopia

Directory of Open Access Journals (Sweden)

Gewei eLian

2015-04-01

Full Text Available The actin cytoskeleton regulates many important cellular processes in the brain, including cell division and proliferation, migration, and cytokinesis and differentiation. These developmental processes can be regulated through actin dependent vesicle and organelle movement, cell signaling, and the establishment and maintenance of cell junctions and cell shape. Many of these processes are mediated by extensive and intimate interactions of actin with cellular membranes and proteins. Disruption in the actin cytoskeleton in the brain gives rise to periventricular heterotopia (PH, a malformation of cortical development, characterized by abnormal neurons clustered deep in the brain along the lateral ventricles. This disorder can give rise to seizures, dyslexia and psychiatric disturbances. Anatomically, PH is characterized by a smaller brain (impaired proliferation, heterotopia (impaired initial migration and disruption along the neuroependymal lining (impaired cell-cell adhesion. Genes causal for PH have also been implicated in actin-dependent processes. The current review provides mechanistic insight into actin cytoskeletal regulation of cortical development in the context of this malformation of cortical development.

Does sleep deprivation impair orthopaedic surgeons' cognitive and psychomotor performance?

Science.gov (United States)

O'Brien, Michael J; O'Toole, Robert V; Newell, Mary Zadnik; Lydecker, Alison D; Nascone, Jason; Sciadini, Marcus; Pollak, Andrew; Turen, Clifford; Eglseder, W Andrew

2012-11-07

Sleep deprivation may slow reaction time, cloud judgment, and impair the ability to think. Our purpose was to study the cognitive and psychomotor performances of orthopaedic trauma surgeons on the basis of the amount of sleep that they obtained. We prospectively studied the performances of thirty-two orthopaedic trauma surgeons (residents, fellows, and attending surgeons) over two four-week periods at an urban academic trauma center. Testing sessions used handheld computers to administer validated cognitive and psychomotor function tests. We conducted a multivariate analysis to examine the independent association between test performance and multiple covariates, including the amount of sleep the night before testing. Our analysis demonstrated that orthopaedic surgeons who had slept four hours or less the night before the test had 1.43 times the odds (95% confidence interval, 1.04 to 1.95; p = 0.03) of committing at least one error on an individual test compared with orthopaedic surgeons who had slept more than four hours the previous night. The Running Memory test, which assesses sustained attention, concentration, and working memory, was most sensitive to deterioration in performance in participants who had had four hours of sleep or less; when controlling for other covariates, the test demonstrated a 72% increase in the odds of making at least one error (odds ratio, 1.72 [95% confidence interval, 1.02 to 2.90]; p = 0.04). No significant decrease in performance with sleep deprivation was shown with the other three tests. Orthopaedic trauma surgeons showed deterioration in performance on a validated cognitive task when they had slept four hours or less the previous night. It is unknown how performance on this test relates to surgical performance.

Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance.

Science.gov (United States)

McCauley, Peter; Kalachev, Leonid V; Mollicone, Daniel J; Banks, Siobhan; Dinges, David F; Van Dongen, Hans P A

2013-12-01

Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation--and thereby sensitivity to neurobehavioral impairment from sleep loss--is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation--and thus sensitivity to sleep loss--depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work.

Sleep deprivation impairs spatial working memory and reduces hippocampal AMPA receptor phosphorylation

NARCIS (Netherlands)

Hagewoud, Roelina; Havekes, Robbert; Novati, Arianna; Keijser, Jan N.; van der Zee, Eddy A.; Meerlo, Peter

2010-01-01

Sleep is important for brain function and cognitive performance. Sleep deprivation (SD) may affect subsequent learning capacity and ability to form new memories, particularly in the case of hippocampus-dependent tasks. In the present study we examined whether SD for 6 or 12 h during the normal

Cocaine- and amphetamine-regulated transcript facilitates the neurite outgrowth in cortical neurons after oxygen and glucose deprivation through PTN-dependent pathway.

Science.gov (United States)

Wang, Y; Qiu, B; Liu, J; Zhu, Wei-Guo; Zhu, S

2014-09-26

Cocaine- and amphetamine-regulated transcript (CART) is a neuropeptide that plays neuroprotective roles in cerebral ischemia and reperfusion (I/R) injury in animal models or oxygen and glucose deprivation (OGD) in cultured neurons. Recent data suggest that intranasal CART treatment facilitates neuroregeneration in stroke brain. However, little is known about the effects of post-treatment with CART during the neuronal recovery after OGD and reoxygenation in cultured primary cortical neurons. The present study was to investigate the role of CART treated after OGD injury in neurons. Primary mouse cortical neurons were subjected to OGD and then treated with CART. Our data show that post-treatment with CART reduced the neuronal apoptosis caused by OGD injury. In addition, CART repaired OGD-impaired cortical neurons by increasing the expression of growth-associated protein 43 (GAP43), which promotes neurite outgrowth. This effect depends on pleiotrophin (PTN) as siRNA-mediated PTN knockdown totally abolished the increase in CART-stimulated GAP43 protein levels. In summary, our findings demonstrate that CART repairs the neuronal injury after OGD by facilitating neurite outgrowth through PTN-dependent pathway. The role for CART in neurite outgrowth makes it a new potential therapeutic agent for the treatment of neurodegenerative diseases. Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

Ascent to moderate altitude impairs overnight memory improvements.

Science.gov (United States)

Tesler, Noemi; Latshang, Tsogyal D; Lo Cascio, Christian M; Stadelmann, Katrin; Stoewhas, Anne-Christin; Kohler, Malcolm; Bloch, Konrad E; Achermann, Peter; Huber, Reto

2015-02-01

Several studies showed beneficial effects of sleep on memory performance. Slow waves, the electroencephalographic characteristic of deep sleep, reflected on the neuronal level by synchronous slow oscillations, seem crucial for these benefits. Traveling to moderate altitudes decreases deep sleep. In a randomized cross-over design healthy male subjects performed a visuo-motor learning task in Zurich (490 m) and at Davos Jakobshorn (2590 m) in random order. Memory performance was assessed immediately after learning, before sleep, and in the morning after a night of sleep. Sleep EEG recordings were performed during the nights. Our findings show an altitude induced reduction of sleep dependent memory performance. Moreover, this impaired sleep dependent memory performance was associated with reduced slow wave derived measures of neuronal synchronization. Our results are consistent with a critical role of slow waves for the beneficial effects of sleep on memory that is susceptible to natural environmental influences. Copyright © 2014 Elsevier Inc. All rights reserved.

Impaired cortical processing of inspiratory loads in children with chronic respiratory defects

Directory of Open Access Journals (Sweden)

Clément Annick

2007-09-01

Full Text Available Abstract Background Inspiratory occlusion evoked cortical potentials (the respiratory related-evoked potentials, RREPs bear witness of the processing of changes in respiratory mechanics by the brain. Their impairment in children having suffered near-fatal asthma supports the hypothesis that relates asthma severity with the ability of the patients to perceive respiratory changes. It is not known whether or not chronic respiratory defects are associated with an alteration in brain processing of inspiratory loads. The aim of the present study was to compare the presence, the latencies and the amplitudes of the P1, N1, P2, and N2 components of the RREPs in children with chronic lung or neuromuscular disease. Methods RREPs were recorded in patients with stable asthma (n = 21, cystic fibrosis (n = 32, and neuromuscular disease (n = 16 and in healthy controls (n = 11. Results The 4 RREP components were significantly less frequently observed in the 3 groups of patients than in the controls. Within the patient groups, the N1 and the P2 components were significantly less frequently observed in the patients with asthma (16/21 for both components and cystic fibrosis (20/32 and 14/32 than in the patients with neuromuscular disease (15/16 and 16/16. When present, the latencies and amplitudes of the 4 components were similar in the patients and controls. Conclusion Chronic ventilatory defects in children are associated with an impaired cortical processing of afferent respiratory signals.

Impairment due to combined sleep restriction and alcohol is not mitigated by decaying breath alcohol concentration or rest breaks.

Science.gov (United States)

Manousakis, Jessica E; Anderson, Clare

2017-09-01

Epidemiological and laboratory-based driving simulator studies have shown the detrimental impact of moderate, legal levels of alcohol consumption on driving performance in sleepy drivers. As less is known about the time course of decaying alcohol alongside performance impairment, our study examined impairment and recovery of performance alongside decaying levels of alcohol, with and without sleep restriction. Sixteen healthy young males (18-27 years) underwent 4 counterbalanced conditions: Baseline, Alcohol (breath alcohol concentration [BrAC] batteries commenced 1 hr after consumption and were completed every 30 min for 2 hr (1:30 p.m.-3:30 p.m.). The Combined condition impaired subjective and objective sleepiness. Here, performance deficits peaked 90 min after alcohol consumption or 30 min after the BrAC peak. Performance did not return to baseline levels until 2.5 hr following consumption, despite receiving rest breaks in between testing. These findings suggest that (a) falling BrACs are an inadequate guide for performance/safety and (b) rest breaks without sleep are not a safety measure for mitigating performance impairment when consuming alcohol following restricted sleep. Copyright © 2017 John Wiley & Sons, Ltd.

Long-term exposure to noise impairs cortical sound processing and attention control.

Science.gov (United States)

Kujala, Teija; Shtyrov, Yury; Winkler, Istvan; Saher, Marieke; Tervaniemi, Mari; Sallinen, Mikael; Teder-Sälejärvi, Wolfgang; Alho, Kimmo; Reinikainen, Kalevi; Näätänen, Risto

2004-11-01

Long-term exposure to noise impairs human health, causing pathological changes in the inner ear as well as other anatomical and physiological deficits. Numerous individuals are daily exposed to excessive noise. However, there is a lack of systematic research on the effects of noise on cortical function. Here we report data showing that long-term exposure to noise has a persistent effect on central auditory processing and leads to concurrent behavioral deficits. We found that speech-sound discrimination was impaired in noise-exposed individuals, as indicated by behavioral responses and the mismatch negativity brain response. Furthermore, irrelevant sounds increased the distractibility of the noise-exposed subjects, which was shown by increased interference in task performance and aberrant brain responses. These results demonstrate that long-term exposure to noise has long-lasting detrimental effects on central auditory processing and attention control.

Tai chi qigong as a means to improve night-time sleep quality among older adults with cognitive impairment: a pilot randomized controlled trial

Directory of Open Access Journals (Sweden)

Chan AWK

2016-09-01

Full Text Available Aileen WK Chan, Doris SF Yu, KC Choi, Diana TF Lee, Janet WH Sit, Helen YL Chan The Nethersole School of Nursing, The Chinese University of Hong Kong, Hong Kong SAR, People’s Republic of China Purpose: Age-related cognitive decline is a growing public health concern worldwide. More than a quarter of adults with cognitive impairment experience sleep disturbance. The objective of this pilot study was to evaluate the preliminary effects of tai chi qigong (TCQ on improving the night-time sleep quality of older adults with cognitive impairment. Participants: Older adults with cognitive impairment who complain of sleep disturbance. Methods: A randomized controlled trial with two groups. Fifty-two subjects were recruited from two district elderly community centers and randomly assigned to either the TCQ group (n=27 or the control group (n=25. The intervention group received TCQ training consisting of two 60-minute sessions each week for 2 months. The control group was advised to maintain their usual activities. Sleep quality was measured by the Chinese Pittsburgh Sleep Quality Index. Quality of life was measured by Short-form 12, cognitive functions measured by mini-mental state examination, and subjective memory deficits measured by the memory inventory for Chinese. Results: Data were collected at baseline, 2 months, and 6 months. Significant results were noted at 6 months in the Chinese Pittsburgh Sleep Quality Index global score (P=0.004, sleep duration (P=0.003, habitual sleep efficiency (P=0.002, and the Short-form 12 mental health component (P<0.001. The TCQ participants reported better sleep quality and a better (quality of life mental health component than the control group. Conclusion: TCQ can be considered a useful nonpharmacological approach for improving sleep quality in older adults with cognitive impairment.Clinical trial registration: CUHK_CCT00448 (https://www2.ccrb.cuhk.edu.hk/registry/public/287. Keywords: cognitive decline, mind�

Obstructive sleep apnea and cognitive impairment: Addressing the blood–brain barrier

Science.gov (United States)

Lim, Diane C.; Pack, Allan I.

2013-01-01

SUMMARY Increasing data support a connection between obstructive sleep apnea (OSA) and cognitive impairment but a causal link has yet to be established. Although neuronal loss has been linked to cognitive impairment, emerging theories propose that changes in synaptic plasticity can cause cognitive impairment. Studies demonstrate that disruption to the blood–brain barrier (BBB), which is uniquely structured to tightly maintain homeostasis inside the brain, leads to changes in the brain’s microenvironment and affects synaptic plasticity. Cyclical intermittent hypoxia is a stressor that could disrupt the BBB via molecular responses already known to occur in either OSA patients or animal models of intermittent hypoxia. However, we do not yet know if or how intermittent hypoxia can cause cognitive impairment by mechanisms operating at the BBB. Therefore, we propose that initially, adaptive homeostatic responses at the BBB occur in response to increased oxygen and nutrient demand, specifically through regulation of influx and efflux BBB transporters that alter microvessel permeability. We further hypothesize that although these responses are initially adaptive, these changes in BBB transporters can have long-term consequences that disrupt the brain’s microenvironment and alter synaptic plasticity leading to cognitive impairment. PMID:23541562

Circadian Rhythm Sleep Disorders

Directory of Open Access Journals (Sweden)

Erhan Akinci

2016-06-01

Full Text Available The circadian rhythm sleep disorders define the clinical conditions where sleep and ndash;wake rhythm is disrupted despite optimum environmental and social conditions. They occur as a result of the changes in endogenous circadian hours or non-compatibility of environmental factors or social life with endogenous circadian rhythm. The sleep and ndash;wake rhythm is disrupted continuously or in repeating phases depending on lack of balance between internal and external cycles. This condition leads to functional impairments which cause insomnia, excessive sleepiness or both in people. Application of detailed sleep anamnesis and sleep diary with actigraphy record, if possible, will be sufficient for diagnosis. The treatment aims to align endogenous circadian rhythm with environmental conditions. The purpose of this article is to review pathology, clinical characteristics, diagnosis and treatment of circadian rhythm disorder. [Psikiyatride Guncel Yaklasimlar - Current Approaches in Psychiatry 2016; 8(2: 178-189

Acute cortical deafness in a child with MELAS syndrome.

Science.gov (United States)

Pittet, Marie P; Idan, Roni B; Kern, Ilse; Guinand, Nils; Van, Hélène Cao; Toso, Seema; Fluss, Joël

2016-05-01

Auditory impairment in mitochondrial disorders are usually due to peripheral sensorineural dysfunction. Central deafness is only rarely reported. We report here an 11-year-old boy with MELAS syndrome who presented with subacute deafness after waking up from sleep. Peripheral hearing loss was rapidly excluded. A brain MRI documented bilateral stroke-like lesions predominantly affecting the superior temporal lobe, including the primary auditory cortex, confirming the central nature of deafness. Slow recovery was observed in the following weeks. This case serves to illustrate the numerous challenges caused by MELAS and the unusual occurrence of acute cortical deafness, that to our knowledge has not be described so far in a child in this setting.

A cortical–hippocampal–cortical loop of information processing during memory consolidation

Science.gov (United States)

Rothschild, Gideon; Eban, Elad; Frank, Loren M

2018-01-01

Hippocampal replay during sharp-wave ripple events (SWRs) is thought to drive memory consolidation in hippocampal and cortical circuits. Changes in neocortical activity can precede SWR events, but whether and how these changes influence the content of replay remains unknown. Here we show that during sleep there is a rapid cortical–hippocampal–cortical loop of information flow around the times of SWRs. We recorded neural activity in auditory cortex (AC) and hippocampus of rats as they learned a sound-guided task and during sleep. We found that patterned activation in AC precedes and predicts the subsequent content of hippocampal activity during SWRs, while hippocampal patterns during SWRs predict subsequent AC activity. Delivering sounds during sleep biased AC activity patterns, and sound-biased AC patterns predicted subsequent hippocampal activity. These findings suggest that activation of specific cortical representations during sleep influences the identity of the memories that are consolidated into long-term stores. PMID:27941790

Consolidation through the looking-glass: sleep-dependent proactive interference on visuomotor adaptation in children.

Science.gov (United States)

Urbain, Charline; Houyoux, Emeline; Albouy, Geneviève; Peigneux, Philippe

2014-02-01

Although a beneficial role of post-training sleep for declarative memory has been consistently evidenced in children, as in adults, available data suggest that procedural memory consolidation does not benefit from sleep in children. However, besides the absence of performance gains in children, sleep-dependent plasticity processes involved in procedural memory consolidation might be expressed through differential interference effects on the learning of novel but related procedural material. To test this hypothesis, 32 10-12-year-old children were trained on a motor rotation adaptation task. After either a sleep or a wake period, they were first retested on the same rotation applied at learning, thus assessing offline sleep-dependent changes in performance, then on the opposite (unlearned) rotation to assess sleep-dependent modulations in proactive interference coming from the consolidated visuomotor memory trace. Results show that children gradually improve performance over the learning session, showing effective adaptation to the imposed rotation. In line with previous findings, no sleep-dependent changes in performance were observed for the learned rotation. However, presentation of the opposite, unlearned deviation elicited significantly higher interference effects after post-training sleep than wakefulness in children. Considering that a definite feature of procedural motor memory and skill acquisition is the implementation of highly automatized motor behaviour, thus lacking flexibility, our results suggest a better integration and/or automation or motor adaptation skills after post-training sleep, eventually resulting in higher proactive interference effects on untrained material. © 2013 European Sleep Research Society.

Sleep and Cognitive Decline: A Strong Bidirectional Relationship. It Is Time for Specific Recommendations on Routine Assessment and the Management of Sleep Disorders in Patients with Mild Cognitive Impairment and Dementia.

