normal human sleep, an overview

Med Clin N Am 88 (2004) 551–565

Normal human sleep: an overview

Max Hirshkowitz, PhD, DABSMa,b,c,d,*aDepartment of Psychiatry, Baylor College of Medicine, 1 Baylor Plaza,

Houston, TX 77030, USAbDepartment of Medicine, Baylor College of Medicine, 1 Baylor Plaza,

Houston, TX 77030, USAcHouston Veterans Affairs Medical Center–Sleep, Center 111i, 2002 Holcombe Boulevard,

Houston, TX 77030, USAdMethodist Hospital Sleep Diagnostic Laboratory, Houston, TX, USA

Sleep can be defined many ways; however, the basic core concepts remainthe same. First and foremost is that sleep is a brain process. The body restsbut the brain sleeps. This is not to say the body does not require sleep; thereare essential body processes that occur only when the brain is asleep.Nonetheless, the brain is what does the sleeping. The second core concept isthat sleep is not a unitary phenomenon. There are several types of sleep, eachwith their own particular characteristics, functions, and regulatory systems.Selective deprivation of one type of sleep usually provokes rebound duringrecovery. Finally, some sleep processes are active and involve significantcortical activation [1,2]. The activation level may exceed that occurringduring some states of wakefulness. Because sleep is a brain process, thetraditional approach to studying sleep began by measuring brain activity.

The first great step forward toward the modern understanding ofhuman sleep was taken by Berger [3]. In addition to being the father ofelectroencephalography (EEG), he also made the first sleep recording andnoted that the alpha rhythm disappeared when his subject fell asleep.Essentially, this operational definition for sleep onset remains even to thepresent day. Alpha cessation marks the transition from wakefulness to sleep,assuming the individual has eyes closed and is not engaged in effortfulmental activity. This important step toward the modern understanding ofnormal human sleep established differential electroencephalographic (andpresumably brain activity) correlates of sleep and wakefulness. In so doing,it set up the basic paradigm for studying human sleep and sleep disorders.

* Houston Veterans Affairs Medical Center–Sleep Center 111i, 2002 Holcombe

Boulevard, Houston, TX 77030.

E-mail address: [email protected]

0025-7125/04/$ - see front matter. Published by Elsevier Inc.

doi:10.1016/j.mcna.2004.01.001

mailto:[email protected]

552 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

The second major step occurred within a decade when the firstcontinuous overnight EEG sleep recordings in humans were published in1937 by Loomis et al [4]. The information on miles of paper tracingsrecorded with their 8-ft-long drum polygraph were summarized accordinga data reduction scheme they called ‘‘sleep staging.’’ The sleep stageclassification system (stages A, B, C, D, and E) was largely based onpredominant EEG activity within a fixed time domain, or epoch. EEGactivity includes beta activity (>13 Hz); sleep spindles (12–14 Hz bursts);alpha rhythm (8–13 Hz, sometimes slower); theta rhythm (4–7 Hz); saw-tooth theta waves (4–7 Hz, with notched appearance); delta rhythm (\4Hz); and slow waves (\2 Hz). Sleep stages were then graphically illustratedin a manner remarkably similar to what is still done today.

It took another 15 years to pass the next major milestone. Aserinsky andKleitman [5] added the final piece to the brainwave correlate sleep puzzle bydiscovering episodic electro-oculographic (EOG) activity occurring approx-imately every 90 to 120 minutes during stage B sleep. Initially this EOGactivation was suspected to be a recording artifact; however, continuedefforts verified that actual eye movements were occurring. These jerky eyemovements (as Aserinsky called them) eventually became known as rapideye movements (REMs). Subsequent studies revealed dreaming in 20 of the27 instances when individuals were awakened from REM sleep [5]. The EEGcorrelates of dreaming were established, arming researchers with a labora-tory tool to unlock the mysteries of dreaming (as Freud [6] called it, ‘‘theroyal road to the unconscious’’), or so it was thought.

Hundreds of studies attempted to exploit the REM-dreaming paradigm;however, no unified ‘‘dream theory’’ emerged. Some Freudian concepts wereverified (eg, daytime residue), whereas others were not. The two majorcompeting modern theories are the neurophysiologically grounded activa-tion-synthesis hypothesis and the cognitive dream theory. The activation-synthesis hypothesis considers dreaming as epiphenomenologic, created bya cortex trying its best to interpret incoming random subcortical activity. Bycontrast, the cognitive theories consider dreaming an extension of daytimethought albeit governed by a different grammar and looser rules [7,8].

