The effect of sleep restriction therapy for insomnia on REM sleep fragmentation: A secondary analysis of a randomised controlled trial.

Rapid eye movement sleep fragmentation is hypothesised to be a reliable feature of insomnia, which may contribute to emotion dysregulation. Sleep restriction therapy, an effective intervention for insomnia, has the potential to reduce rapid eye movement sleep fragmentation through its manipulation of basic sleep-wake processes. We performed secondary data analysis of a randomised controlled trial to examine whether sleep restriction therapy reduces rapid eye movement sleep fragmentation in comparison to a matched control arm. Participants (n = 56; 39 female, mean age = 40.78 ± 9.08 years) were randomly allocated to 4 weeks of sleep restriction therapy or 4 weeks of time in bed regularisation. Ambulatory polysomnographic recordings were performed at baseline, week 1 and week 4. Arousals during rapid eye movement and non-rapid eye movement sleep were scored blind to group allocation. The following rapid eye movement sleep fragmentation index was the primary outcome: index 1 = (rapid eye movement arousals + rapid eye movement awakenings + non-rapid eye movement intrusions)/rapid eye movement duration in hours. Secondary outcomes were two further indices of rapid eye movement sleep fragmentation: index 2 = (rapid eye movement arousals + rapid eye movement awakenings)/rapid eye movement duration in hours; and index 3 = rapid eye movement arousals/rapid eye movement duration in hours. A non-rapid eye movement fragmentation index was also calculated (non-rapid eye movement arousals/non-rapid eye movement duration in hours). Linear-mixed models were fitted to assess between-group differences. There was no significant group difference for the primary rapid eye movement fragmentation index at week 1 (p = 0.097, d = -0.31) or week 4 (p = 0.741, d = -0.06). There was some indication that secondary indices of rapid eye movement fragmentation decreased more in the sleep restriction therapy group relative to control at week 1 (index 2: p = 0.023, d = -0.46; index 3: p = 0.051, d = -0.39), but not at week 4 (d ≤ 0.13). No group effects were found for arousals during non-rapid eye movement sleep. We did not find clear evidence that sleep restriction therapy modifies rapid eye movement sleep fragmentation. Small-to-medium effect sizes in the hypothesised direction, across several indices of rapid eye movement fragmentation during early treatment, demand further investigation in future studies.

Altered functional connectivity after acute sleep deprivation reveals potential locations for noninvasive brain stimulation techniques.

BACKGROUNDS: Non-invasive brain stimulation (NIBS) techniques are emerging as efficacious treatments for sleep deprivation (SD). However, the stimulation location of NIBS (e.g. transcranial magnetic stimulation and transcranial direct current stimulation) on intervening acute SD is limited in previous studies. In this study, we aimed to investigate potentially effective targets of NIBS on intervening acute SD. METHODS: We firstly performed a meta-analysis of 95 functional magnetic resonance imaging studies to find SD-related brain regions as regions of interest (ROI). Subsequently, we used resting-state functional connectivity analysis in 32 young individuals suffering from 24 h SD to identify brain surface regions associated with the ROIs. Finally, we applied 10-20 system coordinates to locate scalp sites for NIBS corresponding to the brain surface regions. RESULTS: We identified the bilateral dorsolateral prefrontal cortex, bilateral inferior frontal gyrus, left supplementary motor area, precentral, right precuneus, bilateral inferior parietal gyrus, right middle temporal gyrus, and superior frontal gyrus as potential targets of NIBS for intervening SD. The 10-20 system coordinates corresponding to these brain surface regions were identified as potential sites for NIBS. CONCLUSIONS: In conclusion, we identified several potential targets which could provide alternative stimulation locations for the use of NIBS on young patients suffering from acute SD.

Study on acupuncture improving sleep deprivation comorbid with cognitive dysfunction based on rs-fMRI: A protocol for systematic review and meta-analysis.

