Sleep deprivation,the process and state of partial or complete lack of normal sleep caused by various factors,is prevalent at present.Seriously impairing the physical and mental health,sleep deprivation has become a public health problem that cannot be ignored.Studies have demonstrated that blood-brain barrier impairment is the key pathophysiological process of a variety of neurological diseases.Although clinical and basic studies have suggested that sleep deprivation can induce blood-brain barrier impairment,the underlying mechanisms remain to be elucidated.This review summarizes the advances in the mechanisms of blood-brain barrier impairment induced by sleep deprivation.
Humans ; Sleep Deprivation/complications* ; Blood-Brain Barrier ; Brain

Sleep deprivation (SD) has been taken as an independent predictor for cardiovascular risks, which was closely related to the increased morbidity and mortality in coronary heart disease (CHD). In this article, after reviewing the impact of modern medical method sleep deprivation on CHD and studies on principle method recipe medicines for preventing and treating CHD, the authors observed the autonomic nerve dysfunction, hormonal metabolism dysfunction, endothelial dysfunction and inflammatory responses after sleep deprivation, which can cause or aggravate CHD. On the basis of the traditional Chinese medicine theories of "heart dominating the blood and vessels and the mind", the authors considered that traditional Chinese medicines can tonify heart and soothe the nerves, reducing all of the risk factors through multi-target and multi-pathway, and improve sleep and decrease the risk factors caused by sleep deprivation, which provides a new idea for the prevention and treatment of CHD.
Animals ; Coronary Disease ; drug therapy ; etiology ; prevention & control ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Sleep Deprivation ; complications

Research on the effect of sleep deprivation (SD) is an approach to shedding light on the working mechanism of sleep for cognitive brain function. To explore how SD affects cognitive function, a number of measures involving psychology, brain imaging and electrophysiology, have been adopted in this area. Research groups from domestic and verseas have focused on many aspects of cognitive science and have acquired initial results, but uniform conclusion has not been made because of mixed factors. Starting from the mechanism of SD, this paper summarizes the progress in the search of effect of SD, including the neurophysiologic change by brain imaging and the use of EEG for evaluating the decline of cognitive function, and then analyzes the main influential factors and orientation of future research in this area.
Brain ; physiopathology ; Cognition ; physiology ; Cognition Disorders ; etiology ; physiopathology ; Electroencephalography ; methods ; Event-Related Potentials, P300 ; physiology ; Humans ; Sleep Deprivation ; complications ; physiopathology

Sleep deprivation (SD) has been associated with an increased morbidity and mortality of coronary heart disease (CHD). SD could induce autonomic nervous dysfunction, hypertension, arrhythmia, hormonal dysregulation, oxidative stress, endothelial dysfunction, inflammation and metabolic disorder in CHD patients. This paper reviewed the study results of SD in clinical trials and animal experiments and concluded that SD was associated with cardiovascular risk factors, which aggravated CHD in pathogenesis and outcomes.
Autonomic Nervous System Diseases ; etiology ; Coronary Artery Disease ; etiology ; Humans ; Hypertension ; etiology ; Metabolic Diseases ; etiology ; Oxidative Stress ; Sleep Deprivation ; complications

Animals ; Extinction, Psychological ; physiology ; Fear ; physiology ; Male ; Mental Recall ; physiology ; Rats ; Rats, Sprague-Dawley ; Sleep Deprivation ; complications ; physiopathology ; Sleep, REM ; physiology

Sleep loss can severely impact on the integrity of cognitive functions. This review highlights the recent functional neuroimaging studies on the brain's response while performing cognitive tasks when deprived of sleep. Among sleep-deprived healthy volunteers, reduced attention, accompanied by lowered parieto-occipital activation, may underlie performance decrements seen in other "higher cognitive domains". Functional neuroimaging in this setting has increased our understanding of how the brain responds to, and compensates for, sleep loss. Functional neuroimaging may also provide a safe, reproducible and non-invasive means to evaluate the cognitive and neural impact of therapeutic interventions designed to treat sleep disorders and/ or to reduce the negative cognitive impact of sleep loss.
Attention ; Brain ; anatomy & histology ; pathology ; Cognition Disorders ; etiology ; pathology ; Continuous Positive Airway Pressure ; Emotions ; Humans ; Magnetic Resonance Imaging ; Sleep Apnea, Obstructive ; complications ; pathology ; therapy ; Sleep Deprivation ; complications ; pathology ; physiopathology ; Sleep Initiation and Maintenance Disorders ; complications ; physiopathology ; Task Performance and Analysis

AIMTo explore the effects of sleep deprivation (SD) on myocardium and its antioxygen index.

METHODS35 Sprague Dawley rats were randomly divided into five groups: Cage control, Tank control, SD 2 d, SD 4 d and SD 6 d. The "flower pot" technique was used to establish rats sleep deprivation model followed by record of surface electrocardiogram, detection of myocardium morphology changes under microscope and transmission electron microscope and investigation of MDA content and SOD activity of myocardial mitochondria.

RESULTSAfter sleep deprivation, heart rate increased and ECG showed ischemia of myocardium; subcellular organelles such as chromosome, endoplasmic reticulum, mitochondria, intercalated disk impaired, myofibril lysis or necrosis, and lipid peroxidation reaction effects spread widely; edema, bleeding of the microvessels and invasion of the monocytes could be seen in the lumen. The MDA level increased and SOD activity increased followed by a decreased trend.

CONCLUSIONSleep deprivation can induce damage on myocardium, and the stress especially oxygen stress caused by SD may be the possible mechanism.

Animals ; Electrocardiography ; Female ; Male ; Myocardial Ischemia ; etiology ; pathology ; physiopathology ; Oxidative Stress ; physiology ; Rats ; Rats, Sprague-Dawley ; Sleep Deprivation ; complications ; Superoxide Dismutase ; metabolism

Parkinson's disease (PD) is a multifaceted disease in which environmental variables combined with genetic predisposition cause dopaminergic (DAergic) neuron loss in the substantia nigra pars compacta. The mutation of leucine-rich repeat kinase 2 (Lrrk2) is the most common autosomal dominant mutation in PD, and it has also been reported in sporadic cases. A growing body of research suggests that circadian rhythm disruption, particularly sleep-wake abnormality, is common during the early phase of PD. Our present study aimed to evaluate the impact of sleep deprivation (SD) on motor ability, sleep performance, and PD pathologies in Lrrk2^G2019S transgenic mice. After two months of SD, Lrrk2^G2019S mice at 12 months of age showed an exacerbated PD-like phenotype with motor deficits, a reduced striatal DA level, degenerated DAergic neurons, and altered sleep structure and biological rhythm accompanied by the decreased protein expression level of circadian locomotor output cycles kaput Lrrk2 gene in the brain. All these changes persisted and were even more evident in 18-month-old mice after 6 months of follow-up. Moreover, a significant increase in α-synuclein aggregation was found in SD-treated transgenic mice at 18 months of age. Taken together, our findings indicate that sleep abnormalities, as a risk factor, may contribute to the pathogenesis and progression of PD. Early detection of sleep disorders and improvement of sleep quality may help to delay disease progression and provide long-term clinical benefits.
Animals ; Electroencephalography ; Leucine/genetics* ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics* ; Mice ; Mice, Transgenic ; Mutation ; Parkinson Disease/metabolism* ; Sleep Deprivation/complications* ; alpha-Synuclein/genetics*