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Non-rapid eye movement sleep

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Title: Non-rapid eye movement sleep  
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Non-rapid eye movement sleep

Non-rapid eye movement sleep, or NREM, is, collectively,

  • Rechtschaffen, A; Kales, A (1968). A Manual of Standardized Terminology, Techniques and Scoring System For Sleep Stages of Human Subjects. US Dept of Health, Education, and Welfare; National Institutes of Health. 
  • M. Massimini, G. Tononi, et al., "Breakdown of Cortical Effective Connectivity During Sleep," Science, vol. 309, 2005, pp. 2228–32.
  • P. Cicogna, V. Natale, M. Occhionero, and M. Bosinelli, "Slow Wave and REM Sleep Mentation," Sleep Research Online, vol. 3, no. 2, 2000, pp. 67–72.
  • D. Foulkes et al., "Ego Functions and Dreaming During Sleep Onset," in Charles Tart, ed., Altered States of Consciousness, p. 75.
  • Rock, Andrea (2004). The Mind at Night.  
  • Warren, Jeff (2007). "The Slow Wave". The Head Trip: Adventures on the Wheel of Consciousness.  
  • Iber, C; Ancoli-Israel, S; Chesson, A; Quan, SF. for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester: American Academy of Sleep Medicine; 2007.
  • Manni, Raffaele. "Rapid Eye Movement Sleep, Non-rapid Eye Movement Sleep, Dreams, and Hallucinations". 2005;7:196-197.

Further reading

"sleep." Encyclopædia Britannica. Encyclopædia Britannica Online. Encyclopædia Britannica Inc., 2011. Web. 05 Dec. 2011..

  1. ^ OConnell, C. (2010, Mar 09). Why do some people sleepwalk? Irish Times, pp. 7. Retrieved from http://ezproxy.qa.proquest.com/docview/309237844?accountid=14771.
  2. ^ Manni,Raffaele. "Rapid Eye Movement Sleep, Non-rapid Eye Movement Sleep, Dreams, and Hallucinations". 2005;7:196-197.
  3. ^ Manni,Raffaele. "Rapid Eye Movement Sleep, Non-rapid Eye Movement Sleep, Dreams, and Hallucinations". 2005;7:196-197.
  4. ^ Andreasen, Nancy C.; Black, Donald W. (2006). Introductory Textbook of Psychiatry. American Psychiatric.  
  5. ^ McNamara, Patrick; Johnson, Patricia; McLaren, Deirdre; Harris, Erica; Beauharnais, Catherine (2010). "Rem And Nrem Sleep Mentation". International Review of Neurobiology (Elsevier Inc) 92: 69–86.  
  6. ^ Manni,Raffaele. "Rapid Eye Movement Sleep, Non-rapid Eye Movement Sleep, Dreams, and Hallucinations". 2005;7:196-197.
  7. ^ Hiatt John F., Floyd Thomas C., Katz Paul H., Feinberg Irwin. "Further Evidence of Abnormal Non-Rapid-Eye-Movement Sleep in Schizophrenia" (1985). Volume 42. New York: Northport.
  8. ^ Schulz, Hartmut (2008). "Rethinking sleep analysis. Comment on the AASM Manual for the Scoring of Sleep and Associated Events". J Clin Sleep Med (American Academy of Sleep Medicine) 4 (2): 99–103.  
  9. ^ Green, Simon (2011). Biological Rhythms, Sleep and Hypnosis. New York: Palgrave MacMillan.  
  10. ^ National Institute of Neurological Disorders and Stroke, Understanding sleep
  11. ^ Green, Simon (2011). Biological Rhythms, Sleep and Hypnosis. New York: Palgrave Macmillan.  
  12. ^ "Glossary. A resource from the Division of Sleep Medicine at Harvard Medical School, Produced in partnership with WGBH Educational Foundation". Harvard University. 2008. Retrieved 2009-03-11. The 1968 categorization of the combined Sleep Stages 3–4 was reclassified in 2007 as Stage N3. 
  13. ^ McNamara, P.; McLaren, D.; Durso, K. (June 2007). "Representation of the Self in REM and NREM Dreams". Dreaming 17 (2): 113–126.  
  14. ^ Cline, John. "Sleep Spindles". Psychology Today. 
  15. ^ Jordan, Paul. "NREM Sleep: Stages 1, 2, and 3". 
  16. ^ "Revisiting the K-Complex and Appraisal to Scientific Debate". Dormigivilia. 
  17. ^ Dement W, Kleitman N. The relation of eye movements during sleep to dream activity: an objective method for the study of dream. J. Exp. Psychol. 1957; 53: 339–4
  18. ^ Suzuki H; Uchiyama M; Tagaya H et al. Dreaming during nonrapid eye movement sleep in the absence of prior rapid eye movement sleep. SLEEP 2004;27(8):1486-90.
  19. ^ Schenck, Carlos. "Sleep and Parasomnias". National Sleep Foundation. 
  20. ^ "Selective slow-wave sleep (SWS) deprivation and SWS rebound: do we need a fixed SWS amount per night?". 1999.  
  21. ^ Maquet, Pierre, "Understanding non rapid eye movement sleep through neuroimaging." World Journal of Biological Psychiatry: June 2010, 11 (S1), p. 9-15, http://informahealthcare.com/doi/abs/10.3109/15622971003637736