The next major refinement to sleep state description came later in the1950s when Jouvet [9] observed postural changes in cat corresponded todifferent sleep states. He then electromyographically (EMG) verified muscleatonia accompanying REM sleep in normal animals. This functional para-lysis, detectable by EMG recording, was the final step toward developingwhat is now standard recording practice for determining human sleep stage.Jouvet [9] also introduced the concept that REM sleep was a third state ofconsciousness and not just another component of the basic rest activitycycle. From one perspective, sleep generally represents an altered state inneurologic organization (compared with wakefulness). During wakefulnessthe nervous system supports an active brain in an active body. Undernormal circumstances, an individual is conscious of the surroundings and

553M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

responsive to the environment. During sleep, for the most part environ-mental responsiveness is lost and one becomes unconscious. Sleep wastraditionally regarded as a deactivated (or inactive) brain in an inactivebody. With the discovery of REM sleep muscle atonia (presumably ac-companying dreaming), another organizational state could be postulated:an active brain in an inactive body.

The final step for defining normal human sleep was the development,publication, and widespread agreement to use A Manual of StandardizedTerminology, Techniques and Scoring System for Sleep Stages of HumanSubjects (Standardized Manual) [10]. Commonly referred to as the ‘‘R&Ksystem,’’ after the two editors Rechtschaffen and Kales, this work includescontributions from a veritable pantheon of scientists and clinicians drivenby devoted interest in human sleep and its disorders. The group includesRalph J. Berger, William C. Dement, Allan Jacobson, Laverne C. Johnson,Michel Jouvet, Anthony Kales, Lawrence J. Monroe, Ian Oswald, AllanRechtschaffen, Howard P. Roffwarg, Bedrich Roth, and Richard D. Walter.In 1968, the United States Government Printing Office published theStandardized Manual. It was later reprinted by the Brain InformationService (University of California, Los Angeles, CA).

The Standardized Manual was pivotal in the field and the key to itssuccess was final agreement and consensus. This is not to say thatparticipants did not heatedly disagree; they did. Some participants arguedthat one EEG channel was inadequate, that chin EMG was questionablyuseful, that delta amplitude criteria were arbitrary, and so forth. In the heatof the arguments, Allan Rechtschaffen reportedly barred the doors anddecreed that no one could leave until they came to agreement; they did.Indeed, if each participant had returned to their laboratory and ignored theguideline in favor of continuing to do things according to their own practice,the project would not have succeeded. For the most part, the rules forscoring already existed as the Dement-Kleitman system and the Williams-Karacan system. Some modifications, explications, and simplifications weremade in the interest of improving recording ease and scoring reliability. Inthe end, however, the critical ingredient was consensus, without which theattempt at standardization would have failed.

Normal human sleep: definitions

Electroencephalography activity recorded from central (C3 or C4) andoccipital (O3 or O4) derivations, EOG activity from right and left eye(recorded from the outer canthi), and submental EMG are used to definesleep stage. In standard practice, each 30 seconds of recording (one epoch) iscategorized as wakefulness (W) or sleep stage 1, 2, 3, 4, or REM. Epochlength was a convention based on paper polygraph tracings. These tracingswere usually recorded at a chart speed of 10 mm/s; therefore, each resulting


polygraph page was 30 seconds in duration. Because each polygraph page isnumbered, it was a matter of convenience to summarize sleep state for each30-second page. Although paper polysomnograms have mostly gone theway of the dinosaurs, the practice of 30-second epoch sleep staging con-tinues, notwithstanding computerized polygraph systems’ ability easily toresize pages and alter temporal resolution.

