Monogram: Sleep and Disorders of Sleep Shyam Narayan Arya, BB Thakur
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Normal SleepCHAPTER 1

Shyam Narayan Arya
 
INTRODUCTION
It is a common knowledge that humans spend a third of their lives asleep
Sleep is essential for normal functioning of both psyche (mind) and soma (body). Lack of sleep leads to daytime drowsiness. Memory lapses, lack of concentration and mood alterations are common consequences of insomnia or lack of sleep. Lack of sleep may also cause proneness to accidents, poor performance of work and breaches in interpersonal relationship.1,2
Animals deprived of sleep will experience metabolic abnormalities and die.3 Even in human beings, a rare disorder known as fatal familial insomnia in which almost total loss of sleep occurs, leads to an early death. Sleep is also related to memory and learning. An improvement of performance on several tasks involving memory consolidation and procedural learning after good sleep has been clearly shown, and the improvements seen after sleep are generally greater than those found after a period of rest without sleep, suggesting a special influence of sleep on learning.4
 
LOSS OF SLEEP RESULTS IN ABNORMAL HORMONE RHYTHM4
Sleep is characterized by diminished responsiveness to, and perceptual disengagement from the environment. Superficially speaking it may be compared to a state of coma with the exception that it is readily reversible. However, from a neurophysiologic standpoint it bears no resemblance to state of coma (Fig. 1.1).
During sleep, the brain is highly active and undergoes characteristic changes not only in nervous system, but throughout the body. This is very clearly shown in the polysomnogram which records the EEG, EOG (Electro-oculogram) from the left and right outer canthus, EMG of submentalis muscle, nasal air flow rate, respiratory efforts, oxygen saturation (by pulse oxymetry) and in some cases, EMG from tibialis anterior muscle.5
Even though sleep is such a prerequisite for a good quality of life (QOL), we know little about the type, duration, and features of sleep. Brain-circuits involved are complex and new information is emerging daily.4
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Figure 1.1: Patient undergoing polysomnography (Source: American academy of sleep medicine slide set. Sleep apnea, diagnosis, and treatment. In: Westchester IL (Ed): American academy of sleep medicine; 2001). Produced from Clinical Management of Insomnia In: Doghramji K, Doghramji. pp (Eds). Professional Communication with thanks).
2Optimal and ideal duration of sleep is said to be between 7–8 hours. Persons who habitually sleep for less than 5 to 6 hours are likely to report that they sleep less than they would like to and that they are more dissatisfied with life.4
However, the amount of sleep needed for each individual is simply the amount that is sufficient to be able to perform day time activities satisfactorily after feeling refreshed on waking.
 
