International Review of Psychiatry, August 2005; 17(4): 213–228

Sleep physiology and pathology: Pertinence to psychiatry

CONSTANTIN R. SOLDATOS & THOMAS J. PAPARRIGOPOULOS

Athens University Medical School, Department of Psychiatry, Athens, Greece

Summary
Sleep should not be considered a behavioural state characterized by brain inertia; instead, it is a highly dynamic process
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involving numerous brainstem areas and all physiological systems of the body. Our understanding of the underlying
mechanisms responsible for sleep regulation has considerably advanced since the discovery of rapid eye movement (REM)
sleep, about half a century ago. Based on standardized electroencephalographic, electro-oculographic and electromyographic
features, two distinct main states periodically alternating throughout the night have been identified: REM and non-REM
sleep; the latter is further distinguished into stages 1, 2, 3 and 4. Computerized analysis of sleep recordings yielded more
detailed information on sleep physiology and pathology. Although still preliminary, neuroimaging studies promise to
elucidate the functional alterations of neuronal substrates during sleep. Regarding sleep disorders, which account for a
substantial individual and socio-economic burden, considerable progress has been achieved in terms of their classification,
assessment, clinical diagnosis and treatment. Specific sleep disorders within the three major categories, that is, ‘dysomnias’,
‘parasomnias’, and ‘sleep disorders associated with mental, neurologic, or other medical conditions’, exhibit characteristic
clinical features; sleep laboratory recordings considerably assist to definitely diagnose several among them. Pertinence of
sleep medicine for psychiatrists is obvious, taking into consideration that psychiatric disorders account for the largest
diagnostic group of patients with sleep problems. In fact, the basics of this interdisciplinary field should be of special concern
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both to medical students and clinicians of diverse backgrounds who are interested in acquiring the necessary skills to globally
and comprehensively understand and eventually effectively treat their patients.

Introduction Miller & Turner, 1988; Mellinger, Balter &

‘In whatever disease sleep is laborious, it is a deadly
symptom’
Hippocrates, Aphorisms, II
The elusive nature of sleep and dreaming has always
fascinated people. Their impact upon physical,
mental and emotional well-being of individuals had
been recognized long ago. Some of the world’s
greatest and most influential personalities such as
Hippocrates and Freud attempted explanations of
physiological basis of sleep and dreaming, yet their
understanding remained limited and rudimentary
(Freud, 1953; Jones & Withington, 1931); lack of
appropriate technology for the investigation of sleep
did not permit the development of truly scientific
knowledge until recently.
Accumulated evidence from worldwide large-scale
epidemiological studies, show that approximately a
third of the population either suffer from or are prone
to develop one or more sleep problems within
a given year (Bixler, Kales, Soldatos, Kales &
Healey, 1979; Gallup Organization, 1995; Lack,
Uhlenhuth, 1985; Quera-Salva, Orluc, Goldenberg
& Guilleminault, 1991; Soldatos, Allaert, Ohta &
Dikeos, 2005). Obviously, this has a considerable
negative impact on the general health status and
quality of life of the affected individuals. Besides,
these sleep-related problems cause a substantial
socio-economic burden through direct treatment
costs as well as collateral undesirable consequences,
such as absenteeism, accidents, and so forth (Léger,
Levy & Paillard, 1999; Ohayon & Smirne, 2002;
Roth & Ancoli-Israel, 1999; Stoller, 1994; Walsh &
Ustun, 1999) Chronic sleep problems have been
closely associated either with comorbid psychiatric
disorders, such as depression, alcoholism and sub-
stance abuse, or multiple medical conditions (Berlin,
Litovitz, Diaz & Ahmed, 1984; Buysse et al., 1994;
Ford & Kamerow, 1989; Ford & Cooper-Patrick,
2001; McCall, Reboussin & Cohen, 2000; Tan,
J.D. Kales, A. Kales, Soldatos & Bixler, 1984); this
comorbidity further increases the overall burden to
patients, their families and society at large. Yet, sleep
disorders are notably under-recognized or under-
estimated and, therefore, often left untreated.

Correspondence: Constantin R. Soldatos, MD, Professor of Psychiatry, Athens University Medical School, Department
of Psychiatry, Eginition Hospital, 74 Vas Sofias Avenue, 115 28, Athens, Greece. Tel: þ30 210 7289 324.
Fax: þ30 210 7251 312. E-mail: egslelabath@hol.gr
ISSN 0954–0261 print/ISSN 1369–1627 online ß 2005 Institute of Psychiatry
DOI: 10.1080/09540260500104565
 214 C. R. Soldatos & T. J. Paparrigopoulos
Furthermore, disturbed sleep may be either a
prodromal/first presenting symptom or evidence of
aggravation of several somatic and mental diseases
(Fava, Grandi, Canestrari & Molnar, 1990; Jackson,
Cavanagh & Scott, 2003; Katz & McHorney, 1998;
Perlis, Giles, Buysse, Tu & Kupfer, 1997; Smith &
Tarrier, 1992; Wong & Lam, 1999).
Sleep medicine is a multidisciplinary field wherein a
unique cross-fertilization takes place. It involves
physicians of diverse background, such as psychiatry,
neurology, pulmonology, otolaryngology, internal
medicine, paediatrics and dentistry. In recent years,
although the medical profession has recognized that
sleep and its disorders considerably contribute to
medical morbidity, relatively few physicians are
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familiar with sleep disorders medicine. Consequently,
there is a large gap between the increased interest
among physicians on sleep disorders and their skills to
recognize them efficiently; moreover, the incorpora-
tion of sleep medicine into the medical curriculum is
deficient (Kryger, Lavie & Rosen, 1999).
All of the above dictate the need for a compre-
hensive presentation of the basic sleep-related issues
pertinent to clinical medicine and psychiatry. Finally,
from a research perspective, elucidation of sleep
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mechanisms and its disturbances may provide new
insight into the physiology and pathophysiology not
only of psychiatric and neurologic disorders, but also
of the functioning of the central nervous system in
general.
Overview of sleep physiology
Sleep architecture
The contemporary scientific study of sleep begun
half a century ago with the discovery of rapid eye
movement sleep (REM) by E. Aserinsky, N.
Kleitman, and W. Dement (Aserinsky & Kleitman,
1953; Dement & Kleitman, 1957). Following 15
years of groundbreaking research, which established
the interdisciplinary field of hypnology, a consensus
was reached in 1968 on standardized and reliable
criteria for monitoring sleep in the laboratory and
for scoring hypnograms (Rechtschaffen & Kales,
1968). The basic hypnogram, alternatively called
polysomnogram (PSG), consists of three electrophys-
iological recordings: electroencephalogram (EEG),
electro-oculogram (EOG) and electromyogram
(EMG). However, a number of other electrophysi-
ological recordings (electrocardiogram, respiratory
kinesiometry, oxymetry, penial plythesmography,
etc.,) can be executed in parallel, according to specific
clinical and/or research criteria (American Sleep
Disorders Association, 1997; Broughton, 1982;
Kryger, Roth & Dement, 2000; Rechtschaffen &
Kales, 1968).
