W Wo or rl ld d P Ps sy yc ch hi ia at tr ry y 4 4: :3 3 - - October 2005
Sleep disorders in psychiatric practice
WALDEMAR SZELENBERGER1,2, CONSTANTIN SOLDATOS1,3
Over the last years, a large body of evidence has accumulated showing that complaints of disordered sleep are quite prevalent in the com-
munity. Insomnia is by far the most common disturbance and is often associated with concurrent psychiatric illness, in particular anxi-
ety and mood disorders. On the other hand, sleep complaints are frequently present among psychiatric patients and have been incorpo-
rated in the official diagnostic criteria for many mental disorders, such as major depression, post-traumatic stress disorder, generalized
anxiety disorder and substance-related disorders. Estimates of the prevalence of sleep disorders diverge widely, because these disorders
have been variously conceptualized. Currently, however, three different classifications for sleep disorders establish reliable diagnostic cri-
teria and allow for more consistency in clinical research. In particular, the ICD-10 diagnostic criteria for insomnia helped to establish a
consensus among sleep specialists by defining accurately this clinical condition, i.e. by conceptualizing it as the subjective complaint of
insufficient or non-restorative sleep, which is the important feature, not the actual amount of time spent asleep. Alongside the evolution
of taxonomic systems, the development of specific diagnostic tools, such as rating scales for measuring clinical manifestations of sleep dis-
orders, has contributed significantly to the growth in the field. For instance, the risk factors responsible for the development of chronic
insomnia, its consequences, and the complex relationship between insomnia and psychopathology, have been considerably clarified. In
terms of the polysomnographic aberrations observed in various mental disorders, these, although proven not to be pathognomonic for any
of them, have been considerably refined over the last decade, and certain general sleep patterns for some specific disorders have emerged.
Finally, substantial advances have been made in the elucidation of the neuropsychobiological substrate of disturbed sleep. Thus, hyper-
arousal has been identified as the cardinal feature of chronic insomnia, which is associated with an around-the-clock activation of both
major components of the stress system, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system.
Key words: Sleep disorders, insomnia, psychopathology, polysomnography, neurobiology
1WPA Section on Psychiatry and Sleep Wakefulness Disorders
2Department of Psychiatry, Medical University of Warsaw, Poland
3Department of Psychiatry, University of Athens, Greece
A complaint of disordered sleep is quite common.
Bixler et al (1) were among the first to carry out compre-
hensive epidemiological studies using a sample represen-
tative of the general population. They found that a current
complaint of insomnia was reported by 32.2% of the re-
spondents. In addition, 7.1% of the respondents suffered
from excessive sleep, either current or past, 11.2% had a
problem with nightmares and 2.5% reported having sleep-
walking, either current or past.
Concurrent psychiatric diagnoses are common in indi-
viduals with sleep disturbances. In their 1989 study, Ford
and Kamerow (2) demonstrated that 40% of respondents
with insomnia and 46.5% of respondents with hypersom-
nia had a psychiatric disorder, compared with 16.4% of
individuals with no sleep complaints. Anxiety disorders
were found to be the most common mental disorders, in
both insomnia and hypersomnia (23.9% and 27.6%,
respectively). The prevalence of major depression, alcohol
abuse or other substance abuse was also increased.
Insomnia has been found to be associated with psychi-
atric illness in two thirds of patients presenting at a sleep dis-
orders center, and more than half of them had a mood dis-
order (3). In another study, insomnia related to psychiatric
disorder was the most frequent diagnosis in patients referred
because of insomnia to five sleep medicine centers (4).
Patients with sleep complaints are frequently seen in
psychiatric practice. Insomnia is the most prevalent sleep
disorder not only in the general population, but also
among psychiatric patients. For instance, Berlin et al (5)
found that, of 100 patients referred from a general hospital
for psychiatric consultation, 72 had insomnia. In a study by
McCall et al (6), 93% of depressed inpatients complained
of insomnia. Disturbed sleep is a diagnostic criterion for
many mental disorders, such as depressive episode, post-
traumatic stress disorder (PTSD), generalized anxiety dis-
order and substance-related disorders (7-9).
As indicated above, one of three adults may report cur-
rent trouble in falling or staying asleep or problem with
waking up too early (1) but, when a more restrictive defi-
nition was used, the frequency of reported insomnia was
in the range of 7.5 to 10.2% (2,10). Similarly, when sleep
disturbances were required to last 2 weeks within the pre-
vious 6 months, to interfere with daytime functioning, and
not to be related to a mental disorder or medical condi-
tion, the frequency of reported insomnia was only 3.2%
(2). Therefore, a need to develop widely accepted diag-
nostic criteria is self-evident.
