Sleep and memory
The relationship between sleep and memory has been studied since at least the early 19th century. Memory, the cognitive process of storing and retrieving past experiences, learning and recognition,[1] is a product of brain plasticity, the structural changes within synapses that create associations between stimuli. Stimuli are encoded within milliseconds; however, the long-term maintenance of memories can take additional minutes, days, or even years to fully consolidate and become a stable memory that is accessible (more resistant to change or interference). Therefore, the formation of a specific memory occurs rapidly, but the evolution of a memory is often an ongoing process.
Memory processes have been shown to be stabilized and enhanced (sped up and/or integrated) and memories better
History
In 1801, David Hartley first suggested that dreaming altered the associative planetary links within the brain during rapid eye movement (REM) periods of the sleep cycle. The idea that sleep had a mentally restorative effect, sorting out and consolidating memories and ideas, was intellectually acceptable by the end of the 19th century. In ‘Peter and Wendy’,
The first semi-multiple-systematic study of the connection between sleep and memory was conducted in 1924 by Jenkins and Dallenbach, for the purpose of testing Hermann Ebbinghaus' memory decay theory.[1] Their results showed that memory retention was much better after a period of sleep compared to the same time interval spent awake. It was not until 1953, however, when sleep was delineated into rapid eye movement sleep and non-rapid eye movement sleep, that studies focusing on the effect of specific sleep stages on memory were conducted.[1] As behavioral characteristics of the effects of sleep and memory are becoming increasingly understood and supported, researchers are turning to the weakly understood neural basis of sleep and memory.[4]
Sleep cycles
Sleep progresses in a cycle which consists of five stages. Four of these stages are collectively referred to as non-rapid eye movement (NREM) sleep whereas the last cycle is a rapid eye movement period. A cycle takes approximately 90–110 minutes to complete. Wakefulness is found through an electroencephalogram (
- Pre-sleep is the period of decreased perceptual awareness where brain activity is characterized by alpha waveswhich are more rhythmic, higher in amplitude and lower in frequency compared to beta waves.
- Stage one is characterized by light sleep and lasts roughly 10 minutes. Brain waves gradually transition to theta waves.
- Stage two also contains theta waves; however, random short bursts of increased frequency called sleep spindlesare a defining characteristic of this stage.
- Stage three and four are very similar and together are considered to be "deep sleep". In these stages brain activity transitions to delta waveswhich are the lowest in frequency and highest in amplitude. These two stages combined are also called slow wave sleep (SWS).
- Stage five, REM sleep, is one of the most interesting stages as brain wave patterns are similar to those seen in relaxed wakefulness. This is referred to as "active sleep" and is the period when most dreaming occurs. REM sleep is also thought to play a role in the cognitive development of infants and children as they spend much more of their sleep in REM periods opposed to adults.[5]
During the first half of the night, the largest portion of sleep is spent as SWS, but as the night progresses SWS stages decrease in length while REM stages increase.[6]
Memory terms
Stabilization vs. enhancement
Stabilization of a memory is the anchoring of a memory in place, in which a weak connection is established. Stabilization of procedural memories can even occur during waking hours, suggesting that specific non-declarative tasks are enhanced in the absence of sleep.[4] When memories are said to be enhanced, however, the connection is strengthened by rehearsal as well as connecting it to other related memories thereby making the retrieval more efficient. Whereas stabilization of non-declarative memories can be seen to occur during a wakeful state, enhancement of these sensory and motor memories has most been found to occur during nocturnal sleep.[4]
Use-dependent processes vs. experience-dependent processes
Brain activity that occurs during sleep is assessed in two ways: Use-dependency, and Experience-dependency.[7] Use-dependent brain activity is a result of the neuronal usage that occurred during the previous waking hours. Essentially it is neuronal regeneration, activity that occurs whether the person has learnt anything new or not.[7]
Experience-dependent brain activity is a result of a new situation, environment, or learned task or fact that has taken place in the pre-sleep period. This is the type of brain activity that denotes memory consolidation/enhancement.[7]
It is often hard to distinguish between the two in an experimental setting because the setting alone is a new environment. This new environment would be seen in the sleeping brain activity along with the newly learned task. To avoid this, most experimenters insist participants spend one day in the experimental condition before testing begins so the setting is not novel once the experiment begins. This ensures the collected data for experience-dependent brain activity is purely from the novel task.