The hypnogram is the tool for sleep staging by
20–40 s epochs. There are two main states of sleep:
REM and NREM, the latter being distinguished
into stages 1, 2, 3 and 4 depending on various
hypnopolygraphic characteristics (figure 1). Sleep
begins with a few minutes of stage 1 (a relatively low-
voltage, mixed-frequency EEG pattern, occurring as
a transitional stage throughout the night), followed
by a longer period of stage 2 (a stage characterized by
higher voltage theta and delta EEG waves, as well as
specific EEG waveforms, i.e., sleep spindles and
K complexes, typical of stage 2 sleep); in turn, stage
2 is followed by an even longer period of stages 3 and
4, known as slow-wave sleep (SWS; dominated by
low frequency 1–3 Hz, high amplitude >75 mV delta
and theta waves). Then, at about 90 min following
sleep onset, stage REM occurs usually lasting for a
few minutes. This successive occurrence of sleep
stages completes the first sleep cycle. A full night’s
sleep comprises 3–5 sleep cycles; from cycle to cycle,
REM periods last longer while the amount of SWS
decreases and it is almost absent by the end of the
night (figure 2) (Bixler, Robertson & Soldatos, 1987;
Carskadon & Dement, 2000; Rechtschaffen & Kales,
1968).
In young adults, about 20% of total sleep time is
occupied by stage REM, about 60% by stage 2,
about 15% by stages 3 and 4 and about 5% by
stage 1. Further, 70–80% of awakenings from stage
REM are accompanied by dream recollection, while
awakenings from NREM sleep are characterized
either by absence of dream recollection or by a
fragmentary and thought-like mentation. During
NREM, a general slowing of body functions occurs
which is maintained throughout NREM. In contrast,
during REM sleep, which is characterized by
episodic bursts of rapid eye movements and muscle
atonia, physiological processes rise at higher levels
than during NREM sleep and in some instances they
reach awakening levels (Bixler et al., 1987;
Carskadon & Dement, 2000).
The first attempts at automated analysis of the
hypnogram were mainly directed towards replicating
the Rechtschaffen and Kales scoring criteria in order
to curtail visual scoring time and produce objective
EEG analysis. Initially, automation concerned
primarily sleep staging and to a lesser degree the
detection of body movements and specific respira-
tory events; however, no particular consideration was
taken for the internal architecture (microstructure) of
stage 2, SWS and REM sleep (Agarwal & Gotman,
2002; Kubicki & Herrmann, 1996; Penzel &
Conradt, 2000).
As long as automated polysomnography evolved
from period-amplitude analysis and spectral analysis
of the EEG to more elaborate methods, such as
pattern recognition, wave detection, expert system
 Sleep physiology and pathology 215
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Figure 1. Polysomnographic features of NREM (stages 1–4) and REM sleep stages. Progression of NREM sleep is characterized by EEG
activity of increasing amplitude and decreasing amplitude, whereas REM sleep is characterized by a low-amplitude, fast-frequency
EEG pattern, bursts of eye movements, and a markedly decreased level of muscle tonus (modified from Kales, 1968).
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Figure 2. Characteristic sleep architecture changes across the lifespan. A typical sleep cycle is defined as the sequence of sleep stages ending
with a REM period. Lasting approximately 90 min, the sleep cycle is repeated 4–6 times each night. As shown in the figure, REM sleep
remains considerably stable from childhood through old age, whereas stage 4 markedly decreases with age (modified from Kales, 1968).
 216 C. R. Soldatos & T. J. Paparrigopoulos
and neural network approaches, interest was gradu-
ally focused on specific EEG waveforms, such as
sleep spindles (series of rhythmic waves in the
12–14 Hz range that last from 0.5–3 s and are
typically dominant during sleep stage 2), rapid eye
movements, and delta wave activity. However, the
microstructure of sleep is still virtually unknown,
and although several methods of computerized
analysis are now available, none of them has
gained particular popularity in clinical practice;
thus, visual review of any automatically generated
results is still essential in the proper assessment
of polysomnograms (Agarwal & Gotman, 2002;
Kubicki & Herrmann, 1996; Penzel & Conradt,
2000).
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To date, automated techniques have been used to
investigate several delta waveband parameters (i.e.,
frequency measures, total power, production
rhythm, absolute wave count, and distribution
throughout the night), in psychiatric and neurologi-
Few studies have quantified the characteristics of
sleep spindles either in normal subjects or in groups
of patients. So far, findings from the limited number
of subjects who have been studied show that sleep
spindle density is altered in various pathological
conditions. Thus, it is drastically decreased in
several neurodegenerative diseases (Montplaisir,
Petit, Lorrain, Gauthier & Nielsen, 1995; Mouret,
1975; Prinz et al., 1982; Reynolds et al., 1985) and
depression (De Maertelaer, Hoffman, Lemaire &
Mendlewicz, 1987; Goetz et al., 1983), but increased
during the first NREM period in schizophrenic
patients (Hiatt et al., 1985).
Automated EEG can further increase our under-
standing of the mechanisms underlying several
sleep disorders. For instance, it has been recently
shown through quantitative EEG analysis that
patients with idiopathic REM sleep behaviour
disorder may present an impairment of cortical
activity compared to controls during REM sleep,
cal disorders. Results have been inconsistent;
although there is strong evidence that decreased
delta production is characteristic of depression,
schizophrenia, and dementia (Armitage, Calhoun,
Rush & Roffwarg, 1992; Hiatt, Floyd, Katz &
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Feinberg, 1985; Keshavan et al., 1998; Kupfer,
Frank, McEachran & Grochocinski, 1990). Espe-
cially in depression, this abnormality was further
defined as a lower level of delta wave intensity during
the first NREM period than in the second
NREM period, which is contrary to what happens
in normal individuals (Kupfer et al., 1990).
Furthermore, it has been postulated that a decreased
delta sleep ratio across the life cycle is a trait
characteristic of depression (Lauer, Schreiber,
Holsboer & Krieg, 1995; Linkowski, Kerkhofs,
Hauspie & Mendlewicz, 1991; Thase, Fasiczka,
Berman, Simons & Reynolds, 1998). Also, certain
computerized sleep EEG patterns may be relatively
specific to depression, such as an elevated fast-
frequency activity in the right hemisphere and a
reduced beta and theta interhemispheric coherence
(Armitage, 1995). In somnambulism, studies using
spectral EEG analysis, showed similar findings, that
is, lower delta power in the first sleep cycle and a
slower decline throughout the successive sleep cycles
(Gaudreau, Joncas, Zadra & Montplaisir, 2000;
Guilleminault, Poyares, Aftab & Palombini, 2001).