Sleep stages

Wakefulness (also called stage W or stage 0) with eyes closed isaccompanied by an EEG rhythm predominantly in the alpha range (Fig. 1).Some individuals do not have distinct alpha activity and transition quicklyto a low-voltage, mixed-frequency activity. Opening the eyes or engagingin a significant mental task (for example counting backward by threesbeginning with the number 2481) diminishes or blocks the alpha activity.Fairly high muscle activity can be present and eye movements may occur(both rapid and slow). Sleep onset epoch is determined when alphadecreases to duration of less than 50% of an epoch or a vertex wave, K-complex, sleep spindle, or delta activity occurs; otherwise, wakefulness isscored. Stage 1 sleep is scored when low-voltage mixed-frequency EEG ispresent but there are no K complexes, spindles, or REMs. Stage 1 sleepis a nonalpha state with EEG activity that is deltaless and spindleless;however, vertex sharp waves may be present. Stage 2 sleep epochs areclassified when there are sleep spindles or K complexes but high amplitude(75 lV or greater) delta EEG activity occupies less than 20% of the epoch.Stage 3 is designated when there is 20% to 50% delta (or slow wave activity)in an epoch. Stage 4 is scored when delta (or slow wave) activity covers morethan 50% of an epoch. REM sleep is scored when eye movements andmuscle atonia accompanying a stage 1 EEG pattern. Saw-tooth theta wavesmay also accompany REM sleep. In addition to REMs, other physiologicactivities accompany REM sleep including middle ear muscle activity,periorbital integrated potentials, and sleep-related erections. There are

Fig. 1. Wakefulness EEG-EOG-EMG polysomnographic tracings. Shown is a 30-second

tracing of right (EOGR) and left (EOGL) electro-oculograms; submentalis electromyogram

(EMGSM); and monopolar central (C3-A2) and occipital (O3-A2) electroencephalograms.


periods within REM sleep when eye movement activity and presumablyother phasic event activity are high. At other times, REM-like backgroundEEG activity continues with very little phasic activity. These two phases ofREM sleep are called ‘‘phasic REM sleep’’ and ‘‘tonic REM sleep’’ (Fig. 2).Stages 1, 2, 3, and 4 are sometimes collectively referred to as non-REMsleep. Stages 1 and 2 are sometimes referred to as light sleep, whereas stages3 and 4 are often combined and called slow wave sleep or deep sleep (Figs. 3and 4). Table 1 summarizes EEG-EOG-EMG characteristics for wakeful-ness and the different sleep stages.

The normal sleep pattern: generalizations

A healthy young adult good sleeper has 95% sleep efficiency (ie, 5% orless of the total time in bed is spent awake). Sleep onset is swift (less than 15minutes) and nocturnal awakenings few and brief. Stage 2 sleep accounts forapproximately half the night’s sleep, and REM sleep accounts for another20% to 25%. A nightly total of 1% to 5% of stage 1 sleep is distributed atthe wakefulness-sleep transition and at light sleep transitions. The remainingsleep is distributed between slow wave sleep stages 3 and 4. Only minordifferences are found for sleep stage distributions between young adult menand women.

Fig. 2. Tonic and phasic REM sleep EEG-EOG-EMG polysomnographic tracings. Each panel

shows a 30-second tracing of right (EOGR) and left (EOGL) electro-oculograms; submentalis

electromyogram (EMGSM); and monopolar central (C3-A2) and occipital (O3-A2) electro-

encephalograms.


Individuals do not have single blocks of each sleep stage and thenawaken. The normal pattern involves having repeated 90- to 120-minute-long cycles of non-REM and REM sleep. With each cycle reoccurrence thereare usually systematic alterations in cycle properties. Sleep architecturerefers to the progression and continuity of sleep through the sleep cycles ona given night. Fig. 5 shows a typical night with normal sleep architecture ina healthy young adult and the percentages of each sleep stage. The followingfive generalizations can be made about normal sleep architecture:

1. Sleep is entered through non-REM sleep2. Non-REM and REM sleep alternate approximately every 90 to 120

minutes3. Slow wave sleep predominates in the first third of the night4. REM sleep predominates in the last half of the night5. REM sleep occurs in four to six discrete episodes each night with

episodes generally lengthening as sleep period progresses

Age-related changes

Sleep pattern changes as a function of aging. Globally, there is a gradualdecline in overall total sleep time. Aging, especially after middle age, isassociated with greater wakefulness intermixed with sleep (fragmentation).

Fig. 3. Light sleep. Stages 1 and 2 EEG-EOG-EMG polysomnographic tracings. Each panel

shows a 30-second tracing of right (EOGR) and left (EOGL) electro-oculograms; submentalis

electromyogram (EMGSM); and monopolar central (C3-A2) and occipital (O3-A2) electro-

encephalograms.