Consolidation
Consolidation of a memory is a process that takes an initially unstable representation and encodes it in a more sturdy, effective and efficient manner. In this new state, the memory is less susceptible to interference.[1] There are essentially three phases of memory consolidation and all are thought to be facilitated by sleep or not sleep:
- Stabilization is the encoding of a memory which takes only 6 milliseconds.[1]
- Enhancement is the continual process of consolidation which can occur over minutes, 7 hours, days but not longer.[1] Post-sleep behavioural activities can be seen to show significant improvements in the absence of practice.[1]
- Integration can also take hours or years and is the process of connecting recently encoded memories into existing memory networks.[1]
Reconsolidation
Reconsolidation of a memory involves the retrieval of an already consolidated memory (explicit or implicit), into short-term or working memory. Here it is brought into a labile state where subsequent information can interfere with what is currently in memory, therefore altering the memory. This is known as retroactive interference, and is an extremely significant issue for court and eyewitness testimonies.[8]
Pre-training vs post-training sleep deprivation
Researchers approach the study of sleep and memory from different angles. Some studies measure the effects of sleep deprivation after a novel task is taught (the subject learns the task and is sleep deprived afterwards). This is referred to as post-training sleep deprivation. Conversely, other experiments have been conducted that measure the effects of sleep deprivation before a task has been taught (the subject is sleep-deprived and then learns a task). This is referred to as pre-training sleep deprivation.
Offline memory processing
This is the processing of memories out of conscious awareness. For example, after someone has been reading a book, their brain continues to process the experience during other activities. This "offline" processing likewise occurs during sleep.[8]
Methods of measuring memory
Behavioral measures
- A self-ordered pointing task is a task of memory where a participant is presented with a number of images (or words) which are arranged on a display. Several trials are presented, each with a different arrangement and containing some of the previous words or images. The task for the participant is to point to a word or image they had not previously pointed to in other trials.[9]
- In a recency discrimination task participants are shown two trials of image presentation and then a third trial containing a mixture of images from the first and second trial. Their task is to determine whether the image was from the most recent presentation or the previous one.[9]
- In a route retrieval task spatial learning occurs where a participant virtual tours a particular place (such as a town or maze). Participants are asked to virtually tour the same thing at a later time while brain imaging is used to measure activity.[10]
- A paired word associative task consists of two phases. During the first phase (acquisition), the responses of the paired-associate task are learned and become recallable. In the second phase (associative phase), the subject learns to pair each response to a separate stimulus. For example, a visual cue would provide information as to what words must be recalled after the stimulus and words are removed.[11]
- In a mirror tracing task participants are asked to trace several figures as fast and as accurately as possible which they can only see in a mirror. Speed is recorded as well as how much they deviate from the original image (accuracy).[11]
- In the Morris water maze task rats are used to test their spatial learning in two kinds of conditions: spatial and nonspatial. In the spatial condition, a platform is hidden by using murky water and in the nonspatial condition, the platform is visible. The spatial condition the rat must rely on their spatial memory to find the platform whereas the nonspatial condition is used for comparison purposes.[12]
- The serial reaction time task (SRT task) is a task whereby subjects face a computer screen where several markers are displayed that are spatially related to relevant markers on their keyboard. The subjects are asked to react as fast and accurately as possible to the appearance of a stimulus below one of the markers. Subjects can be trained on the task with either explicit instructions (e.g. there are colour sequences presented which must be learned) or implicit ones (e.g. the experimenter does not mention colour sequences, thus leaving the subjects to believe that they are taking place in a speed test). When this task is used in sleep studies, after a time delay, subjects are tested for retention.[13]
- In the reach-to-grasp task rodents learned a skilled forelimb task. 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.[14]
- In a neuroprosthetic task rodents trained to perform a simple brain–machine interface task in which the activity of a set of motor cortical units was used to control a mechanical arm attached to a feeding spout. After successful learning, task-related units specifically experienced increased locking and coherency to slow-wave activity (SWA) during sleep. The time spent in SWA predicted the performance gains upon awakening.[15]
- In a block tapping task participants are asked to type a sequence of five numbers with their dominant or non-dominant hand (specified in experiment), for an allotted period of time, followed by a rest period. A number of these trials occur and the computer records the number of sequences completed to assess speed and the error rate to assess accuracy.[1]
- A finger tapping test is commonly used when a pure motor task is needed. A finger tapping test requires subjects to continuously press four keys (typically numerical keys) on a keypad with their nondominant hand in a sequence, such as 4-3-1-2-4, for a given amount of time. Testing is done by determining the number of errors made.[16]
Neural imaging measures
Neuroimaging can be classified into two categories, both used in varying situations depending on what type of information is needed. Structural imaging deals predominately with the structure of the brain (
Functional magnetic resonance imaging (fMRI) is a type of brain imaging that measures the change of oxygen in the blood due to the activity of neurons. The resulting data can be visualized as a picture of the brain with colored representations of activation.