Regarding REM sleep microstructure, automated
analysis has indicated an increased rate of eye
movement generation (REM activity and density)
during the first REM period both in depression and
schizophrenia, whereas a normal or decreased
production of REMs compared to controls has
been reported in dementia and mental retardation
(Benca, Obermeyer, Thisted & Gillin, 1992; Espie
et al., 1998; Kupfer, 1984).
that is, a lower  power in the occipital region, as well
as during wakefulness, and a higher  power in
the frontal, temporal, and occipital regions (Fantini
et al., 2003).
In conclusion, only if the microstructure of the
sleep EEG can be analyzed using advanced technol-
ogy, will automated sleep analysis go beyond the
relatively limited information obtained from the
visual scoring according to Rechtschaffen and
Kales. Even then, we may need to understand the
importance of microstructure elements through their
correlation with a number of other physiological and/
or clinical parameters.
Physiological changes during sleep
During the transition from wakefulness to NREM
sleep, certain changes in the autonomic nervous
system activation occur, that is, generally, a decrease
in the sympathetic tone and an increase in the
parasympathetic tone. Most typically, these changes
are reflected in the reduction of heart rate, cardiac
output, and blood pressure. In contrast to NREM
sleep, REM sleep is associated with high levels of
sympathetic activity, although this seems to depend
on the presence or absence of phasic phenomena
during REM sleep. Thus, during phasic REM sleep,
a manifest increase and/or variability in heart and
respiratory rates are observed, as well as an increase
in systemic blood pressure and in peripheral
vasoconstriction. Irregular breathing and prolonged
apnoeic events may also occur during this phase.
Penile erections in men are also characteristic of
REM sleep, and their recording through penile
plethysmography can be useful in the differential
diagnosis between psychogenic and organic impo-
tence (Carskadon & Dement, 2000; Krieger, 2000;

Lugaresi & Parmeggiani, 1997; Verrier, Harper &
Hobson, 2000).
Sleep is a period of heightened neuroendocrine
activity; the secretion of several hypothalamic-
pituitary hormones is under circadian regulation
and closely related to the sleep-wake cycle. Thus,
ACTH and cortisol levels peak during the last third
of the night; in contrast, growth hormone levels peak
during the first two hours of sleep, that is, in close
association with the preponderance of SWS.
Many other hormones (such as thyroid-stimulating
hormone, prolactin, gonadotrophins, antidiuretic
hormone) show secretory peaks during sleep while
melatonin’s total secretion occurs exclusively during
the night and it has as its primary function to control
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the circadian rhythm and entrain the body functions
to the light-dark cycle (Brzezinski, 1997; Steiger,
2002; Van Cauter, 2000).
Most of the recently developed functional neuro-
imaging techniques (i.e., single photon emission
tomography, positron emission tomography, func-
tional magnetic resonance imaging, magneto-
encephalographic tomography and near infrared
spectroscopy) have been applied in humans to
explore dynamic brain changes during sleep and
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enable comparisons between the awake state and
NREM and REM sleep. Each technique has its own
advantages and disadvantages, in terms of feasibility,
spatial and temporal resolution, safety and cost
(Nofzinger, 2004).
Neuroimaging techniques, by measuring changes
in brain metabolism and cerebral blood flow, have
shown remarkable functional alterations in the
extensive neuronal circuitry during NREM sleep,
REM sleep and wakefulness. Thus, NREM sleep is
characterized by a widespread decline in function in
the association cortex of the frontal, parietal and
temporal lobes, as well as in the thalamus, dorsal
pons and mesencephalon, cerebellum, basal ganglia,
and basal forebrain; REM sleep instead, has been
associated with an increase in the function of the
limbic and paralimbic cortex relative to waking, and
a relative decrease in the dorso-lateral prefrontal
cortex, parietal cortex, as well as the posterior
cingulate cortex and precuneus. More specifically,
during REM sleep significant activations were found
in the pontine tegmentum, thalamic nuclei, amygda-
loid complexes, hippocampus, anterior cingulate
cortex, and in the temporo-occipital areas of the
posterior cortices. Furthermore, awakening from
NREM sleep has been demonstrated to be associated
with changes in brain activation. Thus, a functional
neuroimaging study suggested that the early
awakening process is associated with reactivation of
centrencephalic areas, whereas full recovery of the
awake state is due to anterior cortical reactivation
(Drummond, Smith, Orff, Chengazi & Perlis, 2004;
Sleep physiology and pathology 217
Maquet, 2000; Nofzinger et al., 2002; Nofzinger,
2004).
During the last years, attempts at acquiring
simultaneous EEG/functional magnetic resonance
imaging monitoring during sleep yielded interesting
results and, purportedly, the potential exists for
mapping electrophysiological activity with unprece-
dented spatio-temporal resolution. To date, some
research groups have successfully used this method-
ology for sleep staging, but they did not address the
association of functional magnetic resonance
imaging changes with specific sleep phenomena
(Born et al., 2002; Czisch et al., 2002; Lovblad
et al., 1999; Portas et al., 2000).
The aforementioned recent advances in the study
of sleep, although preliminary as yet, enhance our
knowledge on the physiology/pathophysiology of
sleep and promise a rewarding future for sleep
research.
Sleep/wakefulness regulation
Three mutually interacting neuronal systems
involved in sleep/wake and REM/NREM sleep
production and regulation have been identified: an
arousal system, a NREM sleep system, and a REM
sleep system.
The wakefulness promoting or arousal system
resides in the ascending reticular activating system
(ARAS), which originates in the brainstem. A dense
neuronal network arising from ARAS projects into
various brainstem (pontine cholinergic nuclei,
serotoninergic dorsal raphe nuclei, noradrenergic
nuclei of locus coeruleus) and forebrain areas (mid-
line and medial thalamus with widespread cortical
projections, amygdala) serving the maintenance of
wakefulness. The hypothalamus, where the supra-
chiasmatic nuclei are located, is also heavily involved
in the circadian control of arousal; histaminergic,
hypocretin/orexin, dopaminergic and glutamatergic
neurons are to be found in this area (Jones, 2000;
Steriade & McCarley, 1990).
The principal region responsible for NREM sleep
is the ventrolateral preoptic area, which contains
GABA-ergic and galaninergic neurons; this area
inhibits the arousal system of the posterior hypotha-
lamus, while receiving afferent fibres from several
systems that modulate arousal. The major structures
responsible for REM sleep are the cholinergic
laterodorsal and pendunculopontine tegmental
nuclei of the pons, which are inhibited by the
activation of the monoaminergic wakefulness-
promoting systems and vice versa they are disin-
hibited as long as the activity of these monoaminergic
systems declines during sleep. In turn, the activation
of the pontine REM sleep promoting centres induces
cortical arousal, as evidenced by the characteristic
 218 C. R. Soldatos & T. J. Paparrigopoulos
desynchronized EEG (low amplitude, high-mixed
frequency EEG) during REM sleep (Hobson,
Stickgold & Pace-Schott, 1998; Jones, 2000;
McGinty & Szymusiak, 2001; Reinoso-Suárez,
De Andrés, Rodrigo-Angulo & Garzón, 2001;
Siegel, 2000).