Science.gov (United States)

Guarnieri, Biancamaria; Sorbi, Sandro

2015-01-01

Sleep disturbances and disruption of the neural regulation of the sleep-wake rhythm appear to be involved in the cellular and molecular mechanisms of cognitive decline. Although sleep problems are highly prevalent in mild cognitive impairment (MCI) and many types of dementia, they have not been systematically investigated in the clinical setting and are often only investigated by sleep specialists upon individual request. This review discusses sleep disorders in the context of cognitive decline and provides an overview of the clinical diagnosis and management of these disorders in patients with dementia and MCI. Key Messages: Sleep disorders are largely underestimated and do not receive sufficient attention in the global management of dementia patients. Sleep disturbances have a significant impact on cognitive and physical functions in individuals with cognitive decline and may be associated with important psychological distress and depression. They are positively associated with the severity of behavioral problems and cognitive impairment. The recent recommendations by the Sleep Study Group of the Italian Dementia Research Association can be used as a guideline for the clinical assessment and management of sleep disorders in MCI and dementia patients. Sleep disorders should be carefully investigated using an in-depth sleep history, physical examination, questionnaires and clinical scales and should be validated with the support of a direct caregiver. The recommendations for older adults can be used as a framework to guide the diagnosis and treatment of sleep disorders in individuals with dementia and MCI. The management strategy should be based on the choice of different treatments for each sleep problem present in the same patient, while avoiding adverse interactions between treatments. © 2015 S. Karger AG, Basel.

Dynamic Circadian Modulation in a Biomathematical Model for the Effects of Sleep and Sleep Loss on Waking Neurobehavioral Performance

Science.gov (United States)

McCauley, Peter; Kalachev, Leonid V.; Mollicone, Daniel J.; Banks, Siobhan; Dinges, David F.; Van Dongen, Hans P. A.

2013-01-01

Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation—and thereby sensitivity to neurobehavioral impairment from sleep loss—is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation—and thus sensitivity to sleep loss—depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work. Citation: McCauley P; Kalachev LV; Mollicone DJ; Banks S; Dinges DF; Van Dongen HPA. Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance. SLEEP 2013;36(12):1987-1997. PMID:24293775

Sleep extension improves neurocognitive functions in chronically sleep-deprived obese individuals.

Directory of Open Access Journals (Sweden)

Eliane A Lucassen

Full Text Available Sleep deprivation and obesity, are associated with neurocognitive impairments. Effects of sleep deprivation and obesity on cognition are unknown, and the cognitive long-term effects of improvement of sleep have not been prospectively assessed in short sleeping, obese individuals.To characterize neurocognitive functions and assess its reversibility.Prospective cohort study.Tertiary Referral Research Clinical Center.A cohort of 121 short-sleeping (<6.5 h/night obese (BMI 30-55 kg/m(2 men and pre-menopausal women.Sleep extension (468±88 days with life-style modifications.Neurocognitive functions, sleep quality and sleep duration.At baseline, 44% of the individuals had an impaired global deficit score (t-score 0-39. Impaired global deficit score was associated with worse subjective sleep quality (p = 0.02, and lower urinary dopamine levels (p = 0.001. Memory was impaired in 33%; attention in 35%; motor skills in 42%; and executive function in 51% of individuals. At the final evaluation (N = 74, subjective sleep quality improved by 24% (p<0.001, self-reported sleep duration increased by 11% by questionnaires (p<0.001 and by 4% by diaries (p = 0.04, and daytime sleepiness tended to improve (p = 0.10. Global cognitive function and attention improved by 7% and 10%, respectively (both p = 0.001, and memory and executive functions tended to improve (p = 0.07 and p = 0.06. Serum cortisol increased by 17% (p = 0.02. In a multivariate mixed model, subjective sleep quality and sleep efficiency, urinary free cortisol and dopamine and plasma total ghrelin accounted for 1/5 of the variability in global cognitive function.Drop-out rate.Chronically sleep-deprived obese individuals exhibit substantial neurocognitive deficits that are partially reversible upon improvement of sleep in a non-pharmacological way. These findings have clinical implications for large segments of the US population.www.ClinicalTrials.gov NCT00261898

Fear memory consolidation in sleep requires protein kinase A.

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Cho, Jiyeon; Sypniewski, Krzysztof A; Arai, Shoko; Yamada, Kazuo; Ogawa, Sonoko; Pavlides, Constantine

2018-05-01

It is well established that protein kinase A (PKA) is involved in hippocampal dependent memory consolidation. Sleep is also known to play an important role in this process. However, whether sleep-dependent memory consolidation involves PKA activation has not been clearly determined. Using behavioral observation, animals were categorized into sleep and awake groups. We show that intrahippocampal injections of the PKA inhibitor Rp-cAMPs in post-contextual fear conditioning sleep produced a suppression of long-term fear memory, while injections of Rp-cAMPs during an awake state, at a similar time point, had no effect. In contrast, injections of the PKA activator Sp-cAMPs in awake state, rescued sleep deprivation-induced memory impairments. These results suggest that following learning, PKA activation specifically in sleep is required for the consolidation of long-term memory. © 2018 Cho et al.; Published by Cold Spring Harbor Laboratory Press.

Unihemispheric sleep and asymmetrical sleep: behavioral, neurophysiological, and functional perspectives

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Mascetti GG

2016-07-01

Full Text Available Gian Gastone Mascetti Department of General Psychology, University of Padova, Padova, Italy Abstract: Sleep is a behavior characterized by a typical body posture, both eyes' closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent

Eight weeks of citicoline treatment does not perturb sleep/wake cycles in cocaine-dependent adults.

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Bracken, Bethany K; Penetar, David M; Rodolico, John; Ryan, Elizabeth T; Lukas, Scott E

2011-06-01

Citicoline (cytidine-5'-diphosphate) is a mononucleotide composed of ribose, cytosine, pyrophosphate, and choline, and is involved in the biosynthesis of the structural phosopholipids of cell membranes. Treatment with citicoline, improves memory in patients with dementia, and reduces damage to the brain after traumatic brain injury or stroke. Recent research has been conducted to assess whether citicoline is an effective treatment for cocaine dependence. In cocaine-dependent individuals, withdrawal from cocaine is associated with disturbed sleep, which may contribute to the high rate of relapse to cocaine use. Therefore, it is important to know the impact of citicoline on the sleep/wake cycle in these individuals in order to rate its overall efficacy. In this double-blind, placebo-controlled trial, the effects of citicoline treatment on the sleep/wake cycles of cocaine dependent participants were assessed. The results of the current study are reported as part of a larger study, consisting of an eight-week treatment period to assess the efficacy of longer-term treatment with citicoline at decreasing cocaine consumption in cocaine-dependent polydrug using participants. In this non-abstinent, cocaine-dependent population, citicoline had no effect on any of the sleep parameters measured including sleep efficiency, sleep latency, total sleep time, number of waking episodes, time awake per episode, amount of time in bed spent moving, number of sleep episodes, time asleep per episode, and amount of time in bed spent immobile. These data suggest that eight weeks of citicoline administration does not disturb sleep/wake cycles of cocaine-dependent individuals. Copyright © 2011 Elsevier Inc. All rights reserved.

Brain Damage and Motor Cortex Impairment in Chronic Obstructive Pulmonary Disease: Implication of Nonrapid Eye Movement Sleep Desaturation.

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Alexandre, Francois; Heraud, Nelly; Sanchez, Anthony M J; Tremey, Emilie; Oliver, Nicolas; Guerin, Philippe; Varray, Alain

2016-02-01

Nonrapid eye movement (NREM) sleep desaturation may cause neuronal damage due to the withdrawal of cerebrovascular reactivity. The current study (1) assessed the prevalence of NREM sleep desaturation in nonhypoxemic patients with chronic obstructive pulmonary disease (COPD) and (2) compared a biological marker of cerebral lesion and neuromuscular function in patients with and without NREM sleep desaturation. One hundred fifteen patients with COPD (Global Initiative for Chronic Obstructive Lung Disease [GOLD] grades 2 and 3), resting PaO2 of 60-80 mmHg, aged between 40 and 80 y, and without sleep apnea (apnea-hypopnea index sleep recordings. In addition, twenty-nine patients (substudy) were assessed i) for brain impairment by serum S100B (biological marker of cerebral lesion), and ii) for neuromuscular function via motor cortex activation and excitability and maximal voluntary quadriceps strength measurement. A total of 51.3% patients (n = 59) had NREM sleep desaturation (NREMDes). Serum S100B was higher in the NREMDes patients of the substudy (n = 14): 45.1 [Q1: 37.7, Q3: 62.8] versus 32.9 [Q1: 25.7, Q3: 39.5] pg.ml(-1) (P = 0.028). Motor cortex activation and excitability were lower in NREMDes patients (both P = 0.03), but muscle strength was comparable between groups (P = 0.58). Over half the nonhypoxemic COPD patients exhibited NREM sleep desaturation associated with higher values of the cerebral lesion biomarker and lower neural drive reaching the quadriceps during maximal voluntary contraction. The lack of muscle strength differences between groups suggests a compensatory mechanism(s). Altogether, the results are consistent with an involvement of NREM sleep desaturation in COPD brain impairment. The study was registered at www.clinicaltrials.gov as NCT01679782. © 2016 Associated Professional Sleep Societies, LLC.

Viii. Attachment and sleep among toddlers: disentangling attachment security and dependency.

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Bélanger, Marie-Ève; Bernier, Annie; Simard, Valérie; Bordeleau, Stéphanie; Carrier, Julie

2015-03-01

Many scholars have proposed that parent-child attachment security should favor child sleep. Research has yet, however, to provide convincing support for this hypothesis. The current study used objective measures of sleep and attachment to assess the longitudinal links between mother-child attachment security and subsequent sleep, controlling for child dependency. Sixty-two middle-class families (30 girls) were met twice, when children were 15 months (Wave 1; W1) and 2 years of age (Wave 2; W2). At W1, mother-child attachment was assessed with the observer version of the Attachment Q-Sort. At W2, children wore an actigraph monitor for 72 hr. Results indicated that children more securely attached to their mothers subsequently slept more at night and had higher sleep efficiency, and these predictions were not confounded by child dependency. These findings suggest a unique role for secure attachment relationships in the development of young children's sleep regulation, while addressing methodological issues that have long precluded consensus in this literature. © 2015 The Society for Research in Child Development, Inc.

Unihemispheric sleep and asymmetrical sleep: behavioral, neurophysiological, and functional perspectives.

Science.gov (United States)

Mascetti, Gian Gastone

2016-01-01

Sleep is a behavior characterized by a typical body posture, both eyes' closure, raised sensory threshold, distinctive electrographic signs, and a marked decrease of motor activity. In addition, sleep is a periodically necessary behavior and therefore, in the majority of animals, it involves the whole brain and body. However, certain marine mammals and species of birds show a different sleep behavior, in which one cerebral hemisphere sleeps while the other is awake. In dolphins, eared seals, and manatees, unihemispheric sleep allows them to have the benefits of sleep, breathing, thermoregulation, and vigilance. In birds, antipredation vigilance is the main function of unihemispheric sleep, but in domestic chicks, it is also associated with brain lateralization or dominance in the control of behavior. Compared to bihemispheric sleep, unihemispheric sleep would mean a reduction of the time spent sleeping and of the associated recovery processes. However, the behavior and health of aquatic mammals and birds does not seem at all impaired by the reduction of sleep. The neural mechanisms of unihemispheric sleep are unknown, but assuming that the neural structures involved in sleep in cetaceans, seals, and birds are similar to those of terrestrial mammals, it is suggested that they involve the interaction of structures of the hypothalamus, basal forebrain, and brain stem. The neural mechanisms promoting wakefulness dominate one side of the brain, while those promoting sleep predominates the other side. For cetaceans, unihemispheric sleep is the only way to sleep, while in seals and birds, unihemispheric sleep events are intermingled with bihemispheric and rapid eye movement sleep events. Electroencephalogram hemispheric asymmetries are also reported during bihemispheric sleep, at awakening, and at sleep onset, as well as being associated with a use-dependent process (local sleep).

Functional neuroimaging and behavioral correlates of capacity decline in visual short-term memory after sleep deprivation.

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Chee, Michael W L; Chuah, Y M Lisa

2007-05-29

Sleep deprivation (SD) impairs short-term memory, but it is unclear whether this is because of reduced storage capacity or processes contributing to appropriate information encoding. We evaluated 30 individuals twice, once after a night of normal sleep and again after 24 h of SD. In each session, we evaluated visual memory capacity by presenting arrays of one to eight colored squares. Additionally, we measured cortical responses to varying visual array sizes without engaging memory. The magnitude of intraparietal sulcus activation and memory capacity after normal sleep were highly correlated. SD elicited a pattern of activation in both tasks, indicating that deficits in visual processing and visual attention accompany and could account for loss of short-term memory capacity. Additionally, a comparison between better and poorer performers showed that preservation of precuneus and temporoparietal junction deactivation with increasing memory load corresponds to less performance decline when one is sleep-deprived.

Dreaming of a Learning Task is Associated with Enhanced Sleep-Dependent Memory Consolidation

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Wamsley, Erin J.; Tucker, Matthew; Payne, Jessica D.; Benavides, Joseph; Stickgold, Robert

2010-01-01

Summary It is now well established that post-learning sleep is beneficial for human memory performance [1–5]. Meanwhile, human and animal studies demonstrate that learning-related neural activity is re-expressed during post-training non-rapid eye movement sleep (NREM) [6–9]. NREM sleep processes appear to be particularly beneficial for hippocampus-dependent forms of memory [1–3, 10]. These observations suggest that learning triggers the reactivation and reorganization of memory traces during sleep, a systems-level process that in turn enhances behavioral performance. Here, we hypothesized that dreaming about a learning experience during NREM sleep would be associated with improved performance on a hippocampus-dependent spatial memory task. Subjects (n=99) were trained on a virtual navigation task, and then retested on the same task 5 hours after initial training. Improved performance at retest was strongly associated with task-related dream imagery during an intervening afternoon nap. Task-related thoughts during wakefulness, in contrast, did not predict improved performance. These observations suggest that sleep-dependent memory consolidation in humans is facilitated by the offline reactivation of recently formed memories, and furthermore, that dream experiences reflect this memory processing. That similar effects were not seen during wakefulness suggests that these mnemonic processes are specific to the sleep state. PMID:20417102

Spontaneous hemodynamic oscillations during human sleep and sleep stage transitions characterized with near-infrared spectroscopy.

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Tiina Näsi

Full Text Available Understanding the interaction between the nervous system and cerebral vasculature is fundamental to forming a complete picture of the neurophysiology of sleep and its role in maintaining physiological homeostasis. However, the intrinsic hemodynamics of slow-wave sleep (SWS are still poorly known. We carried out 30 all-night sleep measurements with combined near-infrared spectroscopy (NIRS and polysomnography to investigate spontaneous hemodynamic behavior in SWS compared to light (LS and rapid-eye-movement sleep (REM. In particular, we concentrated on slow oscillations (3-150 mHz in oxy- and deoxyhemoglobin concentrations, heart rate, arterial oxygen saturation, and the pulsation amplitude of the photoplethysmographic signal. We also analyzed the behavior of these variables during sleep stage transitions. The results indicate that slow spontaneous cortical and systemic hemodynamic activity is reduced in SWS compared to LS, REM, and wakefulness. This behavior may be explained by neuronal synchronization observed in electrophysiological studies of SWS and a reduction in autonomic nervous system activity. Also, sleep stage transitions are asymmetric, so that the SWS-to-LS and LS-to-REM transitions, which are associated with an increase in the complexity of cortical electrophysiological activity, are characterized by more dramatic hemodynamic changes than the opposite transitions. Thus, it appears that while the onset of SWS and termination of REM occur only as gradual processes over time, the termination of SWS and onset of REM may be triggered more abruptly by a particular physiological event or condition. The results suggest that scalp hemodynamic changes should be considered alongside cortical hemodynamic changes in NIRS sleep studies to assess the interaction between the autonomic and central nervous systems.

Congenital olfactory impairment is linked to cortical changes in prefrontal and limbic brain regions

DEFF Research Database (Denmark)

Karstensen, Helena Gásdal; Vestergaard, Martin; Baaré, William F C

2018-01-01

differently in individuals who suffer from lifelong olfactory deprivation relative to healthy normosmic individuals. To address this question, we examined if regional variations in gray matter volume were associated with smell ability in seventeen individuals with isolated congenital olfactory impairment (COI...... in left middle frontal gyrus and right superior frontal sulcus (SFS). COI subjects with severe olfactory impairment (anosmia) had reduced grey matter volume in the left mOFC and increased volume in right piriform cortex and SFS. Within the COI group olfactory ability, measured with the "Sniffin' Sticks...... piriform cortex, while olfactory identification was negatively associated with right SFS volume. Our findings suggest that lifelong olfactory deprivation trigger changes in the cortical volume of prefrontal and limbic brain regions previously linked to olfactory memory....

Language experience enhances early cortical pitch-dependent responses

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Krishnan, Ananthanarayan; Gandour, Jackson T.; Ananthakrishnan, Saradha; Vijayaraghavan, Venkatakrishnan

2014-01-01

Pitch processing at cortical and subcortical stages of processing is shaped by language experience. We recently demonstrated that specific components of the cortical pitch response (CPR) index the more rapidly-changing portions of the high rising Tone 2 of Mandarin Chinese, in addition to marking pitch onset and sound offset. In this study, we examine how language experience (Mandarin vs. English) shapes the processing of different temporal attributes of pitch reflected in the CPR components using stimuli representative of within-category variants of Tone 2. Results showed that the magnitude of CPR components (Na-Pb and Pb-Nb) and the correlation between these two components and pitch acceleration were stronger for the Chinese listeners compared to English listeners for stimuli that fell within the range of Tone 2 citation forms. Discriminant function analysis revealed that the Na-Pb component was more than twice as important as Pb-Nb in grouping listeners by language affiliation. In addition, a stronger stimulus-dependent, rightward asymmetry was observed for the Chinese group at the temporal, but not frontal, electrode sites. This finding may reflect selective recruitment of experience-dependent, pitch-specific mechanisms in right auditory cortex to extract more complex, time-varying pitch patterns. Taken together, these findings suggest that long-term language experience shapes early sensory level processing of pitch in the auditory cortex, and that the sensitivity of the CPR may vary depending on the relative linguistic importance of specific temporal attributes of dynamic pitch. PMID:25506127

Frontal Lobe Contusion in Mice Chronically Impairs Prefrontal-Dependent Behavior.