Molecular measures
Although this may be seen as similar to neuroimaging techniques, molecular measures help to enhance areas of activation that would otherwise be indecipherable to neuroimaging. One such technique that aids in both the temporal and visual resolution of fMRI is the
Methods of measuring sleep
Electrophysiological measures
The main method of measuring sleep in humans is polysomnography (PSG). For this method, participants often must come into a lab where researchers can use PSG to measure things such as total sleep time, sleep efficiency, wake after sleep onset, and sleep fragmentation. PSG can monitor various body functions including brain activity (electroencephalography), eye movement (electrooculography), muscle movement (electromyography), and heart rhythm (electrocardiography).
- Electroencephalography (EEG) is a procedure that records electrical activity along the scalp. This procedure cannot record activity from individual neurons, but instead measures the overall average electrical activity in the brain.
- Electrooculography (EOG) measures the difference in electrical potential between the front and the back of the eye. This does not measure a response to individual visual stimuli, but instead measures general eye movement.
- electromyographmeasures the electrical potential of muscle cells to monitor muscle movement.
- Electrocardiography (ECG or EKG) measures the electrical depolarization of the heart muscles using various electrodes placed near the chest and limbs. This measure of depolarization can be used to monitor heart rhythm.
Behavioural measures
Actigraphy is a common and minimally invasive way to measure sleep architecture. Actigraphy has only one method of recording, movement. This movement can be analyzed using different actigraphic programs. As such, an actigraph can often be worn similarly to a watch, or around the waist as a belt. Because it is minimally invasive and relatively inexpensive, this method allows for recordings outside of a lab setting and for many days at a time. But, actigraphy often over estimates sleep time (de Souza 2003 and Kanady 2011).
Competing theories
Most studies point to the specific deficits in declarative memories that form pre or post REM sleep deprivation. Conversely, deficits in non-declarative memory occur pre or post NREM sleep deprivation. This is the stage specific enhancement theory.[7] There is also a proposed dual-step memory hypothesis suggesting that optimal learning occurs when the memory trace is initially processed in SWS and then REM sleep. Support for this is shown in many experiments where memory improvement is greater with either SWS or REM sleep compared to sleep deprivation, but memory is even more accurate when the sleep period contains both SWS and REM sleep.[7]
Declarative memory
Temporal memory
Temporal memory consists of three main categories,[21] although they are still debated by psychologists and neurobiologists; the categories are immediate memory, short-term and long-term memory.[22] Immediate memory is when a memory is recalled based on recently presented information. Short-term memory is what is used when retaining information that had been presented within seconds or minutes prior. A type of short-term memory is known as working memory, which is the ability to retain information that is necessary to carry out sequential actions. Long-term memory is the retention of information for longer periods of time, such as days, weeks or even a lifetime.