The above neuronal systems are in a mutual
interplay in order to modulate sleep and wakefulness.
The two-process model of sleep regulation has been
advanced since 1982 and it has been most influential
ever since (Borbély, 1982). This model explains the
timing of the alternation between sleep and wakeful-
ness as the result of the interaction of two processes:
a homeostatic process governed by the accumulated
need for sleep (process S), and a circadian process
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(process C) keeping track of environmental cues.
The drive of process S increases exponentially during
wakefulness and declines during sleep. Thus, the
waxing and waning of process S is limited by two
thresholds, namely, a sleep threshold and wake
threshold (Borbély & Achermann, 1999). Evidence
provided from non-REM sleep deprivation experi-
ments supports this theoretical construct (Dijk &
Beersma, 1989). On the other hand, process C, that
is, the circadian component of this regulating
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mechanism, is under the control of the 24-hour
rhythmic oscillation of a pacemaker, which resides in
the suprachiasmatic nuclei of the hypothalamus.
This pacemaker is principally responsible for the
regulation of body temperature and melatonin’s
diurnal secretion (Czeisler & Khalsa, 2000; Moore,
1997). As a result, the propensity for sleep varies
multifactorially throughout the day.
By taking the risk of oversimplification, it can be
proposed that the predominant neurotransmitters
participating in the maintenance of the state of
wakefulness are acetylcholine, norepinephrine and
serotonin; GABA and to a lesser extent norepineph-
rine and serotonin are the prime neurotransmitters
involved in NREM sleep; finally, REM sleep appears
to be closely connected with acetylcholine. However,
there is evidence that many more neurotransmitters/
neuromodulators may play a role as well (e.g.,
hypocretin/orexin, histamine, glutamate, aspartate,
galanine, substance P, etc.,); furthermore, recent
data point to the importance of the neuromodulator
adenosine as a crucial modulator of homeostatic
sleep, that is, of the sleepiness that occurs following
prolonged wakefulness (Kryger et al., 2000; Porkka-
Heiskanen, Alanko, Kalinchuk & Stenberg, 2002).
Clinical aspects of sleep pathology
Sleep disorders classification
With the accumulation of knowledge on sleep
physiology and pathology over the last three decades,
the need for a generally accepted classification of
sleep disorders became apparent. Such a classifica-
tion is expected to increase diagnostic precision,
improve comparability of epidemiological data and
provide greater homogeneity of clinical and research
patient samples.
Currently, three main classifications for sleep
disorders are available: the revised edition of the
International Classification of Sleep Disorders
(ICSD-Revised) produced by the American
Academy of Sleep Medicine (2001), the DSM-
IV-TR sleep disorders section produced by the
American Psychiatric Association (2000) and the
sleep disorders section of the 10th International
Classification of Diseases (ICD-10) which is still
in effect ever since it was officially established by
the World Health Organization (1992).
According to the ICSD-Revised, four main
categories of sleep disorders are identified: (a) the
dyssomnias, that is, disorders characterized either by
insomnia or excessive sleepiness; (b) the parasom-
nias, that is, behavioural aberrations and undesirable
phenomena that intrude into the sleep process; (c)
sleep disorders associated with mental, neurologic,
or other medical disorders; and (d) a category of
‘proposed’ sleep disorders. In total, the ICSD-
Revised comprises 88 distinct diagnostic entities.
The ICSD-Revised is a comprehensive classification,
which comprises a large body of information relative
to the diagnostic criteria, severity and duration,
clinical features, course, epidemiological character-
istics, pathology, polysomnographic, and other
laboratory features, and differential diagnosis of
each specific sleep disorder (American Academy
of Sleep Medicine, 2001).
The DSM-IV-TR sleep disorders section consists
of: (a) primary sleep disorders, subdivided into
dyssomnias and parasomnias; (b) sleep disorders
related to another mental disorder; and (c) other
sleep disorders, for example, sleep disorder due to a
general medical condition and substance-induced
sleep disorder (American Psychiatric Association,
2000). In ICD-10, non-organic sleep disorders
are listed in a special section of chapter V with
mental and behavioural disorders. This section
(F51.0–F51.9) comprises the dysomnias, wherein
the predominant disturbance is in the amount,
quality, or timing of sleep due primarily to emotional
causes (insomnia, hypersomnia, disorder of sleep–
wake schedule), the parasomnias (sleepwalking,
sleep terrors, nightmares), and several other non-
organic sleep disorders. Non-psychogenic sleep
disorders, such as narcolepsy or sleep apnoea, are
placed in chapter VI of ICD-10 (World Health
Organization, 1992). These two classification
systems are less detailed and structured than the
ICSD classification, which is addressed mainly

to sleep specialists. All three classification systems,
however, are based practically on the same principles
and they follow quite similar diagnostic guidelines.
Assessing disordered sleep
Assessing patients with sleep disorders is a rather
complex, time-consuming procedure that requires
history-taking expertise, special clinical skills and
appropriate use of laboratory testing. Objective
polysomnographic recordings and subjective mon-
itoring of sleep problems, through the use of specially
designed scales and questionnaires, may be of help in
certain cases.
Similar to other medical fields, a thorough clinical
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history and physical examination, as well as a
detailed psychiatric assessment are crucial for the
formulation of an accurate diagnosis; moreover,
screening for substance use and medication should
be accomplished, and information on sleep–wake
habits needs to be collected. If deemed necessary, a
laboratory workup should be ordered and a brain
imaging study (CT-scan, MRI) undertaken.
Foremost, a close and trustful physician-patient
relationship is a prerequisite.
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Two main diagnostic tools are used to objectively
assess sleep disorders: polysomnography (described
above) and actigraphy, that is, a method developed
for activity monitoring by means of a simple-to-wear
electronic device in order to identify the presence
or absence of body motility throughout the 24-h
rest-activity cycle (Ancoli-Israel et al., 2003).
Polysomnography is applied either for the all-night
study of sleep, as detailed elsewhere in this chapter,
or for the so-called Multiple Sleep Latency Test
(MSLT). This test measures sleep tendency in
standard conditions favouring sleep onset. It is a
well-validated clinical and experimental method for
the objective assessment of an individual’s level of
daytime sleepiness and documents sleep onset REM
episodes. The individual during the daytime is given
five 15-minute opportunities to nap every two hours
following awakening from nocturnal sleep.
Polysomnographically recorded sleep onset latency
is calculated for each MSLT trial; a mean sleep
latency below 10 min is considered to be definitely
abnormal. Two early onset REM sleep episodes
(i.e., anytime during a 15-minute recording period)
are also considered abnormal and indicative of
narcolepsy (Carskadon et al., 1986). A variation
of the MSLT, the Maintenance of Wakefulness
Test (MWT), which measures the individual’s
ability to resist falling asleep, may alternatively be
used (Doghramji et al., 1997).