BACKGROUND: Sleep deprivation often lead to changes in attention, memory, mood, alertness, and metabolism. Especially, it is often accompanied by cognitive impairment of the brain. Acupuncture is safe and effective for improving cognitive function, but its underlying mechanism is not fully understood. Resting-state functional magnetic resonance imaging is an important means to study brain activity changes. However, the results are inconsistent and lack systematic evaluation and analysis. METHODS: We will search 9 databases, including PubMed, EMBASE, EBSCOhost-Medline, Web of Science, Cochrane Library, China National Knowledge Infrastructure, VIP Database and Wan-Fang Database, Chinese Biomedical Literature Database, and 2 clinical trials register platforms: Chinese Clinical Trial Registry, ClinicalTrials.gov (www.ClinicalTrials.gov/) from inception to November 1, 2022. We will use the Review Manager 5.4 software provided by the Cochrane Collaborative Network for statistical analysis. We then assessed the quality and risk of the included studies and observed the outcome measures. RESULTS: This study will analyze the effect of acupuncture on brain activity changes, improvement of sleep duration, and cognitive impairment. CONCLUSION: This meta-analysis aims to investigate the efficacy of acupuncture on brain activity changes in sleep deprivation comorbid with cognitive dysfunction, so as to provide effective evidence for clarifying its pathogenesis.

Effects of electroacupuncture on the ventral tegmental area- nucleus accumbens dopamine pathway in rats with chronic sleep deprivation.

BACKGROUND: Insomnia is a well-recognized clinical sleep disorder in the adult population. It has been established that acupuncture has a clinical effects in the treatment of insomnia; however, research on the underlying neural circuits involved in these effects is limited. METHODS: The modified multiple platform method (MMPM) was used to establish a rat model of chronic sleep deprivation (CSD). Forty rats were randomly divided into a control (Con) group, (untreated) CSD group, electroacupuncture-treated CSD group (CSD + EA) and estazolam-treated CSD group (CSD + Estazolam group) with n = 10 per group. In the CSD + EA group, EA was delivered at Yintang and unilateral HT7 (left and right treated every other day) with continuous waves (2 Hz frequency) for 30 min/day over 7 consecutive days. In the CSD + Estazolam groups, estazolam was administered by oral gavage (0.1 mg/kg) for 7 consecutive days. The open field test (OFT) was used to observe behavioral changes. Immunofluorescence assays and enzyme-linked immunosorbent assay (ELISA) were used to observe the effects of EA on the ventral tegmental area (VTA)-nucleus accumbens (NAc) dopamine (DA) pathway. We also assessed the effects of EA on the expression of dopamine D1 receptor (D1R) and dopamine D2 receptor (D2R) in the NAc, which are the downstream targets of the VTA-NAc DA pathway. RESULTS: After CSD was established by MMPM, rats exhibited increased autonomous activity and increased excitability of the VTA-NAc DA pathway, with increased VTA and NAc DA content, increased D1R expression and decreased D2R expression in the NAc. EA appeared to reduce the autonomous ability of CSD rats, leading to lower DA content in the VTA and NAc, reduced expression of D1R in the NAc and increased expression of D2R. Most importantly, EA produced effects similar to estazolam with respect to the general condition of rats with CSD and regulation of the VTA-NAc DA pathway. CONCLUSIONS: The therapeutic effect of EA in chronic insomnia may be mediated by reduced excitability of the VTA-NAc DA pathway, with lower DA content in the VTA and NAc, downregulated expression of D1R in the NAc and increased expression of D2R.

Effect of sleep deprivation plus existing therapies on depression: A systematic review and meta-analysis of randomized controlled trials.