In a study, participants were placed into four groups: two control groups given either
Verbal learning
A blood-oxygen-level dependent (BOLD)
Cognitive performance
Cerebral activation during performance on three cognitive tasks (verbal learning, arithmetic, and divided attention) were compared after both normal sleep and 35 hours of total sleep deprivation (TSD) in a study by Drummond and Brown. Use of fMRI measured these differences in the brain. In the verbal learning task,
Slow wave sleep (SWS)
Macroscopic brain systems
The most prominent population pattern in the hippocampus during nREM is called sharp wave ripples (SPW-R). SPW-Rs are the most synchronous neuronal patterns in the mammalian brain. As many as 15-30 percent of neurons in 50-200 ms fire synchronously in the CA3-CA2-CA1, subicular complex and entorhinal cortex during SWP-R (as opposed to ~1 percent during active waking and REM). Neurons within SPW-R are sequentially organized and many of the fast sequences are related to the order of neuronal firing during the pre-sleep experience of the animal. For example, when the rat explores a maze, place cell sequences in the different arms of the maze are replayed either in a forward (as during the experience itself) or reverse order, but compressed in time several-fold. SPW-R are temporally linked to both sleep spindles and slow oscillations of the neocortex. Interfering with SPW-Rs or its coupling with neocortical slow oscillations results in memory impairment, which can be as severe as surgically damaging the hippocampus and/or associated structures. SPW-R is therefore the most prominent physiological biomarker of episodic (i.e., hippocampus-dependent) memory consolidation (Buzsaki 2015).
Neural forebrain reverberation correlation
Researchers used rats in order to investigate the effects of novel tactile objects on the long-term evolution of the major rodent forebrain loops essential in species-specific behaviours, including such structures as the
Neural hippocampal reverberation correlations
A study by Peigneux et al., (2004) noted that the firing sequences in the hippocampal ensembles during spatial learning are also active during sleep, which shows that post training sleep has a role in processing spatial memories. This study was done to prove that the same hippocampal areas are activated in humans during route learning in a virtual town, and are reactivated during subsequent
Based on the active system consolidation hypothesis, repeated reactivations of newly encoded information in hippocampus during slow oscillations in NREM sleep mediate the stabilization and gradual integration of declarative memory with pre-existing knowledge networks on the cortical level.[33] It assumes the hippocampus might hold information only temporarily and in fast-learning rate, whereas the neocortex is related to long-term storage and slow-learning rate.[25][26][28][29][34] This dialogue between hippocampus and neocortex occurs in parallel with hippocampal sharp-wave ripples and thalamo-cortical spindles, synchrony that drives the formation of spindle-ripple event which seems to be a prerequisite for the formation of long-term memories.[26][27][29][34]
Decreases in acetylcholine
In this study, two groups of participants took part in a two-night counterbalanced study. Two tasks were learned by all participants between 10:00-10:30pm. The declarative task was a paired-associate word list of 40 German semantically related word pairs. The non-declarative task was a mirror-tracing task. At 11:00pm all participants were put on a two-hour infusion of either physostigmine or a placebo. Physostigmine is an acetylcholinesterase inhibitor; it is a drug that inhibits the breakdown of the inhibitory neurotransmitter acetylcholine, thereby allowing it to remain active longer in the synapses. The sleep group was put to bed while the other group stayed awake. Testing of both tasks took place at 2:45am, 30 minutes after the sleep group had been woken up; a sleep which had been rich in slow-wave sleep (SWS). Results showed that the increased ACh negatively affected recall memory (declarative task), in the sleep condition compared to participants given the placebo.[11] Specifically, recall after sleep for the placebo group showed an increase of 5.2 ± 0.8 words compared to an increase of only 2.1 ± 0.6 words when participants were given the acetylcholinesterase inhibitor. Conversely, neither speed nor accuracy declined in the non-declarative mirror task when participants were given physostigmine, and neither task performance was affected in the wake groups when physostigmine was administered. This suggests that the purpose of ACh suppression during SWS allows for hippocampus-dependent declarative memory consolidation; high levels of ACh during SWS blocks memory replay on a hippocampal level.[11]
- Note: There was no correlation between the amount of SWS and level of recall. Memory consolidation can be disrupted, however, if large parts of SWS are missing.
Increases in sleep spindles
A study using 49 rats indicated the increase of sleep spindles during slow-wave sleep following learning. It gave evidence to the increase of spindle frequency during non-REM sleep following paired associate of motor-skill learning tasks. Using an EEG, sleep spindles were detected and shown to be present only during slow-wave sleep. Beginning with a preliminary study, rats underwent six hours of monitored sleep, after a period of learning. Results showed that during the first hour following learning, there was the most evident effect on learning-modulated sleep spindle density. However, this increase in spindle density was not dependent on the training condition. In other words, there was an increase in spindles regardless of how the rats were trained. EEG patterns showed a significant difference in the density of sleep spindles compared to the density of a control group of rats, who did not undergo any training before their sleep spindles were measured. This effect of increased spindle density only lasted for the first hour into sleep following training, and then disappeared within the second hour into sleep.