Besides certain special purpose self-rated
analogue rating scales, several instruments have
been developed for the subjective assessment
Sleep physiology and pathology 219
of clinical manifestations of sleep disorders. Among
others, they include the Leeds Sleep Evaluation
Questionnaire (Parrott & Hindmarch, 1980), the St.
Mary’s Hospital Sleep Questionnaire (Ellis et al.,
1981), the Sleep Problems Scale (Jenkins, Stanton,
Niemcryk & Rose, 1988), the Pittsburgh Sleep
Quality Index (Buysse, Reynolds, Monk, Berman &
Kupfer, 1989), the Karolinska Sleep Diary
(Åkerstedt, Hume, Minors & Waterhouse, 1994)
and the more recently developed Athens Insomnia
Scale (Soldatos, Dikeos & Paparrigopoulos, 2000,
2003), the only psychometric instrument which has
been validated not only for the measurement of the
intensity of insomnia, but also for its diagnosis based
on the ICD-10 criteria. The Stanford Sleepiness
Scale (Hoddes, Zarcone, Smythe, Phillips &
Dement, 1973) and the Epworth Sleepiness Scale
(Johns, 1991) are the more commonly used instru-
ments for the self-report of sleepiness behaviours that
may impair adequate functioning. Finally, some
extensive questionnaires such as the Sleep
Disorders Questionnaire (SDQ) (Douglass et al.,
1994), which can be used for the screening of
patients, cover a wide range of disorders occurring
during sleep.
Defining the clinical complaints of sleep disorders
. The complaint of insomnia. Most physicians
would consider insomnia a rather well defined
condition; yet, a consensus regarding its exact
definition seems to be difficult to reach. This is
reflected in the various classification systems in
use over the past two decades. Initially, the
diagnosis of insomnia solely required the sleep
laboratory criterion of reduced sleep quantity.
Subsequently, however, all classifications assigned
equal importance to reduced sleep quantity and
impaired sleep quality as subjectively assessed
by the patient (Soldatos, 2002). An additional
complicating issue is whether insomnia should be
considered a symptom or a disease, since to a
large extent insomnia is associated with concomi-
tant conditions such as various medical and
psychiatric diseases; this distinction carries signifi-
cant implications both for the pathophysiology
of insomnia and for its appropriate treatment
(Chokroverty, 2000; Hajak, 2000; Hohagen et al.,
1993). In general, insomnia secondary to various
conditions is diagnosed far more frequently
than primary insomnia, where no underlying
etiological factor can be readily identified.
Primary insomnia, as a distinct disorder, is often
referred to as ‘psychophysiological insomnia’ or
‘idiopathic insomnia’ (American Academy of
Sleep Medicine, 2001; Billiard & Bentley, 2004;
 220 C. R. Soldatos & T. J. Paparrigopoulos
A. Kales & J. Kales, 1984; Soldatos, 1994, 2002).
Although still preliminary, recent studies are
beginning to clarify how insomnia associated with
concomitant conditions can be distinguished from
primary insomnia. For instance, awake EEG as
well as PSG computerized evaluations have shown
distinct differences in brain electrical activity and
sleep structure in primary insomnia compared to
insomnia secondary to major depression (Perlis
et al., 2001a; Perlis, Smith, Andrews, Orff &
Giles, 2001b; Staner et al., 2003). Moreover,
sleep disturbances seem to diverge depending on
the type of the underlying psychiatric disorder
(Benca et al., 1992). Yet, it is still unclear
whether hyperarousal, which is a well-established
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pivotal factor for the initiation and perpetuation of
primary insomnia, plays also an important role in
insomnia secondary to other conditions (e.g.,
depression) (Billard & Bentley, 2004; Roth &
Drake, 2004). Whatever the case may be, from
a taxonomic and phenomenological standpoint,
insomnia is defined as the complaint either of
difficulty falling asleep or maintaining sleep, or
of poor quality of sleep that occurs at least three
times per week for at least one month and either
For personal use only.
causes marked distress or interferes with ordinary
activities in daily living. It should be underscored
that insomnia is a subjective complaint of
insufficient or non-restorative sleep; this complaint
per se is important, not the actual amount of time
spent asleep (Billard & Bentley, 2004; Soldatos,
2002; World Health Organization, 1992). Based
on the ICSD-Revised, insomnia is classified into
mild, moderate, and severe insomnia, according
to the symptom severity and its consequences,
that is, impairment of social or occupational
functioning and association with feelings of rest-
lessness, irritability, anxiety, daytime fatigue,
and tiredness (American Academy of Sleep
Medicine, 2001). However, insomnia can be also
classified according to its duration (transient: <1
month, short-term: >1 month and <6 months,
chronic: >6 months), clinical characteristics (sleep
onset, sleep maintenance, early morning insom-
nia), and etiology (primary versus secondary)
(American Academy of Sleep Medicine, 2000;
Estivill et al., 2003).
. Excessive daytime sleepiness. Excessive daytime
sleepiness or hypersomnia is a term used to
describe the tendency of an individual to doze off
or fall asleep during various, most often sedentary,
daytime situations. The lifetime prevalence of
hypersomnia among young adults in the general
population has been estimated to be around 16.3%
(Breslau, Roth, Rosenthal & Andreski, 1996).
However, hypersomnia must be differentiated from
fatigue, which very often is a symptom either
of multiple medical conditions or of various
psychiatric disorders. According to the ICSD-
Revised, there are three levels of sleepiness,
namely, mild, moderate and severe, depending
on the intensity of the symptoms, the frequency of
the episodes, the functional impairment they
produce, and the mean sleep latency recorded
during the MSLT. Thus, sleepiness is considered
to be mild when sleep episodes occur only during
times of rest or when little attention is required
(e.g., while watching television, reading whilst
lying down in a quiet room, being a passenger in
a vehicle), may not occur on a daily basis, and
produce a minor impairment of social or occupa-
tional function. This degree of sleepiness is usually
associated with a MSLT mean sleep latency of 10–
15 min. Moderate sleepiness is characterized by
daily sleep episodes that occur during very mild
physical activities requiring, at most, a moderate
degree of attention (e.g., concerts, movies, meet-
ings, etc.,) and produce a moderate impairment of
functioning. In such cases, 5–10 min mean sleep
latency on the MSLT is recorded. Finally, sleepi-
ness is regarded to be severe when sleep episodes
are present daily at times of physical activities that
require mild to moderate attention (e.g., eating,
during conversation, walking, driving, etc.,) and
cause a marked impairment of functioning; it is
usually associated with a MSLT mean sleep
latency of less than 5 min (American Academy of
Sleep Medicine, 2001). Excessive daytime sleepi-
ness may result either from inadequate amount of
sleep or from an increased drive to sleep. Inade-
quate sleep is usually due to shift work or delayed
sleep phase syndrome, which are disorders that
arise from imposed sleep schedules that are out of
phase with the internal circadian rhythms. Dis-
rupted sleep with subsequent daytime sleepiness,
however, is most often the result of obstructive
sleep apnoea, periodic limb movement disorder,
and the intake of certain pharmacological agents
such as stimulants, steroids and antidepressants.