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Austin Chou

Full Text Available Traumatic brain injury (TBI is a major cause of chronic disability in the world. Moderate to severe TBI often results in damage to the frontal lobe region and leads to cognitive, emotional, and social behavioral sequelae that negatively affect quality of life. More specifically, TBI patients often develop persistent deficits in social behavior, anxiety, and executive functions such as attention, mental flexibility, and task switching. These deficits are intrinsically associated with prefrontal cortex (PFC functionality. Currently, there is a lack of analogous, behaviorally characterized TBI models for investigating frontal lobe injuries despite the prevalence of focal contusions to the frontal lobe in TBI patients. We used the controlled cortical impact (CCI model in mice to generate a frontal lobe contusion and studied behavioral changes associated with PFC function. We found that unilateral frontal lobe contusion in mice produced long-term impairments to social recognition and reversal learning while having only a minor effect on anxiety and completely sparing rule shifting and hippocampal-dependent behavior.

The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T2* mapping at 7 T MRI

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Céline Louapre, MD, PhD

2016-01-01

Location of pathology across the cortical width and mantle showed selective correlation with impairment in differing cognitive domains. These findings may guide studies at lower field strength designed to develop surrogate markers of cognitive impairment in MS.

Sleep disturbance in family caregivers of children who depend on medical technology: A systematic review.

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Keilty, Krista; Cohen, Eyal; Ho, Michelle; Spalding, Karen; Stremler, Robyn

2015-01-01

Society relies on family caregivers of children who depend on medical technology (e.g. mechanical ventilation), to provide highly skilled and vigilant care in their homes 24 hours per day. Sleep disturbance is among the most common complaints of these caregivers. The purpose of this review is to systematically examine studies reporting on sleep outcomes in family caregivers of technology dependent children. All relevant databases were systematically searched: MEDLINE, EMBASE, PsycINFO and CINAHL. Given the heterogeneity of the studies, a qualitative analysis was completed and thus results of this review are presented as a narrative. Thirteen studies were retrieved that met eligibility criteria for inclusion. All of the studies reported on family caregivers of children with medical complexity living at home. Moreover, all of the studies relied entirely on self-report, not objective sleep measures. No intervention studies were found. Sleep disturbance was found to be common (51-100%) along with caregiver reports of poor sleep quality. Sleep quantity was seldom measured, but was found in the few studies that did, to be approximately 6 hours, or less than recommendations for optimal health and daytime function. Multiple caregiver, child and environmental factors were also identified that may negatively influence caregiver sleep, health and daytime function. Findings of this review suggest that family caregivers of children with medical complexity who depend on medical technology achieve poor sleep quality and quantity that may place them at risk of the negative consequences of sleep deprivation. Recommendations for practice include that health care providers routinely assess for sleep disturbance in this vulnerable population. The review also suggests that studies using objective sleep measurement are needed to more fully characterize sleep and inform the development of targeted interventions to promote sleep in family caregivers of technology dependent children.

Automatic, ECG-based detection of autonomic arousals and their association with cortical arousals, leg movements, and respiratory events in sleep

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Olsen, Mads; Schneider, Logan Douglas; Cheung, Joseph

2018-01-01

The current definition of sleep arousals neglects to address the diversity of arousals and their systemic cohesion. Autonomic arousals (AA) are autonomic activations often associated with cortical arousals (CA), but they may also occur in isolation in relation to a respiratory event, a leg movement...... event or spontaneously, without any other physiological associations. AA should be acknowledged as essential events to understand and explore the systemic implications of arousals. We developed an automatic AA detection algorithm based on intelligent feature selection and advanced machine learning using...... or respiratory events. This indicates that most FP constitute autonomic activations that are indistinguishable from those with cortical cohesion. The proposed algorithm provides an automatic system trained in a clinical environment, which can be utilized to analyse the systemic and clinical impacts of arousals....

Inhibition of synaptically evoked cortical acetylcholine release by adenosine: an in vivo microdialysis study in the rat.

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Materi, L M; Rasmusson, D D; Semba, K

2000-01-01

The release of cortical acetylcholine from the intracortical axonal terminals of cholinergic basal forebrain neurons is closely associated with electroencephalographic activity. One factor which may act to reduce cortical acetylcholine release and promote sleep is adenosine. Using in vivo microdialysis, we examined the effect of adenosine and selective adenosine receptor agonists and antagonists on cortical acetylcholine release evoked by electrical stimulation of the pedunculopontine tegmental nucleus in urethane anesthetized rats. All drugs were administered locally within the cortex by reverse dialysis. None of the drugs tested altered basal release of acetylcholine in the cortex. Adenosine significantly reduced evoked cortical acetylcholine efflux in a concentration-dependent manner. This was mimicked by the adenosine A(1) receptor selective agonist N(6)-cyclopentyladenosine and blocked by the selective A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). The A(2A) receptor agonist 2-[p-(2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenosi ne hydrochloride (CGS 21680) did not alter evoked cortical acetylcholine release even in the presence of DPCPX. Administered alone, neither DPCPX nor the non-selective adenosine receptor antagonist caffeine affected evoked cortical acetylcholine efflux. Simultaneous delivery of the adenosine uptake inhibitors dipyridamole and S-(4-nitrobenzyl)-6-thioinosine significantly reduced evoked cortical acetylcholine release, and this effect was blocked by the simultaneous administration of caffeine. These data indicate that activation of the A(1) adenosine receptor inhibits acetylcholine release in the cortex in vivo while the A(2A) receptor does not influence acetylcholine efflux. Such inhibition of cortical acetylcholine release by adenosine may contribute to an increased propensity to sleep during prolonged wakefulness.

Dose-Dependent Cortical Thinning After Partial Brain Irradiation in High-Grade Glioma

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Karunamuni, Roshan [Department of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, California (United States); Bartsch, Hauke; White, Nathan S. [Department of Radiology, University of California San Diego, La Jolla, California (United States); Moiseenko, Vitali; Carmona, Ruben; Marshall, Deborah C.; Seibert, Tyler M. [Department of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, California (United States); McDonald, Carrie R. [Department of Psychiatry, University of California San Diego, La Jolla, California (United States); Farid, Nikdokht; Krishnan, Anithapriya; Kuperman, Joshua [Department of Radiology, University of California San Diego, La Jolla, California (United States); Mell, Loren [Department of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, California (United States); Brewer, James B.; Dale, Anders M. [Department of Radiology, University of California San Diego, La Jolla, California (United States); Hattangadi-Gluth, Jona A., E-mail: jhattangadi@ucsd.edu [Department of Radiation Medicine and Applied Sciences, University of California San Diego, La Jolla, California (United States)

2016-02-01

Purpose: Radiation-induced cognitive deficits may be mediated by tissue damage to cortical regions. Volumetric changes in cortex can be reliably measured using high-resolution magnetic resonance imaging (MRI). We used these methods to study the association between radiation therapy (RT) dose and change in cortical thickness in high-grade glioma (HGG) patients. Methods and Materials: We performed a voxel-wise analysis of MRI from 15 HGG patients who underwent fractionated partial brain RT. Three-dimensional MRI was acquired pre- and 1 year post RT. Cortex was parceled with well-validated segmentation software. Surgical cavities were censored. Each cortical voxel was assigned a change in cortical thickness between time points, RT dose value, and neuroanatomic label by lobe. Effects of dose, neuroanatomic location, age, and chemotherapy on cortical thickness were tested using linear mixed effects (LME) modeling. Results: Cortical atrophy was seen after 1 year post RT with greater effects at higher doses. Estimates from LME modeling showed that cortical thickness decreased by −0.0033 mm (P<.001) for every 1-Gy increase in RT dose. Temporal and limbic cortex exhibited the largest changes in cortical thickness per Gy compared to that in other regions (P<.001). Age and chemotherapy were not significantly associated with change in cortical thickness. Conclusions: We found dose-dependent thinning of the cerebral cortex, with varying neuroanatomical regional sensitivity, 1 year after fractionated partial brain RT. The magnitude of thinning parallels 1-year atrophy rates seen in neurodegenerative diseases and may contribute to cognitive decline following high-dose RT.

Filtering the reality: functional dissociation of lateral and medial pain systems during sleep in humans.

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Bastuji, Hélène; Mazza, Stéphanie; Perchet, Caroline; Frot, Maud; Mauguière, François; Magnin, Michel; Garcia-Larrea, Luis

2012-11-01

Behavioral reactions to sensory stimuli during sleep are scarce despite preservation of sizeable cortical responses. To further understand such dissociation, we recorded intracortical field potentials to painful laser pulses in humans during waking and all-night sleep. Recordings were obtained from the three cortical structures receiving 95% of the spinothalamic cortical input in primates, namely the parietal operculum, posterior insula, and mid-anterior cingulate cortex. The dynamics of responses during sleep differed among cortical sites. In sleep Stage 2, evoked potential amplitudes were similarly attenuated relative to waking in all three cortical regions. During paradoxical, or rapid eye movements (REM), sleep, opercular and insular potentials remained stable in comparison with Stage 2, whereas the responses from mid-anterior cingulate abated drastically, and decreasing below background noise in half of the subjects. Thus, while the lateral operculo-insular system subserving sensory analysis of somatic stimuli remained active during paradoxical-REM sleep, mid-anterior cingulate processes related to orienting and avoidance behavior were suppressed. Dissociation between sensory and orienting-motor networks might explain why nociceptive stimuli can be either neglected or incorporated into dreams without awakening the subject. Copyright © 2011 Wiley Periodicals, Inc.

Learning-Dependent Plasticity of the Barrel Cortex Is Impaired by Restricting GABA-Ergic Transmission.

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Posluszny, Anna; Liguz-Lecznar, Monika; Turzynska, Danuta; Zakrzewska, Renata; Bielecki, Maksymilian; Kossut, Malgorzata

2015-01-01

Experience-induced plastic changes in the cerebral cortex are accompanied by alterations in excitatory and inhibitory transmission. Increased excitatory drive, necessary for plasticity, precedes the occurrence of plastic change, while decreased inhibitory signaling often facilitates plasticity. However, an increase of inhibitory interactions was noted in some instances of experience-dependent changes. We previously reported an increase in the number of inhibitory markers in the barrel cortex of mice after fear conditioning engaging vibrissae, observed concurrently with enlargement of the cortical representational area of the row of vibrissae receiving conditioned stimulus (CS). We also observed that an increase of GABA level accompanied the conditioning. Here, to find whether unaltered GABAergic signaling is necessary for learning-dependent rewiring in the murine barrel cortex, we locally decreased GABA production in the barrel cortex or reduced transmission through GABAA receptors (GABAARs) at the time of the conditioning. Injections of 3-mercaptopropionic acid (3-MPA), an inhibitor of glutamic acid decarboxylase (GAD), into the barrel cortex prevented learning-induced enlargement of the conditioned vibrissae representation. A similar effect was observed after injection of gabazine, an antagonist of GABAARs. At the behavioral level, consistent conditioned response (cessation of head movements in response to CS) was impaired. These results show that appropriate functioning of the GABAergic system is required for both manifestation of functional cortical representation plasticity and for the development of a conditioned response.

Functional neuroimaging insights into the physiology of human sleep.

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Dang-Vu, Thien Thanh; Schabus, Manuel; Desseilles, Martin; Sterpenich, Virginie; Bonjean, Maxime; Maquet, Pierre

2010-12-01

Functional brain imaging has been used in humans to noninvasively investigate the neural mechanisms underlying the generation of sleep stages. On the one hand, REM sleep has been associated with the activation of the pons, thalamus, limbic areas, and temporo-occipital cortices, and the deactivation of prefrontal areas, in line with theories of REM sleep generation and dreaming properties. On the other hand, during non-REM (NREM) sleep, decreases in brain activity have been consistently found in the brainstem, thalamus, and in several cortical areas including the medial prefrontal cortex (MPFC), in agreement with a homeostatic need for brain energy recovery. Benefiting from a better temporal resolution, more recent studies have characterized the brain activations related to phasic events within specific sleep stages. In particular, they have demonstrated that NREM sleep oscillations (spindles and slow waves) are indeed associated with increases in brain activity in specific subcortical and cortical areas involved in the generation or modulation of these waves. These data highlight that, even during NREM sleep, brain activity is increased, yet regionally specific and transient. Besides refining the understanding of sleep mechanisms, functional brain imaging has also advanced the description of the functional properties of sleep. For instance, it has been shown that the sleeping brain is still able to process external information and even detect the pertinence of its content. The relationship between sleep and memory has also been refined using neuroimaging, demonstrating post-learning reactivation during sleep, as well as the reorganization of memory representation on the systems level, sometimes with long-lasting effects on subsequent memory performance. Further imaging studies should focus on clarifying the role of specific sleep patterns for the processing of external stimuli, as well as the consolidation of freshly encoded information during sleep.

Basal Forebrain Gating by Somatostatin Neurons Drives Prefrontal Cortical Activity.

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Espinosa, Nelson; Alonso, Alejandra; Morales, Cristian; Espinosa, Pedro; Chávez, Andrés E; Fuentealba, Pablo

2017-11-17

The basal forebrain provides modulatory input to the cortex regulating brain states and cognitive processing. Somatostatin-expressing neurons constitute a heterogeneous GABAergic population known to functionally inhibit basal forebrain cortically projecting cells thus favoring sleep and cortical synchronization. However, it remains unclear if somatostatin cells can regulate population activity patterns in the basal forebrain and modulate cortical dynamics. Here, we demonstrate that somatostatin neurons regulate the corticopetal synaptic output of the basal forebrain impinging on cortical activity and behavior. Optogenetic inactivation of somatostatin neurons in vivo rapidly modified neural activity in the basal forebrain, with the consequent enhancement and desynchronization of activity in the prefrontal cortex, reflected in both neuronal spiking and network oscillations. Cortical activation was partially dependent on cholinergic transmission, suppressing slow waves and potentiating gamma oscillations. In addition, recruitment dynamics was cell type-specific, with interneurons showing similar temporal profiles, but stronger responses than pyramidal cells. Finally, optogenetic stimulation of quiescent animals during resting periods prompted locomotor activity, suggesting generalized cortical activation and increased arousal. Altogether, we provide physiological and behavioral evidence indicating that somatostatin neurons are pivotal in gating the synaptic output of the basal forebrain, thus indirectly controlling cortical operations via both cholinergic and non-cholinergic mechanisms. © The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala.

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Mirante, Osvaldo; Brandalise, Federico; Bohacek, Johannes; Mansuy, Isabelle M

2014-01-01

N-methyl-D-aspartate receptor (NMDAR)-dependent long-term depression (LTD) in the lateral nucleus of the amygdala (LA) is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced post-synaptically at the thalamic input but presynaptically at the cortical input, since post-synaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD).

Conversion Discriminative Analysis on Mild Cognitive Impairment Using Multiple Cortical Features from MR Images

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Shengwen Guo

2017-05-01

Full Text Available Neuroimaging measurements derived from magnetic resonance imaging provide important information required for detecting changes related to the progression of mild cognitive impairment (MCI. Cortical features and changes play a crucial role in revealing unique anatomical patterns of brain regions, and further differentiate MCI patients from normal states. Four cortical features, namely, gray matter volume, cortical thickness, surface area, and mean curvature, were explored for discriminative analysis among three groups including the stable MCI (sMCI, the converted MCI (cMCI, and the normal control (NC groups. In this study, 158 subjects (72 NC, 46 sMCI, and 40 cMCI were selected from the Alzheimer's Disease Neuroimaging Initiative. A sparse-constrained regression model based on the l2-1-norm was introduced to reduce the feature dimensionality and retrieve essential features for the discrimination of the three groups by using a support vector machine (SVM. An optimized strategy of feature addition based on the weight of each feature was adopted for the SVM classifier in order to achieve the best classification performance. The baseline cortical features combined with the longitudinal measurements for 2 years of follow-up data yielded prominent classification results. In particular, the cortical thickness produced a classification with 98.84% accuracy, 97.5% sensitivity, and 100% specificity for the sMCI–cMCI comparison; 92.37% accuracy, 84.78% sensitivity, and 97.22% specificity for the cMCI–NC comparison; and 93.75% accuracy, 92.5% sensitivity, and 94.44% specificity for the sMCI–NC comparison. The best performances obtained by the SVM classifier using the essential features were 5–40% more than those using all of the retained features. The feasibility of the cortical features for the recognition of anatomical patterns was certified; thus, the proposed method has the potential to improve the clinical diagnosis of sub-types of MCI and

A Controlled Trial of CPAP Therapy on Metabolic Control in Individuals with Impaired Glucose Tolerance and Sleep Apnea

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Weinstock, Tanya G.; Wang, Xuelei; Rueschman, Michael; Ismail-Beigi, Faramarz; Aylor, Joan; Babineau, Denise C.; Mehra, Reena; Redline, Susan

2012-01-01

Study Objectives: To address whether treatment of sleep apnea improves glucose tolerance. Design: Randomized, double-blind crossover study. Setting: Sleep clinic referrals. Patients: 50 subjects with moderate to severe sleep apnea (AHI > 15) and impaired glucose tolerance. Interventions: Subjects were randomized to 8 weeks of CPAP or sham CPAP, followed by the alternate therapy after a one-month washout. After each treatment, subjects underwent 2-hour OGTT, polysomnography, actigraphy, and measurements of indices of glucose control. Measurements and Results: The primary outcome was normalization of the mean 2-h OGTT; a secondary outcome was improvement in the Insulin Sensitivity Index (ISI (0,120). Subjects were 42% men, mean age of 54 (10), BMI of 39 (8), and AHI of 44 (27). Baseline fasting glucose was 104 (12), and mean 2-h OGTT was 110 (57) mg/dL. Seven subjects normalized their mean 2-h OGTT after CPAP but not after sham CPAP, while 5 subjects normalized after sham CPAP but not after CPAP. Overall, there was no improvement in ISI (0,120) between CPAP and sham CPAP (3.6%; 95% CI: [-2.2%, 9.7%]; P = 0.22). However, in those subjects with baseline AHI ≥ 30 (n = 25), there was a 13.3% (95% CI: [5.2%, 22.1%]; P CPAP compared to sham CPAP. Conclusions: This study did not show that IGT normalizes after CPAP in subjects with moderate sleep apnea and obesity. However, insulin sensitivity improved in those with AHI ≥ 30, suggesting beneficial metabolic effects of CPAP in severe sleep apnea. Clinical Trials Information: ClinicalTrials.gov Identifier: NCT01385995. Citation: Weinstock TG; Wang X; Rueschman M; Ismail-Beigi F; Aylor J; Babineau DC; Mehra R; Redline S. A controlled trial of CPAP therapy on metabolic control in individuals with impaired glucose tolerance and sleep apnea. SLEEP 2012;35(5):617-625. PMID:22547887

Effects of Sleep Deprivation on Hypoglycemia-Induced Cognitive Impairment and Recovery in Adults With Type 1 Diabetes.