BACKGROUNDS: Depression is the most common mental disorder in the world. Sleep deprivation (SD) is a well-known antidepressant. Several recombination protocols (including medications, bright light treatment [BLT], cognitive-behavioral therapy, sleep phrase advance/sleep phrase delay [SPA/SPD], and repetitive transcranial magnetic stimulation [rTMS]) have been developed to improve and maintain the effect of SD. However, relapse after recovery sleep has been reported, and different recombination protocols result in different outcomes. METHODS: The Embase, Cochrane, PubMed, CBM, Web of Science, and CINAHL databases were searched for clinical trials assessing depression and SD. Three independent reviewers classified forty-three abstracts. The Hamilton Depression Rating Scale was used to assess the outcomes. RESULTS: Compared with existing therapy, patients receiving SD displayed a significant improvement in clinician-rated depressive symptoms (MD -1.48 [95 % CI -2.60, -0.37], p < 0.05). A significant decrease was found in the subgroups of SD plus SPA/SPD (odds ratio 3.90 [95 % CI 1.66, 9.17], p < 0.05), total sleep deprivation[TSD] plus BLT (MD -3.28 [95 % CI -5.06, -1.50], p < 0.05), and partial sleep deprivation[PSD] plus rTMS (MD -7.94 [95 % CI -11.44, -4.45], p < 0.05). No significant differences were observed in the other subgroups. CONCLUSIONS: Adding SD to existing therapies showed a positive outcome in improving depression treatment, which provides evidence for the use of SD in treating depression. Further studies are needed to determine the precise effects of SD plus other interventions.

Cervical transcutaneous vagal nerve stimulation (ctVNS) improves human cognitive performance under sleep deprivation stress.

Fatigue is a pervasive public health and safety issue. Common fatigue countermeasures include caffeine or other chemical stimulants. These can be effective in limited circumstances but other non-pharmacological fatigue countermeasures such as non-invasive electrical neuromodulation have shown promise. It is reasonable to suspect that other types of non-invasive neuromodulation may be similarly effective or perhaps even superior. The objective of this research was to evaluate the efficacy of cervical transcutaneous vagal nerve stimulation (ctVNS) to mitigate the negative effects of fatigue on cognition and mood. Two groups (active or sham stimulation) of twenty participants in each group completed 34 h of sustained wakefulness. The ctVNS group performed significantly better on arousal, multi-tasking, and reported significantly lower fatigue ratings compared to sham for the duration of the study. CtVNS could be a powerful fatigue countermeasure tool that is easy to administer, long-lasting, and has fewer side-effects compared to common pharmacological interventions.

Sleep deprivation therapy to reset the circadian pacemaker in a non-24-hour sleep-wake disorder: a case report.

NONE: Non-24-hour sleep-wake disorder is 1 of several chronic circadian rhythm sleep-wake disorders. It is defined as progressive daily shifts in sleep onset and wake times. It mainly affects patients who are sight-impaired, is relatively rare in sighted patients, and is difficult to treat, with no guidelines. This case report discusses non-24-hour sleep-wake disorder in a sighted young man who complained of alternating severe insomnia and excessive sleepiness, with a sleep agenda and actigraphic data showing a daily delay of approximately 2 hours. A novel therapy by total sleep deprivation followed by a combination of morning light therapy and nocturnal melatonin administration was efficient in stopping his free-running sleep-wake pattern both immediately and in the long term. The treatment combination for 6 months resulted in stable circadian entrainment to a 24-hour cycle. Compliance with chronotherapy was maintained over the course of follow-up.

At the intersection of sleep deficiency and opioid use: mechanisms and therapeutic opportunities.

Due to the ongoing opioid epidemic, innovative scientific perspectives and approaches are urgently needed to reduce the unprecedented personal and societal burdens of nonmedical and recreational opioid use. One promising opportunity is to focus on the relationship between sleep deficiency and opioid use. In this review, we examine empirical evidence: (1) at the interface of sleep deficiency and opioid use, including hypothesized bidirectional associations between sleep efficiency and opioid abstinence; (2) as to whether normalization of sleep deficiency might directly or indirectly improve opioid abstinence (and vice versa); and (3) regarding mechanisms that could link improvements in sleep to opioid abstinence. Based on available data, we identify candidate sleep-restorative therapeutic approaches that should be examined in rigorous clinical trials.

Mild regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on spatial memory.