Table 1

EEG-EOG-EMG characteristics of sleep and wakefulness

Stage EEG characteristics EOG EMG muscle activity

W Predominant alpha activity (more than

50% of the epoch) mixed with EEG

beta.

Slow and rapid High

1 Alpha activity is replaced by

predominant low-voltage,

mixed-frequency background activity

sometimes with vertex sharp waves.

Slow Decreased from awake

2 Sleep spindles and K complexes in

a background EEG that has less than

20% delta activity.

None Decreased from awake

3 Slow waves (EEG delta activity)

comprise 20%–50% of the epoch;

sleep spindles usually are present.


4 More than 50% of the epoch has EEG

delta activity.


REM Low-voltage, mixed-frequency

background activity; saw-tooth theta

waves may be present.

Rapid Nearly absent

Abbreviations: EEG, electroencephalographic; EMG, electromyographic; EOG, electro-

oculographic; REM, rapid eye movement.

Fig. 4. Slow wave sleep. Stages 3 and 4 EEG-EOG-EMG polysomnographic tracings. Each

panel shows a 30-second tracing of right (EOGR) and left (EOGL) electro-oculograms;

submentalis electromyogram (EMGSM); and monopolar central (C3-A2) and occipital (O3-A2)

electroencephalograms.


In generally, the elderly spend more time in bed but less time sleeping.Some of the sleep disturbances are produced by increasing sleep-relatedpathophysiology (eg, arousals from sleep apnea). Some proportion of age-associated deterioration in the sleep pattern may directly relate to the agingprocess and not to secondary factors compromising sleep. REM sleeppercentage (of total sleep time) changes dramatically during the first fewdecades of life. It decreases from more than 50% at birth to 20% to 25% atadolescence. REM sleep then stabilizes, with some additional declineoccurring after age 65 years. By contrast, slow wave sleep begins to declineafter adolescence and continues to decline as a function of age, disappearingcompletely in some elderly individuals.

The difficulty defining normal

The first difficulty encountered when attempting to determine the normalsleep pattern is that sleep is altered by the processes used for measurement.The delayed sleep onset, general disruption, and decreased REM or slowwave sleep percentages found when an individual sleeps in a newenvironment (eg, the sleep laboratory) provides a good example ofHeisenberg’s uncertainty principle. This laboratory-adaptation consequenceis so commonly observed it has been named the ‘‘first-night effect.’’ Tocharacterize normal sleep, first-night data are often discarded. Nonetheless,age-specific normative values have been derived empirically for both firstand succeeding nights. Polysomnographic data from large samples acrosswide age ranges can be obtained [11–16]. The many studies performed byWilliams et al [17] were eventually combined to provide the first completesource of sleep normative data. These data were published in 1974 in thebook EEG of Human Sleep [17]. The intent of Williams et al [17] was toprovide a reference standard against which individual patient data could becompared. They reasoned that to know if sleep is abnormal, one first needs

Fig. 5. Sleep architecture (A) and composition (B) in a normal, healthy young adult.


to know the range of normal values. Over many years, beginning at theUniversity of Florida at Gainesville and continuing at the Veterans AffairsMedical Center in Houston, data were methodically collected, scored,tabulated, and analyzed. These data, nearly 30 years old, are still used asnormative values by many clinicians.

There are, however, three important issues to consider when using EEGof Human Sleep data as normative values. First, polysomnograms were notrecorded according to recommendations in the Standardized Manual. TheFlorida group, later the Houston group, used a different recording montagethat included frontal, central, and occipital EEG derivations but did notinclude submentalis EMG and summarized to 1-minute epochs. Second, therecordings were not scored using the R&K system but rather a modifica-tion of the Dement-Kleitman system [18] called the Weaver-1 (after thelaboratory’s long-time chief technologist Ralph Weaver). Delta activity wasscored from a bipolar frontal tracing (F1-F7); alpha activity was scoredfrom a bipolar occipital tracing (O3-OZPZ); and other waveforms werescored from a monopolar central tracing (C3-A2). The third and perhapsmost important issue is that the values presented do not include the first-night results. Eliminating the first night because it is likely contaminated bya laboratory adaptation effect is completely reasonable for a scientificexploration designed to characterize normal sleep. Using such values createsa biased comparison, however, when compared with a patient’s first night inthe laboratory. This problem exists for most data samples available in thepublished literature.