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Inkster, Berit E; Zammitt, Nicola N; Ritchie, Stuart J; Deary, Ian J; Morrison, Ian; Frier, Brian M

2016-05-01

To ascertain whether hypoglycemia in association with sleep deprivation causes greater cognitive dysfunction than hypoglycemia alone and protracts cognitive recovery after normoglycemia is restored. Fourteen adults with type 1 diabetes underwent a hyperinsulinemic, hypoglycemic clamp on two separate occasions. Before one glucose clamp, the participants stayed awake overnight to induce sleep deprivation. Participants were randomized and counterbalanced to the experimental condition. Cognitive function tests were performed before and during hypoglycemia and for 90 min after restoration of normoglycemia. Cognitive impairment during hypoglycemia did not differ significantly between the sleep-deprived and non-sleep-deprived conditions. However, in the sleep-deprived state, digit symbol substitution scores and choice reaction times were significantly poorer during recovery (P sleep deprivation, such as tiredness, were removed. Hypoglycemia per se produced a significant decrement in cognitive function; coexisting sleep deprivation did not have an additive effect. However, after restoration of normoglycemia, preceding sleep deprivation was associated with persistence of hypoglycemic symptoms and greater and more prolonged cognitive dysfunction during the recovery period. © 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.

Reduced cortical complexity in children with Prader-Willi Syndrome and its association with cognitive impairment and developmental delay.

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Lukoshe, Akvile; Hokken-Koelega, Anita C; van der Lugt, Aad; White, Tonya

2014-01-01

Prader-Willi Syndrome (PWS) is a complex neurogenetic disorder with symptoms involving not only hypothalamic, but also a global, central nervous system dysfunction. Previously, qualitative studies reported polymicrogyria in adults with PWS. However, there have been no quantitative neuroimaging studies of cortical morphology in PWS and no studies to date in children with PWS. Thus, our aim was to investigate and quantify cortical complexity in children with PWS compared to healthy controls. In addition, we investigated differences between genetic subtypes of PWS and the relationship between cortical complexity and intelligence within the PWS group. High-resolution structural magnetic resonance images were acquired in 24 children with genetically confirmed PWS (12 carrying a deletion (DEL), 12 with maternal uniparental disomy (mUPD)) and 11 age- and sex-matched typically developing siblings as healthy controls. Local gyrification index (lGI) was obtained using the FreeSurfer software suite. Four large clusters, two in each hemisphere, comprising frontal, parietal and temporal lobes, had lower lGI in children with PWS, compared to healthy controls. Clusters with lower lGI also had significantly lower cortical surface area in children with PWS. No differences in cortical thickness of the clusters were found between the PWS and healthy controls. lGI correlated significantly with cortical surface area, but not with cortical thickness. Within the PWS group, lGI in both hemispheres correlated with Total IQ and Verbal IQ, but not with Performance IQ. Children with mUPD, compared to children with DEL, had two small clusters with lower lGI in the right hemisphere. lGI of these clusters correlated with cortical surface area, but not with cortical thickness or IQ. These results suggest that lower cortical complexity in children with PWS partially underlies cognitive impairment and developmental delay, probably due to alterations in gene networks that play a prominent role in

Disruption of Transient Serotonin Accumulation by Non-Serotonin-Producing Neurons Impairs Cortical Map Development

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Xiaoning Chen

2015-01-01

Full Text Available Polymorphisms that alter serotonin transporter SERT expression and functionality increase the risks for autism and psychiatric traits. Here, we investigate how SERT controls serotonin signaling in developing CNS in mice. SERT is transiently expressed in specific sets of glutamatergic neurons and uptakes extrasynaptic serotonin during perinatal CNS development. We show that SERT expression in glutamatergic thalamocortical axons (TCAs dictates sensory map architecture. Knockout of SERT in TCAs causes lasting alterations in TCA patterning, spatial organizations of cortical neurons, and dendritic arborization in sensory cortex. Pharmacological reduction of serotonin synthesis during the first postnatal week rescues sensory maps in SERTGluΔ mice. Furthermore, knockdown of SERT expression in serotonin-producing neurons does not impair barrel maps. We propose that spatiotemporal SERT expression in non-serotonin-producing neurons represents a determinant in early life genetic programming of cortical circuits. Perturbing this SERT function could be involved in the origin of sensory and cognitive deficits associated with neurodevelopmental disorders.

Correlation of Sleep Disturbance and Cognitive Impairment in Patients with Parkinson’s Disease

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Eun Ja Kim

2014-04-01

Full Text Available Objective Cognitive impairment is a common nonmotor symptom of Parkinson’s disease (PD and is associated with high mortality, caregiver distress, and nursing home placement. The risk factors for cognitive decline in PD patients include advanced age, longer disease duration, rapid eye movement sleep behavior disorder, hallucinations, excessive daytime sleepiness, and nontremor symptoms including bradykinesia, rigidity, postural instability, and gait disturbance. We conducted a cross-sectional study to determine which types of sleep disturbances are related to cognitive function in PD patients. Methods A total of 71 PD patients (29 males, mean age 66.46 ± 8.87 years were recruited. All patients underwent the Mini- Mental State Examination (MMSE and the Korean Version of the Montreal Cognitive Assessments (MoCA-K to assess global cognitive function. Sleep disorders were evaluated with the Stanford Sleepiness Scale, Epworth Sleepiness Scale, Insomnia Severity Index (ISI, Pittsburg Sleep Quality Index, and Parkinson’s Disease Sleep Scale in Korea (PDSS. Results The ISI was correlated with the MMSE, and total PDSS scores were correlated with the MMSE and the MoCA-K. In each item of the PDSS, nocturnal restlessness, vivid dreams, hallucinations, and nocturnal motor symptoms were positively correlated with the MMSE, and nocturnal restlessness and vivid dreams were significantly related to the MoCA-K. Vivid dreams and nocturnal restlessness are considered the most powerful correlation factors with global cognitive function, because they commonly had significant correlation to cognition assessed with both the MMSE and the MoCA-K. Conclusions We found a correlation between global cognitive function and sleep disturbances, including vivid dreams and nocturnal restlessness, in PD patients.

Alcohol Dependence and Its Relationship With Insomnia and Other Sleep Disorders.

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Chakravorty, Subhajit; Chaudhary, Ninad S; Brower, Kirk J

2016-11-01

Sleep-related complaints are widely prevalent in those with alcohol dependence (AD). AD is associated not only with insomnia, but also with multiple sleep-related disorders as a growing body of literature has demonstrated. This article will review the various aspects of insomnia associated with AD. In addition, the association of AD with other sleep-related disorders will be briefly reviewed. The association of AD with insomnia is bidirectional in nature. The etiopathogenesis of insomnia has demonstrated multiple associations and is an active focus of research. Treatment with cognitive behavioral therapy for insomnia is showing promise as an optimal intervention. In addition, AD may be associated with circadian abnormalities, short sleep duration, obstructive sleep apnea, and sleep-related movement disorder. The burgeoning knowledge on insomnia associated with moderate-to-severe alcohol use disorder has expanded our understanding of its underlying neurobiology, clinical features, and treatment options. Copyright © 2016 by the Research Society on Alcoholism.

Dreaming of a Learning Task Is Associated with Enhanced Sleep-Dependent Memory Consolidation

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Wamsley, Erin J.; Tucker, Matthew; Payne, Jessica D.; Benavides, Joseph A.; Stickgold, Robert

2010-01-01

It is now well established that post-learning sleep is beneficial for human memory performance [1–5]. Meanwhile, human and animal studies demonstrate that learning-related neural activity is re-expressed during post-training non-rapid eye movement sleep (NREM) [6–9]. NREM sleep processes appear to be particularly beneficial for hippocampus-dependent forms of memory [1–3, 10]. These observations suggest that learning triggers the reactivation and reorganization of memory traces during sleep, a...

Transcranial electrical currents to probe EEG brain rhythms and memory consolidation during sleep in humans.

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Lisa Marshall

Full Text Available Previously the application of a weak electric anodal current oscillating with a frequency of the sleep slow oscillation (∼0.75 Hz during non-rapid eye movement sleep (NonREM sleep boosted endogenous slow oscillation activity and enhanced sleep-associated memory consolidation. The slow oscillations occurring during NonREM sleep and theta oscillations present during REM sleep have been considered of critical relevance for memory formation. Here transcranial direct current stimulation (tDCS oscillating at 5 Hz, i.e., within the theta frequency range (theta-tDCS is applied during NonREM and REM sleep. Theta-tDCS during NonREM sleep produced a global decrease in slow oscillatory activity conjoint with a local reduction of frontal slow EEG spindle power (8-12 Hz and a decrement in consolidation of declarative memory, underlining the relevance of these cortical oscillations for sleep-dependent memory consolidation. In contrast, during REM sleep theta-tDCS appears to increase global gamma (25-45 Hz activity, indicating a clear brain state-dependency of theta-tDCS. More generally, results demonstrate the suitability of oscillating-tDCS as a tool to analyze functions of endogenous EEG rhythms and underlying endogenous electric fields as well as the interactions between EEG rhythms of different frequencies.

Sex-dependent effects of sleep deprivation on myocardial sensitivity to ischemic injury.

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Zoladz, Phillip R; Krivenko, Anna; Eisenmann, Eric D; Bui, Albert D; Seeley, Sarah L; Fry, Megan E; Johnson, Brandon L; Rorabaugh, Boyd R

2016-01-01

Sleep deprivation is associated with increased risk of myocardial infarction. However, it is unknown whether the effects of sleep deprivation are limited to increasing the likelihood of experiencing a myocardial infarction or if sleep deprivation also increases the extent of myocardial injury. In this study, rats were deprived of paradoxical sleep for 96 h using the platform-over-water method. Control rats were subjected to the same condition except the control platform was large enough for the rats to sleep. Hearts from sleep deprived and control rats were subjected to 20 min ischemia on a Langendorff isolated heart system. Infarct size and post ischemic recovery of contractile function were unaffected by sleep deprivation in male hearts. In contrast, hearts from sleep-deprived females exhibited significantly larger infarcts than hearts from control females. Post ischemic recovery of rate pressure product and + dP/dT were significantly attenuated by sleep deprivation in female hearts, and post ischemic recovery of end diastolic pressure was significantly elevated in hearts from sleep deprived females compared to control females, indicating that post ischemic recovery of both systolic and diastolic function were worsened by sleep deprivation. These data provide evidence that sleep deprivation increases the extent of ischemia-induced injury in a sex-dependent manner.

Multidrug Resistance-Related Protein 1 (MRP1) Function and Localization Depend on Cortical Actin

NARCIS (Netherlands)

Hummel, Ina; Klappe, Karin; Ercan, Cigdem; Kok, Jan Willem

MRP1 (ABCC1) is known to be localized in lipid rafts. Here we show in two different cell lines that localization of Mrp1/MRP1 (Abcc1/ABCC1) in lipid rafts and its function as an efflux pump are dependent on cortical actin. Latrunculin B disrupts both cortical actin and actin stress fibers. This

Increased frontal sleep slow wave activity in adolescents with major depression

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Noemi Tesler

2016-01-01

Full Text Available Sleep slow wave activity (SWA, the major electrophysiological characteristic of deep sleep, mirrors both cortical restructuring and functioning. The incidence of Major Depressive Disorder (MDD substantially rises during the vulnerable developmental phase of adolescence, where essential cortical restructuring is taking place. The goal of this study was to assess characteristics of SWA topography in adolescents with MDD, in order to assess abnormalities in both cortical restructuring and functioning on a local level. All night high-density EEG was recorded in 15 patients meeting DSM-5 criteria for MDD and 15 sex- and age-matched healthy controls. The actual symptom severity was assessed using the Children's Depression Rating Scale—Revised (CDRS-R. Topographical power maps were calculated based on the average SWA of the first non-rapid eye movement (NREM sleep episode. Depressed adolescents exhibited significantly more SWA in a cluster of frontal electrodes compared to controls. SWA over frontal brain regions correlated positively with the CDRS-R subscore “morbid thoughts”. Self-reported sleep latency was significantly higher in depressed adolescents compared to controls whereas sleep architecture did not differ between the groups. Higher frontal SWA in depressed adolescents may represent a promising biomarker tracing cortical regions of intense use and/or restructuring.

(Mis)perception of sleep in insomnia: a puzzle and a resolution.

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Harvey, Allison G; Tang, Nicole K Y

2012-01-01

Insomnia is prevalent, causing severe distress and impairment. This review focuses on illuminating the puzzling finding that many insomnia patients misperceive their sleep. They overestimate their sleep onset latency (SOL) and underestimate their total sleep time (TST), relative to objective measures. This tendency is ubiquitous (although not universal). Resolving this puzzle has clinical, theoretical, and public health importance. There are implications for assessment, definition, and treatment. Moreover, solving the puzzle creates an opportunity for real-world applications of theories from clinical, perceptual, and social psychology as well as neuroscience. Herein we evaluate 13 possible resolutions to the puzzle. Specifically, we consider the possible contribution, to misperception, of (1) features inherent to the context of sleep (e.g., darkness); (2) the definition of sleep onset, which may lack sensitivity for insomnia patients; (3) insomnia being an exaggerated sleep complaint; (4) psychological distress causing magnification; (5) a deficit in time estimation ability; (6) sleep being misperceived as wake; (7) worry and selective attention toward sleep-related threats; (8) a memory bias influenced by current symptoms and emotions, a confirmation bias/belief bias, or a recall bias linked to the intensity/recency of symptoms; (9) heightened physiological arousal; (10) elevated cortical arousal; (11) the presence of brief awakenings; (12) a fault in neuronal circuitry; and (13) there being 2 insomnia subtypes (one with and one without misperception). The best supported resolutions were misperception of sleep as wake, worry, and brief awakenings. A deficit in time estimation ability was not supported. We conclude by proposing several integrative solutions.

Enhancement of sleep slow waves: underlying mechanisms and practical consequences.

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Michele eBellesi

2014-10-01

Full Text Available Even modest sleep restriction, especially the loss of sleep slow wave activity, is invariably associated with slower EEG activity during wake, the occurrence of local sleep in an otherwise awake brain, and impaired performance due to cognitive and memory deficits. Recent studies not only confirm the beneficial role of sleep in memory consolidation, but also point to a specific role for sleep slow waves. Thus, the implementation of methods to enhance sleep slow waves without unwanted arousals or lightening of sleep could have significant practical implications. Here we first review the evidence that it is possible to enhance sleep slow waves in humans using transcranial direct-current stimulation and transcranial magnetic stimulation. Since these methods are currently impractical and their safety is questionable, especially for chronic long-term exposure, we then discuss novel data suggesting that it is possible to enhance slow waves using sensory stimuli. We consider the physiology of the K-complex, a peripheral evoked slow wave, and show that, among different sensory modalities, acoustic stimulation is the most effective in increasing the magnitude of slow waves, likely through the activation of non-lemniscal ascending pathways to the thalamo-cortical system. In addition, we discuss how intensity and frequency of the acoustic stimuli, as well as exact timing and pattern of stimulation, affect sleep enhancement. Finally, we discuss automated algorithms that read the EEG and, in real-time, adjust the stimulation parameters in a closed-loop manner to obtain an increase in sleep slow waves and avoid undesirable arousals. In conclusion, while discussing the mechanisms that underlie the generation of sleep slow waves, we review the converging evidence showing that acoustic stimulation is safe and represents an ideal tool for slow wave sleep enhancement.

Impaired driving simulation in patients with Periodic Limb Movement Disorder and patients with Obstructive Sleep Apnea Syndrome

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Gieteling, Esther W.; Bakker, Marije S.; Hoekema, Aarnoud; Maurits, Natasha M.; Brouwer, Wiebo H.; van der Hoeven, Johannes H.

Background: Excessive daytime sleepiness (EDS) is considered to be responsible for increased collision rate and impaired driving simulator performance in Obstructive Sleep Apnea Syndrome (OSAS) patients. Periodic Limb Movement Disorder (PLMD) patients also frequently report EDS and may also have

Distinct molecular components for thalamic- and cortical-dependent plasticity in the lateral amygdala

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Osvaldo eMirante

2014-07-01

Full Text Available N-methyl-D-aspartate receptor (NMDAR-dependent long-term depression (LTD in the lateral nucleus of the amygdala (LA is a form of synaptic plasticity thought to be a cellular substrate for the extinction of fear memory. The LA receives converging inputs from the sensory thalamus and neocortex that are weakened following fear extinction. Combining field and patch-clamp electrophysiological recordings in mice, we show that a paired-pulse low-frequency stimulation can induce a robust LTD at thalamic and cortical inputs to LA, and we identify different underlying molecular components at these pathways. We show that while LTD depends on NMDARs and activation of the protein phosphatases PP2B and PP1 at both pathways, it requires NR2B-containing NMDARs at the thalamic pathway, but NR2C/D-containing NMDARs at the cortical pathway. LTD appears to be induced postsynaptically at the thalamic input but presynaptically at the cortical input, since postsynaptic calcium chelation and NMDAR blockade prevent thalamic but not cortical LTD. These results highlight distinct molecular features of LTD in LA that may be relevant for traumatic memory and its erasure, and for pathologies such as post-traumatic stress disorder (PTSD.

