Med Clin N Am 88 (2004) 551–565

Normal human sleep: an overview

Max Hirshkowitz, PhD, DABSMa,b,c,d,*
a
Department of Psychiatry, Baylor College of Medicine, 1 Baylor Plaza,
Houston, TX 77030, USA
b
Department of Medicine, Baylor College of Medicine, 1 Baylor Plaza,
Houston, TX 77030, USA
c
Houston Veterans Affairs Medical Center–Sleep, Center 111i, 2002 Holcombe Boulevard,
Houston, TX 77030, USA
d
Methodist Hospital Sleep Diagnostic Laboratory, Houston, TX, USA

Sleep can be defined many ways; however, the basic core concepts remain
the same. First and foremost is that sleep is a brain process. The body rests
but the brain sleeps. This is not to say the body does not require sleep; there
are essential body processes that occur only when the brain is asleep.
Nonetheless, the brain is what does the sleeping. The second core concept is
that sleep is not a unitary phenomenon. There are several types of sleep, each
with their own particular characteristics, functions, and regulatory systems.
Selective deprivation of one type of sleep usually provokes rebound during
recovery. Finally, some sleep processes are active and involve significant
cortical activation [1,2]. The activation level may exceed that occurring
during some states of wakefulness. Because sleep is a brain process, the
traditional approach to studying sleep began by measuring brain activity.
The first great step forward toward the modern understanding of
human sleep was taken by Berger [3]. In addition to being the father of
electroencephalography (EEG), he also made the first sleep recording and
noted that the alpha rhythm disappeared when his subject fell asleep.
Essentially, this operational definition for sleep onset remains even to the
present day. Alpha cessation marks the transition from wakefulness to sleep,
assuming the individual has eyes closed and is not engaged in effortful
mental activity. This important step toward the modern understanding of
normal human sleep established differential electroencephalographic (and
presumably 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: maxh@bcm.tmc.edu

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

doi:10.1016/j.mcna.2004.01.001
552 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

The second major step occurred within a decade when the first
continuous overnight EEG sleep recordings in humans were published in
1937 by Loomis et al [4]. The information on miles of paper tracings
recorded with their 8-ft-long drum polygraph were summarized according
a data reduction scheme they called ‘‘sleep staging.’’ The sleep stage
classification system (stages A, B, C, D, and E) was largely based on
predominant EEG activity within a fixed time domain, or epoch. EEG
activity 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 (\4
Hz); and slow waves (\2 Hz). Sleep stages were then graphically illustrated
in a manner remarkably similar to what is still done today.
It took another 15 years to pass the next major milestone. Aserinsky and
Kleitman [5] added the final piece to the brainwave correlate sleep puzzle by
discovering episodic electro-oculographic (EOG) activity occurring approx-
imately every 90 to 120 minutes during stage B sleep. Initially this EOG
activation was suspected to be a recording artifact; however, continued
efforts verified that actual eye movements were occurring. These jerky eye
movements (as Aserinsky called them) eventually became known as rapid
eye movements (REMs). Subsequent studies revealed dreaming in 20 of the
27 instances when individuals were awakened from REM sleep [5]. The EEG
correlates of dreaming were established, arming researchers with a labora-
tory tool to unlock the mysteries of dreaming (as Freud [6] called it, ‘‘the
royal 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 were
verified (eg, daytime residue), whereas others were not. The two major
competing modern theories are the neurophysiologically grounded activa-
tion-synthesis hypothesis and the cognitive dream theory. The activation-
synthesis hypothesis considers dreaming as epiphenomenologic, created by
a cortex trying its best to interpret incoming random subcortical activity. By
contrast, the cognitive theories consider dreaming an extension of daytime
thought albeit governed by a different grammar and looser rules [7,8].
The next major refinement to sleep state description came later in the
1950s when Jouvet [9] observed postural changes in cat corresponded to
different sleep states. He then electromyographically (EMG) verified muscle
atonia accompanying REM sleep in normal animals. This functional para-
lysis, detectable by EMG recording, was the final step toward developing
what is now standard recording practice for determining human sleep stage.
Jouvet [9] also introduced the concept that REM sleep was a third state of
consciousness and not just another component of the basic rest activity
cycle. From one perspective, sleep generally represents an altered state in
neurologic organization (compared with wakefulness). During wakefulness
the nervous system supports an active brain in an active body. Under
normal circumstances, an individual is conscious of the surroundings and
 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565 553