Reward learning and memory
In a study by Fischer and Born, 2009,
Non-declarative memory
Sleep deprivation
ERK phosphorylation
Extracellular signal-related kinases, also known as classical MAP kinase, are a group of protein kinases located in neurons. These proteins are activated or deactivated by phosphorylation (adding of a phosphate group using ATP), in response to neurotransmitters and growth factors.[12] This can result in subsequent protein to protein interactions and signal transductions (neurotransmitters or hormones transmit to cells), which ultimately controls all cellular processes including gene transcription and cell cycles (important in learning and memory). A study tested four groups of rats in the Morris Water Maze, two groups in the spatial task (hidden platform) and two groups in the non-spatial task (visible platform.) The effects of six hours of total sleep deprivation (TSD) were assessed for the experimental group (one spatial group, one non-spatial group) in both tasks. Six hours after the TSD period (or sleep period for controls), the groups of rats were trained on either task then tested 24 hours later. In addition, the levels of total ERK phosphorylation (ERK 1 and ERK 2), protein phosphate 1 (PP1), and MAPK phosphatase 2 (latter two both involved in dephosphorylation) were assessed by decapitating four other groups of mice, (two sleep deprived and two non-sleep deprived), and removing their hippocampuses after the six hours of TSD, or two hours after TSD (eight hours total). Results showed that TSD did not impair learning of the spatial task, but it did impair memory. With regards to the non-spatial task, learning again was no different in the TSD; however, memory in the TSD group was actually slightly better, although not quite significantly. Analysis of the hippocampus showed that TSD significantly decreased the levels of total ERK phosphorylation by about 30%. TSD did not affect proteins in the cortex which indicates that the decreases in ERK levels were due to impaired signal transduction in the hippocampus. In addition, neither PP1 or MAPK phosphatase 2 levels were increased suggesting that the decreases in ERK were not due to dephosphorylation but instead a result of TSD. Therefore, it is proposed that TSD has aversive effects on the cellular processes (ERK: gene transcription etc.), underlying sleep-dependent memory plasticity.[12]
REM sleep
PGO waves
In animals, the appearance of ponto-geniculo-occipital waves (
Implicit face memory
Faces are an important part of one's social life. To be able to recognize, respond and act towards a person requires unconscious memory encoding and retrieval processes. Facial stimuli are processed in the
Macroscopic brain systems
Previous research has shown REM sleep to reactivate cortical neural assemblies post-training on a serial reaction time task (SRT), in other words REM sleep replays the processing that occurred while one learnt an implicit task in the previous waking hours.[42] However, control subjects did not complete a SRT task, thus researchers could not assume the reactivation of certain networks to be a result of the implicitly learned sequence/grammar as it could simply be due to elementary visuomotor processing which was obtained in both groups. To answer this question the experiment was redone and another group was added who also took part in the SRT task. They experienced no sequence to the SRT task (random group), whereas the experimental group did experience a sequence (probabilistic group), although without conscious awareness. Results of PET scans indicate that bilateral cuneus were significantly more activated during SRT practice as well as post-training REM sleep in the Probabilistic group than the Random group.[42] In addition, this activation was significantly increased during REM sleep versus the SRT task. This suggests that specific brain regions are specifically engaged in the post-processing of sequential information. This is further supported by the fact that regional CBF (rCBF) during post-training REM sleep are modulated by the level of high-order, but not low-order learning obtained prior to sleep. Therefore, brain regions that take part in a learning process are modulated by both the sequential structure of the learned material (increased activation in cuneus), and the amount of high-order learning (rCBF).[42]
REM sleep deprivation and neurotrophic factors
The effects of REM sleep deprivation (RSD) on neurotrophic factors, specifically
Macroscopic brain system reorganization