Another general issue for determining normative values is whether oneshould require a fixed time in bed at set times, a fixed duration for timein bed, or variable time in bed set according to an individual’s routine.Standardizing set times, although attractive from a laboratory operationperspective, creates an artificial situation. The individual may be sleepingout of their normal routine and have disturbed sleep. Similarly, having a setduration for time in bed may artificially increase the amount of wakefulnessor REM sleep. Having an individual sleep according to their own scheduleattempts to obtain data will less measurement bias; however, it producesgreater variation in many parameters (eg, total sleep time).

Normal human sleep: actuarial data

Data presented here were recorded as part of a variety of prospectiveresearch projects. Table 2 shows first-night polysomnographic results forsubjects divided into five nonoverlapping age groups. Table 3 shows resultsfrom the following night from the same subjects. All subjects were normalhealthy volunteers. Informed consent was obtained from each subject.Subjects were recruited through media advertising, health fairs, posters, andreferral channels.

Tab

Nor

N= 49) 50–59 y (N = 41) � 60 y (N = 29)

SD Mean SD Mean SD

Gen

T 49.4 393.0 51.1 395.7 42.8

Sl 14.0 8.7 11.4 15.3 14.9

T 54.6 331.6 63.6 298.4 61.3

Sl 10.8 84.3 11.1 75.4 13.2

L 22.2 4.3 11.1 4.2 9.8

N 5.3 11.4 4.5 14.1 6.7

A 0.8 1.8 0.7 2.2 1.0

N 18.8 46.3 12.7 50.8 21.9

Non

St 3.3 5.5 3.0 6.1 3.5

St 11.7 54.2 10.2 51.0 9.1

St 2.4 3.0 2.4 2.5 2.3

St 6.5 4.1 5.6 2.6 3.4

REM

R 6.4 17.6 5.9 13.2 5.7

R 0.9 3.8 0.9 3.6 1.3

R 33.7 78.7 32.6 59.2 26.8

M 7.1 20.3 6.3 16.3 6.5

R 11.1 89.7 10.7 90.3 12.1

a

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mative sleep values for first night sleeping in the laboratory

Age group (no. of subjects)

20–29 y (N = 44) 30–39 y (N = 23) 40–49 y (

Mean SD Mean SD Mean

eral, sleep continuity, and integrity measures

ime in bed (minutes) 404.9 44.1 393.1 58.2 404.2

eep latency (minutes) 11.8 13.1 13.4 10.1 14.2

otal sleep time (minutes) 347.3 62.5 340.0 70.8 329.4

eep efficiency indexa 86.2 14.2 86.4 11.6 81.7

atency to arising (minutes) 2.0 7.7 9.7 22.7 7.1

umber of awakenings 9.6 8.2 7.7 4.2 11.6

wakenings per hour 1.5 1.2 1.3 0.8 1.8

umber of sleep stage shifts 47.1 23.6 39.9 11.8 46.7

-REM sleep stage percentages

age 1 percentage of time in bed 4.1 3.0 3.4 2.1 5.4




sleep measures

EM sleep percentage of time in bed 17.8 7.1 18.2 7.9 15.8

EM sleep episodes (number) 3.3 1.0 3.4 1.0 3.5

EMSEb duration (minutes) 77.0 31.2 79.5 40.7 74.2

ean REMSE duration (minutes) 23.1 8.4 23.6 14.1 21.1

EM sleep efficiency indexc 91.0 18.7 93.4 8.7 88.1

Sleep efficiency is total sleep time percentage of time in bed.

REMSE is REM sleep episode.

REM sleep efficiency index is total REM sleep time percentage of total REM sleep episodes d

Tabl

Norm

N= 49) 50–59 y (N = 41) �60 y (N = 29)