Normal Stages and Architecture of Sleep
“Recording the EEG and other physiological variables such as muscle activity from submentalis and tibialis anterior (anterior) muscles and eye-movements from outer canthi of both eyes by polysomnogram gives information about different stages of sleep and their pattern of occurrences.”4 This pattern varies from person to person but usually consists of four or five cycles of quiet sleep known as non rapid eye movement (NREM), alternating with rapideye-movement (REM) sleep or paradoxical sleep.1,4 This paradoxical sleep is distinct from paradoxical insomnia in which the person sleeps well but feels he does not. In paradoxical insomnia, to be described in next chapter, the person is said to have sleep-state-misperception or subjective insomnia.
In 1937, Loomis6 was the first to observe that sleep is not a homogenous state during the whole night and described different stages of sleep based on overnight EEG recording of a healthy person. In 1953, Aesrinsky7 and Kleitman observed a special state of sleep termed rapid eye movement sleep (REM sleep) during which rapid binocularly symmetrical eye movements occur. EEG pattern during REM sleep is similar to one observed during wakefulness and both respiratory and heart rates are increased in contrast to other sleep stages.
From overnight recording of EEG and electro-oculogram, Kleitman and Demant8 specified the cyclic pattern of rapid eye movements (REM) and non rapid eye movement (NREM) sleep. The first part of night is characterised by periods of deep quiet sleep (N REM sleep) with more and longer periods of cycles of REM sleep in the latter half of the night. One cycle of REM and NREM lasts for about 90–100 minutes. This is known as ultradian rhythm of sleep. Kleitman also divided non-REM sleep into four stages 1.2.3.4 ranging from light sleep in stage 1 to the deepest in stage 4. Some authorities divide non REM sleep into 3 stages only.9
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Figure 1.2: Polysomnography of patient in stage 1 sleep
Abbreviations: cps, cycles per second; EEG, electroencephalogram; EMG, electromyogram; L-EOG, left electro-oculogram; R-EOG, right electrooculogram. In this patient, ≥ 50% of the epoch contains O activity (3 to 7 cps); there may be a activity with <50% of the epoch. slow3
In stage 1 (Fig. 1.2), the EEG is characterized by low voltage mixed frequency with 3–7 cycles per second 3–7 Hz-range and α-activity of one to ten seconds minutes (9–10 Hz). Relatively high tone of submentalis and tibialis anterior muscles is evident.
(Source: Reproduced from Clinical Management of Insomnia by Doghramji KL, Doghramji pp (Eds) Professional Communications with thanks)
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Figure 1.3: Polysomnography of patient in stage 2 sleep
Abbreviations: cps, cycles per second; EEG, electroencephalogram; EmG, electromyogram; L-EOG, left electro-oculogram; R-EOG, right electro-oculogram.
In this patient, background EEG is θ (3 to 7 cps). K-complexes and spindles occur episodically. Mirrored EEG is the EOG leads. High tonic submental EMG is evident.
Illustrated guide to polysomnography: Normal sleep, CD-Rom. Avilable at: http//aasmnet.org/sleepEdSeries.aspx. Accessed December 13, 2006
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Figure 1.4: Polysomnography of patient in stage 3 sleep
Abbreviations: EEG, electroencephalogram; EMG, electromyogram; L-EOG, left electro-oculogram; R-EOG right electro-oculogram.
In this patient, >50% of the epoch will have scorable δ activity. EOG channels will mirror and activity. Submental muscle tone may be slightly reduced.
Illustrated guide to polysomnography: Normal sleep, CD-Rom. Available at: http//aasmnet.org/sleepEdSeries.aspx. Accessed December 13, 2006.4
In stage 2 (Fig. 1.3), the sleep spindles (12–14 Hz. range) and K-complexes appear. The K-complex is sharp negative wave followed by a slower positive wave with high amplitude. The duration of these patterns should be 0.5 sec at minimum and the interval between two successive sleep spindles or K-complexes should be less than 3 minutes; mirrored EEG in EOG leads and high tonic submentalis in EMG are evident.
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Figure 1.5: Polysomnography of patient in stage 4 sleep
Abbreviations: EEG, electroencephalogram; EMG, electromyogram; L-EOG, left electro-oculogram; R-EOG, right electro-oculogram.
In this patient, >50% of the epoch will have scorable δ EEG activity. The EOG leads will mirror all of the δ EEG activity. Submental EMC activity will be slightly reduced from that of light sleep.
Illustrated guide to polysomnography: Normal sleep, CD-Rom. Available at: http//aasmnet.org/sleepEdSeries.aspx. Accessed December 13, 2006.
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Figure 1.6: Polysomnography of patient in REM sleep
Abbreviations: EEG, electroencephalogram; EMG, electromyogram; L-EOG, left electro-oculogram; REM-EOG, right electro-oculogram.
In this patient rapid eye movements, mixed frequency, EEG and low tonic submental EMG are evident
Illustrated guide to polysomnography: Normal sleep, CD-Rom. Available at: http//aasmnet.org/sleepEdSeries.aspx. Accessed December 13, 2006.5
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Figure 1.7: Sleep architecture of a normal adult
Abbreviations: REM, rapid eye movement
The horizontal axis portrays hours of sleep
Source: Erman MK. J Cin Psychiatry. 2001; 62 (suppl 10): 9-17
(Source: Reproduced from Doghramji & Doghramji's book referred to before, with thanks)
In stage 3 (Fig. 1.4), approximately 25–50% of the epoch of EEG records show high voltage slow waves of 2 Hz, with amplitude of 75μv (Delta activity). Sleep spindles and K-complexes also occur. EOG channels will mirror Delta (∂) activity. Submental tone may be slightly low now.
In stage 4 (Fig. 1.5), more than 50% of the epoch will have theta activity (2Hz.) or slower activity with amplitude greater than 75μv. Otherwise, the EEG has same amplitude as in stage 3. The EOG leads will mirror all of the (∂) theta activity. Submentalis EMG will show further reduction of tone compared to the earlier stages of sleep.
(Reproduced from the book Doghramji as referred to earlier with thanks)
EEG of the REM sleep (Fig. 1.6) shows low voltage rapid complexes. Bursts of rapid eye movements are seen at intervals in EOG, which stand out prominently against the background of the low voltage rapid complexes in EEG. Low tonic submental EMG are evident.
The sleep architecture of normal adult has also been depicted by Erman (2001). This is shown in Figure 1.7 as histogram.9
 