With the accumulation of knowledge over the years,
insomnia has been variously conceptualized. To date, no
definition has gained universal acceptance. ICD-10 defines
the clinical condition of insomnia as follows: the complaint
is either of difficulty falling asleep or maintaining sleep, or
of poor quality of sleep; the disturbance has occurred at
least three times per week for at least 1 month; the unsatis-
factory quantity and/or quality of sleep either causes
marked distress or interferes with ordinary activities in daily
living. Thus, ICD-10 diagnostic criteria help to establish the
threshold of significant sleep disturbance. It should be
stressed that insomnia is a subjective complaint of insuffi-
cient or non-restorative sleep, and this complaint is impor-
tant, not the actual amount of time spent asleep (11).
Needless to say, a universally accepted classification of
sleep disorders would also increase diagnostic precision,
improve comparability of epidemiological studies and pro-
vide greater homogeneity of research samples. Such a need
has been long recognized. The first classification system
was published in 1979 (12). Currently, three different classi-
fications for sleep disorders are available: the revised edi-
tion of the International Classification of Sleep Disorders
(ICSD, 13), the DSM-IV sleep disorders section and the
section of ICD-10 dealing with non-organic sleep disorders.
The revised edition of the ICSD comprises 88 syn-
dromes. They are divided into the following categories (13):
• Dyssomnias, i.e. the disorders of initiating and main-
taining sleep and the disorders of excessive sleepiness.
• Parasomnias, i.e. undesirable phenomena that occur
predominantly during sleep.
• Sleep disorders associated with mental, neurologic, or
other medical disorders.
• Proposed sleep disorders.
The ICSD differs from other classifications also in that
it includes polysomnographic diagnostic criteria.
The DSM-IV sleep disorders section (7) consists of:
• Primary sleep disorders, subdivided into dyssomnias
• Sleep disorders related to another mental disorder.
• Other sleep disorders, e.g., sleep disorder due to a gen-
eral medical condition and substance-induced sleep
In ICD-10, non-organic sleep disorders are listed with
mental and behavioral disorders. The section of non-organic
sleep disorders is divided into: a) dyssomnias, i.e. predomi-
nant disturbance in the amount, quality, or timing of sleep
due to emotional causes (non-organic insomnia, non-organ-
ic hypersomnia, non-organic disorder of sleep-wake sched-
ule), and b) parasomnias, i.e. abnormal episodic events
occurring during sleep (sleepwalking, sleep terrors, night-
mares). Non-psychogenic sleep disorders, such as narcolep-
sy or sleep apnoea, are placed in chapter 6 of ICD-10 (8).
The National Institute of Mental Health classification of
insomnia (14) may be helpful in treatment planning. In this
classification, insomnia has been divided into: a) transient
insomnia lasting several days and related to minor situa-
tional stress; b) short-term insomnia lasting up to three
weeks and associated with acute personal loss in work or
family life, and c) long-term insomnia. It should be noted
that both transient and short-term insomnia are physiolog-
ical reactions occurring in normal sleepers, while long-
term insomnia is a disorder of multiple causes.
The development of specific diagnostic tools has con-
tributed significantly to the growth in the field. For the
past sixty years, polysomnography has been the main
method of sleep analysis and the main diagnostic tool in
sleep medicine. Standardized scoring systems for sleep
stages had landmark significance, allowing to compare the
results between laboratories. From the 1960s onwards,
Rechtschaffen and Kales scoring criteria (15) have been
the gold standard, despite the development of alternative
methods of sleep description.
Altered sleep has to be regarded as a 24-hour disorder.
Therefore, night-time recordings may be followed by day-
time tests such as the Multiple Sleep Latency Test, a neu-
rophysiological technique developed to quantify sleep ten-
Rating scales for measuring clinical manifestations of
sleep disorders have also been developed. Among many
others, they include the Pittsburgh Sleep Quality Index
(PSQI), designed to evaluate self-rated sleep quality (17);
the Sleep Problems Scale (18); the Stanford Sleepiness
Scale, the first tool developed to measure self-rated day-
time hypersomnolence (19); and the Epworth Sleepiness
Scale, employed to evaluate chronic excessive daytime
sleepiness (20). Recently, the Athens Insomnia Scale, an
instrument quantifying the severity of insomnia based on
the ICD-10 criteria and consisting of either 8 items or only
5 items in the brief version, was produced (11,21,22). In
addition, many other psychobiological measures can be
utilized, since sleep medicine emerges from and depends
upon a multidisciplinary approach.