responsive to the environment. During sleep, for the most part environ-
mental responsiveness is lost and one becomes unconscious. Sleep was
traditionally regarded as a deactivated (or inactive) brain in an inactive
body. 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 Standardized
Terminology, Techniques and Scoring System for Sleep Stages of Human
Subjects (Standardized Manual) [10]. Commonly referred to as the ‘‘R&K
system,’’ after the two editors Rechtschaffen and Kales, this work includes
contributions from a veritable pantheon of scientists and clinicians driven
by devoted interest in human sleep and its disorders. The group includes
Ralph J. Berger, William C. Dement, Allan Jacobson, Laverne C. Johnson,
Michel Jouvet, Anthony Kales, Lawrence J. Monroe, Ian Oswald, Allan
Rechtschaffen, Howard P. Roffwarg, Bedrich Roth, and Richard D. Walter.
In 1968, the United States Government Printing Office published the
Standardized Manual. It was later reprinted by the Brain Information
Service (University of California, Los Angeles, CA).
The Standardized Manual was pivotal in the field and the key to its
success was final agreement and consensus. This is not to say that
participants did not heatedly disagree; they did. Some participants argued
that one EEG channel was inadequate, that chin EMG was questionably
useful, that delta amplitude criteria were arbitrary, and so forth. In the heat
of the arguments, Allan Rechtschaffen reportedly barred the doors and
decreed that no one could leave until they came to agreement; they did.
Indeed, if each participant had returned to their laboratory and ignored the
guideline in favor of continuing to do things according to their own practice,
the project would not have succeeded. For the most part, the rules for
scoring already existed as the Dement-Kleitman system and the Williams-
Karacan system. Some modifications, explications, and simplifications were
made in the interest of improving recording ease and scoring reliability. In
the end, however, the critical ingredient was consensus, without which the
attempt at standardization would have failed.

Normal human sleep: definitions

Electroencephalography activity recorded from central (C3 or C4) and
occipital (O3 or O4) derivations, EOG activity from right and left eye
(recorded from the outer canthi), and submental EMG are used to define
sleep stage. In standard practice, each 30 seconds of recording (one epoch) is
categorized as wakefulness (W) or sleep stage 1, 2, 3, 4, or REM. Epoch
length was a convention based on paper polygraph tracings. These tracings
were usually recorded at a chart speed of 10 mm/s; therefore, each resulting
554 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

polygraph page was 30 seconds in duration. Because each polygraph page is

numbered, it was a matter of convenience to summarize sleep state for each
30-second page. Although paper polysomnograms have mostly gone the
way of the dinosaurs, the practice of 30-second epoch sleep staging con-
tinues, notwithstanding computerized polygraph systems’ ability easily to
resize pages and alter temporal resolution.

Sleep stages
Wakefulness (also called stage W or stage 0) with eyes closed is
accompanied by an EEG rhythm predominantly in the alpha range (Fig. 1).
Some individuals do not have distinct alpha activity and transition quickly
to a low-voltage, mixed-frequency activity. Opening the eyes or engaging
in a significant mental task (for example counting backward by threes
beginning 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 alpha
decreases to duration of less than 50% of an epoch or a vertex wave, K-
complex, sleep spindle, or delta activity occurs; otherwise, wakefulness is
scored. Stage 1 sleep is scored when low-voltage mixed-frequency EEG is
present but there are no K complexes, spindles, or REMs. Stage 1 sleep
is a nonalpha state with EEG activity that is deltaless and spindleless;
however, vertex sharp waves may be present. Stage 2 sleep epochs are
classified 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 more
than 50% of an epoch. REM sleep is scored when eye movements and
muscle atonia accompanying a stage 1 EEG pattern. Saw-tooth theta waves
may also accompany REM sleep. In addition to REMs, other physiologic
activities 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.
 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565 555