Sleep deprivation impairs recall of social transmission of food preference in rats

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Wooden JI

2014-11-01

Full Text Available Jessica I Wooden,1,2 Jennifer Pido,1 Hunter Mathews,1 Ryan Kieltyka,1 Bertha Montemayor,1 Christopher P Ward1,3 1Department of Psychology, University of Houston-Clear Lake, 2Department of Psychology, University of Houston, 3Menninger Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, Houston, TX, USAAbstract: Evidence indicates that sleep plays an important role in learning and memory, and disruption of sleep especially seems to interfere with hippocampal memory processes. Social transmission of food preference (STFP, a natural test of paired associative learning, has been shown to be dependent on the hippocampus. While social transmission of food preference is not a novel task, it has not been used to examine the role of sleep in memory consolidation. Male Sprague-Dawley rats were randomly divided into three groups: cage control; sleep-deprived; and device control. Demonstrator rats were given powdered food mixed with a target spice. Test rats then interacted with demonstrator rats before being given a two choice test of powered food with the target spice or a novel spice. Sleep-deprived rats were then placed in an automated device that prevented sleep for 24 hours. After sleep deprivation, animals were given a preference test again to determine memory for the target spice at both 24 hours and 72 hours. Polysomnography was used to validate the method of sleep deprivation. During immediate preference testing, rats demonstrated a clear preference for the food containing the target spice. Rats that experienced 24 hours of sleep deprivation following the initial testing indicated a significant reduction in the recall of the target spice at 24 and 72 hours. The cage control and device animals maintained their preference for food containing the target spice. Therefore, the loss of sleep interfered with memory consolidation for food preference learned via social transmission.Keywords: hippocampus, learning, consolidation

Prediction of Alzheimer’s disease in mild cognitive impairment using sulcal morphology and cortical thickness

DEFF Research Database (Denmark)

Plocharski, Maciej; Østergaard, Lasse Riis

2019-01-01

converters, or MCIc). The purpose of this study was to predict future AD-conversion in patients with MCI using machine learning with sulcal morphology and cortical thickness measures as classification features. 32 sulci per subject were extracted from 1.5T T1-weighted ADNI database MRI scans of 90 MCIc......Mild cognitive impairment (MCI) is an intermediate condition between healthy ageing and dementia. The amnestic MCI is often a high risk factor for subsequent Alzheimer’s disease (AD) conversion. Some MCI patients never develop AD (MCI non-converters, or MCInc), but some do progress to AD (MCI...... subjects as future converters, (89.7% sensitivity, 84.4% specificity, 0.94 AUC), using 10-fold cross-validation. These results using sulcal and cortical features are superior to the state-of-the-art methods. The most discriminating predictive features were observed in the temporal and frontal lobes...

Short-term immobilization influences use-dependent cortical plasticity and fine motor performance.

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Opie, George M; Evans, Alexandra; Ridding, Michael C; Semmler, John G

2016-08-25

Short-term immobilization that reduces muscle use for 8-10h is known to influence cortical excitability and motor performance. However, the mechanisms through which this is achieved, and whether these changes can be used to modify cortical plasticity and motor skill learning, are not known. The purpose of this study was to investigate the influence of short-term immobilization on use-dependent cortical plasticity, motor learning and retention. Twenty-one adults were divided into control and immobilized groups, both of which underwent two experimental sessions on consecutive days. Within each session, transcranial magnetic stimulation (TMS) was used to assess motor-evoked potential (MEP) amplitudes, short- (SICI) and long-interval intracortical inhibition (LICI), and intracortical facilitation (ICF) before and after a grooved pegboard task. Prior to the second training session, the immobilized group underwent 8h of left hand immobilization targeting the index finger, while control subjects were allowed normal limb use. Immobilization produced a reduction in MEP amplitudes, but no change in SICI, LICI or ICF. While motor performance improved for both groups in each session, the level of performance was greater 24-h later in control, but not immobilized subjects. Furthermore, training-related MEP facilitation was greater after, compared with before, immobilization. These results indicate that immobilization can modulate use-dependent plasticity and the retention of motor skills. They also suggest that changes in intracortical excitability are unlikely to contribute to the immobilization-induced modification of cortical excitability. Copyright © 2016. Published by Elsevier Ltd.

Anosognosia in mild cognitive impairment: Relationship to activation of cortical midline structures involved in self-appraisal

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Ries, Michele L.; Jabbar, Britta M.; Schmitz, Taylor W.; Trivedi, Mehul A.; Gleason, Carey E.; Carlsson, Cynthia M.; Rowley, Howard A.; Asthana, Sanjay; Johnson, Sterling C.

2009-01-01

Awareness of cognitive dysfunction shown by individuals with Mild Cognitive Impairment (MCI), a condition conferring risk for Alzheimer’s disease (AD), is variable. Anosognosia, or unawareness of loss of function, is beginning to be recognized as an important clinical symptom of MCI. However, little is known about the brain substrates underlying this symptom. We hypothesized that MCI participants’ activation of cortical midline structures (CMS) during self-appraisal would covary with level of insight into cognitive difficulties (indexed by a discrepancy score between patient and informant ratings of cognitive decline in each MCI participant). To address this hypothesis, we first compared 16 MCI participants and 16 age-matched controls, examining brain regions showing conjoint or differential BOLD response during self-appraisal. Second, we used regression to investigate the relationship between awareness of deficit in MCI and BOLD activity during self-appraisal, controlling for extent of memory impairment. Between-group comparisons indicated that MCI participants show subtly attenuated CMS activity during self-appraisal. Regression analysis revealed a highly-significant relationship between BOLD response during self-appraisal and self-awareness of deficit in MCI. This finding highlights the level of anosognosia in MCI as an important predictor of response to self-appraisal in cortical midline structures, brain regions vulnerable to changes in early AD. PMID:17445294

Modulation of Sleep Homeostasis by Corticotropin Releasing Hormone in REM Sleep-Deprived Rats

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Ricardo Borges Machado

2010-01-01

Full Text Available Studies have shown that sleep recovery following different protocols of forced waking varies according to the level of stress inherent to each method. Sleep deprivation activates the hypothalamic-pituitary-adrenal axis and increased corticotropin-releasing hormone (CRH impairs sleep. The purpose of the present study was to evaluate how manipulations of the CRH system during the sleep deprivation period interferes with subsequent sleep rebound. Throughout 96 hours of sleep deprivation, separate groups of rats were treated i.c.v. with vehicle, CRH or with alphahelical CRH9−41, a CRH receptor blocker, twice/day, at 07:00 h and 19:00 h. Both treatments impaired sleep homeostasis, especially in regards to length of rapid eye movement sleep (REM and theta/delta ratio and induced a later decrease in NREM and REM sleep and increased waking bouts. These changes suggest that activation of the CRH system impact negatively on the homeostatic sleep response to prolonged forced waking. These results indicate that indeed, activation of the HPA axis—at least at the hypothalamic level—is capable to reduce the sleep rebound induced by sleep deprivation.

Role of hippocampal and prefrontal cortical signaling pathways in dextromethorphan effect on morphine-induced memory impairment in rats.

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Ghasemzadeh, Zahra; Rezayof, Ameneh

2016-02-01

Evidence suggests that dextromethorphan (DM), an NMDA receptor antagonist, induces memory impairment. Considering that DM is widely used in cough-treating medications, and the co-abuse of DM with morphine has recently been reported, the aims of the present study was (1) to investigate whether there is a functional interaction between morphine and DM in passive avoidance learning and (2) to assess the possible role of the hippocampal and prefrontal cortical (PFC) signaling pathways in the effects of the drugs on memory formation. Our findings indicated that post-training or pre-test administration of morphine (2 and 6 mg/kg) or DM (10-30 mg/kg) impaired memory consolidation and retrieval which was associated with the attenuation of the levels of phosphorylated Ca(2+)/calmodulin-dependent protein kinase II (p-CAMKII) and cAMP responsive element-binding protein (p-CREB) in the targeted sites. Moreover, the memory impairment induced by post-training administration of morphine was reversed by pre-test administration of the same dose of morphine or DM (30 mg/kg), indicating state-dependent learning (SDL) and a cross-SDL between the drugs. It is important to note that the levels of p-CAMKII/CAMKII and p-CREB/CREB in the hippocampus and the PFC increased in drugs-induced SDL. In addition, DM administration potentiated morphine-induced SDL which was related to the enhanced levels of hippocampal and PFC CAMKII-CREB signaling pathways. It can be concluded that there is a relationship between the hippocampus and the PFC in the effect of DM and/or morphine on memory retrieval. Moreover, a cross SDL can be induced between the co-administration of DM and morphine. Interestingly, CAMKII-CREB signaling pathways also mediate the drugs-induced SDL. Copyright © 2015 Elsevier Inc. All rights reserved.

Electroencephalographic findings related with mild cognitive impairment in idiopathic rapid eye movement sleep behavior disorder.

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Sasai, Taeko; Matsuura, Masato; Inoue, Yuichi

2013-12-01

Mild cognitive impairment (MCI) and electroencephalographic (EEG) slowing have been reported as common findings of idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) and α-synucleinopathies. The objective of this study is to clarify the relation between MCI and physiological markers in iRBD. Cross-sectional study. Yoyogi Sleep Disorder Center. Thirty-one patients with iRBD including 17 younger patients with iRBD (younger than 70 y) and 17 control patients for the younger patients with iRBD. N/A. Montreal Cognitive Assessment (MoCA) and n-polysomnogram (PSG) were conducted of all participants. In patients with iRBD, the factors associated with MCI were explored among parameters of REM sleep without atonia (RWA), score of Sniffin' Sticks Test (threshold-discrimination-identification [TDI] score), RBD morbidity, and RBD severity evaluated with the Japanese version of the RBD questionnaire (RBDQ-JP). The younger iRBD group showed significantly lower alpha power during wake and lower MoCA score than the age-matched control group. MCI was detected in 13 of 17 patients (76.5%) on MoCA in this group. Among patients wtih iRBD, the MoCA score negatively correlated with age, proportion of slow wave sleep, TDI score, and EEG spectral power. Multiple regression analysis provided the following equation: MoCA score = 50.871-0.116*age -5.307*log (δ power during REM sleep) + 0.086*TDI score (R² = 0.598, P sleep), and 0.357 for TDI score (F = 9.900, P sleep and olfactory dysfunction, was revealed to be associated with cognitive decline in idiopathic rapid eye movement sleep behavior disorder.

The 5-HT6 receptor antagonist idalopirdine potentiates the effects of donepezil on gamma oscillations in the frontal cortex of anesthetized and awake rats without affecting sleep-wake architecture.

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Amat-Foraster, Maria; Leiser, Steven C; Herrik, Kjartan F; Richard, Nelly; Agerskov, Claus; Bundgaard, Christoffer; Bastlund, Jesper F; de Jong, Inge E M

2017-02-01

The 5-HT 6 receptor is a promising target for cognitive disorders, in particular for Alzheimer's disease (AD). The high affinity and selective 5-HT 6 receptor antagonist idalopirdine (Lu AE58054) is currently in development for mild-moderate AD as adjunct therapy to acetylcholinesterase inhibitors (AChEIs). We studied the effects of idalopirdine alone and in combination with the AChEI donepezil on cortical function using two in vivo electrophysiological methods. Neuronal network oscillations in the frontal cortex were measured during electrical stimulation of the brainstem nucleus pontis oralis (nPO) in the anesthetized rat and by an electroencephalogram (EEG) in the awake, freely moving rat. In conjunction with the EEG study, we investigated the effects of idalopirdine and donepezil on sleep-wake architecture using telemetric polysomnography. Idalopirdine (2 mg/kg i.v.) increased gamma power in the medial prefrontal cortex (mPFC) during nPO stimulation. Donepezil (0.3 and 1 mg/kg i.v.) also increased cortical gamma power and pretreatment with idalopirdine (2 mg/kg i.v.) potentiated and prolonged the effects of donepezil. Similarly, donepezil (1 and 3 mg/kg s.c.) dose-dependently increased frontal cortical gamma power in the freely moving rat and pretreatment with idalopirdine (10 mg/kg p.o.) augmented the effect of donepezil 1 mg/kg. Analysis of the sleep-wake architecture showed that donepezil (1 and 3 mg/kg s.c.) dose-dependently delayed sleep onset and decreased the time spent in both REM and non REM sleep stages. In contrast, idalopirdine (10 mg/kg p.o.) did not affect sleep-wake architecture nor the effects of donepezil. In summary, we show that idalopirdine potentiates the effects of donepezil on frontal cortical gamma oscillations, a pharmacodynamic biomarker associated with cognition, without modifying the effects of donepezil on sleep. The increased cortical excitability may contribute to the procognitive effects of idalopirdine in donepezil

Increased EEG sigma and beta power during NREM sleep in primary insomnia.

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Spiegelhalder, Kai; Regen, Wolfram; Feige, Bernd; Holz, Johannes; Piosczyk, Hannah; Baglioni, Chiara; Riemann, Dieter; Nissen, Christoph

2012-12-01

The hyperarousal model of primary insomnia suggests that a deficit of attenuating arousal during sleep might cause the experience of non-restorative sleep. In the current study, we examined EEG spectral power values for standard frequency bands as indices of cortical arousal and sleep protecting mechanisms during sleep in 25 patients with primary insomnia and 29 good sleeper controls. Patients with primary insomnia demonstrated significantly elevated spectral power values in the EEG beta and sigma frequency band during NREM stage 2 sleep. No differences were observed in other frequency bands or during REM sleep. Based on prior studies suggesting that EEG beta activity represents a marker of cortical arousal and EEG sleep spindle (sigma) activity is an index of sleep protective mechanisms, our findings may provide further evidence for the concept that a simultaneous activation of wake-promoting and sleep-protecting neural activity patterns contributes to the experience of non-restorative sleep in primary insomnia. Copyright © 2012 Elsevier B.V. All rights reserved.

Adaptation of sensorimotor coupling in postural control is impaired by sleep deprivation.

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Stefane A Aguiar

Full Text Available The purpose of the study was to investigate the effects of sleep deprivation (SD in adaptation of the coupling between visual information and body sway in young adults' postural control due to changes in optic flow characteristics. Fifteen young adults were kept awake for approximately 25 hours and formed the SD group, while fifteen adults who slept normally the night before the experiment participated as part of the control group. All participants stood as still as possible in a moving room before and after being exposed to one trial with higher amplitude and velocity of room movement. Postural performance and the coupling between visual information, provided by a moving room, and body sway were examined. Results showed that after an abrupt change in visual cues, larger amplitude, and higher velocity of the room, the influence of room motion on body sway was decreased in both groups. However, such a decrease was less pronounced in sleep deprived as compared to control subjects. Sleep deprived adults were able to adapt motor responses to the environmental change provided by the increase in room motion amplitude. Nevertheless, they were not as efficient as control subjects in doing so, which demonstrates that SD impairs the ability to adapt sensorimotor coupling while controlling posture when a perturbation occurs.

Formation and suppression of acoustic memories during human sleep.

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Andrillon, Thomas; Pressnitzer, Daniel; Léger, Damien; Kouider, Sid

2017-08-08

Sleep and memory are deeply related, but the nature of the neuroplastic processes induced by sleep remains unclear. Here, we report that memory traces can be both formed or suppressed during sleep, depending on sleep phase. We played samples of acoustic noise to sleeping human listeners. Repeated exposure to a novel noise during Rapid Eye Movements (REM) or light non-REM (NREM) sleep leads to improvements in behavioral performance upon awakening. Strikingly, the same exposure during deep NREM sleep leads to impaired performance upon awakening. Electroencephalographic markers of learning extracted during sleep confirm a dissociation between sleep facilitating memory formation (light NREM and REM sleep) and sleep suppressing learning (deep NREM sleep). We can trace these neural changes back to transient sleep events, such as spindles for memory facilitation and slow waves for suppression. Thus, highly selective memory processes are active during human sleep, with intertwined episodes of facilitative and suppressive plasticity.Though memory and sleep are related, it is still unclear whether new memories can be formed during sleep. Here, authors show that people could learn new sounds during REM or light non-REM sleep, but that learning was suppressed when sounds were played during deep NREM sleep.

REM sleep respiratory behaviours mental content in narcoleptic lucid dreamers.

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Oudiette, Delphine; Dodet, Pauline; Ledard, Nahema; Artru, Emilie; Rachidi, Inès; Similowski, Thomas; Arnulf, Isabelle

2018-02-08

Breathing is irregular during rapid eye-movement (REM) sleep, whereas it is stable during non-REM sleep. Why this is so remains a mystery. We propose that irregular breathing has a cortical origin and reflects the mental content of dreams, which often accompany REM sleep. We tested 21 patients with narcolepsy who had the exceptional ability to lucid dream in REM sleep, a condition in which one is conscious of dreaming during the dream and can signal lucidity with an ocular code. Sleep and respiration were monitored during multiple naps. Participants were instructed to modify their dream scenario so that it involved vocalizations or an apnoea, -two behaviours that require a cortical control of ventilation when executed during wakefulness. Most participants (86%) were able to signal lucidity in at least one nap. In 50% of the lucid naps, we found a clear congruence between the dream report (e.g., diving under water) and the observed respiratory behaviour (e.g., central apnoea) and, in several cases, a preparatory breath before the respiratory behaviour. This suggests that the cortico-subcortical networks involved in voluntary respiratory movements are preserved during REM sleep and that breathing irregularities during this stage have a cortical/subcortical origin that reflects dream content.

Transcranial magnetic stimulation and sleep disorders: pathophysiologic insights.

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Nardone, Raffaele; Höller, Yvonne; Brigo, Francesco; Tezzon, Frediano; Golaszewski, Stefan; Trinka, Eugen

2013-11-01

The neural mechanisms underlying the development of the most common intrinsic sleep disorders are not completely known. Therefore, there is a great need for noninvasive tools which can be used to better understand the pathophysiology of these diseases. Transcranial magnetic stimulation (TMS) offers a method to noninvasively investigate the functional integrity of the motor cortex and its corticospinal projections in neurologic and psychiatric diseases. To date, TMS studies have revealed cortical and corticospinal dysfunction in several sleep disorders, with cortical hyperexcitability being a characteristic feature in some disorders (i.e., the restless legs syndrome) and cortical hypoexcitability being a well-established finding in others (i.e., obstructive sleep apnea syndrome narcolepsy). Several research groups also have applied TMS to evaluate the effects of pharmacologic agents, such as dopaminergic agent or wake-promoting substances. Our review will focus on the mechanisms underlying the generation of abnormal TMS measures in the different types of sleep disorders, the contribution of TMS in enhancing the understanding of their pathophysiology, and the potential diagnostic utility of TMS techniques. We also briefly discussed the possible future implications for improving therapeutic approaches. Copyright © 2013 Elsevier B.V. All rights reserved.

cGMP-dependent protein kinase I, the circadian clock, sleep and learning

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Feil, Robert; Hölter, Sabine M; Weindl, Karin; Wurst, Wolfgang; Langmesser, Sonja; Gerling, Andrea; Feil, Susanne; Albrecht, Urs

2009-01-01

The second messenger cGMP controls cardiovascular and gastrointestinal homeostasis in mammals. However, its physiological relevance in the nervous system is poorly understood.1 Now, we have reported that the cGMP-dependent protein kinase type I (PRKG1) is implicated in the regulation of the timing and quality of sleep and wakefulness.2 Prkg1 mutant mice showed altered distribution of sleep and wakefulness as well as reduction in rapid-eye-movement sleep (REMS) duration and in non-REMS consoli...

Adenosine and sleep

International Nuclear Information System (INIS)

Yanik, G.M. Jr.