Vulnerable areas like the hippocampus are sensitive to insults such as sleep deprivation (SD); they are also susceptible to environmental enrichment. Much evidence is accumulating that chronic sleep deprivation causes alterations in the hippocampus that responsible for spatial memory. However, there is conflicting about the differences between acute and chronic SD results. The purpose of this study was to determine the protective effects of mild treadmill exercise on acute SD rats. Four groups were created as control, exercise, sleep deprivation, exercise + sleep deprivation. Multiple platforms method was used to induce REM sleep deprivation (RD) for 48 h. The exercise was applied fivedaysperweekforfour weeks(5 × 4). For the first and second weeks, the length of the exercise was 15 min in two sessions (5 min interval) followed by 15 min in three, 15 min in four sessions. Morris water maze (MWM) was used as a spatial memory test. Gene level was determined by using the qPCR technique. Malondialdehyde (MDA) content in the hippocampus was measured as an extent of peroxidative damage to lipids by using the ELISA method. 48 h RD impaired long-term spatial memory significantly. Mild, regular treadmill exercise ameliorated the detrimental effects of acute sleep deprivation on memory. There was no significant difference in MDA between groups. Hippocampal gene expression did not show any changes in all groups. Lack of correlation between memory impairment and levels of genes in the hippocampus is likely to be related to the differences in behavioral and genetic mechanisms.

Climate change and epilepsy: Insights from clinical and basic science studies.

Climate change is with us. As professionals who place value on evidence-based practice, climate change is something we cannot ignore. The current pandemic of the novel coronavirus, SARS-CoV-2, has demonstrated how global crises can arise suddenly and have a significant impact on public health. Global warming, a chronic process punctuated by acute episodes of extreme weather events, is an insidious global health crisis needing at least as much attention. Many neurological diseases are complex chronic conditions influenced at many levels by changes in the environment. This review aimed to collate and evaluate reports from clinical and basic science about the relationship between climate change and epilepsy. The keywords climate change, seasonal variation, temperature, humidity, thermoregulation, biorhythm, gene, circadian rhythm, heat, and weather were used to search the published evidence. A number of climatic variables are associated with increased seizure frequency in people with epilepsy. Climate change-induced increase in seizure precipitants such as fevers, stress, and sleep deprivation (e.g. as a result of more frequent extreme weather events) or vector-borne infections may trigger or exacerbate seizures, lead to deterioration of seizure control, and affect neurological, cerebrovascular, or cardiovascular comorbidities and risk of sudden unexpected death in epilepsy. Risks are likely to be modified by many factors, ranging from individual genetic variation and temperature-dependent channel function, to housing quality and global supply chains. According to the results of the limited number of experimental studies with animal models of seizures or epilepsy, different seizure types appear to have distinct susceptibility to seasonal influences. Increased body temperature, whether in the context of fever or not, has a critical role in seizure threshold and seizure-related brain damage. Links between climate change and epilepsy are likely to be multifactorial, complex, and often indirect, which makes predictions difficult. We need more data on possible climate-driven altered risks for seizures, epilepsy, and epileptogenesis, to identify underlying mechanisms at systems, cellular, and molecular levels for better understanding of the impact of climate change on epilepsy. Further focussed data would help us to develop evidence for mitigation methods to do more to protect people with epilepsy from the effects of climate change.

Effects of transcranial direct current stimulation on performance and recovery sleep during acute sleep deprivation: a pilot study.

BACKGROUND: Previous studies claimed that transcranial direct current stimulation (tDCS) over the left dorsolateral prefrontal cortex (DLPFC) improves cognition in neuropsychiatric patients with cognitive impairment, schizophrenia, organic hypersomnia, etc, but few studies evaluated the effects of tDCS on cognitive improvement following sleep deprivation. The objective of this study was to determine whether tDCS (anode on the left DLPFC and cathode on the right DLPFC with a 2-mA current for 30 min) improves cognition following sleep deprivation. METHODS: Seven participants received active tDCS and eight participants received sham tDCS when their cognition declined during at least 30 h of sleep deprivation. All participants completed the psychomotor vigilance task, Trail Making Tests A and B, digit cancellation test, Stroop color word test, the Brief Visuospatial Memory Test-Revised and a procedural game every 2 h during the sleep deprivation and after recovery sleep. RESULTS: Compared to the sham stimulation, active tDCS (anode on the left DLPFC and cathode on the right DLPFC at a 2-mA current for 30 min) had beneficial effects on attention, memory, executive function, processing speed, and the ability to inhibit cognitive interference, and improved in subjective drowsiness and fatigue following sleep deprivation. The lasting effect of a single tDCS on cognition during sleep deprivation was greater than 2 h. In all participants, tDCS did not disturb recovery sleep, and cognitive performance recovered to the baseline levels after recovery sleep. CONCLUSIONS: The study results indicate that tDCS can improve cognition following sleep deprivation and does not disturb recovery sleep or cognitive performance after recovery sleep. The possible pathophysiological mechanisms might be related to the modulation of the corticothalamic pathway. We believe that tDCS can be applied in the treatment of sleep disorders involving sleepiness. TRIAL REGISTRATION NUMBER: ChiCTR2000029420. DATE OF REGISTRATION: 2020-1-31.