References

A study was done involving an experimental and a control group to have them learn to navigate a 3D maze. The blood flow in the parahippocampal gyrus increased in conjunction with the individual's performance through the 3D maze. Participants were then trained in the maze for 4 hours and later, during the various sleep cycles of nonREM sleep, REM sleep and wakefulness, they were scanned twelve times using a PET scan during the night. The PET scan demonstrated a higher blood flow in the hippocampus during SWS/non-REM sleep due to the training from the previous day while the control group exhibited no increased blood flow and they had not received the training the prior day. The brain activity during sleep, according to this study, would show the events of the previous day do make a difference. One theory suggests a model of Hippocampal-neocortical dialogue. "Two stages of hippocampal activity have been proposed, the first being the recording of the memory during waking and the second involving the playback of the memory during nonREM sleep. This process of reactivation of memory firing sequences is believed to gradually reinforce initially weak connections between neocortical sites allowing the original information to be activated in the cortex independently of the hippocampus, and thus ensuring refreshed encoding capacity of the hippocampus." Maquet concluded that the areas of the brain involved with information processing and memory have increased brain activity during the slow wave sleep period. Events experienced in the previous day have more efficient and clearer memory recall the next day thus indicating that the memory regions of the brain are activated during SWS/non-REM sleep instead of being dormant as previously thought.[21]

Slow Wave Sleep (SWS) is a highly active state unlike a state of brain quiescence as previously thought. Brain imaging data has shown that during nonREM sleep the regional brain activity is influenced by the waking experience just passed.

After sleep deprivation there is usually a sharp rebound of SWS, suggesting there is a "need" for this stage.[20]

The highest arousal thresholds (e.g. difficulty of awakening, such as by a sound of a particular volume) are observed in stage 3. A person will typically feel groggy when awoken from this stage, and indeed, cognitive tests administered after awakening from stage 3 indicate that mental performance is somewhat impaired for periods up to 30 minutes or so, relative to awakenings from other stages. This phenomenon has been called "sleep inertia."

Slow-wave sleep (SWS) is made up of the deepest stage of NREM, and is often referred to as deep sleep.

Slow-wave sleep

Stage 3: Stage 4 Sleep. EEG highlighted by red box.


Stage 2: Stage 2 Sleep. EEG highlighted by red box. Sleep spindles highlighted by red line.


Stage 1: Stage1 Sleep. EEG highlighted by red box.

The figures represent 30-second epochs (30 seconds of data). They represent data from both eyes, chin, EEG, legs, microphone, intercostal EMG, sternocleidomastoid activity, nasal/oral air flow, thoracic effort, abdominal effort, EKG, oxymetry, and body position, in that order. EEG is highlighted by the red box. Sleep spindles in the stage 2 figure are underlined in red.

Polysomnography (PSG) is a test used in the study of sleep; the test result is called a polysomnogram. Below are images of the NREM stages 1, 2 and 4 (prior to the merging of stages 3 and 4).

Polysomnography

Some examples of parasomnias are somnambulism (sleep walking), somniloquy (sleep talking), sleep eating, nightmares or night terrors, sleep paralysis, and sexsomnia (or "sleep sex"). Many of these have a genetic component, and can be quite damaging to the person with the behavior or their bed partner. Parasomnias are most common in children, but most children have been found to outgrow them with age. However, if not outgrown, they can cause other serious problems with everyday life.[19]

The occurrence of parasomnias is very common in the last stage of NREM sleep. A parasomnia is a sleep behavior that affects the function, quality, or timing of sleep. It is caused by a physiological activation in which the person's brain is caught between the stages of falling asleep and waking from sleep. The autonomous nervous system, cognitive process, and motor system are activated during sleep or while the person wakes up from sleep.