Walker and Stickgold hypothesized that after initial memory acquisition, sleep reorganizes memory representation at a macro-brain systems level.[1] Their experiment consisted of two groups; the night-sleep group was taught a motor sequence block tapping task at night, put to sleep and then retested 12 hours later. The day-wake group was taught the same task in the morning and tested 12 hours later with no intervening sleep. FMRI was used to measure brain activity during retest. Results indicated significantly fewer errors/sequence in the night-sleep group compared to the day wake group. FMRI output for the night-sleep group indicated increased activation in the right primary motor cortex/M1/Prefrontal Gyrus (contra lateral to the hand they were block tapping with), right anterior medial prefrontal lobe, right hippocampus (long-term memory, spatial memory), right ventral striatum (olfactory tubercle, nucleus accumbens), as well as regions of the cerebellum (lobules V1, V11). In the day-wake group, fMRI showed "decreased" signal activation bilaterally in the parietal cortices (integrates multiple modalities), in addition to the left insular cortex (regulation of homeostasis), left temporal pole (most anterior of temporal cortex), and the left inferior fronto-polar cortex.[1] Previous investigations have shown that signal increases indicate brain plasticity. The increased signal activity seen in M1 after sleep corresponds to increased activity in this area seen during practice; however, an individual must practice for longer periods than they would have to sleep in order to obtain the same level of M1 signal increases. Therefore, it is suggested that sleep enhances the cortical representation of motor tasks by brain system expansion, as seen by increased signal activity.[1]
Working memory
Considered to be a mental workspace enabling temporary storage and retrieval of information,
Sleep deprivation
Sleep deprivation, whether it is total sleep deprivation or partial sleep deprivation, can impair working memory in measures of memory, speed of cognitive processing, attention and task switching. Casement et al. found that when subjects were asked to recognize digits displayed on a screen by typing them on a keypad, the working memory speed of subjects whose sleep was restricted to four hours a night (approximately 50% of their normal sleep amount) were 58% slower than control groups who were allowed their full eight hours of sleep.[45]
Synaptic plasticity
The brain is an ever-changing, plastic, model of information sharing and processing. In order for the brain to incorporate new experiences into a refined
Neurotransmitter regulation
The changes in quantity of a certain neurotransmitter as well as how the post-synaptic terminal responds to this change are underlying mechanisms of brain plasticity.
Gene expression
Recently, approximately one hundred genes whose brain expression is increased during periods of sleep have been found.
Alternative sleep schedules
Motor skills learning
The impact of daytime naps was looked at by Walker and Stickgold (2005).[52] The experimental group was given a 60-90 minute afternoon nap (one full cycle), after a motor skills task learned that morning, while the control group received no nap. The nap group improved 16% when tested after their nap, while the no-nap group made no significant improvements. However, it seemed to all even out after that same night's sleep; the no-nap group improved 24% and the nap group improved only 7% more for a total of 23%, virtually identical. With regards to motor skills learning, naps seem to only speed up skill enhancement, not increase the amount of enhancement.[52]
Visuals skills learning
Much like motor skills learning, verbal skills learning increased after a daytime nap period. Researchers Mednick and colleagues have shown that if a visual skills task (find task) is taught in the morning and repeatedly tested throughout the day, individuals will actually become worse at the task. The individuals that were allowed a 30-60 minute nap seemed to gain stabilization of the skill, as no deterioration occurred. If allowed a 60-90 minute nap (
Shift workers
Sleep and aging
Sleep often becomes deregulated in the elderly, a problem which can lead to or exacerbate pre-existing memory decline.
Healthy older adults
The positive correlation between sleep and memory breaks down with aging. In general, older adults suffer from decreased sleep efficiency.[55] The amount of time and density of REM sleep and SWS decreases with age.[56][57][58] Consequently, it is common that the elderly receive no increase in memory after a period of rest.[59]
To combat this, donepezil has been tested in healthy elderly patients where it was shown to increase time spent in REM sleep and improve following day memory recall.[60]
Alzheimer's disease
Alzheimers disease is thought to be caused by the abnormal buildup of proteins around brain cells which disrupt the activity of neurotransmitters.[61] Patients with Alzheimer's disease experience more sleep disruption than the healthy elderly. Studies have shown that in patients with Alzheimer's disease, there is a decrease in fast spindles. It has also been reported that spindle density the night before a memory test correlates positively with accuracy on an immediate recall task.[56] A positive correlation between time spent in SWS and next day autobiographical memory recall has also been reported in Alzheimer's patients.[62]
See also
- Effects of sleep deprivation on cognitive performance
- Emotion and memory
- Memory and aging
- Memory and social interactions
- Memory improvement
- Sleep study
- Biphasic and polyphasic sleep
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