Last but not least, narcolepsy—a disorder char-
acterized by loss of orexin cells in the hypothala-
mus, undetectable CSF orexin, and associated
with the presence of HLA DQB1*0602 antigen—
and the idiopathic hypersomnia, are the main
underlying causes of excessive drive to sleep
(Guilleminault & Brooks, 2001; Mignot, 2004;
Roth & Roehrs, 1996). Regarding hypersomnia,
which occurs in the course of psychiatric condi-
tions, it should be mentioned that it is a common
symptom of affective disorders (up to 10–15% of
cases; particularly in seasonal affective disorder
and atypical depression), schizophrenia and
other chronic psychotic disorders, substance
abuse, and so forth (Reynolds & Kupfer, 1987;

Vgontzas, Bixler, Kales, Criley & Vela-Bueno,
2000).
. Aberrant behaviours during sleep. Several undesir-
able physical phenomena may occur during sleep.
These aberrant behaviours, which are called
parasomnias, are not abnormalities of the process
driving sleep and awake states per se. Dramatic
autonomic nervous system changes and motor
activity are usually the predominant features of this
group of disorders. The parasomnias are subdi-
vided into arousal disorders, sleep-wake transition
disorders, parasomnias usually associated with
REM sleep, and other parasomnias, according to
the sleep stage they originate from. Numerous
of them are manifestations of untimely central
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nervous system activation, thus challenging the
concept that wakefulness and NREM or REM
sleep are always mutually exclusive states. In this
context, the intrusion of wakefulness into NREM
sleep explains confusional arousals, automatic
behaviours during sleep, and so forth. The tonic
and phasic components of REM sleep may also
become dissociated giving rise to the occasional
persistence of motor activity during REM sleep
(Kryger et al., 2000; Mahowald & Schenck, 2000;
For personal use only.
Mahowald, Bornemann & Schenck, 2004; Malow,
2002; Montplaisir, 2004). The subgroup of arousal
disorders consists of the characteristic disorders of
sleepwalking, sleep terrors, and confusional
arousals. In general, these conditions most often
occur during NREM sleep and they are character-
ized by more or less complex motor automatisms
following an impaired arousal from sleep,
confusion, and amnesia for the episode (Kales
et al., 1980; A. Kales, Soldatos & J.D. Kales,
1987). The subgroup of sleep-wake transition
disorders includes disorders that occur in the
transition from wakefulness to sleep or vice versa,
such as rhythmic movement disorder, sleep-talk-
ing, and nocturnal leg cramps. The parasomnias
usually associated with REM sleep include dis-
orders, such as nightmares, sleep paralysis, sleep-
related painful erections, REM-sleep-related sinus
arrest, and REM-sleep behaviour disorder. Finally,
a number of other parasomnias (e.g., sleep
enuresis, nocturnal paroxysmal dystonia) involving
different systems may occur anytime during sleep
(American Academy of Sleep Medicine, 2001).
Aberrant behaviours during sleep may also be part
of disorders that are not typically classified as
parasomnias. In such cases, although the primary
complaint may be insomnia or hypersomnia,
a variety of concomitant symptoms may be
present. For instance, during sleep apnoea or
hypoventilation syndrome, loud snoring, cessation
of respiration and whole-body movements
occur; during periodic limb movement disorder,
Sleep physiology and pathology 221
repetitive highly stereotyped limb muscle
movements are present, and during restless legs
syndrome, undesirable leg sensations usually oc-
curring before sleep onset cause an almost
irresistible urge to move the legs. Finally, patho-
logical phenomena during sleep may occur in the
context of diverse mental, neurologic or other
medical disorders, only to mention nocturnal
epilepsy, sleep-related asthma and sleep-related
gastroesophageal reflux among others (American
Academy of Sleep Medicine, 2001).
Polysomnographic aspects of sleep pathology
Polysomnographic findings in selected dyssomnias
Although most dyssomnias can be diagnosed
through direct observation and detailed clinical
history, polysomnography may considerably assist
the definite diagnosis of certain sleep disorders, such
as narcolepsy and obstructive sleep apnoea.
In narcolepsy, all-night polysomnography may
reveal a short sleep latency of less than 10 min
and a REM period appearing within 20 min after
sleep onset, which can be associated with reports
of hypnagogic hallucinations or sleep paralysis. An
increased amount of stage 1 sleep and frequent
awakenings may also be present. The multiple sleep
latency test (MSLT) may objectively provide
evidence for the characteristic excessive daytime
sleepiness and demonstrate the presence of sleep-
onset REM periods. Sleep latencies of less than
10 min (typically below 5 min) and two or more
sleep-onset REM periods are found in most narco-
leptic patients (American Sleep Disorders
Association, 1997; American Academy of Sleep
Medicine, 2001).
In obstructive sleep apnoea syndrome, besides the
standard polysomnographic monitoring, nasal and
oral airflow, respiratory movements, electrocardio-
gram and blood oxygen saturation should also be
measured. Sleep studies demonstrate apnoeic epi-
sodes that typically last for 20–40 s or even longer, in
the presence of respiratory muscle effort. These
episodes usually occur during stages 1 and 2 of sleep,
or during REM sleep; they are characterized by a
reduction of airflow of greater than 50%, which is
associated with a reduction in the arterial oxygen
saturation levels and a concomitant transient eleva-
tion of carbon dioxide. Changes in cardiac rhythm
occur frequently during the apnoeic episodes and
gastroesophageal reflux may take place in some
patients. The apnoeic or hypopnoeic events may
severely disrupt sleep and result in excessive daytime
sleepiness, with abnormal mean sleep latencies on the
MSLT, that is, below 10 min (American Sleep
Disorders Association, 1997; American Academy
 222 C. R. Soldatos & T. J. Paparrigopoulos
of Sleep Medicine, 2001; Malhotra & White, 2002;
Roehrs & Roth, 1992).
Polysomnographic findings in selected parasomnias
Sleep terrors and sleepwalking occur in stage 3 and/
or stage 4 sleep, usually in the first third of the night
when SWS is more abundant; however, episodes can
occur in SWS at any time of the night. Sleep terrors
and episodes of partial arousal from SWS are
accompanied by accelerated heart rate, increased
respiratory rate, and signs of autonomic hyperarousal
(American Academy of Sleep Medicine, 2001;
Broughton, 2000; A. Kales, Jacobson, Paulson,
J.D. Kales & Walter, 1966).
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Nightmares occur during REM sleep as evidenced
by polysomnography, which shows an abrupt
awakening from REM sleep. Often, the REM
sleep episode is of long duration (more than
10 min) and is associated with an increased REM
density. Sometimes, nightmares secondary to a
traumatic life event may also occur during stage 2
non-REM sleep. Yet, as a rule, the diagnosis of
a nightmare can be accomplished based on the
information obtained during a careful sleep history
For personal use only.
