睡眠剥夺对健康青年男性工作记忆的影响及莫达非尼的干预作用

目的 探讨不同时间睡眠剥夺对健康青年男性工作记忆的影响,以及莫达非尼对睡眠剥夺的对抗作用. 方法 10名健康男性青年志愿者进行间隔1周的3次36 h睡眠剥夺,第一次不服药,为剥夺组,后2次志愿者交叉服用莫达非尼和安慰剂(于睡眠剥夺14 h和24h 2次服用1.每次服药后3 h进行工作记忆任务测试(倒数n项测验),剥夺组也在同样的时间进行测试.把睡眠剥夺前清醒时设为正常对照组.并进行测试. 结果 剥夺组的1-back任务的第2次测试平均反应时间较第1次测试明显延长,2-back任务的第2次测试平均反应时间、错误率较第1次测试明显增高,差异均有统计学意义(P＜0.05).剥夺组的l-back任务的第2次测试错误率与平均反应时间均比正常对照组明显增高,2-back任务的两次测试平均反应时间和错误率较正常对照组明显增高,差异均有统计学意义(P＜0.05).莫达非尼组的1-back任务的第2次测试平均反应时间较剥夺组明显降低,2-back任务的两次测试平均反应时间和错误率较剥夺组明显降低,差异均有统计学意义(P＜0.05). 结论 睡眠剥夺后工作记忆受到损害,并随着剥夺时间延长,受损加重.莫达非尼对睡眠剥夺后的工作记忆损害有明显的改善作用.     

睡眠剥夺对健康人注意力的影响

目的探讨睡眠剥夺对健康人注意力的影响。方法对10名健康青年男性志愿者进行32h(第1d8:00～第2d16:00)睡眠剥夺,并在睡眠剥夺前、后各17h和32h分别进行4次持续性操作任务(CPT)、选择性注意力(Stroop测验)的测试。结果在CPT和Stroop试验测试中,睡眠剥夺后2次测试的反应时间显著长于睡眠剥夺前,错误率显著高于睡眠剥夺前(均P<0.05),睡眠剥夺后第2次测试平均反应时间和错误率较第1次测试显著增加(均P<0.05)。结论健康人睡眠剥夺后注意力明显下降,并且睡眠剥夺时间越长越明显。     

Geranylgeranylacetone, an inducer of HSP 70, attenuates REM sleep rebound after sleep deprivation

The effect of pretreatment of geranylgeranylacetone (GGA), an inducer of heat shock protein (HSP) 70, on responses in sleep and core body temperature (Tcore) against sleep deprivation (SD) was examined in rats. After 3 days of GGA or vehicle injection, a 6-h period of SD was performed. During the recovery period, both rapid-eye movement (REM) and non-REM (NREM) sleep were increased in both GGA- and vehicle-injected rats. However, in GGA-injected rats, REM-sleep rebound was significantly suppressed, while NREM-sleep rebound remained unaffected. In addition, the increase of Tcore caused by SD was also attenuated in GGA-injected rats. In the hippocampus, both SD and the GGA pretreatment induced an increase in the expression of HSP70 mRNA, indicating that the SD functions as a stress for hippocampal neurons and that the GGA induces HSP70 expression. The findings suggest that pretreatment with GGA suppresses REM sleep rebound and the response of Tcore against SD.     

How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay

Total sleep deprivation (TSD) leads to an immediate amelioration of depressed mood in approximately 70 % of patients with the melancholic subtype of depression. The clinical utility of this procedure is limited, as the improvement usually subsides after the next night of sleep. In the present study, 40 depressed inpatients, being free of psychoactive medication for at least 7 days and who had responded to a TSD were then distributed (according to a matched-pair design) to a sleep phase advance (SPA = time in bed scheduled from 1700–2400 hrs) or a sleep phase delay (SPD = time in bed from 0200–0700 hrs) with a succeeding shift back (for one hour in the SPA group per day) respectively shift forward (for 30 minutes in the SPD group per day), until the initial sleep phase (2300–0600 hrs) was reached after seven days again. Based on previous observations it was hypothesized that a phase advance of the sleep period should prevent responders to TSD from relapsing. Whereas 75% of the TSD responders were stabilized by the phase advanced condition and did not relapse over a period of seven days, only 40% of the patients in the phase delayed condition did not relapse. Polysomnography during the course of the study gave no evidence that the unusual sleep schedules caused prolonged sleep deprivation. Abnormalities of REM sleep persisted both in the clinical responders and non-responders after the sleep wake manipulation. It is concluded that the clinical effectiveness of TSD can be significantly improved by combining TSD with a following phase advance of the sleep period. Received: 3 May 1999 / Accepted: 12 July 1999     