Parasomnias

However, because the diaphragm is largely driven by the autonomous system, it is relatively spared of non-REM inhibition. As such, the suction pressures it generates stay the same. This narrows the upper airway during sleep, increasing resistance and making airflow through the upper airway turbulent and noisy. For example, one way to determine whether a person is sleeping is to listen to their breathing - once the person falls asleep, their breathing becomes noticeably louder. Not surprisingly, the increased tendency of the upper airway to collapse during breathing in sleep can lead to snoring, a vibration of the tissues in the upper airway. This problem is exacerbated in overweight people when sleeping on the back, as extra fat tissue may weigh down on the airway, closing it. This can lead to sleep apnea.

  1. The upper airway becomes more floppy.
  2. The rhythmic innervation results in weaker muscle contractions because the intracellular calcium levels are lowered, as the removal of tonic innervation hyperpolarizes motoneurons, and consequently, muscle cells.

During non-REM sleep, the tonic drive to most respiratory muscles of the upper airway is inhibited. This has two consequences:

Muscle movements during non-REM

Research has also shown that dreams during the NREM stage most commonly occur during the morning hours which is also the time period with the highest occurrence of REM sleep. This was found through a study involving subjects taking naps over specific intervals of time and being forcefully awakened, their sleep was separated into naps including only REM sleep and only NREM sleep using polysomnography. This implies that the polysomnographic occurrence of REM sleep is not required for dreaming. Rather, the actual mechanisms that create REM sleep cause changes to one's sleep experience. Through these changes, by morning, a sub-cortical activation occurs during NREM that is comparable to the type that occurs during REM. It is this sub-cortical activation that results in dreaming during the NREM stage during the morning hours.[18]

Although study participants' reports of intense dream vividness during REM sleep and increased recollection of dreams occurring during that phase suggest that dreaming most commonly occurs during that stage,[17] dreaming can also occur during NREM sleep.

Dreaming during NREM

K-complexes are single long delta waves that last for only a second.[15] They are also unique to NREM sleep. They appear spontaneously across the early stages, usually in the second stage, much like the sleep spindles. However, unlike sleep spindles, they can be voluntarily induced by transient noises like a knock at the door. The function of these K-complexes is unknown, but further research still needs to be conducted.[16]

Sleep spindles are unique to NREM sleep. The most spindle activity occurs at the beginning and the end of NREM. Sleep spindles involve activation in the brain in the areas of the thalamus, anterior cingulate and insular cortices, and the superior temporal gyri. They have different lengths. There are slow spindles in the range of 11 – 13 Hz that are associated with increased activity in the superior frontal gyrus, and fast spindles in the range of 13 – 15 Hz that are associated with recruitment of sensorimotor processing cortical regions, as well as recruitment of the mesial frontal cortex and hippocampus. There is no clear answer as to what these sleep spindles mean, but ongoing research hopes to illuminate their function.[14]

Sleep spindles and K-complexes

  • Stage 1 – occurs mostly in the beginning of sleep, with slow eye movement. This state is sometimes referred to as relaxed wakefulness.[9] Alpha waves disappear and the theta wave appears. People aroused from this stage often believe that they have been fully awake. During the transition into stage-1 sleep, it is common to experience hypnic jerks.[10]
  • Stage 2 – no eye movement occurs, and dreaming is very rare. The sleeper is quite easily awakened. EEG recordings tend to show characteristic "sleep spindles", which are short bursts of high frequency brain activity,[11] and "K-complexes" during this stage.
  • Stage 3 – previously divided into stages 3 and 4, is deep sleep, slow-wave sleep (SWS). Stage 3 was formerly the transition between stage 2 and stage 4 where delta waves, associated with "deep" sleep, began to occur, while delta waves dominated in stage 4. In 2007, these were combined into just stage 3 for all of deep sleep.[12] Dreaming is more common in this stage than in other stages of NREM sleep though not as common as in REM sleep. The content of SWS dreams tends to be disconnected, less vivid, and less memorable than those that occur during REM sleep.[13] This is also the stage during which parasomnias most commonly occur. Various education systems e.g. the VCAA of Australian Victorian education practice still practice the stages 3 & 4 separation.

NREM sleep was divided into four stages in the Rechtschaffen and Kales (R&K) standardization of 1968. That has been reduced to three in the 2007 update by The American Academy of Sleep Medicine (AASM).[8]

Stages of NREM sleep

Contents

  • Stages of NREM sleep 1
  • Sleep spindles and K-complexes 2
  • Dreaming during NREM 3
  • Muscle movements during non-REM 4
  • Parasomnias 5
  • Polysomnography 6
  • Slow-wave sleep 7
  • References 8
  • Further reading 9

[7] It has been found through several experiments that low levels of stage 3 sleep are found in about 40-50% of acute and chronic schizophrenics who typically portray abnormal non-rapid eye movement sleep.[6] The differences in the REM and NREM activity reported is believed to arise from differences in the memory stages that happen during the two methods of sleep.[5]

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