The Relative Distribution of Sleep Changes with Age
Delta sleep (2–3 Hz) or slow wave sleep is maximal in children and diminishes markedly with age especially during adolescence. Seniors may have little or no delta sleep. The loss of delta sleep with age may be consequences of diminution in cortical synaptic activity. In contrast, stage-1 sleep increases with age. With aging, there is a general tendency toward sleep fragmentation, characterized by an increase in the frequency of brief arousals and awareness.10
To summarise1012 normal sleep in adults is divided into NREM and REM sleep. NREM is further divided into N1, N2, N3, and N4. It is to be noted that N3 and N4 are periods of deep sleep in which delta waves are seen. Hence, as N3 and N4 stages progress, stronger stimulus are required to result in an awakening. Stage of REM-sleep has tonic and phasic components. The phasic component is a sympathetically driven state characterized by rapid eye movements, muscle twitches, and respiratory variability. Tonic REM is a parasympathetically driven state, with eye no movement. However, the REM period length and density of movements increase throughtout the sleep cycle.
While falling off to sleep, wakefulness usually transitions into light NREM sleep. NREM sleep typically begins in the lighter stages N1 and N2 and progressively deepens to N3 and N4 or slow wave sleep, as evidenced by higher voltage delta waves. During N3 and N4 (slow wave sleep) stages of sleep, delta waves account for more than 20% of the sleep EEG. REM sleep follows NREM sleep and occur 4 to 5 times during a normal 8 hour sleep-period. The first 6REM period of the night may be less than 10 minutes in duration while the last may exceed 60 minutes. The NREM-REM cycle vary in length from 70–100 minutes initially to 80–120 minutes later in the night.
In adults, N1 is considered a transition between wake and sleep. It occurs upon falling asleep and during brief arousal periods during normal sleep and usually accounts for 2–5% of total sleep time. Stage N2 occurs throughout the sleep period and represents 45–55 % of total sleep-time. Stages N3 and N4 occur mostly in its first third of the night and constitute 5–15% of total sleep time. REM represents 20–25% of total sleep time and occurs in 4 to 5 periods throughout the night. Thus, sleep is a cyclic phenomenon with 4 to 5 REM periods during the night accounting for about one-fourth of total night's sleep (1.5–2 hours). The first REM period occurs about 80–120 minutes after onset of sleep and lasts about 10 minutes. Later REM periods are longer (15–40 minutes) and occur mostly in the last several hours of sleep. Most stage 4 (deepest) sleep occurs in the first several hours. Age related changes in normal sleep include an unchanging percentage of REM sleep and marked decrease in stages 3 and stages 4 sleep with an increase in wakeful periods during the night.
 