periods within REM sleep when eye movement activity and presumably
other phasic event activity are high. At other times, REM-like background
EEG activity continues with very little phasic activity. These two phases of
REM 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-REM
sleep. Stages 1 and 2 are sometimes referred to as light sleep, whereas stages
3 and 4 are often combined and called slow wave sleep or deep sleep (Figs. 3
and 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% or
less of the total time in bed is spent awake). Sleep onset is swift (less than 15
minutes) and nocturnal awakenings few and brief. Stage 2 sleep accounts for
approximately half the night’s sleep, and REM sleep accounts for another
20% to 25%. A nightly total of 1% to 5% of stage 1 sleep is distributed at
the wakefulness-sleep transition and at light sleep transitions. The remaining
sleep is distributed between slow wave sleep stages 3 and 4. Only minor
differences are found for sleep stage distributions between young adult men
and 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.
556 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

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.

Individuals do not have single blocks of each sleep stage and then
awaken. The normal pattern involves having repeated 90- to 120-minute-
long cycles of non-REM and REM sleep. With each cycle reoccurrence there
are usually systematic alterations in cycle properties. Sleep architecture
refers to the progression and continuity of sleep through the sleep cycles on
a given night. Fig. 5 shows a typical night with normal sleep architecture in
a healthy young adult and the percentages of each sleep stage. The following
five generalizations can be made about normal sleep architecture:
1. Sleep is entered through non-REM sleep
2. Non-REM and REM sleep alternate approximately every 90 to 120
minutes
3. Slow wave sleep predominates in the first third of the night
4. REM sleep predominates in the last half of the night
5. 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 gradual
decline in overall total sleep time. Aging, especially after middle age, is
associated with greater wakefulness intermixed with sleep (fragmentation).
 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565 557

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.

Table 1
EEG-EOG-EMG characteristics of sleep and wakefulness
Stage EEG characteristics EOG EMG muscle activity
W Predominant alpha activity (more than Slow and rapid High
50% of the epoch) mixed with EEG
beta.
1 Alpha activity is replaced by Slow Decreased from awake
predominant low-voltage,
mixed-frequency background activity
sometimes with vertex sharp waves.
2 Sleep spindles and K complexes in None Decreased from awake
a background EEG that has less than
20% delta activity.
3 Slow waves (EEG delta activity) None Decreased from awake
comprise 20%–50% of the epoch;
sleep spindles usually are present.
4 More than 50% of the epoch has EEG None Decreased from awake
delta activity.
REM Low-voltage, mixed-frequency Rapid Nearly absent
background activity; saw-tooth theta
waves may be present.
Abbreviations: EEG, electroencephalographic; EMG, electromyographic; EOG, electro-
oculographic; REM, rapid eye movement.
558 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

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

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

The difficulty defining normal

The first difficulty encountered when attempting to determine the normal
sleep pattern is that sleep is altered by the processes used for measurement.
The delayed sleep onset, general disruption, and decreased REM or slow
wave sleep percentages found when an individual sleeps in a new
environment (eg, the sleep laboratory) provides a good example of
Heisenberg’s uncertainty principle. This laboratory-adaptation consequence
is so commonly observed it has been named the ‘‘first-night effect.’’ To
characterize normal sleep, first-night data are often discarded. Nonetheless,
age-specific normative values have been derived empirically for both first
and succeeding nights. Polysomnographic data from large samples across
wide age ranges can be obtained [11–16]. The many studies performed by
Williams et al [17] were eventually combined to provide the first complete
source of sleep normative data. These data were published in 1974 in the
book EEG of Human Sleep [17]. The intent of Williams et al [17] was to
provide a reference standard against which individual patient data could be
compared. They reasoned that to know if sleep is abnormal, one first needs
 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565 559