Regular aerobic exercise counteracts endothelial vasomotor dysfunction associated with insufficient sleep.

Insufficient sleep is associated with endothelial vasomotor dysfunction and increased cardiovascular risk. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn, reducing cardiovascular risk. We tested the hypotheses that regular aerobic exercise would 1) improve endothelial vasodilation and 2) decrease endothelin (ET)-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep <7 h/night. Thirty-six healthy, middle-aged adults were studied: 16 with normal sleep duration (age: 57 ± 2 yr; sleep duration: 7.4 ± 0.1 h/night) and 20 with short sleep duration (age: 56 ± 1 yr; sleep duration: 6.2 ± 0.1 h/night). The 20 short sleepers completed a 3-mo aerobic exercise training intervention. Forearm blood flow was determined (via plethysmography) in response to intra-arterial acetylcholine (ACh), BQ-123 (ETA receptor antagonist), ACh + BQ-123, and sodium nitroprusside. Forearm blood flow responses to ACh were lower (∼20%; P < 0.05) in the short (from 4.2 ± 0.2 to 10.5 ± 0.6 mL/100 mL tissue/min) versus normal (4.2 ± 0.2 to 12.7 ± 0.6 mL/100 mL tissue/min) sleepers. In response to BQ-123, the short-sleep group had a significantly greater increase in resting forearm blood flow than the normal-sleep group (∼25% vs. ∼8%). ACh + BQ-123 resulted in a significant (∼25%) increase in the ACh-mediated vasodilation in the short-sleep group only. After exercise training, although nightly sleep duration was unchanged (6.4 ± 0.1 h/night), ACh-mediated vasodilation was significantly higher (∼20%), ET-1-mediated vasoconstriction was significantly lower (∼80%), and the vasodilator response to ACh was not increased with ETA receptor blockade. Regular aerobic exercise, independent of changes in nightly sleep duration, can counteract insufficient sleep-related endothelial vasomotor dysfunction.NEW & NOTEWORTHY Habitual insufficient nightly sleep (<7 h/night) is associated with increased risk of cardiovascular disease and events. Endothelial dysfunction, specifically reduced endothelium-dependent vasodilation and increased endothelin (ET)-1-mediated vasoconstriction, is considered to be a major contributing mechanism underlying increased vascular risk with insufficient sleep. In contrast to insufficient sleep, regular aerobic exercise enhances endothelial vasomotor function, reducing the risk of cardiovascular disease and associated events. In the present study, we determined the effects of aerobic exercise training on endothelium-dependent vasodilation and ET-1 vasoconstriction in adults who habitually sleep <7 h/night. After exercise training, although nightly sleep duration was unchanged, endothelium-dependent vasodilation was significantly enhanced and ET-1-mediated vasoconstrictor tone was significantly reduced in adults who sleep <7 h/night. Regular aerobic exercise training can mitigate insufficient sleep-related endothelial vasomotor dysfunction and, in turn, potentially reduce the cardiovascular risk associated with habitual insufficient nightly sleep.

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives.

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health.Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/.

Reducing Delirium in Hospitalized Adults Through a Structured Sleep Promotion Program.