Effects of chronic sleep deprivation on central cholinergic receptors in rat brain

Rats subjected to chronic total sleep deprivation (TSD) by the disk-over-water method have shown very large, sustained rebounds in paradoxical sleep (PS) (also known as REM sleep). Other studies have indicated that cholinergic mechanisms are involved in the instigation and maintenance of PS. Hypothetically, the large PS rebounds could be mediated by an upregulation of cholinergic receptors during TSD. To evaluate this hypothesis, regional brain cholinergic receptors were compared in rats subjected to 10-day TSD by the disk-over-water method (TSD rats), yoked control (TSC) rats which received the same physical stimulation but with much smaller reductions in sleep, and home cage control (HCC) rats. l-[³H]nicotine and [³H]quinuclidinyl benzilate were used as specific cholinergic radioligands for nicotinic and muscarinic receptor binding assays, respectively. Nicotinic receptor binding was not significantly different among groups for any of the brain regions assayed, including frontal cortex, parietal cortex, thalamus, amygdala, hippocampus, anterior hypothalamus, posterior hypothalamus, caudate, limbic system (including septal area, olfactory tubercle, and nucleus accumbens), midbrain, pons, and medulla. Thus, there was no evidence that changes in nicotinic receptors mediate the PS rebounds. For muscarinic receptor binding, TSD rats differed significantly from control rats only in showing a higher binding affinity than TSC rats in the limbic system and a lower binding density than HCC rats in the hippocampus. On the other hand, significant differences in muscarinic receptor binding sites between rats selectively deprived of PS and their yoked controls were found only for the septal area. Although chronic sleep deprivation resulted in a few regionally specific changes in muscarinic receptor binding, compared to the large PS rebounds during recovery from chronic sleep deprivation, the changes in receptor binding were very small and were not apparent in the region most intimately related to the cholinergic instigation of PS, i.e., the pons. Thus, there was no substantial evidence that PS rebounds are mediated via cholinergic receptor upregulation.     

DST in healthy volunteers and after sleep deprivation

The dexamethasone suppression test (DST) was performed in 46 healthy volunteers and repeated in nine of them following total sleep deprivation (TSD). While only 2 postdexamethasone cortisol values were insufficiently suppressed (greater than 5 micrograms %) in control DSTs, 5 postdexamethasone cortisol values were above 5 micrograms % following TSD. The mean postdexamethasone value was increased from 1.55 +/- 1.06 to 4.47 +/- 5.86 micrograms % following TSD at 8.00 h. The authors conclude that sleep deprivation as a therapeutic approach and prolonged sleeplessness may bias DST results.     

Manipulating REM sleep in older adults by selective REM sleep deprivation and physiological as well as pharmacological REM sleep augmentation methods