to know the range of normal values. Over many years, beginning at the
University of Florida at Gainesville and continuing at the Veterans Affairs
Medical Center in Houston, data were methodically collected, scored,
tabulated, and analyzed. These data, nearly 30 years old, are still used as
normative values by many clinicians.
There are, however, three important issues to consider when using EEG
of Human Sleep data as normative values. First, polysomnograms were not
recorded according to recommendations in the Standardized Manual. The
Florida group, later the Houston group, used a different recording montage
that included frontal, central, and occipital EEG derivations but did not
include submentalis EMG and summarized to 1-minute epochs. Second, the
recordings were not scored using the R&K system but rather a modifica-
tion of the Dement-Kleitman system [18] called the Weaver-1 (after the
laboratory’s long-time chief technologist Ralph Weaver). Delta activity was
scored from a bipolar frontal tracing (F1-F7); alpha activity was scored
from a bipolar occipital tracing (O3-OZPZ); and other waveforms were
scored from a monopolar central tracing (C3-A2). The third and perhaps
most important issue is that the values presented do not include the first-
night results. Eliminating the first night because it is likely contaminated by
a laboratory adaptation effect is completely reasonable for a scientific
exploration designed to characterize normal sleep. Using such values creates
a biased comparison, however, when compared with a patient’s first night in
the laboratory. This problem exists for most data samples available in the
published literature.
Another general issue for determining normative values is whether one
should require a fixed time in bed at set times, a fixed duration for time
in bed, or variable time in bed set according to an individual’s routine.
Standardizing set times, although attractive from a laboratory operation
perspective, creates an artificial situation. The individual may be sleeping
out of their normal routine and have disturbed sleep. Similarly, having a set
duration for time in bed may artificially increase the amount of wakefulness
or REM sleep. Having an individual sleep according to their own schedule
attempts to obtain data will less measurement bias; however, it produces
greater variation in many parameters (eg, total sleep time).

Normal human sleep: actuarial data

Data presented here were recorded as part of a variety of prospective
research projects. Table 2 shows first-night polysomnographic results for
subjects divided into five nonoverlapping age groups. Table 3 shows results
from the following night from the same subjects. All subjects were normal
healthy volunteers. Informed consent was obtained from each subject.
Subjects were recruited through media advertising, health fairs, posters, and
referral channels.
 560
Table 2
Normative 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 (N = 49) 50–59 y (N = 41)  60 y (N = 29)
Mean SD Mean SD Mean SD Mean SD Mean SD

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

General, sleep continuity, and integrity measures
Time in bed (minutes) 404.9 44.1 393.1 58.2 404.2 49.4 393.0 51.1 395.7 42.8
Sleep latency (minutes) 11.8 13.1 13.4 10.1 14.2 14.0 8.7 11.4 15.3 14.9
Total sleep time (minutes) 347.3 62.5 340.0 70.8 329.4 54.6 331.6 63.6 298.4 61.3
Sleep efficiency indexa 86.2 14.2 86.4 11.6 81.7 10.8 84.3 11.1 75.4 13.2
Latency to arising (minutes) 2.0 7.7 9.7 22.7 7.1 22.2 4.3 11.1 4.2 9.8
Number of awakenings 9.6 8.2 7.7 4.2 11.6 5.3 11.4 4.5 14.1 6.7
Awakenings per hour 1.5 1.2 1.3 0.8 1.8 0.8 1.8 0.7 2.2 1.0
Number of sleep stage shifts 47.1 23.6 39.9 11.8 46.7 18.8 46.3 12.7 50.8 21.9
Non-REM sleep stage percentages
Stage 1 percentage of time in bed 4.1 3.0 3.4 2.1 5.4 3.3 5.5 3.0 6.1 3.5
Stage 2 percentage of time in bed 48.7 9.2 49.7 10.1 51.8 11.7 54.2 10.2 51.0 9.1
Stage 3 percentage of time in bed 3.4 1.9 4.3 1.9 2.9 2.4 3.0 2.4 2.5 2.3
Stage 4 percentage of time in bed 12.1 5.4 10.9 6.5 5.7 6.5 4.1 5.6 2.6 3.4
REM sleep measures
REM sleep percentage of time in bed 17.8 7.1 18.2 7.9 15.8 6.4 17.6 5.9 13.2 5.7
REM sleep episodes (number) 3.3 1.0 3.4 1.0 3.5 0.9 3.8 0.9 3.6 1.3
REMSEb duration (minutes) 77.0 31.2 79.5 40.7 74.2 33.7 78.7 32.6 59.2 26.8
Mean REMSE duration (minutes) 23.1 8.4 23.6 14.1 21.1 7.1 20.3 6.3 16.3 6.5
REM sleep efficiency indexc 91.0 18.7 93.4 8.7 88.1 11.1 89.7 10.7 90.3 12.1
a
Sleep efficiency is total sleep time percentage of time in bed.
b
REMSE is REM sleep episode.
c
REM sleep efficiency index is total REM sleep time percentage of total REM sleep episodes duration.
Table 3
Normative 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 (N = 49) 50–59 y (N = 41) 60 y (N = 29)