1987-01-01

Behavioral and biochemical approaches have been used to determine the relative contribution of endogenous adenosine and adenosine receptors to the sleep-wake cycle in the rat. Adenosine concentrations in specific areas of the rat brain were not affected by 24 hours of total sleep deprivation, or by 24 or 48 hours of REM sleep deprivation. In order to assess the effect of REM sleep deprivation on adenosine A 1 receptors, 3 H-L-PIA binding was measured. The Bmax values for 3 H-L-PIA binding to membrane preparations of the cortices and corpus striata from 48 hour REM sleep-deprived animals were increased 14.8% and 23%, respectively. These increases were not maintained following the cessation of sleep deprivation and recovered within 2 hours. The results of a 96 hour REM deprivation experiment were similar to those of the 48 hour REM sleep deprivation experiment. However, these increases were not evident in similar structures taken from stress control animals, and conclusively demonstrated that the changes in 3 H-L-PIA binding resulted from REM sleep deprivation and not from stress

Reduced cortical complexity in children with Prader-Willi Syndrome and its association with cognitive impairment and developmental delay.

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Akvile Lukoshe

Full Text Available BACKGROUND: Prader-Willi Syndrome (PWS is a complex neurogenetic disorder with symptoms involving not only hypothalamic, but also a global, central nervous system dysfunction. Previously, qualitative studies reported polymicrogyria in adults with PWS. However, there have been no quantitative neuroimaging studies of cortical morphology in PWS and no studies to date in children with PWS. Thus, our aim was to investigate and quantify cortical complexity in children with PWS compared to healthy controls. In addition, we investigated differences between genetic subtypes of PWS and the relationship between cortical complexity and intelligence within the PWS group. METHODS: High-resolution structural magnetic resonance images were acquired in 24 children with genetically confirmed PWS (12 carrying a deletion (DEL, 12 with maternal uniparental disomy (mUPD and 11 age- and sex-matched typically developing siblings as healthy controls. Local gyrification index (lGI was obtained using the FreeSurfer software suite. RESULTS: Four large clusters, two in each hemisphere, comprising frontal, parietal and temporal lobes, had lower lGI in children with PWS, compared to healthy controls. Clusters with lower lGI also had significantly lower cortical surface area in children with PWS. No differences in cortical thickness of the clusters were found between the PWS and healthy controls. lGI correlated significantly with cortical surface area, but not with cortical thickness. Within the PWS group, lGI in both hemispheres correlated with Total IQ and Verbal IQ, but not with Performance IQ. Children with mUPD, compared to children with DEL, had two small clusters with lower lGI in the right hemisphere. lGI of these clusters correlated with cortical surface area, but not with cortical thickness or IQ. CONCLUSIONS: These results suggest that lower cortical complexity in children with PWS partially underlies cognitive impairment and developmental delay, probably due to

Relating Cortical Wave Dynamics to Learning and Remembering

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Eduardo Mercado III

2014-12-01

Full Text Available Electrical waves propagate across sensory and motor cortices in stereotypical patterns. These waves have been described as potentially facilitating sensory processing when they travel through sensory cortex, as guiding movement preparation and performance when they travel across motor cortex, and as possibly promoting synaptic plasticity and the consolidation of memory traces, especially during sleep. Here, an alternative theoretical framework is suggested that integrates Pavlovian hypotheses about learning and cortical function with concepts from contemporary proceduralist theories of memory. The proposed framework postulates that sensory-evoked cortical waves are gradually modified across repeated experiences such that the waves more effectively differentiate sensory events, and so that the waves are more likely to reverberate. It is argued that the qualities of cortical waves—their origins, form, intensity, speed, periodicity, extent, and trajectories —are a function of both the structural organization of neural circuits and ongoing reverberations resulting from previously experienced events. It is hypothesized that experience-dependent cortical plasticity, both in the short- and long-term, modulates the qualities of cortical waves, thereby enabling individuals to make progressively more precise distinctions between complex sensory events, and to reconstruct components of previously experienced events. Unlike most current neurobiological theories of learning and memory mechanisms, this hypothesis does not assume that synaptic plasticity, or any other form of neural plasticity, serves to store physical records of previously experienced events for later reactivation. Rather, the reorganization of cortical circuits may alter the potential for certain wave patterns to arise and persist. Understanding what factors determine the spatiotemporal dynamics of cortical waves, how structural changes affect their qualities, and how wave dynamics

Sleeping dendrites: fiber-optic measurements of dendritic calcium activity in freely moving and sleeping animals

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Julie Seibt

2014-03-01

Full Text Available Dendrites are the post-synaptic sites of most excitatory and inhibitory synapses in the brain, making them the main location of cortical information processing and synaptic plasticity. Although current hypotheses suggest a central role for sleep in proper cognitive function and brain plasticity, virtually nothing is known about changes in dendritic activity across the sleep-wake cycle and how waking experience modifies this activity. To start addressing these questions, we developed a method that allows long-term recordings of EEGs/EMG combined with in vivo cortical calcium (Ca2+ activity in freely moving and sleeping rats. We measured Ca2+ activity from populations of dendrites of layer (L 5 pyramidal neurons (n = 13 rats that we compared with Ca2+ activity from populations of neurons in L2/3 (n = 11 rats. L5 and L2/3 neurons were labelled using bolus injection of OGB1-AM or GCaMP6 (1. Ca2+ signals were detected using a fiber-optic system (cannula diameter = 400µm, transmitting the changes in fluorescence to a photodiode. Ca2+ fluctuations could then be correlated with ongoing changes in brain oscillatory activity during 5 major brain states: active wake [AW], quiet wake [QW], NREM, REM and NREM-REM transition (or intermediate state, [IS]. Our Ca2+ recordings show large transients in L5 dendrites and L2/3 neurons that oscillate predominantly at frequencies In summary, we show that this technique is successful in monitoring fluctuations in ongoing dendritic Ca2+ activity during natural brain states and allows, in principle, to combine behavioral measurement with imaging from various brain regions (e.g. deep structures in freely behaving animals. Using this method, we show that Ca2+ transients from populations of L2/3 neurons and L5 dendrites are deferentially regulated across the sleep/wake cycle, with dendritic activity being the highest during the IS sleep. Our correlation analysis suggests that specific sleep EEG activity during NREM and IS

Cortical drive to breathe in amyotrophic lateral sclerosis: a dyspnoea-worsening defence?

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Georges, Marjolaine; Morawiec, Elise; Raux, Mathieu; Gonzalez-Bermejo, Jésus; Pradat, Pierre-François; Similowski, Thomas; Morélot-Panzini, Capucine

2016-06-01

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease causing diaphragm weakness that can be partially compensated by inspiratory neck muscle recruitment. This disappears during sleep, which is compatible with a cortical contribution to the drive to breathe. We hypothesised that ALS patients with respiratory failure exhibit respiratory-related cortical activity, relieved by noninvasive ventilation (NIV) and related to dyspnoea.We studied 14 ALS patients with respiratory failure. Electroencephalographic recordings (EEGs) and electromyographic recordings of inspiratory neck muscles were performed during spontaneous breathing and NIV. Dyspnoea was evaluated using the Multidimensional Dyspnea Profile.Eight patients exhibited slow EEG negativities preceding inspiration (pre-inspiratory potentials) during spontaneous breathing. Pre-inspiratory potentials were attenuated during NIV (p=0.04). Patients without pre-inspiratory potentials presented more advanced forms of ALS and more severe respiratory impairment, but less severe dyspnoea. Patients with pre-inspiratory potentials had stronger inspiratory neck muscle activation and more severe dyspnoea during spontaneous breathing.ALS-related diaphragm weakness can engage cortical resources to augment the neural drive to breathe. This might reflect a compensatory mechanism, with the intensity of dyspnoea a negative consequence. Disease progression and the corresponding neural loss could abolish this phenomenon. A putative cognitive cost should be investigated. Copyright ©ERS 2016.

Learning-enhanced coupling between ripple oscillations in association cortices and hippocampus.

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Khodagholy, Dion; Gelinas, Jennifer N; Buzsáki, György

2017-10-20

Consolidation of declarative memories requires hippocampal-neocortical communication. Although experimental evidence supports the role of sharp-wave ripples in transferring hippocampal information to the neocortex, the exact cortical destinations and the physiological mechanisms of such transfer are not known. We used a conducting polymer-based conformable microelectrode array (NeuroGrid) to record local field potentials and neural spiking across the dorsal cortical surface of the rat brain, combined with silicon probe recordings in the hippocampus, to identify candidate physiological patterns. Parietal, midline, and prefrontal, but not primary cortical areas, displayed localized ripple (100 to 150 hertz) oscillations during sleep, concurrent with hippocampal ripples. Coupling between hippocampal and neocortical ripples was strengthened during sleep following learning. These findings suggest that ripple-ripple coupling supports hippocampal-association cortical transfer of memory traces. Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

Effects of Sleep Deprivation and Aging on Long-Term and Remote Memory in Mice

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Vecsey, Christopher G.; Park, Alan J.; Khatib, Nora; Abel, Ted

2015-01-01

Sleep deprivation (SD) following hippocampus-dependent learning in young mice impairs memory when tested the following day. Here, we examined the effects of SD on remote memory in both young and aged mice. In young mice, we found that memory is still impaired 1 mo after training. SD also impaired memory in aged mice 1 d after training, but, by a…

Slow sleep spindle and procedural memory consolidation in patients with major depressive disorder

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Nishida M

2016-01-01

Full Text Available Masaki Nishida,1 Yusaku Nakashima,2 Toru Nishikawa11Department of Psychiatry and Behavioral Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Yushima, Bunkyo, 2Medical Technology Research Laboratory, Research and Development Division, Medical Business Unit, Sony Corporation, Tokyo, JapanIntroduction: Evidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process.Methods: Healthy control participants (n=17 and patients medicated for major depressive disorder (n=11 were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement. Participants' brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs. Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5–16 Hz and slow-frequency spindle activity (10.5–12.5 Hz.Result: Sleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups.Conclusion: Because the changes in slow

Preserved sleep microstructure in blind individuals

DEFF Research Database (Denmark)

Aubin, Sébrina; Christensen, Julie A.E.; Jennum, Poul

2018-01-01

, as light is the primary zeitgeber of the master biological clock found in the suprachiasmatic nucleus of the hypothalamus. In addition, a greater number of sleep disturbances is often reported in blind individuals. Here, we examined various electroencephalographic microstructural components of sleep, both...... during rapid-eye-movement (REM) sleep and non-REM (NREM) sleep, between blind individuals, including both of early and late onset, and normal-sighted controls. During wakefulness, occipital alpha oscillations were lower, or absent in blind individuals. During sleep, differences were observed across...... electrode derivations between the early and late blind samples, which may reflect altered cortical networking in early blindness. Despite these differences in power spectra density, the electroencephalography microstructure of sleep, including sleep spindles, slow wave activity, and sawtooth waves, remained...

Shaping the aging brain: Role of auditory input patterns in the emergence of auditory cortical impairments

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Brishna Soraya Kamal

2013-09-01

Full Text Available Age-related impairments in the primary auditory cortex (A1 include poor tuning selectivity, neural desynchronization and degraded responses to low-probability sounds. These changes have been largely attributed to reduced inhibition in the aged brain, and are thought to contribute to substantial hearing impairment in both humans and animals. Since many of these changes can be partially reversed with auditory training, it has been speculated that they might not be purely degenerative, but might rather represent negative plastic adjustments to noisy or distorted auditory signals reaching the brain. To test this hypothesis, we examined the impact of exposing young adult rats to 8 weeks of low-grade broadband noise on several aspects of A1 function and structure. We then characterized the same A1 elements in aging rats for comparison. We found that the impact of noise exposure on A1 tuning selectivity, temporal processing of auditory signal and responses to oddball tones was almost indistinguishable from the effect of natural aging. Moreover, noise exposure resulted in a reduction in the population of parvalbumin inhibitory interneurons and cortical myelin as previously documented in the aged group. Most of these changes reversed after returning the rats to a quiet environment. These results support the hypothesis that age-related changes in A1 have a strong activity-dependent component and indicate that the presence or absence of clear auditory input patterns might be a key factor in sustaining adult A1 function.

Auditory cortical function during verbal episodic memory encoding in Alzheimer's disease.

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Dhanjal, Novraj S; Warren, Jane E; Patel, Maneesh C; Wise, Richard J S

2013-02-01

Episodic memory encoding of a verbal message depends upon initial registration, which requires sustained auditory attention followed by deep semantic processing of the message. Motivated by previous data demonstrating modulation of auditory cortical activity during sustained attention to auditory stimuli, we investigated the response of the human auditory cortex during encoding of sentences to episodic memory. Subsequently, we investigated this response in patients with mild cognitive impairment (MCI) and probable Alzheimer's disease (pAD). Using functional magnetic resonance imaging, 31 healthy participants were studied. The response in 18 MCI and 18 pAD patients was then determined, and compared to 18 matched healthy controls. Subjects heard factual sentences, and subsequent retrieval performance indicated successful registration and episodic encoding. The healthy subjects demonstrated that suppression of auditory cortical responses was related to greater success in encoding heard sentences; and that this was also associated with greater activity in the semantic system. In contrast, there was reduced auditory cortical suppression in patients with MCI, and absence of suppression in pAD. Administration of a central cholinesterase inhibitor (ChI) partially restored the suppression in patients with pAD, and this was associated with an improvement in verbal memory. Verbal episodic memory impairment in AD is associated with altered auditory cortical function, reversible with a ChI. Although these results may indicate the direct influence of pathology in auditory cortex, they are also likely to indicate a partially reversible impairment of feedback from neocortical systems responsible for sustained attention and semantic processing. Copyright © 2012 American Neurological Association.

Objective and subjective measurement of sleep disturbance in female trauma survivors with posttraumatic stress disorder.

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Werner, Kimberly B; Griffin, Michael G; Galovski, Tara E

2016-06-30

Sleep disturbance may be the most often endorsed symptom of posttraumatic stress disorder (PTSD). Much of this research is based on subjective reports from trauma survivors; however, objective measures of sleep-related impairment have yielded findings inconsistent with self-report data. More studies investigating subjective and objective assessments concordantly are needed to understand sleep impairment in PTSD. The current study examined PTSD-related sleep disturbance in a female interpersonal violence cohort with full PTSD diagnoses (N=51) assessing subjective (global and daily diary measures) and objective (actigraphy) sleep measures concurrently. PTSD severity was positively associated with global, subjective reports of sleep impairment and insomnia. Subjective measures of sleep (including global sleep impairment, insomnia, and daily sleep diary reports of total sleep time, sleep efficiency, and sleep onset latency) were moderately to strongly correlated. However, no significant correlations between subjective and objective reports of sleep impairment were found in this cohort. Analyses demonstrated an overall elevation in subjectively reported sleep impairment when compared to objective measurement assessed concurrently. Findings demonstrate a lack of agreement between subjective and objective measurements of sleep in a PTSD-positive female cohort, suggesting objective and subjective sleep impairments are distinct sleep parameters that do not necessarily directly co-vary. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Urotensin II modulates rapid eye movement sleep through activation of brainstem cholinergic neurons

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Huitron-Resendiz, Salvador; Kristensen, Morten Pilgaard; Sánchez-Alavez, Manuel

2005-01-01

administration of UII into the PPT nucleus increases REM sleep without inducing changes in the cortical blood flow. Intracerebroventricular injection of UII enhances both REM sleep and wakefulness and reduces slow-wave sleep 2. Intracerebroventricular, but not local, administration of UII increases cortical...... dorsal tegmental nuclei. This distribution suggests that the UII system is involved in functions regulated by acetylcholine, such as the sleep-wake cycle. Here, we tested the hypothesis that UII influences cholinergic PPT neuron activity and alters rapid eye movement (REM) sleep patterns in rats. Local...... synaptic transmission because it persisted in the presence of TTX and antagonists of ionotropic glutamate, GABA, and glycine receptors. Collectively, these results suggest that UII plays a role in the regulation of REM sleep independently of its cerebrovascular actions by directly activating cholinergic...

Regional cerebral glucose metabolic rate in human sleep assessed by positron emission tomography

International Nuclear Information System (INIS)

Buchsbaum, M.S.; Wu, J.; Hazlett, E.; Sicotte, N.; Bunney, W.E. Jr.; Gillin, J.C.

1989-01-01

The cerebral metabolic rate of glucose was measured during nighttime sleep in 36 normal volunteers using positron emission tomography and fluorine-18-labeled 2-deoxyglucose (FDG). In comparison to waking controls, subjects given FDG during non-rapid eye movement (NREM) sleep showed about a 23% reduction in metabolic rate across the entire brain. This decrease was greater for the frontal than temporal or occipital lobes, and greater for basal ganglia and thalamus than cortex. Subjects in rapid eye movement (REM) sleep tended to have higher cortical metabolic rates than walking subjects. The cingulate gyrus was the only cortical structure to show a significant increase in glucose metabolic rate in REM sleep in comparison to waking. The basal ganglia were relatively more active on the right in REM sleep and symmetrical in NREM sleep

Acute sleep restriction reduces insulin sensitivity in adolescent boys

DEFF Research Database (Denmark)

Klingenberg, Lars; Chaput, Jean-Philippe; Holmbäck, Ulf

2013-01-01

Short sleep duration has been linked to impaired glucose metabolism in many experimental studies. Moreover, studies have reported indications of an increased metabolic stress following sleep restriction.......Short sleep duration has been linked to impaired glucose metabolism in many experimental studies. Moreover, studies have reported indications of an increased metabolic stress following sleep restriction....

Impaired Sleep, Circadian Rhythms and Neurogenesis in Diet-Induced Premature Aging

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Alexander J. Stankiewicz

2017-10-01

Full Text Available Chronic high caloric intake (HCI is a risk factor for multiple major human disorders, from diabetes to neurodegeneration. Mounting evidence suggests a significant contribution of circadian misalignment and sleep alterations to this phenomenon. An inverse temporal relationship between sleep, activity, food intake, and clock mechanisms in nocturnal and diurnal animals suggests that a search for effective therapeutic approaches can benefit from the use of diurnal animal models. Here, we show that, similar to normal aging, HCI leads to the reduction in daily amplitude of expression for core clock genes, a decline in sleep duration, an increase in scoliosis, and anxiety-like behavior. A remarkable decline in adult neurogenesis in 1-year old HCI animals, amounting to only 21% of that in age-matched Control, exceeds age-dependent decline observed in normal 3-year old zebrafish. This is associated with misalignment or reduced amplitude of daily patterns for principal cell cycle regulators, cyclins A and B, and p20, in brain tissue. Together, these data establish HCI in zebrafish as a model for metabolically induced premature aging of sleep, circadian functions, and adult neurogenesis, allowing for a high throughput approach to mechanistic studies and drug trials in a diurnal vertebrate.