SD Mean SD Mean SD

Gene

Ti 50.0 405.5 56.4 406.6 45.8

Sle 9.7 6.1 7.7 8.2 7.7

To 52.4 366.6 58.0 348.8 51.5

Sle 9.8 90.4 7.1 85.8 7.9

La 8.1 2.4 8.8 1.3 2.4

Nu 5.8 9.7 5.2 12.3 6.7

Aw 0.9 1.4 0.8 1.9 1.0

Nu 18.2 45.1 16.3 47.2 14.2

Non-

St 2.8 4.7 3.7 4.0 2.7

St 11.5 56.7 9.9 57.6 8.2

St 2.6 3.7 3.4 2.9 2.5

St 7.0 4.4 5.2 4.8 5.3

REM

RE 7.1 20.9 7.2 16.4 7.4

RE 0.9 4.1 0.9 3.8 1.2

RE 35.1 92.5 29.7 74.7 34.3

M 9.3 23.1 7.4 20.2 9.8

RE 9.8 90.1 9.1 90.2 11.1

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ative sleep values for second night sleeping in the laboratory

Age group (no. of subjects)

20–29 y (N = 44) 30–39 y (N = 23) 40–49 y (

Mean SD Mean SD Mean

ral, sleep continuity, and integrity measures

me in bed (minutes) 397.3 44.5 397.5 49.7 411.7

ep latency (minutes) 6.3 6.9 10.0 10.3 8.4

tal sleep time (minutes) 374.9 44.5 375.8 52.9 370.2

ep efficiency indexa 94.4 4.7 94.4 4.1 90.2

tency to arising (minutes) 0.4 1.0 0.2 0.4 2.5

mber of awakenings 6.3 6.3 4.7 3.7 8.4

akenings per hour 1.0 1.0 0.7 0.6 1.3

mber of sleep stage shifts 44.4 23.6 36.2 14.8 43.5

REM sleep stage percentages





sleep measures

M sleep percentage of time in bed 22.2 6.1 23.1 6.7 20.4

M sleep episodes (number) 3.6 0.8 3.6 0.8 3.8

MSE duration (minutes) 94.3 27.4 99.1 32.9 94.0

ean REMSE duration (minutes) 27.2 8.9 27.9 9.7 25.4

M sleep efficiency indexb 94.0 7.9 93.6 7.7 90.5

Sleep efficiency is total sleep time percentage of time in bed.

REM sleep efficiency index is total REM sleep time percentage of total REM sleep episodes d


Although individual protocols differed, all had two consecutive nightsat the beginning of the study, one for adaptation and one for baseline.Polysomnograms were recorded and scored according to the StandardizedManual. Grass Model 78, Grass Model 8-10, Nihon Kohden, and GrassHeritage polysomnograph systems were used. In most cases, subjects wereinstrumented for respiratory, leg movement, or other evaluations.

Subjects reported to the laboratory 1 to 2 hours before scheduledbedtime. Bedtimes and arising times were scheduled, as much as possible,according to the subject’s normal routine. On arrival at the laboratory, eachsubject completed a brief presleep questionnaire and had monitoring devicesattached by the night technologist. Polysomnographic calibrations werepreformed before each recording. Subjects slept in temperature-controlled,sound-attenuated, electrically shielded, private bedrooms and were contin-uously monitored throughout the night. On awakening at the end of thescheduled sleep period, monitoring devices were removed and the subjectcompleted a postsleep questionnaire.

Mechanism regulating and governing normal sleep

There are three basic mechanisms coordinating and governing sleep andwakefulness: (1) autonomic nervous system balance, (2) homeostatic sleepdrive, and (3) circadian rhythms. These mechanisms maintain sleep andwakefulness in a dynamic balance but also allow for adaptation to suddenshifts in the time and duration of sleep.

Autonomic nervous system balance

In general, sleep requires decreased sympathetic activation and increasedparasympathetic balance. Consequently, anything that increases sympa-thetic outflow can disturb sleep and it matters little whether the origin isexogenous or endogenous [19]. That is, both drinking coffee at bedtime(exogenous) and anxious rumination (endogenous) may keep one awake byautonomic mechanisms. This feature of autonomic regulation likely hassurvival value. When emergencies occur in the middle of the night, thereneeds to be a mechanism to promote quick response and sustained alerting.The survival value may be why autonomic activations commence rapidlybut dissipate slowly. Unfortunately, this mechanism may go awry andcontribute to insomnia. For example, if one gets ‘‘worked up’’ aboutsomething right before bedtime, they may toss and turn for an hour. Ritualscan help promote progressive relaxation and gradual reorientation awayfrom daytime stressors and toward nocturnal tranquility. In children whosleep well, elaborate presleep rituals are common and may include a bedtimestory; a light snack; teeth brushing; prayers; and having a favorite stuffedanimal toy, pillow, and blanket. The latter also provides sleep-onset