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

Mean SD Mean SD Mean SD Mean SD Mean SD
General, sleep continuity, and integrity measures
Time in bed (minutes) 397.3 44.5 397.5 49.7 411.7 50.0 405.5 56.4 406.6 45.8
Sleep latency (minutes) 6.3 6.9 10.0 10.3 8.4 9.7 6.1 7.7 8.2 7.7
Total sleep time (minutes) 374.9 44.5 375.8 52.9 370.2 52.4 366.6 58.0 348.8 51.5
Sleep efficiency indexa 94.4 4.7 94.4 4.1 90.2 9.8 90.4 7.1 85.8 7.9
Latency to arising (minutes) 0.4 1.0 0.2 0.4 2.5 8.1 2.4 8.8 1.3 2.4
Number of awakenings 6.3 6.3 4.7 3.7 8.4 5.8 9.7 5.2 12.3 6.7
Awakenings per hour 1.0 1.0 0.7 0.6 1.3 0.9 1.4 0.8 1.9 1.0
Number of sleep stage shifts 44.4 23.6 36.2 14.8 43.5 18.2 45.1 16.3 47.2 14.2
Non-REM sleep stage percentages
Stage 1 percentage of time in bed 3.0 2.1 2.5 2.1 4.3 2.8 4.7 3.7 4.0 2.7
Stage 2 percentage of time in bed 50.5 8.7 52.8 9.1 54.6 11.5 56.7 9.9 57.6 8.2
Stage 3 percentage of time in bed 4.6 2.6 3.8 1.7 3.4 2.6 3.7 3.4 2.9 2.5
Stage 4 percentage of time in bed 14.2 6.3 12.3 7.6 7.5 7.0 4.4 5.2 4.8 5.3
REM sleep measures
REM sleep percentage of time in bed 22.2 6.1 23.1 6.7 20.4 7.1 20.9 7.2 16.4 7.4
REM sleep episodes (number) 3.6 0.8 3.6 0.8 3.8 0.9 4.1 0.9 3.8 1.2
REMSE duration (minutes) 94.3 27.4 99.1 32.9 94.0 35.1 92.5 29.7 74.7 34.3
Mean REMSE duration (minutes) 27.2 8.9 27.9 9.7 25.4 9.3 23.1 7.4 20.2 9.8
REM sleep efficiency indexb 94.0 7.9 93.6 7.7 90.5 9.8 90.1 9.1 90.2 11.1
a
Sleep efficiency is total sleep time percentage of time in bed.
b
REM sleep efficiency index is total REM sleep time percentage of total REM sleep episodes duration.

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Although individual protocols differed, all had two consecutive nights

at the beginning of the study, one for adaptation and one for baseline.
Polysomnograms were recorded and scored according to the Standardized
Manual. Grass Model 78, Grass Model 8-10, Nihon Kohden, and Grass
Heritage polysomnograph systems were used. In most cases, subjects were
instrumented for respiratory, leg movement, or other evaluations.
Subjects reported to the laboratory 1 to 2 hours before scheduled
bedtime. Bedtimes and arising times were scheduled, as much as possible,
according to the subject’s normal routine. On arrival at the laboratory, each
subject completed a brief presleep questionnaire and had monitoring devices
attached by the night technologist. Polysomnographic calibrations were
preformed 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 the
scheduled sleep period, monitoring devices were removed and the subject
completed a postsleep questionnaire.