Morning administration of oral methamphetamine dose-dependently disrupts nighttime sleep in recreational stimulant users.

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Herrmann, Evan S; Johnson, Patrick S; Bruner, Natalie R; Vandrey, Ryan; Johnson, Matthew W

2017-09-01

Use of amphetamine-type stimulants (e.g., methamphetamine) is associated with acute sleep disruptions. No prior reports have characterized the acute effects of methamphetamine on sleep using polysomnography, the gold standard for objective sleep monitoring. Recreational stimulant users (n=19) completed a baseline assessment, which included questionnaires assessing demographic and substance use characteristics, and the Pittsburgh Sleep Quality Index (PSQI), which assesses sleep quality over the past month. Participants were administered 0mg (placebo), 20mg, or 40mg oral methamphetamine at 08:15h on study days, using a double-blind, randomized, within-subjects design. Sleep was monitored using polysomnography from 22:20 that evening until 06:15 the following morning. PSQI scores indicated more than half of participants reported poor sleep quality at baseline. Methamphetamine dose-dependently increased sleep latency, and decreased total sleep time, sleep efficiency, time in NREM 2 sleep, number of REM periods, and total time in REM sleep. Sleep under placebo conditions was consistent with what would be expected from healthy adults. Morning oral administration of methamphetamine produces robust disruptions in nighttime sleep. Future research should examine relations between stimulant use and sleep disruption in naturalistic settings, with regard to both stimulant abuse and licit prescription use. Copyright © 2017. Published by Elsevier B.V.

Visuo-Spatial Imagery Impairment in Posterior Cortical Atrophy: A Cognitive and SPECT Study

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Simona Gardini

2011-01-01

Full Text Available This study investigated the cognitive profile and the cerebral perfusion pattern in a highly educated 70 year old gentleman with posterior cortical atrophy (PCA. Visuo-perceptual abilities, spatial memory, spatial representation and navigation, visuo-spatial mental imagery, semantic and episodic-autobiographical memory were assessed. Regional cerebral blood flow (rCBF was imaged with SPECT. Cognitive testing showed visual-perceptual impairment, apperceptive visual and landmark agnosia, topographical disorientation with way-finding deficits, impaired map learning and poor mental image generation. Semantic memory was normal, while episodic-autobiographical memory was impaired. Reduced rCBF was found mainly in the right hemisphere, in the precentral gyrus, posterior cingulate and middle temporal gyri, cuneus and precuneus, in the left superior temporal and lingual gyri and in the parahippocampus bilaterally. Hypoperfusion in occipito-parietal regions was associated with visuo-spatial deficits, whereas deficits in visuo-spatial mental imagery might reflect dysfunction related to hypoperfusion in the parahippocampus and precuneus, structures which are responsible for spatial and imagery processing. Dissociating performance between preserved semantic memory and poor episodic-autobiographical recall is consistent with a pattern of normal perfusion in frontal and anterior temporal regions but abnormal rCBF in the parahippocampi. The present findings indicate that PCA involves visuo-spatial imagery deficits and provide further validation to current neuro-cognitive models of spatial representation and topographical disorientation.

Exploring Interventions for Sleep Disorders in Adolescent Cannabis Users

Directory of Open Access Journals (Sweden)

Tzvi Furer

2018-02-01

Full Text Available This review summarizes the available literature on the intersection of adolescent cannabis use and sleep disturbances, along with interventions for adolescent cannabis users who suffer sleep impairments. Adolescents are susceptible to various sleep disorders, which are often exacerbated by the use of substances such as cannabis. The relationship between cannabis and sleep is bidirectional. Interventions to improve sleep impairments among adolescent cannabis users to date have demonstrated limited efficacy, although few studies indicating the benefits of behavioral interventions—such as Cognitive Behavior Therapy for Insomnia or Mindfulness Based Stress Reduction—appear promising in the treatment of sleep disorders, which are present for users of cannabis. Further research is necessary to elucidate the precise mechanisms by which cannabis use coexists with sleep impairments, along with effective interventions for those users who suffer sleep difficulties.

Experience-dependent phase-reversal of hippocampal neuron firing during REM sleep.

Science.gov (United States)

Poe, G R; Nitz, D A; McNaughton, B L; Barnes, C A

2000-02-07

The idea that sleep could serve a cognitive function has remained popular since Freud stated that dreams were "not nonsense" but a time to sort out experiences [S. Freud, Letter to Wilhelm Fliess, May 1897, in The Origins of Psychoanalysis - Personal Letters of Sigmund Freud, M. Bonaparte, A. Freud, E. Kris (Eds.), Translated by E. Mosbacher, J. Strachey, Basic Books and Imago Publishing, 1954]. Rapid eye movement (REM) sleep, which is associated with dream reports, is now known to be is important for acquisition of some tasks [A. Karni, D. Tanne, B.S. Rubenstein, J.J.M. Askenasy, D. Sagi, Dependence on REM sleep of overnight improvement of a perceptual skill, Science 265 (1994) 679-682; C. Smith, Sleep states and learning: a review of the animal literature, Biobehav. Rev. 9 (1985) 157-168]; although why this is so remains obscure. It has been proposed that memories may be consolidated during REM sleep or that forgetting of unnecessary material occurs in this state [F. Crick, G. Mitchison, The function of dream sleep, Nature 304 (1983) 111-114; D. Marr, Simple memory: a theory for archicortex, Philos. Trans. R. Soc. B. 262 (1971) 23-81]. We studied the firing of multiple single neurons in the hippocampus, a structure that is important for episodic memory, during familiar and novel experiences and in subsequent REM sleep. Cells active in familiar places during waking exhibited a reversal of firing phase relative to local theta oscillations in REM sleep. Because firing-phase can influence whether synapses are strengthened or weakened [C. Holscher, R. Anwyl, M.J. Rowan, Stimulation on the positive phase of hippocampal theta rhythm induces long-term potentiation that can be depotentiated by stimulation on the negative phase in area CA1 in vivo, J. Neurosci. 15 (1977) 6470-6477; P.T. Huerta, J.E. Lisman, Bidirectional synaptic plasticity induced by a single burst during cholinergic theta oscillation in CA1 in vitro, Neuron 15 (1995) 1053-1063; C. Pavlides, Y

Association between Facebook dependence and poor sleep quality: a study in a sample of undergraduate students in Peru.

Science.gov (United States)

Wolniczak, Isabella; Cáceres-DelAguila, José Alonso; Palma-Ardiles, Gabriela; Arroyo, Karen J; Solís-Visscher, Rodrigo; Paredes-Yauri, Stephania; Mego-Aquije, Karina; Bernabe-Ortiz, Antonio

2013-01-01

Internet can accelerate information exchange. Social networks are the most accessed especially Facebook. This kind of networks might create dependency with several negative consequences in people's life. The aim of this study was to assess potential association between Facebook dependence and poor sleep quality. A cross sectional study was performed enrolling undergraduate students of the Universidad Peruana de Ciencias Aplicadas, Lima, Peru. The Internet Addiction Questionnaire, adapted to the Facebook case, and the Pittsburgh Sleep Quality Index, were used. A global score of 6 or greater was defined as the cutoff to determine poor sleep quality. Generalized linear model were used to determine prevalence ratios (PR) and 95% confidence intervals (95%CI). A total of 418 students were analyzed; of them, 322 (77.0%) were women, with a mean age of 20.1 (SD: 2.5) years. Facebook dependence was found in 8.6% (95% CI: 5.9%-11.3%), whereas poor sleep quality was present in 55.0% (95% CI: 50.2%-59.8%). A significant association between Facebook dependence and poor sleep quality mainly explained by daytime dysfunction was found (PR = 1.31; IC95%: 1.04-1.67) after adjusting for age, sex and years in the faculty. There is a relationship between Facebook dependence and poor quality of sleep. More than half of students reported poor sleep quality. Strategies to moderate the use of this social network and to improve sleep quality in this population are needed.

Associations between subjective sleep quality and brain volume in Gulf War veterans.

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Chao, Linda L; Mohlenhoff, Brian S; Weiner, Michael W; Neylan, Thomas C

2014-03-01

To investigate whether subjective sleep quality is associated with brain volume independent of comorbid psychiatric conditions. Cross-sectional. Department of Veterans Affairs (VA) Medical Center. One hundred forty-four Gulf War Veterans (mean age 45 years; range: 31-70 years; 14% female). None. Total cortical, lobar gray matter, and hippocampal volumes were quantified from 1.5 Tesla magnetic resonance images using Freesurfer version 4.5. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). Multiple linear regressions were used to determine the association of sleep quality with total and regional brain volumes. The global PSQI score was positively correlated with lifetime and current posttraumatic stress disorder (PTSD) and current depressive symptoms (P sleep quality. Poorer subjective sleep quality was associated with reduced total cortical and regional frontal lobe volumes independent of comorbid psychiatric conditions. Future work will be needed to examine if effective treatment of disturbed sleep leads to improved structural and functional integrity of the frontal lobes.

Trait- and pre-sleep-state-dependent arousal in insomnia disorders: what role may sleep reactivity and sleep-related metacognitions play? A pilot study.

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Palagini, Laura; Mauri, Mauro; Dell'Osso, Liliana; Riemann, Dieter; Drake, Christopher L

2016-09-01

Research into the cause of chronic insomnia has identified hyperarousal as a key factor, which is likely to have both trait and state components. Sleep-related cognition, metacognition, and sleep reactivity also play an important role in insomnia. Our aim was to investigate how these insomnia-related constructs are associated with trait predisposition and pre-sleep arousal in subjects with an insomnia disorder. Fifty-three individuals with insomnia disorder (according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) (F = 33; 52 + 10)) and 30 healthy controls (F = 18; 51.8 + 12 years) were evaluated with a set of questionnaires, including the Ford Insomnia Response to Stress Test (FIRST), Metacognition Questionnaire - Insomnia (MCQI), Arousal Predisposition Scale (APS), and Pre-sleep Arousal Scale (PSAS). Statistical analyses included multiple regression to elucidate the independent determinants of APS and PSAS. Participants with insomnia presented higher FIRST, MCQI, APS, PSAS scores (p-values insomnia, APS and cognitive PSAS were best determined by MCQI (respectively, B = 0.09, p = 0.001, B = 0.08, p = 0.02), somatic PSAS by cognitive arousal (PSAS B = 0.35, p = 0.004) CONCLUSIONS: This study suggests that in insomnia disorders, trait predisposition toward hyperarousal and pre-sleep-cognitive-state-dependent arousal may be closely related to sleep-related metacognitive processes. Sleep-related metacognitive processes may be associated with trait hyperarousal within the framework of a mutual relationship, and could, in turn, modulate cognitive pre-sleep-state arousal. A broad range of cognitive and metacognitive processes should be considered when dealing with subjects with insomnia. Copyright © 2016 Elsevier B.V. All rights reserved.

Sleep-Dependent Consolidation of Statistical Learning

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Durrant, Simon J.; Taylor, Charlotte; Cairney, Scott; Lewis, Penelope A.

2011-01-01

The importance of sleep for memory consolidation has been firmly established over the past decade. Recent work has extended this by suggesting that sleep is also critical for the integration of disparate fragments of information into a unified schema, and for the abstraction of underlying rules. The question of which aspects of sleep play a…

Impact of partial sleep deprivation on immune markers.

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Wilder-Smith, A; Mustafa, F B; Earnest, A; Gen, L; Macary, P A

2013-10-01

Sleep quality is considered to be an important predictor of immunity. Lack of sleep therefore may reduce immunity, thereby increasing the susceptibility to respiratory pathogens. A previous study showed that reduced sleep duration was associated with an increased likelihood of the common cold. It is important to understand the role of sleep in altering immune responses to understand how sleep deprivation leads to an increased susceptibility to the common cold or other respiratory infections. We sought to examine the impact of partial sleep deprivation on various immune markers. Fifty-two healthy volunteers were partially sleep deprived for one night. We took blood samples before the sleep deprivation, immediately after, and 4 and 7 days after sleep deprivation. We measured various immune markers and used a generalized estimating equation (GEE) to examine the differences in the repeated measures. CD4, CD8, CD14, and CD16 all showed significant time-dependent changes, but CD3 did not. The most striking time-dependent change was observed for the mitogen proliferation assay and for HLA-DR. There was a significant decrease in the mitogen proliferation values and HLA-DR immediately after the sleep deprivation experiment, which started to rise again on day 4 and normalized by day 7. The transiently impaired mitogen proliferation, the decreased HLA-DR, the upregulated CD14, and the variations in CD4 and CD8 that we observed in temporal relationship with partial sleep deprivation could be one possible explanation for the increased susceptibility to respiratory infections reported after reduced sleep duration. Copyright © 2013 Elsevier B.V. All rights reserved.

Genetic or pharmacological reduction of PERK enhances cortical-dependent taste learning.

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Ounallah-Saad, Hadile; Sharma, Vijendra; Edry, Efrat; Rosenblum, Kobi

2014-10-29

Protein translation initiation is controlled by levels of eIF2α phosphorylation (p-eIF2α) on Ser51. In addition, increased p-eIF2α levels impair long-term synaptic plasticity and memory consolidation, whereas decreased levels enhance them. Levels of p-eIF2α are determined by four kinases, of which protein kinase RNA-activated (PKR), PKR-like endoplastic reticulum kinase (PERK), and general control nonderepressible 2 are extensively expressed in the mammalian mature brain. Following identification of PERK as the major kinase to determine basal levels of p-eIF2α in primary neuronal cultures, we tested its function as a physiological constraint of memory consolidation in the cortex, the brain structure suggested to store, at least in part, long-term memories in the mammalian brain. To that aim, insular cortex (IC)-dependent positive and negative forms of taste learning were used. Genetic reduction of PERK expression was accomplished by local microinfusion of a lentivirus harboring PERK Short hairpin RNA, and pharmacological inhibition was achieved by local microinfusion of a PERK-specific inhibitor (GSK2606414) to the rat IC. Both genetic reduction of PERK expression and pharmacological inhibition of its activity reduced p-eIF2α levels and enhanced novel taste learning and conditioned taste aversion, but not memory retrieval. Moreover, enhanced extinction was observed together with enhanced associative memory, suggesting increased cortical-dependent behavioral plasticity. The results suggest that, by phosphorylating eIF2α, PERK functions in the cortex as a physiological constraint of memory consolidation, and its downregulation serves as cognitive enhancement. Copyright © 2014 the authors 0270-6474/14/3314624-09$15.00/0.

Sleep deprivation impairs cAMP signalling in the hippocampus

NARCIS (Netherlands)

Vecsey, Christopher G; Baillie, George S; Jaganath, Devan; Havekes, Robbert; Daniels, Andrew; Wimmer, Mathieu; Huang, Ted; Brown, Kim M; Li, Xiang-Yao; Descalzi, Giannina; Kim, Susan S; Chen, Tao; Shang, Yu-Ze; Zhuo, Min; Houslay, Miles D; Abel, Ted

2009-01-01

Millions of people regularly obtain insufficient sleep. Given the effect of sleep deprivation on our lives, understanding the cellular and molecular pathways affected by sleep deprivation is clearly of social and clinical importance. One of the major effects of sleep deprivation on the brain is to

Abeta(1-42) injection causes memory impairment, lowered cortical and serum BDNF levels, and decreased hippocampal 5-HT(2A) levels

DEFF Research Database (Denmark)

Christensen, R; Marcussen, Anders Bue; Wörtwein, Gitta

2008-01-01

was used to monitor Abeta(1-42) induced memory impairment. Memory impairment was seen 22 days after injection of Abeta(1-42) in the experimental group and until termination of the experiments. In the Abeta(1-42) injected animals we saw an abolished increase in serum BDNF levels that was accompanied...... by significant lower BDNF levels in frontal cortex and by an 8.5% reduction in hippocampal 5-HT(2A) receptor levels. A tendency towards lowered cortical 5-HT(2A) was also observed. These results indicate that the Abeta(1-42) associated memory deficit is associated with an impaired BDNF regulation, which...

Propofol Anesthesia and Sleep: A High-Density EEG Study

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Murphy, Michael; Bruno, Marie-Aurelie; Riedner, Brady A.; Boveroux, Pierre; Noirhomme, Quentin; Landsness, Eric C.; Brichant, Jean-Francois; Phillips, Christophe; Massimini, Marcello; Laureys, Steven; Tononi, Giulio; Boly, Melanie

2011-01-01

Study Objectives: The electrophysiological correlates of anesthetic sedation remain poorly understood. We used high-density electroencephalography (hd-EEG) and source modeling to investigate the cortical processes underlying propofol anesthesia and compare them to sleep. Design: 256-channel EEG recordings in humans during propofol anesthesia. Setting: Hospital operating room. Patients or Participants: 8 healthy subjects (4 males) Interventions: N/A Measurements and Results: Initially, propofol induced increases in EEG power from 12–25 Hz. Loss of consciousness (LOC) was accompanied by the appearance of EEG slow waves that resembled the slow waves of NREM sleep. We compared slow waves in propofol to slow waves recorded during natural sleep and found that both populations of waves share similar cortical origins and preferentially propagate along the mesial components of the default network. However, propofol slow waves were spatially blurred compared to sleep slow waves and failed to effectively entrain spindle activity. Propofol also caused an increase in gamma (25–40 Hz) power that persisted throughout LOC. Source modeling analysis showed that this increase in gamma power originated from the anterior and posterior cingulate cortices. During LOC, we found increased gamma functional connectivity between these regions compared to the wakefulness. Conclusions: Propofol anesthesia is a sleep-like state and slow waves are associated with diminished consciousness even in the presence of high gamma activity. Citation: Murphy M; Bruno MA; Riedner BA; Boveroux P; Noirhomme Q; Landsness EC; Brichant JF; Phillips C; Massimini M; Laureys S; Tononi G; Boly M. Propofol anesthesia and sleep: a high-density EEG study. SLEEP 2011;34(3):283-291. PMID:21358845

Increased 20-HETE synthesis explains reduced cerebral blood flow but not impaired neurovascular coupling after cortical spreading depression in rat cerebral cortex

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Fordsmann, Jonas Christoffer; ko, Rebecca; Choi, Hyun B

2013-01-01

Cortical spreading depression (CSD) is associated with release of arachidonic acid (AA), impaired neurovascular coupling, and reduced cerebral blood flow (CBF), caused by cortical vasoconstriction. We tested the hypothesis that the released AA is metabolized by the cytochrome P450 enzyme to produce...... neurovascular coupling after CSD. These findings suggest that CSD-induced increments in 20-HETE cause the reduction in CBF after CSD, and that the attenuation of stimulation-induced CBF responses after CSD has a different mechanism. We suggest that blockade of 20-HETE synthesis may be clinically relevant...