BACKGROUND: Delirium affects approximately 1 in 4 patients during their hospitalization and is associated with numerous complications. Sleep deprivation is a significant risk factor for developing delirium and is a patient dissatisfier. PROBLEM: An internal assessment revealed that up to 25% of all patients on medical-surgical units had a diagnosis of delirium while in the hospital. APPROACH: An evidence-based practice project was implemented to reduce the development of delirium through sleep promotion on 2 inpatient units. A dedicated time was selected, and key strategies were identified to promote sleep with minimal interruptions. OUTCOMES: Delirium decreased by 33% and 45% on the 2 units over 1 year. Overall, patient satisfaction for quietness at night survey responses also increased (P = .0005; CI, 0.05 to 0.67) with ongoing sustainment. CONCLUSIONS: Implementation of a dedicated period to sleep was associated with a reduction in delirium and increased patient satisfaction for quietness at night.

Biological rhythms and chronotherapeutics in depression.

Depressive syndromes are frequent and heterogeneous brain conditions with more than 90% of patients suffering from sleep complaints. Better characterizing this "sleep" domain may allow to both better treat acute episodes with existing chronotherapeutics, but also to prevent the manifestation or recurrences of mood disorders. This work aims to i) review theoretical and fundamental data of chronotherapeutics, and ii) provide practical recommendations. Light therapy (LT) can be used as a first-line monotherapy of moderate to severe depression of all subtypes. LT can be also used as a combination with antidepressant to maximize patients' response rates, which has a clear superiority to antidepressant alone. Sleep deprivation (SD) is a rapid and powerful chronotherapeutic with antidepressant responses within hours in 45-60% of patients with unipolar or bipolar depression. Different strategies should be combined to stabilize the SD antidepressant effect, including concomitant medications, repeated SD, combination with sleep phase advance and/or LT (triple chronotherapy). Melatonin treatment is of interest in remitted patients with mood disorder to prevent relapses or recurrences, if a complaint of insomnia, poor sleep quality or phase delay syndrome is associated. During the acute phase, melatonin could be used as an adjuvant treatment for symptoms of insomnia associated with depression. The cognitive behavioral therapy for insomnia (CBT-I) can be recommend to treat insomnia during euthymic phases. The Interpersonal and social rhythm therapy (IPSRT) is indicated for the acute treatment of bipolar depression and for the prevention of mood episodes. Chronotherapeutics should always be associated with behavioral measures for healthy sleep.

Causes and effects of lack of sleep in hospitalized children. / Causas y efectos en la falta de sueño en niños hospitalizados.

Sleep is a key function that takes up one third of our lives. Sleep deprivation may lead to physical and psychological disorders in the short and long term. Hospitalization, regardless of its cause, does not favor good enough and restorative sleep. It is affected by both external (light, noise) and internal (procedures, drugs, care) factors. The intensive care unit is the place where falling asleep and maintaining sleep is more difficult. This is in addition to disease severity and the characteristics of its structure and functioning. A poor sleep quantity or quality may trigger an acute confusional state, which often affects hospitalized children, known as delirium. Promoting a joint effort among all sectors of the hospital setting targeted at protecting sleep as much as possible is the required task.

El sueño es una función vital en la que transcurre un tercio de nuestras vidas. Su restricción puede provocar trastornos físicos y psíquicos a corto y largo plazo. La internación hospitalaria, sin tener en cuenta la enfermedad que la originó, no favorece un sueño reparador y suficiente. Los factores que interfieren son externos (luz, ruidos) e internos (procedimientos, fármacos, cuidados). La Unidad de Cuidados Intensivos es el lugar con mayor dificultad para la conciliación y el mantenimiento del sueño. Se suma la gravedad de la enfermedad y las características de su estructura y funcionamiento. El deterioro de la cantidad o calidad del sueño podría desencadenar un cuadro de confusión mental agudo que, con frecuencia, afecta a los niños internados, reconocido como delirium. Promover, en el medio institucional, un trabajo conjunto de todos los estamentos para proteger el sueño dentro de lo posible es una tarea por realizar.

Weakly encoded memories due to acute sleep restriction can be rescued after one night of recovery sleep.