Experimental approaches to manipulate REM sleep within the cognitive neuroscience of sleep are usually based on sleep deprivation paradigms and focus on younger adults. In the present study, a traditional selective REM sleep deprivation paradigm as well as two alternative manipulation paradigms targeting REM sleep augmentation were investigated in healthy older adults. The study sample consisted of 107 participants, male and female, between the ages of 60 and 82 years, who had been randomly assigned to five experimental groups. During the study night, a first group was deprived of REM sleep by selective REM sleep awakenings, while a second group was woken during stage 2 NREM sleep in matched frequency. Physiological REM sleep augmentation was realized by REM sleep rebound after selective REM sleep deprivation, pharmacological REM sleep augmentation by administering an acetylcholinesterase inhibitor in a double-blind, placebo-controlled design. Deprivation and augmentation paradigms manipulated REM sleep significantly, the former affecting more global measures such as REM sleep minutes and percentage, the latter more organizational aspects such as stage shifts to REM sleep, REM latency, REM density (only pharmacological augmentation) and phasic REM sleep duration. According to our findings, selective REM sleep deprivation seems to be an efficient method of REM sleep manipulation in healthy older adults. While physiological rebound-based and pharmacological cholinergic REM sleep augmentation methods both failed to affect global measures of REM sleep, their efficiency in manipulating organizational aspects of REM sleep extends the traditional scope of REM sleep manipulation methods within the cognitive neuroscience of sleep.     

Small platform sleep deprivation selectively increases the average duration of rapid eye movement sleep episodes during sleep rebound

The single platform-on-water (flower pot) method is extensively used for depriving rapid eye movement sleep (REMS). Detailed comparison of sleep–wake architecture, recorded during the rebound period after spending three days on either a small or large platform, could separate the effects of REMS deficit from other stress factors caused by the procedure. A further aim of the study was to find the most characteristic REMS parameter of the rebound originating from REMS deficit. Rats were kept on a small or large platform for 72 h. Their fronto-parietal electroencephalogram, electromyogram and motility were recorded during the 24 h rebound at the beginning of the passive phase. A similar period of a home cage group was also recorded. The most typical differences between the two rebound groups were the increased cumulative time and longer average duration of REMS episodes without significant change in the number of these episodes of the small platform animals during the passive phase. Results obtained by cosinor analysis were in accordance with the findings above. Since we did not find any difference in the average duration of REMS episodes comparing the large platform rebound group and the home cage group, we concluded that the increased mean duration of REMS episodes is a selective marker for the rebound caused by small platform sleep deprivation, while other changes in sleep architecture may be the consequence of stress and also some sleep deficit.     

The timing and duration of sleep in partial sleep deprivation therapy of depression

The antidepressant response to partial sleep deprivation early in the night (PSD-E) was compared with the response to partial sleep deprivation late in the night (PSD-L) in 16 drug-free depressed inpatients using a balanced order crossover design. PSD-L had a significantly greater antidepressant effect that PSD-E. The response to PSD-L was sustained and enhanced by a second night of treatment. Patients had significantly shorter sleep durations and reduced REM sleep on PSD-L that did not occur in the PSD-E situation. There was a significant negative correlation between response to PSD and sleep duration, and in particular, REM sleep duration, in the late sleep deprivation situation. Thus, the amount and timing of sleep appear to be factors in the response to PSD, but additional studies are needed to evaluate the relative importance of these parameters.     

Platform sleep deprivation affects deep slow wave sleep in addition to REM sleep

Rats were sleep deprived by the platform method to look for differential effects on light and deep slow wave sleep depending on platform size. Diameters of large and small platforms were 15 cm and 5.1 cm respectively. Sleep was recorded during a baseline light period (09.00-19.00 h), continuously during 48 h of sleep deprivation and during the first lights on recovery period (09.00-19.00 h). In both platform conditions REM sleep was virtually abolished during the first light period (hours 0-10 of sleep deprivation), while NREM sleep was reduced to approximately half of control values. During the second light period (hours 22-34 of sleep deprivation) REM sleep recovered somewhat in the large platform group. Light slow wave sleep (SWS-1) was comparable to baseline while deep slow wave sleep (SWS-2) was still significantly reduced. In the small platform group both SWS-2 and REM sleep was considerably reduced on day 2. Over the whole deprivation period there was an effect of platform size on SWS-1 (higher in the small platform group), and on SWS-2 and REM sleep (lower in the small platform group). During the 9 h light-time recovery sleep there was an REM sleep rebound in both groups. SWS-1 was reduced in both groups while SWS-2 was not significantly increased. The ratio SWS-2/SWS-1 was, however, significantly increased only in the small platform group recovery sleep. The results suggest that platform sleep deprivation deprives the animals of deep slow wave sleep in addition to REM sleep. This has implications for conclusions on REM sleep function based upon REM sleep deprivation.     