(American Academy of Sleep Medicine, 2001).
In REM sleep behaviour disorder, polysomnogra-
phy demonstrates an excessive augmentation of chin
EMG tone or limb phasic EMG twitching during
REM sleep, coupled with prominent and often
prolonged periods of extremity activity on the video
recordings (American Academy of Sleep Medicine,
2001; Mahowald & Schenck, 2000). Frequently
there is also a pronounced increase in REM density
and in the percentage of slow-wave sleep (Fantini
et al., 2003; Olson, Boeve & Silber, 2000; Schenck,
Mahowald & Mahohald, 1997; Sforza, Krieger &
Petiau, 1997). Contrary to what is the case with
nightmare patients, those with REM sleep behaviour
disorder should be invariably recorded in the sleep
laboratory for the confirmation of the diagnosis,
which has been suspected on clinical grounds.
Polysomnographic findings in sleep disorders associated
with psychiatric disorders
In general, there are no pathognomonic
polysomnographic findings for any mental disorder;
however, overall sleep patterns for specific disorders
can be identified, while refined automated sleep
EEG analysis has yielded some interesting results
that offer an insight into their pathophysiological
mechanisms (Kryger et al., 2000).
Patients with affective disorders have been more
extensively studied than any other group of psychia-
tric patients and they have been shown to present
with the most profound, widespread, and stable
sleep abnormalities, either in unipolar or bipolar
depression. Thus, sleep of these patients, is char-
acterized by reduced sleep efficiency (less total sleep
time, increased sleep latency, multiple awakenings
during the night, early morning awakening),
diminished slow-wave sleep with abnormal distribu-
tion throughout the night, a short REM latency
(30–50 min), increased density of REMs, and an
increased amount of REM sleep during the first half
of the night. Biological treatments tend to normalize
most of the above sleep aberrations (Benca et al.,
1992; Kupfer, 1984; Kryger et al., 2000; Kupfer
et al., 1990; Lauer et al., 1995; Riemann, Berger &
Voderholzer, 2001).
Similar sleep abnormalities were also documented
in other psychiatric disorders, including schizophre-
nia, anxiety disorders, dementia, and alcoholism
(Benca et al., 1992). For instance, SWS is reduced
and awakenings are increased in patients with
Alzheimer’s disease, while a significant reduction
of SWS is evidenced in abstinent alcoholics (Benca
et al., 1992; Kryger et al., 2000; Prinz et al., 1982;
Reynolds et al., 1985). Regarding REM sleep
microstructure, namely, rapid eye movements,
delta wave counts, sleep spindle characteristics and
so forth in different disorders, the main findings have
been mentioned previously.
Several studies confirm that psychiatric symptoms
and underlying pathology is reflected in sleep
variables. Accordingly, global severity of psychotic
symptoms has been positively associated with
increased wake time, reduced REM total time,
short REM latencies, and reduced SWS. More
specifically, ‘positive’ symptoms have been asso-
ciated with increased REM density, short REM
latency, reduced sleep efficiency and prolonged sleep
latencies, whereas ‘negative’ symptoms have been
associated with decreased SWS and short REM
latency. Furthermore, poor long-term clinical out-
come of psychosis has been associated with the
presence of a short REM latency and SWS deficits.
In terms of neuro-anatomical correlates, the amount
of SWS has been reported to be inversely correlated
with the lateral ventricular/brain ratio (Benson et al.,
1996; D.P. Van Kammen, W.B. Van Kammen,
Peters, Goetz & Neylan, 1984).
Longitudinal studies as well as family studies
suggest that sleep aberrations in affective disorders
may be a trait characteristic of these disorders. Thus,
sleep of depressed patients in remission is still
disturbed: delta sleep is decreased and REM latency
is shortened; actually, the shorter the REM latency
the higher is the risk for relapse (Thase et al., 1998).
Studies in high risk probands also showed that
short REM latency and SWS deficits may run in
families, and that polysomnographic abnormalities
may precede the clinical expression of depression

(Giles et al., 1989; Goetz, Wolk, Coplan, Ryan &
Weissman, 2001; Lauer et al., 1995; Linkowski et al.,
1991). The different polysomnographic findings
in anxiety disorders, depression, schizophrenia, are
presented in detail in the respective articles of this
issue.
Relevance of sleep disorders for psychiatrists
Epidemiological considerations
Psychiatric disorders account for the largest diag-
nostic group of patients with sleep problems. General
population surveys report that at least 30–50%
of individuals with complaints of insomnia or
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hypersomnia show evidence of primary psychiatric
disorders (Ford & Kamerow, 1989; Ohayon, 1996;
Soldatos, 1994). Anxiety in particular has been
found to be quite common (about 25–40%) in
insomniacs, compared to the general population
(Ford & Kamerow, 1989; Ganguli, Reynolds &
Gilby, 1996; Mellinger et al., 1985). Also, based on
referrals to sleep disorder centres, a psychiatric
disorder is found to be the most frequent cause of
insomnia (Buysse et al., 1994). Moreover, certain
For personal use only.
sleep-wakefulness disorders (e.g., sleep apnoea,
narcolepsy) are often accompanied by secondary
psychopathology (Kales et al., 1982a, 1985).
Disturbed sleep among psychiatric patients
The DSM-IV-TR and ICD-10 classifications
include sleep disturbance as a characteristic symp-
tom among the diagnostic criteria for several
psychiatric disorders, including major depression,
generalized anxiety disorder, and post-traumatic
stress disorder (American Psychiatric Association,
2000; World Health Organization, 1992). Disturbed
sleep is considered a cardinal symptom of affective
disorders in particular. During depression, patients
have difficulty in sleep induction and sleep main-
tenance, and may awake early in the morning; during
episodes of mania, however, although they may sleep
even less than while depressed, they usually do not
present with a subjective complaint of insomnia
(American Psychiatric Association, 2000).
In approximately 30% of patients with major
depression, the sleep disturbance (i.e., insomnia,
hypersomnia mainly in bipolar depression and
seasonal affective disorder, or intense dreams/night-
mares) may be the presenting complaint. Of parti-
cular interest is the observation that insomnia in
patients with depression is a predictor of suicide
tendency; a number of studies have suggested that
patients with both depression and insomnia are
particularly at risk of committing suicide (Agargun,
Kara & Solmaz, 1997). Also, sleep disturbance
Sleep physiology and pathology 223
is the most common prodrome of mania and the
sixth most common prodrome of bipolar depression
(Chang, Ford, Mead, Cooper-Patrick & Klag, 1997;
Jackson et al., 2003). Thus, from a clinical stand-
point, a reduction of sleep duration may have a
predictive value in the early diagnosis of relapse of an
affective episode (Barbini, Bertelli, Colombo &
Smeraldi, 1996; Perlis et al., 1997; Wehr, 1991).