Sleep in Infants3,911,13
In newborns, the total sleep duration in a day can be 14–16 hours. Infants have an overall greater total sleep time than any other age group; their sleep time can be divided into multiple periods. Over the first several months of life, sleep time decreases: by age 5–6 months, sleep consolidates into an overnight period with at least one nap during the day. REM-sleep in infants represents a larger percentage of the total sleep time at the total expense of stage the N3 stage NREM sleep. Until the age of 3–4 months, newborns transition from wake to REM sleep stage. Thereafter wake begins to transition directly into NREM.
Overall electro cortical recorded voltage remains high during sleep, as it does during periods of wakefulness. Sleep spindles begin appearing at the second month of life with a density greater than that seen in adults. After the first year, the spindles begin to decrease in density and progress towards adult pattern. K-complexes develop by 6th month of life.
Sleep in elderly:3,10 In the elderly person, the time spent in stage N3 and N4 decreases and the time in N1 and N2 increases. Latency to fall asleep and the number and duration of overnight arousal periods increase. This often leads to an increase in the total time in bed, which can lead to complaints of insomnia. Sleep fragmentation results from the increase in overnight arousal and may be exacerbated by the increasing number of geriatric medical conditions including sleep apnea, musculoskeletal disorders and cardiopulmonary diseases.11
 
Dreams3
Every one dreams. However, the frequency varies from individual to individual. Dreams are usually only remembered when there is a period of waking during or at the end of a REM-episode. Dream can happen during NREM sleep too, although these may be generally different; they are less story-like, are bizarre and less vivid. Eye movements and twitching during dreams occur in bouts lasting 2–3 minutes (Phase REM) followed by no movements of 1–3 minute's duration, (tonic REM).3 It is possible to suppose that these eye movements seen in REM sleep are scanning of dream images, but this is hard to prove, because when subjects are woken 7during a bout of REM sleep stage, the recall could be related to either of these two stages of REM. More about dreams will be discussed in chapter 2. Nightmares are dreams that have an unpleasant or scary content that often leads to such arousal, that the dreamer awakes in fear and so remembers the content as a nightmare. This is experienced by most people at some stage in their life. Nightmares are more common in children or those with other psychiatric illnesses, especially depression.
 
What Regulates Sleep and Wakefulness
Sleep and wakefulness are regulated through many mechanisms in human body. Only a minor part of this mechanism is known to us; a major part still eludes human understanding. That means we do not understand the “Whys” of sleep. Whatever little is known of sleep physiology is described below:
Sleep is regulated through five mechanisms
  1. Circadian rhythm.
  2. Sleep homeostasis.
  3. Complex neuronal circuits in basal forebrain, hypothalamus and certain brain stem nuclei.
  4. Suppression of reticular activating system.
  5. Depression of (a) Hypothalamic Pituitary Adrenal Axis (HPA-AXIS) and (b) Sympathetic system.
 
Circadian Rhythm of Sleep-wakefulness1216
Just as there are diurnal variations in endocrinal, thermoregulatory, cardiac, pulmonary, renal, gastrointestinal and neurobehavioral functions in the body, so is the variation of sleep awake cycle.10,11 These are known as circadian rhythms.
“While it is now recognised that many peripheral tissues in mammals have circadian clocks that regulate diverse physiologic processes. These independent tissue specific oscillations are co-ordinated by a central neuronal pacemaker located in the suprachiasmatic nuclei of the hypothalamus. Sleep-awake clock is also under these suprachiasmatic nuclei”.3,11,12,14
[Source: Reproduced from book Clinical Management of Insomnia by Doghramji KD, Doghramji pp (Eds), with thanks].
 