Mechanism regulating and governing normal sleep

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

Autonomic nervous system balance

In general, sleep requires decreased sympathetic activation and increased
parasympathetic balance. Consequently, anything that increases sympa-
thetic outflow can disturb sleep and it matters little whether the origin is
exogenous or endogenous [19]. That is, both drinking coffee at bedtime
(exogenous) and anxious rumination (endogenous) may keep one awake by
autonomic mechanisms. This feature of autonomic regulation likely has
survival value. When emergencies occur in the middle of the night, there
needs to be a mechanism to promote quick response and sustained alerting.
The survival value may be why autonomic activations commence rapidly
but dissipate slowly. Unfortunately, this mechanism may go awry and
contribute to insomnia. For example, if one gets ‘‘worked up’’ about
something right before bedtime, they may toss and turn for an hour. Rituals
can help promote progressive relaxation and gradual reorientation away
from daytime stressors and toward nocturnal tranquility. In children who
sleep well, elaborate presleep rituals are common and may include a bedtime
story; a light snack; teeth brushing; prayers; and having a favorite stuffed
animal toy, pillow, and blanket. The latter also provides sleep-onset
 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565 563

association stimuli that likely facilitate conditioning. As an autonomic

process, sleep onset is amenable to classical conditioning. Pavlov was able
to condition a dog to salivate by repeatedly pairing a ringing bell with
food presentation (canines automatically salivate when food is present).
Conditioning sleep onset, or the autonomic properties surrounding it, often
inadvertently occurs. The bed, pillow, or blanket (or stuffed animal toy for
children) 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 stimulus
cue for sleep onset, the parent may find himself or herself having to rock the
baby 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 or
she becomes. Homeostatic regulation of sleepiness is similar to that for
thirst, hunger, and sex. Hypothalamic-generated motivational states direct
behavioral 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 explore
sleep’s function by examining deficits produced by its loss. Sleep deprivation
can be total, partial, or stage-specific. Not surprisingly, sleep loss increases
sleepiness. Sleep loss also seems to diminish coping and sleep-deprived
individuals 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, catecholamine
turnover increases and cortisol rises [20–22].

Circadian rhythms
Most people have noticed that during extended wakefulness, sleepiness
waxes and wanes. Sometimes after staying up all night, the chronobiologic
self-abuser notes a surge of energy at daybreak. Although the person has
been awake longer, they feel less sleepy than they did at 5:00 AM. This
violation in homeostasis reveals another factor governing sleep and
wakefulness: the circadian rhythm. The circadian rhythm is an approximate
daylong rhythm (from the root ‘‘circa’’ + ‘‘dias’’ [approximately a day]).
There are many biologic clocks; however, the one regulating the sleep-wake
circadian rhythm is located in the suprachiasmatic nucleus and the core
body temperature cycle is entrained to this sleep-wake oscillator (which is
why the temperature cycle is commonly used as a marker of circadian
rhythm). In general (1) maximum alertness occurs at temperature peak; (2)
drowsiness ensues when temperature starts to fall; (3) when temperature
reaches nadir, sleepiness can be overwhelming; (4) sleepiness decreases and
564 M. Hirshkowitz / Med Clin N Am 88 (2004) 551–565

alertness increases as temperature begins to rise; and (5) when temperature

reaches maximal level, the cycle begins again [23–25].

When things go awry: abnormal sleep

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

Summary
In this article normal human sleep is discussed. Landmarks leading up to
the understanding of human sleep, EEG definitions, and general character-
istics of normal human sleep are presented. Actuarial laboratory data, for
both night 1 and night 2, are provided with an explanation of how they were
compiled. Finally, the mechanisms governing sleep and wakefulness are
reviewed. This information, normal human sleep, and the mechanisms
regulating it are critical to understanding abnormal sleep associated with
sleep disorders.

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