Effects of REM sleep awakenings and related wakening paradigms on the ultradian sleep cycle and the symptoms in depression

In 1975 Vogel and coworkers published their classical study where they compared selective rapid eye movement (REM) sleep deprivation by brief awakenings to a control intervention paradigm in depressed patients. The superior antidepressive impact of the first procedure was attributed to the REM pressure accumulating during the treatment period. The laborious procedure and the considerable effort necessary to evaluate the sleep profiles in real time have prevented similar experiments so far. Based on artificial neural networks we developed a software for the real time detection of REM sleep. In combination with an alarm system the algorithm allowed us to wake up subjects automatically and to reduce REM sleep by about 50%. The procedure was then compared to a modified nonREM intervention paradigm for a treatment period of ten consecutive nights in depressed patients (n(1)=14, n(2)=13). These simultaneously received moderate dosages of Trimipramine. We found a strong and robust but not significantly different reduction of the average Hamilton rating scores (33 and 41% of baseline levels). While the REM sleep awakenings shortened the sleep cycle duration considerably, our nonREM intervention paradigm lengthened the ultradian alternations. Both effects might be interpreted as a challenge imposed on the nonREM-REM alternating mechanism possibly responsible for the antidepressive impact. A different timing of the control interventions might have caused the discrepancy between our findings and those of Vogel and coworkers.     

全部睡眠剥夺对健康男性青年脑电功率谱的影响

目的 探讨全部睡眠剥夺对健康男性青年脑电功率谱的影响。方法 选身体健康男性青年（１９￣２２岁）自愿受试者２０名,剥夺全部睡眠５０ｈ,定时记录脑电图共８次（间隔６ｈ）,分析各脑区各频段脑电功率。结果 睡眠剥夺５０ｈ后所有脑区（双侧枕区除外）的δ频段（Ｐ〈０．０５￣Ｐ〈０．００１）、θ频段（Ｐ〈０．０１￣Ｐ〈０．００１）功率升高,α２频段功率降低（Ｐ〈０．００１）,并与睡眠剥夺时间呈线性相关（Ｐ〈０．０１￣Ｐ〈０．００１）。例如,Ｆ３区δ、θ和α２频段脑电功率在睡眠剥夺前后分别为３．７８、４．１７;３．６５、４．３４;４．６４和３．９１ｌｎ（μＶ＾２）。脑电功率出现显著变化的时间由早以晚依次为α２频段、θ频段和δ频段。额前区、中央区、顶区和颞中区的改变较早,左半球比右半球早。脑电功率具有显著的随时间变化现象。快波频     

Extracellular serotonin levels in the medullary reticular formation during normal sleep and after REM sleep deprivation

Rapid eye movement (REM) sleep is hypothesized to result from the activity of REM sleep-generating and REM sleep-inhibiting neurons. The serotoninergic (5-HT) neurons of the dorsal raphe nucleus (DRN) represents one such population of REM-sleep inhibiting neurons since they are silent during REM sleep. Consistent with the decrease in activity of 5-HT neurons, the brain extracellular levels of 5-HT are lower during REM sleep compared to wakefulness. It is not known whether serotonin release is also reduced as a consequence of REM sleep rebound. Using microdialysis sampling coupled to HPLC–ECD, we measured the extracellular levels of 5-HT and its metabolite (5-HIAA) in the medial medullary reticular formation (mMRF) of freely behaving rats during normal sleep, REM sleep deprivation as well as during REM sleep rebound. We found that the levels 5-HT and 5-HIAA were significantly decreased by REM sleep deprivation. The reduction of 5-HT release was maintained during REM sleep rebound but the extracellular level of its main metabolite was increased. In addition, even during REM sleep rebound, 5-HT release during sleep was low compared to wakefulness. Taken together these data support the permissive role of 5-HT neurotransmission for REM sleep expression.     