“To quote MS Steven”
“The suprachiasmatic nucleus sets the body clock to 24.2 hours, with both light and dark schedule cues entraining to 24.2 hour cycle.15 The retinohypothalamic tract allows light 8cues to directly influence the suprachiasmatic nucleus. Light is called Zeitgeber, a German word meaning time-giver because it sets the suprachiasmatic clock. A practical purpose has been proposed for the circadian rhythm, using the analogy of the brain being somewhat like a battery charging during sleep and discharging during the wake period”. The nadir (lowest point) of the rhythm is in the early morning. The downswing in circadian rhythm prior to the nadir is thought to assist the brain to remain asleep overnight for full restoration by preventing premature awaking. The morning upswing then facilitates awaking and through the day acts as a counterbalance to sleep and leads to the progressive discharge of wake neuronal activity. After the circadian apex in the early evening, the downswing aids sleep-invitation, sleep offset (awakening) is primarily determined by circadian rhythm. A person who regularly awakens at an early hour will generally not be able to sleep much later than his or her normal walking time even if moderately sleep deprived (Fig. 1.8).
Melatonin is secreted by the pineal gland and modulates the light entrainment. Pineal secretes melatonin maximally during the night.12
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Figure 1.8: Two-process model of sleep-wake regulation
Source: Edgar DM, et al. J Neurosci. 1996;1065-79
 
SLEEP HOMEOSTASIS1416
We know that “milieu-interior” of Claude Bernard or homeostasis is a mechanism to maintain stability in the normal human body status or internal environment of the organism. It is achieved by a system of central mechanisms activated by negative feedback e.g. maintenance of blood sugar. When blood sugar rises after meals, pancreas secretes insulin to neutralise it so that post prandial blood sugar does not exceed a certain level, say 140 mgm/dl. In the same way when one has sleep deprivation, say due to a late night party, the sleep centres produce excessive sleep promoter neuratransmitters e.g. Gama amino butyric acid (GABA), galanin, adenosine, etc. and the person sleeps longer the next night and thus replenishes the sleep deprivation of the previous night. Homeostatic sleep propensity (the need for sleep) for a 9duration to compensate for sleep-deprivation of previous night or nights must be balanced against the circadian element of satisfactory sleep.17 Along with this, corresponding message from the circadian clock, tells the body it needs to sleep.
This is an example of sleep homeostasis. If the sleep-homeostasis is disturbed or deranged, insomnia occurs and the person gets many consequences of sleep-deprivation like decrease in functioning of immune system, cognitive impairment and impairment in other day-time activities like performance at work and so on.
 
NEURONAL CIRCUITS OF SLEEP11,14,1618
Brain becomes less responsive to external stimuli like visual auditory and other environmental stimuli during transition from wake to sleep, which is considered by some to be N1 stage of sleep. Historically, sleep was thought to be a passive state that was initiated through withdrawal of sensory inputs. Currently, sleep is considered an active initiation mechanism that facilitates brain withdrawal16 and both homeostatic factors (factor S) and circadian factors (factor C) interact to determine the timing and quality of sleep.
The sleep centre is situated in the ventrolateral preoptic nucleus (VLPO) of the anterior hypothalamus. It has been proved by PET scan that VLPO becomes active during sleep, which results in production of sleep promoter neurotransmitters like GABA, galanin, adenosine and melatonin which inhibit the wake-centres in the tuberoinfundibular region of brain (the region of base of brain between two optic chiasma that includes the infundibulum, tuber–cinereum and mammillary bodies. The wake centres are widespread, not only encompassing in them the tubermammillary nucleus (tuberinfundibular region) but also lateral hypothalamus and the brain stem nuclei like locus coeruleus, dorsal raphe, laterodorsal tegmental nucleus and pedunculopontine tegmental nucleus. The wake centres by producing wake promoting neurotransmitters nor-epinephrine, serotonin, orexin, dopamine, acetylcholine and histamine, awake the patient after overnight sleep. The hypocretin (OREXIN) is secreted in the lateral hypothalamus.11
The tuberoinfundibular region projects rostrally to the intralaminar nuclei of the thalamus and to the cerebral cortex. So, when the sleep centre becomes active not only are the tuberoinfundibular region depressed but it's cortical projections are also inhibited. This results in functional disconnection between the brain stem and the more rostral thalamus on the one hand and central cortex on the other. A decrease in the ascending thalamo-cortical impulses (cholinergic transmission) occurs leading to decreased cortical responsiveness.
In addition to inhibiting higher cortical consciousness, the impulses flowing to muscles of the trunk and extremities through the pontine reticular inhibitory system inhibits effective transmissions from ascending sensory tracts.
The brain stem nuclei (nucleus coeruleus and dorsal raphe nucleus) inhibit the inferior motor neurone to produce relaxation of the selected muscles of extremities which is so characteristic of deep sleep. In other words, when the tuberoinfundibular region is depressed by inhibitory impulses from VLPO, the sensory impulses from the environmental stimuli, ascending through reticular activating system are not allowed to reach cerebral cortex due to blockage at the tuberoinfundibular region. Thus, the cerebral cortex is functionally disconnected (withdrawn) from environmental stimuli during sleep.
Limbic system is also considered to play an important role in sleep mechanism.10
 