Alterações cognitivas na SAOS Cognitive impairment in obstructive sleep apnea syndrome

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Pedro Felipe Carvalhedo de Bruin

2010-06-01

Full Text Available Alterações da cognição e do desempenho estão bem estabelecidas em pacientes com SAOS, causando um impacto significativo sobre a qualidade de vida e o risco de acidentes nesses indivíduos. Tais alterações são mais profundas nos quadros mais graves de SAOS, o que explica a aparente discrepância na frequência e gravidade desse prejuízo entre estudos com pacientes de clínicas de sono e estudos de base populacional. Vários aspectos podem estar comprometidos, incluindo o processamento cognitivo, a atenção sustentada, as funções executivas e a memória. Entretanto, os mecanismos causais desses déficits não estão inteiramente elucidados, e existem controvérsias, particularmente em relação à contribuição relativa da hipóxia intermitente e da interrupção do sono presentes na SAOS. O impacto da sonolência diurna sobre o desempenho desses pacientes nos diversos testes cognitivos também ainda deve ser determinado, assim como o possível efeito de comorbidades frequentes, incluindo o diabete melito, a hipertensão arterial sistêmica, a doença cardiovascular e a obesidade. Existem evidências convincentes de que o tratamento com CPAP produz uma significativa melhora do desempenho e da cognição, sobretudo nos portadores de SAOS moderada e grave, embora sejam necessários mais estudos acerca do seu impacto a longo prazo.Cognitive and performance impairment is well established in patients with obstructive sleep apnea syndrome (OSAS, having a significant impact on the quality of life and the risk of accidents in these individuals. The severity of the impairment correlates with that of the OSAS, which explains the apparent discrepancy between studies using patients from sleep clinics and population-based studies in terms of the reported frequency and severity of such impairment. Cognitive processing, sustained attention, executive functioning, and memory have all been reported to be impaired in OSAS. However, the causal

Association between Facebook dependence and poor sleep quality: a study in a sample of undergraduate students in Peru.

Directory of Open Access Journals (Sweden)

Isabella Wolniczak

Full Text Available OBJECTIVES: Internet can accelerate information exchange. Social networks are the most accessed especially Facebook. This kind of networks might create dependency with several negative consequences in people's life. The aim of this study was to assess potential association between Facebook dependence and poor sleep quality. METHODOLOGY/PRINCIPAL FINDINGS: A cross sectional study was performed enrolling undergraduate students of the Universidad Peruana de Ciencias Aplicadas, Lima, Peru. The Internet Addiction Questionnaire, adapted to the Facebook case, and the Pittsburgh Sleep Quality Index, were used. A global score of 6 or greater was defined as the cutoff to determine poor sleep quality. Generalized linear model were used to determine prevalence ratios (PR and 95% confidence intervals (95%CI. A total of 418 students were analyzed; of them, 322 (77.0% were women, with a mean age of 20.1 (SD: 2.5 years. Facebook dependence was found in 8.6% (95% CI: 5.9%-11.3%, whereas poor sleep quality was present in 55.0% (95% CI: 50.2%-59.8%. A significant association between Facebook dependence and poor sleep quality mainly explained by daytime dysfunction was found (PR = 1.31; IC95%: 1.04-1.67 after adjusting for age, sex and years in the faculty. CONCLUSIONS: There is a relationship between Facebook dependence and poor quality of sleep. More than half of students reported poor sleep quality. Strategies to moderate the use of this social network and to improve sleep quality in this population are needed.

Association between Facebook Dependence and Poor Sleep Quality: A Study in a Sample of Undergraduate Students in Peru

Science.gov (United States)

Wolniczak, Isabella; Cáceres-DelAguila, José Alonso; Palma-Ardiles, Gabriela; Arroyo, Karen J.; Solís-Visscher, Rodrigo; Paredes-Yauri, Stephania; Mego-Aquije, Karina; Bernabe-Ortiz, Antonio

2013-01-01

Objectives Internet can accelerate information exchange. Social networks are the most accessed especially Facebook. This kind of networks might create dependency with several negative consequences in people’s life. The aim of this study was to assess potential association between Facebook dependence and poor sleep quality. Methodology/Principal Findings A cross sectional study was performed enrolling undergraduate students of the Universidad Peruana de Ciencias Aplicadas, Lima, Peru. The Internet Addiction Questionnaire, adapted to the Facebook case, and the Pittsburgh Sleep Quality Index, were used. A global score of 6 or greater was defined as the cutoff to determine poor sleep quality. Generalized linear model were used to determine prevalence ratios (PR) and 95% confidence intervals (95%CI). A total of 418 students were analyzed; of them, 322 (77.0%) were women, with a mean age of 20.1 (SD: 2.5) years. Facebook dependence was found in 8.6% (95% CI: 5.9%–11.3%), whereas poor sleep quality was present in 55.0% (95% CI: 50.2%–59.8%). A significant association between Facebook dependence and poor sleep quality mainly explained by daytime dysfunction was found (PR = 1.31; IC95%: 1.04–1.67) after adjusting for age, sex and years in the faculty. Conclusions There is a relationship between Facebook dependence and poor quality of sleep. More than half of students reported poor sleep quality. Strategies to moderate the use of this social network and to improve sleep quality in this population are needed. PMID:23554978

Impaired behavioral and neurocognitive function in preschool children with obstructive sleep apnea.

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Landau, Yael E; Bar-Yishay, Orit; Greenberg-Dotan, Sari; Goldbart, Aviv D; Tarasiuk, Ariel; Tal, Asher

2012-02-01

We aimed to examine the hypothesis that behavioral and neurocognitive functions of preschool children with Obstructive Sleep Apnea Syndrome (OSAS) are impaired compared to healthy children, and improve after adenotonsillectomy (TA). A comprehensive assessment battery was used to assess cognitive and behavioral functions, and quality of life in children with OSAS compared to matched controls. 45 children (mean age 45.5 ± 9 months, 73% boys, BMI 15.7 ± 2) with OSAS were compared to 26 healthy children (mean age 48.6 ± 8 months, 46% boys, BMI 16.4 ± 2). Mean AHI in the OSAS group was 13.2 ± 10.7 (ranging from 1.2 to 57). Significantly impaired planning and fluency (executive function) were found in children with OSAS, as well as impaired attention and receptive vocabulary. Parents and teachers described the OSAS group as having significantly more behavior problems. Quality of life questionnaire in children with OSAS (mean 2.3, range 0.7-4.3) was significantly worse compared to controls (mean 0, range: 0-4), P improvement was documented in verbal and motor fluency, sustained attention, and vocabulary. After TA, fewer behavioral problems were seen. Preschool children with OSAS present significantly impaired executive functions, impaired attention and receptive vocabulary, and more behavior problems. One year after TA, the prominent improvements were in behavior and quality of life. These findings suggest that the impact of OSAS on behavioral and cognitive functions begins in early childhood. Copyright © 2011 Wiley Periodicals, Inc.

Stereotypic wheel running decreases cortical activity in mice

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Fisher, Simon P.; Cui, Nanyi; McKillop, Laura E.; Gemignani, Jessica; Bannerman, David M.; Oliver, Peter L.; Peirson, Stuart N.; Vyazovskiy, Vladyslav V.

2016-01-01

Prolonged wakefulness is thought to gradually increase ‘sleep need' and influence subsequent sleep duration and intensity, but the role of specific waking behaviours remains unclear. Here we report the effect of voluntary wheel running during wakefulness on neuronal activity in the motor and somatosensory cortex in mice. We find that stereotypic wheel running is associated with a substantial reduction in firing rates among a large subpopulation of cortical neurons, especially at high speeds. Wheel running also has longer-term effects on spiking activity across periods of wakefulness. Specifically, cortical firing rates are significantly higher towards the end of a spontaneous prolonged waking period. However, this increase is abolished when wakefulness is dominated by running wheel activity. These findings indicate that wake-related changes in firing rates are determined not only by wake duration, but also by specific waking behaviours. PMID:27748455

Sleep disturbances and glucose homeostasis

NARCIS (Netherlands)

Barf, R. Paulien; Scheurink, Anton J.W.

2011-01-01

Sleep disturbances, induced by either lifestyle, shift work or sleeping disorders, have become more prevalent in our 24/7 Western society. Sleep disturbances are associated with impaired health including metabolic diseases such as obesity and type 2 diabetes. The question remains whether there is a

Sleep restriction therapy for insomnia is associated with reduced objective total sleep time, increased daytime somnolence, and objectively impaired vigilance: implications for the clinical management of insomnia disorder.

Science.gov (United States)

Kyle, Simon D; Miller, Christopher B; Rogers, Zoe; Siriwardena, A Niroshan; Macmahon, Kenneth M; Espie, Colin A

2014-02-01

To investigate whether sleep restriction therapy (SRT) is associated with reduced objective total sleep time (TST), increased daytime somnolence, and impaired vigilance. Within-subject, noncontrolled treatment investigation. Sleep research laboratory. Sixteen patients [10 female, mean age = 47.1 (10.8) y] with well-defined psychophysiological insomnia (PI), reporting TST ≤ 6 h. Patients were treated with single-component SRT over a 4-w protocol, sleeping in the laboratory for 2 nights prior to treatment initiation and for 3 nights (SRT night 1, 8, 22) during the acute interventional phase. The psychomotor vigilance task (PVT) was completed at seven defined time points [day 0 (baseline), day 1,7,8,21,22 (acute treatment) and day 84 (3 mo)]. The Epworth Sleepiness Scale (ESS) was completed at baseline, w 1-4, and 3 mo. Subjective sleep outcomes and global insomnia severity significantly improved before and after SRT. There was, however, a robust decrease in PSG-defined TST during acute implementation of SRT, by an average of 91 min on night 1, 78 min on night 8, and 69 min on night 22, relative to baseline (P insomnia.

Ventilatory control sensitivity in patients with obstructive sleep apnea is sleep stage dependent.

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Landry, Shane A; Andara, Christopher; Terrill, Philip I; Joosten, Simon A; Leong, Paul; Mann, Dwayne L; Sands, Scott A; Hamilton, Garun S; Edwards, Bradley A

2018-05-01

The severity of obstructive sleep apnea (OSA) is known to vary according to sleep stage; however, the pathophysiology responsible for this robust observation is incompletely understood. The objective of the present work was to examine how ventilatory control system sensitivity (i.e. loop gain) varies during sleep in patients with OSA. Loop gain was estimated using signals collected from standard diagnostic polysomnographic recordings performed in 44 patients with OSA. Loop gain measurements associated with nonrapid eye movement (NREM) stage 2 (N2), stage 3 (N3), and REM sleep were calculated and compared. The sleep period was also split into three equal duration tertiles to investigate how loop gain changes over the course of sleep. Loop gain was significantly lower (i.e. ventilatory control more stable) in REM (Mean ± SEM: 0.51 ± 0.04) compared with N2 sleep (0.63 ± 0.04; p = 0.001). Differences in loop gain between REM and N3 (p = 0.095), and N2 and N3 (p = 0.247) sleep were not significant. Furthermore, N2 loop gain was significantly lower in the first third (0.57 ± 0.03) of the sleep period compared with later second (0.64 ± 0.03, p = 0.012) and third (0.64 ± 0.03, p = 0.015) tertiles. REM loop gain also tended to increase across the night; however, this trend was not statistically significant [F(2, 12) = 3.49, p = 0.09]. These data suggest that loop gain varies between REM and NREM sleep and modestly increases over the course of sleep. Lower loop gain in REM is unlikely to contribute to the worsened OSA severity typically observed in REM sleep, but may explain the reduced propensity for central sleep apnea in this sleep stage.

Care mapping in clinical neuroscience settings: Cognitive impairment and dependency.

Science.gov (United States)

Leigh, Andrew James; O'Hanlon, Katie; Sheldrick, Russell; Surr, Claire; Hare, Dougal Julian

2015-01-01

Person-centred care can improve the well-being of patients and is therefore a key driver in healthcare developments in the UK. The current study aims to investigate the complex relationship between cognitive impairment, dependency and well-being in people with a wide range of acquired brain and spinal injuries. Sixty-five participants, with varied acquired brain and spinal injuries, were selected by convenience sampling from six inpatient clinical neuroscience settings. Participants were observed using Dementia Care Mapping - Neurorehabilitation (DCM-NR) and categorised based on severity of cognitive impairment. A significant difference in the behaviours participants engaged in, their well-being and dependency was found between the severe cognitive impairment group and the mild, moderate or no cognitive impairment groups. Dependency and cognitive impairment accounted for 23.9% of the variance in well-ill-being scores and 17.2% of the variance in potential for positive engagement. The current study highlights the impact of severe cognitive impairment and dependency on the behaviours patients engaged in and their well-being. It also affirms the utility of DCM-NR in providing insights into patient experience. Consideration is given to developing DCM-NR as a process that may improve person-centred care in neuroscience settings.

Context-dependent modulation of hippocampal and cortical recruitment during remote spatial memory retrieval.

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Lopez, Joëlle; Herbeaux, Karin; Cosquer, Brigitte; Engeln, Michel; Muller, Christophe; Lazarus, Christine; Kelche, Christian; Bontempi, Bruno; Cassel, Jean-Christophe; de Vasconcelos, Anne Pereira

2012-04-01

According to systems consolidation, as hippocampal-dependent memories mature over time, they become additionally (or exclusively) dependent on extra-hippocampal structures. We assessed the recruitment of hippocampal and cortical structures on remote memory retrieval in a performance-degradation resistant (PDR; no performance degradation with time) versus performance-degradation prone (PDP; performance degraded with time) context. Using a water-maze task in two contexts with a hidden platform and three control conditions (home cage, visible platform with or without access to distal cues), we compared neuronal activation (c-Fos imaging) patterns in the dorsal hippocampus and the medial prefrontal cortex (mPFC) after the retrieval of recent (5 days) versus remote (25 days) spatial memory. In the PDR context, the hippocampus exhibited greater c-Fos protein expression on remote than recent memory retrieval, be it in the visible or hidden platform group. In the PDP context, hippocampal activation increased at the remote time point and only in the hidden platform group. In the anterior cingulate cortex, c-Fos expression was greater for remote than for recent memory retrieval and only in the PDR context. The necessity of the mPFC for remote memory retrieval in the PDR context was confirmed using region-specific lidocaine inactivation, which had no impact on recent memory. Conversely, inactivation of the dorsal hippocampus impaired both recent and remote memory in the PDR context, and only recent memory in the PDP context, in which remote memory performance was degraded. While confirming that neuronal circuits supporting spatial memory consolidation are reorganized in a time-dependent manner, our findings further indicate that mPFC and hippocampus recruitment (i) depends on the content and perhaps the strength of the memory and (ii) may be influenced by the environmental conditions (e.g., cue saliency, complexity) in which memories are initially formed and subsequently

Vascular compliance limits during sleep deprivation and recovery sleep.

Science.gov (United States)

Phillips, Derrick J; Schei, Jennifer L; Rector, David M

2013-10-01

Our previous studies showed that evoked hemodynamic responses are smaller during wake compared to sleep; suggesting neural activity is associated with vascular expansion and decreased compliance. We explored whether prolonged activity during sleep deprivation may exacerbate vascular expansion and blunt hemodynamic responses. Evoked auditory responses were generated with periodic 65 dB speaker clicks over a 72-h period and measured with cortical electrodes. Evoked hemodynamic responses were measured simultaneously with optical techniques using three light-emitting diodes, and a photodiode. Animals were housed in separate 30×30×80 cm enclosures, tethered to a commutator system and maintained on a 12-h light/dark cycle. Food and water were available ad libitum. Seven adult female Sprague-Dawley rats. Following a 24-h baseline recording, sleep deprivation was initiated for 0 to 10 h by gentle handling, followed by a 24-h recovery sleep recording. Evoked electrical and hemodynamic responses were measured before, during, and after sleep deprivation. Following deprivation, evoked hemodynamic amplitudes were blunted. Steady-state oxyhemoglobin concentration increased during deprivation and remained high during the initial recovery period before returning to baseline levels after approximately 9-h. Sleep deprivation resulted in blood vessel expansion and decreased compliance while lower basal neural activity during recovery sleep may allow blood vessel compliance to recover. Chronic sleep restriction or sleep deprivation could push the vasculature to critical levels, limiting blood delivery, and leading to metabolic deficits with the potential for neural trauma.

Spatial and reversal learning in the Morris water maze are largely resistant to six hours of REM sleep deprivation following training

Science.gov (United States)

Walsh, Christine M.; Booth, Victoria; Poe, Gina R.

2011-01-01

This first test of the role of REM (rapid eye movement) sleep in reversal spatial learning is also the first attempt to replicate a much cited pair of papers reporting that REM sleep deprivation impairs the consolidation of initial spatial learning in the Morris water maze. We hypothesized that REM sleep deprivation following training would impair both hippocampus-dependent spatial learning and learning a new target location within a familiar environment: reversal learning. A 6-d protocol was divided into the initial spatial learning phase (3.5 d) immediately followed by the reversal phase (2.5 d). During the 6 h following four or 12 training trials/day of initial or reversal learning phases, REM sleep was eliminated and non-REM sleep left intact using the multiple inverted flowerpot method. Contrary to our hypotheses, REM sleep deprivation during four or 12 trials/day of initial spatial or reversal learning did not affect training performance. However, some probe trial measures indicated REM sleep-deprivation–associated impairment in initial spatial learning with four trials/day and enhancement of subsequent reversal learning. In naive animals, REM sleep deprivation during normal initial spatial learning was followed by a lack of preference for the subsequent reversal platform location during the probe. Our findings contradict reports that REM sleep is essential for spatial learning in the Morris water maze and newly reveal that short periods of REM sleep deprivation do not impair concurrent reversal learning. Effects on subsequent reversal learning are consistent with the idea that REM sleep serves the consolidation of incompletely learned items. PMID:21677190