Modafinil reduces microsleep during partial sleep deprivation in depressed patients

Objective

Sleep deprivation (SD) can induce a prompt decrease in depressive symptoms within 24 h. Following the recovery night, however, a relapse into depression occurs in most patients. Recovery sleep, naps and even very short episodes of sleep (microsleep; MS) during SD have been shown to provoke a rapid relapse into depression. This study tested the hypothesis that modafinil reduces MS during SD and stabilizes the treatment response to PSD compared to placebo.

Methods

A total of 28 patients (13 men, 15 women; age 45.1 ± 12.1 years) with a major depressive episode and a cumulative daytime microsleep of five or more minutes were investigated using a double-blind placebo-controlled study design. All patients were treated with a stable mirtazapine monotherapy. A partial SD (PSD) was performed after one week. Additional morning treatment with modafinil vs. placebo started during PSD and was maintained over two weeks. Sleep-EEG and MS episodes were recorded with a portable EEG. Depression severity was assessed using the Hamilton Depression Rating Scale before, during and after PSD and at follow-ups after one and two weeks.

Results

Patients treated with modafinil showed significantly reduced microsleep during PSD (11.63 ± 15.99 min) compared to the placebo group (47.77 ± 65.31 min). This suppression of MS was not associated with the antidepressive effect of PSD.

Conclusions

Compared to placebo, modafinil was efficient in reducing daytime microsleep following partial sleep deprivation but did not enhance the antidepressive effects of PSD and did not stabilize antidepressive effects over two weeks.     

睡眠剥夺对认知影响的研究进展

现代社会,睡眠剥夺(sleep deprivation,SD)是一种常见现象,困扰着很多人,引起人的日间工作能力降低.近年来的研究结果显示,SD可以使认知功能受损,但是其损害机制尚不清楚.本综述将重点阐述SD对行为和中枢系统的影响,进而阐明SD引起认知功能受损的可能机制,并且展望未来的研究方向.     

Effects of sleep deprivation on cognitive functions

Sleep deprivation （SD） is a common condition that afflicts many people in modem life. Deficits in daytime perfor- mance due to SD are experienced universally. Recent evidence indicates that SD causes impairments in cognitive functions. However, the mechanisms that SD impairs cognitive functions are not clear. This review will focus on the behavioral and neural effects of SD with the aim to elucidate the possible mechanisms of SD-induced deterioration in cognitive functions and to identify directions for future research.     

The cholinesterase inhibitor DFP facilitates the expression of paradoxical sleep (PS) propensity in rats subjected to short-term PS deprivation

Short-term paradoxical sleep (PS) deprivation was used to examine the effects of chronic exposure to subtoxic doses of the cholinesterase inhibitor diisopropylfluorophosphate (DFP) on PS regulation. Rats were injected once daily with DFP (0.2 mg/kg per day; s.c.) for 11 consecutive days; control rats received a daily injection of oil vehicle. The experiment was conducted on the 10th and 11th days of treatment, when brain cholinesterase inhibition induced by DFP exposure was maximal. On the 10th day, an 8-h baseline recording was carried out. On the 11th day, a 6-h PS deprivation was carried out by manually awaking rats each time they showed polygraphic signs of PS; recordings were then continued for another 2 h to examine recovery sleep. During deprivation, though they slept less than controls, DFP-treated rats made more attempts to enter PS. After deprivation, their PS rebound had an overall amount comparable to that of the controls, but its time course was shortened: whereas PS elevation was manifested through the 2 h of recovery in the control group, it occurred only during the first hour in the DFP group. These results demonstrate that chronic, low-level DFP exposure facilitated the expression of the PS propensity that accumulated as a result of PS deprivation: it enhanced the tendency for PS during deprivation; it accelerated the rate of compensatory PS expression after deprivation. They support the hypothesis that DFP promotes PS initiation by increasing cholinergic transmission.     

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

BackgroundPrevious 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.MethodsSeven 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.ResultsCompared 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.ConclusionsThe 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 numberChiCTR2000029420.Date of registration2020-1-31.     