Schematic Representation of Mechanism of Sleep
  1. Central neuronal pacemaker in suprachiasmatic nucleus
    (circadian rhythm regulator)
    +
  2. Sleep centre in ventro lateral preoptic nucleus (VLPO) in anterior hypothalamus
    +
  3. Sleep homeostasis
    ↓ Produce
    Sleep promoters e.g., → GABA, galanin, adenosin, melatonin
    ↓ Inhibit
    Awake centres in:-
    1. Nuclei of tuberoinfundibular region (Tuber-cinereum, mammillary bodies and infundibulum) and its projections to cerebral cortex
    2. Lateral hypothalamus (which secretes OREXIN)
    3. Brain stem nuclei: Locus coeruleus, dorsal raphe nucleus, pedunculopontine tegmental nucleus, laterodorsal tegmental nucleus
      ↓ Results in:
      Reduced secretion of awake promoters like, Catecholamine, serotonin, orexin, dopamine, acetychotine, histamine
      Sleep ensues
 
What should be Optimum Duration of Sleep
Human sleep-needs can vary by age and among individuals and sleep is considered to be adequate when there is no daytime sleepiness or dysfunction.
Japanese Prof Ying-Hui-Fu and her colleagues19 bred mice that carried a mutated DEC-2-gene and slept less than normal mice. It is in hypothesised that a considerable amount of sleep-related behavior such as when and how long a person needs to sleep, is regulated by genes. Researchers have discovered some evidence that seems to support this assumption. One gene named as ABCC9, has been identified and has appeared to influence the duration of human sleep.1921
A study by Psychiatry Department of University of California, San Diego19 of more than one million adults found that people who reported sleeping for 6–7 hours each night lived longest (no-30).22 Another study of sleep duration and mortality risk in women showed similar results.22 Several studies23 have on the other hand shown that sleeping more that 7–8 hours per day has been consistently associated with increased mortality.
Researchers at the University of Warwick and University College of London,17 have found lack of sleep more than doubling the risk of cardiovascular disease, but that too much sleep can also be associated with doubling the risk of death though not primarily from cardiovascular24,25 diseases.11
Professor Francesco Cappuecio said,19 “Short sleep has been shown to be a risk factor for weight gain, hypertension and Type 2 diabetes sometimes leading to mortality”.
To quote Dr Shashbank R Joshi26 [in the book “Prevention of Diabetes”, published by Indian College of Physicians and Association of Physicians of India (Banshi Sahoo (Ed)) Mumbai 2013; in chapter 2 “Diabetes Prevention in Native Asian Indians], “Eat Less, Eat on Time, Eat Right, Walk more, SLEEP WELL and Smile to prevent diabetes mellitus” implies clearly that sleeping well is also a prerequisite to prevent diabetes. If you don't sleep well you will be prone to diabetes mellitus.
 
Why do we Need Sleep
Several studies on experimental animals and humans have suggested following attributes to sleep.
 
Restorative Function
The sleeping brain has been shown to remove metabolic waste products at a faster rate than during an awake state.19,27 The metabolic phase during sleep in anabolic. Anabolic hormones such as growth hormone are secreted preferentially during sleep, especially during the slow wave sleep. Sleep has also been theorised to effectively combat the accumulation of free radicals in brain by increasing the efficacy of endogenous anti-oxidant mechanism.19,28
That sleep loss impairs immune functions has been inferred from surrogate markers of immune-mechanism like white blood cell count. Persons deprived of sleep for 24 hours showed 20% decrease in WBC count than in their usual wake state.
Wound healing has been associated with sleep, as sleep deprivation has been shown to hinder the healing of burns on rats.
Conservation of energy by sleep is a common knowledge.
 