association stimuli that likely facilitate conditioning. As an autonomicprocess, sleep onset is amenable to classical conditioning. Pavlov was ableto condition a dog to salivate by repeatedly pairing a ringing bell withfood presentation (canines automatically salivate when food is present).Conditioning sleep onset, or the autonomic properties surrounding it, ofteninadvertently occurs. The bed, pillow, or blanket (or stuffed animal toy forchildren) become conditioned stimuli for sleep onset. In some cases,however, a bedroom stimulus cues an alerting response (producing psycho-physiologic insomnia). Similarly, if a parent becomes the child’s stimuluscue for sleep onset, the parent may find himself or herself having to rock thebaby back to sleep at any and all times of the night.

Homeostatic sleep drive

In general, the longer an individual remains awake, the sleepier he orshe becomes. Homeostatic regulation of sleepiness is similar to that forthirst, hunger, and sex. Hypothalamic-generated motivational states directbehavioral systems to perform actions that reduce drive. Continuous, uninter-rupted, prolonged wakefulness eventually makes sleep irresistible. Sleep-deprivation studies stretch homeostatic mechanisms to their limits to exploresleep’s function by examining deficits produced by its loss. Sleep deprivationcan be total, partial, or stage-specific. Not surprisingly, sleep loss increasessleepiness. Sleep loss also seems to diminish coping and sleep-deprivedindividuals become irritable and easily frustrated. Further deprivation ad-versely affects attention and performance lapses occur. In some individuals,longer-term sleep deprivation may produce hallucinations and on rare oc-casions seizures. Because sleep deprivation is stressful, catecholamineturnover increases and cortisol rises [20–22].

Circadian rhythms

Most people have noticed that during extended wakefulness, sleepinesswaxes and wanes. Sometimes after staying up all night, the chronobiologicself-abuser notes a surge of energy at daybreak. Although the person hasbeen awake longer, they feel less sleepy than they did at 5:00 AM. Thisviolation in homeostasis reveals another factor governing sleep andwakefulness: the circadian rhythm. The circadian rhythm is an approximatedaylong rhythm (from the root ‘‘circa’’ + ‘‘dias’’ [approximately a day]).There are many biologic clocks; however, the one regulating the sleep-wakecircadian rhythm is located in the suprachiasmatic nucleus and the corebody temperature cycle is entrained to this sleep-wake oscillator (which iswhy the temperature cycle is commonly used as a marker of circadianrhythm). In general (1) maximum alertness occurs at temperature peak; (2)drowsiness ensues when temperature starts to fall; (3) when temperaturereaches nadir, sleepiness can be overwhelming; (4) sleepiness decreases and


alertness increases as temperature begins to rise; and (5) when temperaturereaches maximal level, the cycle begins again [23–25].

When things go awry: abnormal sleep

Understanding what constitutes normal sleep is essential to recognizeand assess the severity of abnormal sleep. Although better normative dataare sorely needed, sleep disturbances can be evaluated objectively andquantitatively assessed. Distinct pathophysiology leading to sleep alteration(eg, sleep-disordered breathing provoking awakenings) is one way thatdisorders adversely affect sleep. Other sleep disorders arise from defectiveor impaired mechanisms that regulate and govern sleep. For example, aweak homeostatic drive for sleep likely produces chronic insomnia, whereasthe intrusion of REM sleep phenomena into the waking state underliesnarcolepsy. There are hundreds of sleep laboratories studying abnormalsleep every night. Polysomnograms are being recorded digitally andpreserved in their entirety. If every accredited sleep laboratory contributedone normal man’s and one normal woman’s polysomnogram per year,recorded according to standard protocol, one would not only be able togauge normal sleep better, but one would better understand abnormal sleep.In the meanwhile clinicians can use available actuarial information and thebasic understanding of the sleep process.

Summary

In this article normal human sleep is discussed. Landmarks leading up tothe understanding of human sleep, EEG definitions, and general character-istics of normal human sleep are presented. Actuarial laboratory data, forboth night 1 and night 2, are provided with an explanation of how they werecompiled. Finally, the mechanisms governing sleep and wakefulness arereviewed. This information, normal human sleep, and the mechanismsregulating it are critical to understanding abnormal sleep associated withsleep disorders.

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