Furthermore, it has been advanced that sleep/wake
cycle instability caused by psychosocial stress may
trigger an episode in bipolar patients (Ashman et al.,
1999; Wehr, Sack & Rosenthal, 1987). Lastly it
should be mentioned that induced sleep deprivation
and phase advance of the sleep/wake cycle are
frequently associated with mood elevation and,
therefore, they have been proposed as a therapy for
depression (Wu & Bunney, 1990).
Along with affective disorders, anxiety disorders
are the most frequent psychiatric causes correlated
with sleep disturbance. Patients with generalized
anxiety disorder and panic disorder frequently
present with insomnia (Benca et al., 1992; Ohayon
& Roth, 2003). Moreover, some patients with panic
disorder may have panic attacks during sleep. Nearly
a third of the patients with panic disorder suffer also
from recurrent nocturnal panic attacks (Mellman &
Uhde, 1989). These attacks typically occur during
the transition from stage 2 sleep to SWS, and there is
an abrupt arousal from sleep, which is accompanied
by intense anxiety and autonomic nervous system
hyperarousal. This condition must be differentiated
from several other parasomnias (e.g., night terrors;
American Academy of Sleep Medicine, 2001).
Finally, in post-traumatic stress disorder, sleep
disturbances (i.e., re-experiencing of the traumatic
event in the form of recurrent nightmares and
symptoms of hyperarousal such as difficulty initiating
and maintaining sleep) are among the required
criteria for the diagnosis of the disorder; nightmares
or anxiety arousals are reported by 60–70% of
patients with post-traumatic stress disorder
(American Psychiatric Association, 2000; Van der
Kolk et al., 1984).
In schizophrenia, insomnia, although not included
in the diagnostic criteria, is a common clinical
feature in particular during the acute psychotic
state and exacerbations of the disease; severe
insomnia is one of the prodromal symptoms asso-
ciated with psychotic decompensation. Moreover,
reversal of the sleep–wake cycle with concomitant
severe insomnia and nightmares and terrifying
hypnagogic hallucinations are quite frequent
(Benson & Zarcone, 2000).
Psychoactive substances have a profound effect on
sleep, either during the phase of abuse or following
withdrawal and periods of abstinence. Sleep has been
more extensively studied in alcoholic patients who
 224 C. R. Soldatos & T. J. Paparrigopoulos
commonly report insomnia, diurnal hypersomno-
lence, polyphasic sleep–wake cycles, and several
parasomnias; these symptoms have been also object-
ively documented. Furthermore, alcohol increases
the likelihood of sleep-related breathing disorders,
such as obstructive sleep apnoea-hypopnoea
syndrome, as well as the risk of developing periodic
limb movements (Benca et al., 1992; Gillin &
Drummond, 2000). Sleep disturbances persist for
months or even years following recovery and
continued abstinence from alcohol; it has been
reported that even after 1–2 years of abstinence,
sleep still tends to be shallow and fragmented
(Gillin & Drummond, 2000).
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Psychopathology among patients with sleep disorders
Regarding primary sleep disorders, these are of
special interest to psychiatrists because it has been
repeatedly shown that these conditions are often
associated with the presence of psychopathology
(Kales et al., 1982a, b). For instance, nightmares
are reported by almost one fourth of non-psychotic
patients examined in a psychiatric emergency setting
(Brylowsky, 1990). Nightmares disrupt sleep and can
For personal use only.
cause insomnia and significant psychological distress
(Belicki, 1992); they may be symptoms of an
underlying psychiatric disorder such as post-
traumatic stress disorder, depression, schizophrenia,
or a personality disorder.
Since the first systematic psychopathological study
of somnambulism (Kales et al., 1980), it had been
demonstrated that current adult sleepwalkers
exhibit higher levels of concomitant psychopathology
than control subjects; thus, 72% of the current
sleepwalkers had been given a psychiatric diagnosis,
most frequently that of a personality disorder. This
initial observation was recently supported by the
findings of a recent general population epidemiolog-
ical study where a high comorbidity between mood
and anxiety disorders and night terrors or sleepwalk-
ing compared to healthy individuals was found
(Ohayon, Guilleminault, Zulley, Palombini &
Raab, 1999).
A link between periodic limb movement disorder
(PLMD) and psychiatric disorders has emerged
in several studies. A recent community survey
documented a strong association of PLMD with
stress and the presence of a mental disorder (Ohayon
& Roth, 2002). Increased rates of PLMD have
been reported in patients with attention deficit
hyperactivity disorder (Golan, Shahar, Ravid &
Pillar, 2004; Picchietti et al., 1999), post-traumatic
stress disorder, and those suffering from frequent
nightmares (Germain & Nielsen, 2003; Ross et al.,
1994). Finally, it has been demonstrated that
obstructive sleep apnoea may lead to impaired
daytime functioning with ensuing cognitive and
psychiatric symptoms, such as executive dysfunction,
impaired vigilance, depression, and hyperactivity in
children. Detailed presentation of relevant findings is
made in subsequent articles of the present issue.
All of the above indicate that sleep disorders, most
notably insomnia, are a frequent presenting symp-
tom of several mental disorders. Nonetheless,
epidemiological studies show that the converse is
also true, that is, that the prevalence of any
psychiatric disorder is higher in individuals with
insomnia compared to those without. Thus, the risk
of the occurrence of depression is approximately
four times more likely in insomniacs than in non-
insomniacs (Ford & Kamerow, 1989; Mellinger
et al., 1985); also, individuals presenting with
insomnia at a given time have a 1.6 probability of
suffering from any psychiatric illness compared to
non-insomniacs, whereas that risk rises to 39.8
if insomnia persists one year later (Walsh & Ustun,
1999). These findings raise the important issue
of the bi-directional relationship between insomnia
and psychopathology (Billard & Bentley, 2004;
Riemann & Voderholzer, 2003).
Conclusion
The study of sleep and its disorders has gained
momentum over the past decades and has given rise
to a novel field of medicine that covers a broad range
of scientific knowledge from basic science to clinical
practice; accordingly, sleep medicine should be of
concern both to researchers and clinicians of diverse
background who are interested in acquiring the
necessary skills to globally and comprehensively
understand and eventually effectively treat their
patients.
The present article, wherein the basics of sleep
medicine are dealt with, is but a brief introduction
to this fascinating field. Considerable advances
have been achieved towards the understanding of
sleep physiology and pathology; also, multiple
diagnostic tools and efficient treatments have been
developed (neuroimaging techniques, automated
polysomnography, standardized sleep scales, detailed
systems of classification, novel pharmacological
agents, cognitive-behavioural therapies, special
devices to overcome sleep-related breathing diffi-
culty, and so forth). However, many issues remain
to be addressed in the field of sleep medicine and
need to be further clarified. Last but not least, the
intention of this article is to improve physicians’
awareness of the significance of the study of sleep
and to emphasize that the incorporation of sleep
medicine into medical school curricula, residency
programs and continuing medical education
schemes is badly needed.

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