Ontogenesis (Course of Development of an Individual Organism)
According to Ontogenetic hypothesis of REM sleep, the activity occurring during neonatal REM sleep (or active sleep) seems to be particularly important to developing organism. Studies have shown that deprivation of REM sleep early in life can result in behavioral problems, decreased brain mass and an abnormal amount of neural death19 as REM sleep appears to be important for development of brain. REM sleep occupies the majority of time of sleep in infants who spend most of their time sleeping to ensure proper development of their brain.
 
Memory Proccessing
There are numerous ways in which sleep is related to memory. Working-memory is adversely affected by sleep deprivation. Working memory is important because it keeps information active for further processing and supports higher-level cognitive functions such as decision making, reasoning and episodic memory. In an interesting study, 18 women and 26 men were allowed to sleep for 26 minutes per night for 4 nights. Prior to this, their cognitive function was tested while well-rested. During the day time, following each night of sleep deprivation, their cognitive functions were tested twice a day. It was found that the average working memory span of the sleep deprived group dropped by 38% compared to the controlled group who were allowed normal sleep, i.e. sleep, to their satisfaction. Sleep has an overall role of consolidation and organisation of synaptic connections formed during learning and experience.1912
 
DREAMING
Everyone dreams, the frequency varies from individual to individual. Dreams are usually only remembered when there is a period of waking during or at the end of a REM episode. Dreams can also occur during NREM episodes.
Dreams which occur during REM stage of sleep may be generally different from those which occur during NREM phase in that they are less story like and bizarre and less vivid.4 Eye movements and twitching during dream occur in bouts lasting one to three minutes alternating with periods of no movement for 1 to 3 minutes.
 
Theories of Dream
  1. Dreaming is perceived experience of sensory images and sounds during sleep in a sequence which the dreamer perceives more as an apparent participant than as an observer. Dreaming centres are located in pons.
  2. Another theory is that dreams are caused by the random firing of neurons in the cerebral cortex during the REM-period.
  3. Theory of Dreams by Freud Sigmond: Freud postulated that dreams are the symbolic experience of frustrated desires that have been relegated to the subconscious mind.
  4. Activation Synthesis Theory of Dreaming: It has been proposed by workers like John Allan Hobson and Robert Mc-Carley that dreams are caused by the random firming of cerebral cortical neurons as stated above.
This theory helps to explain the irrationality of brain (mind) during REM sleep as according to this theory the forebrain creates a story in an attempt to reconcile and make sense of nonsensical sensory informations presented to it.19 This theory supports the view that dreams occur during REM phase of sleep.
Sexual Theory of Dreams: It has been hypothesized that parasympathetic nervous system experience increased activity during REM sleep. Some facts e.g., penile erection during dreams substantiate this hypothesis. Penile erection caused by hyperactive parasympathetic system many explain dreams with sexual contents, but penile erection occurs also during non sexual dreams.
All these sum up to a fact that we still do not fully understand the mechanism of dream.
We can suppress or encourage dreams. Suppressants of dreams are: antidepressants, acetaminophen (paracetamol), ibuprofen and alcohol. Alcohol should not however be prescribed as it leads to fragmented non restorative sleep. We can encourage dreaming by melatonin.
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  1. Joshi SR. Diabtes Prevention in Native Asian Indians in ICP Monogram on Prevention of Diabetes, published by Indian College of Physicians and Association of Physicians of India (ed Dr Banshi Saboo). 2013 Unit 6 and 7, Ground floor. Turf Estate, off. Dr E Moses Road, Near Mahalakshmi station (West Mumbai 400011).
  1. “Brain may flush out toxins during sleep (http://www.ninds.nih.gov/news and events/news articles/press release brain sleep 10182013.htm) National Institute of Health. Retrieved 25 october 2013.
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