Sleep is thought to play a complementary role in human memory processing: sleep loss impairs the formation of new memories during the following awake period and, conversely, normal sleep promotes the strengthening of the already encoded memories. However, whether sleep can strengthen deteriorated memories caused by insufficient sleep remains unknown. Here, we showed that sleep restriction in a group of participants caused a reduction in the stability of EEG activity patterns across multiple encoding of the same event during awake, compared with a group of participants that got a full night's sleep. The decrease of neural stability patterns in the sleep-restricted group was associated with higher slow oscillation-spindle coupling during a subsequent night of normal sleep duration, thereby suggesting the instantiation of restorative neural mechanisms adaptively supporting cognition and memory. Importantly, upon awaking, the two groups of participants showed equivalent retrieval accuracy supported by subtle differences in the reinstatement of encoding-related activity: it was longer lasting in sleep-restricted individuals than in controls. In addition, sustained reinstatement over time was associated with increased coupling between spindles and slow oscillations. Taken together, these results suggest that the strength of prior encoding might be an important moderator of memory consolidation during sleep. Supporting this view, spindles nesting in the slow oscillation increased the probability of correct recognition only for weakly encoded memories. Current results demonstrate the benefit that a full night's sleep can induce to impaired memory traces caused by an inadequate amount of sleep.

Perspectives in affective disorders: Clocks and sleep.

Mood disorders are often characterised by alterations in circadian rhythms, sleep disturbances and seasonal exacerbation. Conversely, chronobiological treatments utilise zeitgebers for circadian rhythms such as light to improve mood and stabilise sleep, and manipulations of sleep timing and duration as rapid antidepressant modalities. Although sleep deprivation ("wake therapy") can act within hours, and its mood-elevating effects be maintained by regular morning light administration/medication/earlier sleep, it has not entered the regular guidelines for treating affective disorders as a first-line treatment. The hindrances to using chronotherapeutics may lie in their lack of patentability, few sponsors to carry out large multi-centre trials, non-reimbursement by medical insurance and their perceived difficulty or exotic "alternative" nature. Future use can be promoted by new technology (single-sample phase measurements, phone apps, movement and sleep trackers) that provides ambulatory documentation over long periods and feedback to therapist and patient. Light combinations with cognitive behavioural therapy and sleep hygiene practice may speed up and also maintain response. The urgent need for new antidepressants should hopefully lead to reconsideration and implementation of these non-pharmacological methods, as well as further clinical trials. We review the putative neurochemical mechanisms underlying the antidepressant effect of sleep deprivation and light therapy, and current knowledge linking clocks and sleep with affective disorders: neurotransmitter switching, stress and cortico-limbic reactivity, clock genes, cortical neuroplasticity, connectomics and neuroinflammation. Despite the complexity of multi-system mechanisms, more insight will lead to fine tuning and better application of circadian and sleep-related treatments of depression.

Impact of Sleep Deprivation in the Neurological Intensive Care Unit: A Narrative Review.

Sleep is fundamental for everyday functioning, yet it is often negatively impacted in critically ill patients by the intensive care setting. With a focus on the neurological intensive care unit (NeuroICU), this narrative review summarizes methods of measuring sleep and addresses common causes of sleep disturbance in the hospital including environmental, pharmacological, and patient-related factors. The effects of sleep deprivation on the cardiovascular, pulmonary, immune, endocrine, and neuropsychological systems are discussed, with a focus on short-term deprivation in critically ill populations. Where evidence is lacking in the literature, long-term sleep deprivation studies and the effects of sleep deprivation in healthy individuals are also referenced. Lastly, strategies for the promotion of sleep in the NeuroICU are presented.

Research on freshman and sleeping habits: A text message-based sleep intervention.

OBJECTIVE: Lack of understanding regarding the function of sleep and lack of education regarding healthy sleep practices may hinder college students from getting sufficient quality sleep. The current study examines the effect of a text message based educational intervention aimed at improving sleep quality and sleep hygiene behaviors in freshman undergraduate college students. PARTICIPANTS: 135 undergraduate students were recruited fall of 2016. METHODS: Three discussion groups were held to test and refine the text message content. Students were randomized into a three-group pretest-posttest experimental design. Participants completed measures of sleep quality, sleep hygiene, and sleep knowledge. RESULTS: Data analysis indicated the intervention did not demonstrate significant differences between groups over time on sleep quality, sleep hygiene behaviors, and sleep knowledge. CONCLUSION: More research is needed to understand how best to harness text messaging technology and sleep health education to promote healthy sleep behaviors in college students.