The diagnostic value of the short sleep EEG and other provocative methods following sleep deprivation

Summary One hundred and eighty-five EEGs recorded after deprivation of sleep for 24h were evaluated. Valuable diagnostic information was found in 59% of the EEG recordings; 24% of the EEGs contained seizure activity. The duration of the stages of sleep and the frequency of seizure activity, paroxysmal sharp wave groups and localizing findings were analyzed. The sleep stages A to C (based on the Loomis scale) were reached for about equal duration by an EEG recording of 30–40 min; sleep stage D was reached only shortly and stage E was not observed. Pathological EEG findings appeared for the most part in the sleep stages A and B. Localized findings were pronounced in stage C. No significant differences pertaining to the occurrence and form of EEG patterns were found between patient groups with primary generalized seizures, psychomotor seizures or those with unclarified disturbances of consciousness. The combination of the short sleep EEG following 24h of sleep deprivation with subsequent use of the additional provocative methods of hyperventilation, photostimulation and hydration, yielded, in all, new information in 50% of the patients. Each of these additional methods contributed nearly equally to this information.

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Zusammenfassung Es wurden 185 EEGs nach 24h Schlafentzug ausgewertet. Hiervon enthielten 110 EEGs (59%) diagnostisch weiterführende Befunde. In 24% fand sich Krampfaktivität. Es wurden die Dauer der Schlafstadien, die Häufigkeit des Auftretens von Krampfaktivität, paroxysmalen Steilwellengruppen und Lokalbefunden analysiert. Die Schlaftiefen A bis C (nach Loomis) wurden während einer EEG-Ableitung von 30–40 min gleichmäßig lang, Stadium D nur kurz, Stadium E nicht erreicht. Pathologische EEG-Befunde traten überwiegend in den Schlafstadien A und B auf. Lokalbefunde fanden sich besonders im Stadium C. Zwischen den Patientengruppen mit primär generalisierten Anfällen, psychomotorischen Anfällen sowie Zuständen ungeklärter Bewußtseinsstörung fand sich kein signifikanter Unterschied hinsichtlich Auftreten und Ausprägung der EEG-Veränderungen. Die regelmäßig durchgeführte Hyperventilation und Fotostimulation und die Flüssigkeitsbelastung, die nur bei negativen Vorbefunden zusätzlich durchgeführt wurde, ergaben zusammen in 50% eine neue Information.

     

功能磁共振成像研究睡眠剥夺36小时对健康男性工作记忆的影响

目的 利用功能磁共振成像(functional magnetic resonance imaging,fMRI)技术研究睡眠剥夺36 h对健康男性工作记忆的影响及可能机制.方法 10名健康男性受试者连续36 h睡眠剥夺,睡眠剥夺前后分别接受工作记忆任务测试,同时进行fMRI扫描.fMRI扫描采用2项工作记忆任务,收集获得的行为学结果和fMRI图像,用SPM2软件进行图像分析.比较睡眠剥夺前后工作记忆任务测试及fMRI扫描结果.结果 剥夺后LTR任务的反应时间为(866±102)ms,比剥夺前[(754±91)ms]明显延长(t=2.59,P<0.01),准确率为84.78%±8.71%,比剥夺前(95.31%±3.56%)明显降低(t=3.52,P<0.01);剥夺后PLUS任务的反应时间为(848±94)ms,比剥夺前[(756±79),ms]明显延长(t=2.37,P<0.05),准确率为84.22%±9.66%,比剥夺前(95.70%±4.72%)明显降低(t=3.38,P<0.01);剥夺前在额顶叶、前扣带回和丘脑等工作记忆相关性脑区被激活.PLUS任务较LTR任务激活脑区范围更广,强度更显著.剥夺后顶叶激活降低,前额叶和丘脑的激活增强.结论 睡眠剥夺能够导致工作记忆能力受损.fMRI显示睡眠剥夺后完成工作记忆任务时,在相应脑区顶叶激活降低,前额叶和丘脑激活增强,这可能是睡眠剥夺导致认知功能损害的机制之一.