INSOMNIA AND PSYCHOPATHOLOGY
“It is virtually axiomatic that a disturbance of the mind
can manifest itself in the sleeping state as well as in the
waking state” (23). A wealth of data on sleep in mental dis-
orders has been accumulated to date. Clinical manifesta-
tions of chronic insomnia were thoroughly documented in
a series of journal articles published in the 1970s and 1980s
by Kales’s group, which were integrated into a monograph
on the evaluation and treatment of insomnia (24).
Insomnia is a condition of heterogeneous origin. Multi-
ple diagnoses are the rule, not the exception. Stressful life
events or stressors of everyday life are triggering factors,
and maladaptive habits contribute to the development and
persistence of insomnia. However, some predisposing fac-
tors, such as female gender (25) and family history of sleep
disturbances (26), increase the vulnerability to insomnia.
McCarren et al (27), using the Vietnam Era Registry,
demonstrated that genetic effects were stronger predictors
of self-reported insomnia than combat exposure.
For many years, insomnia has been viewed as a disorder
of minor importance, although it was clear that insomniacs
have poorer physical and mental health, and attempt sui-
cide four times more often than controls (28). Prospective
epidemiological studies consistently report that insomniacs
are at greater risk for developing a depressive disorder. Ford
and Kamerow (2) were the first to demonstrate that indi-
viduals who complained of insomnia at baseline and one
W Wo or rl ld d P Ps sy yc ch hi ia at tr ry y 4 4: :3 3 - - October 2005
year later had a greater risk of developing new depression
over the intervening year. Eaton et al (29) found that sleep
problems identify 47% of the new cases of major depres-
sion occurring in the next year, and sleep problems are a
better predictor of full-blown depression than thoughts of
or wishes for death, feeling of worthlessness and guilt, psy-
chomotor retardation, weight problems or fatigue. In the
Breslau et al (30) study, insomniacs were at nearly four
times higher risk for developing a new depressive disorder
in the following 3.5 years. Data from epidemiological stud-
ies indicate that the risk for developing new anxiety disor-
ders and alcohol abuse is also greater for insomniacs (2).
In a review of ten epidemiological studies on the asso-
ciation between heart disease and insomnia, Schwartz et
al (31) concluded that sleep complaints are a marker for
chronic stress which results in autonomic dysfunction and
increased risk of myocardial infarction.
SLEEP ABERRATIONS IN PSYCHIATRIC DISORDERS
Descriptive data on sleep in depressive disorders are the
best documented results in the field. Disturbed sleep during
an acute depressive episode is characterized by decreased
sleep continuity (increased sleep latency, multiple awaken-
ings, early morning awakening), diminished slow wave
sleep (stage 3 and 4), and shortened latency to the first rapid
eye movement (REM) period, with an increased amount of
REM sleep early in the first half of the night. However, 10-
15% of depressive patients report hypersomnia, together
with complaints of decreased energy and psychomotor
retardation (for a review see 32). In mania, disturbed sleep
continuity, shortened REM latency and greater REM densi-
ty have been found (33).
Sleep abnormalities have been also documented in other
psychiatric disorders, including schizophrenia, anxiety dis-
orders, dementia and alcoholism. Prolonged sleep latency,
decreased sleep continuity, decreased total sleep time,
reduced slow wave sleep, decreased REM latency, reduced
or increased REM sleep, increased REM density are the
most often reported abnormalities in schizophrenia (for a
review see 34). Sleep in generalized anxiety disorder is char-
acterized by decreased depth and continuity (35). Lower
sleep efficiency was demonstrated in outpatients with
obsessive-compulsive disorder (36). DSM-IV and ICD-10
criteria for PTSD include nightmares and difficulty falling
or staying asleep; however, objective sleep studies on PTSD
revealed either no abnormalities or a variability of findings:
reduced total sleep time, decreased sleep efficiency and
delta sleep, reduced or increased REM latency and REM
percentage, increased REM density (37). Slow wave sleep is
reduced, and nocturnal waking is increased in patients with
possible or probable Alzheimer’s disease (38). A consider-
able reduction of slow wave sleep was found in abstinent
alcoholics (39). Polysomnographic variables are not
pathognomonic for any mental disorder (40), although gen-
eral sleep patterns for specific disorders can be identified.
Automated EEG analysis may provide additional informa-
tion. For instance, Ganguli et al (41) found less delta counts
in schizophrenics while their slow wave sleep percent did
not differ from that seen in controls.
Although polysomnography is the most widely used and
the most sensitive state indicator of sleep, no diagnostic
parameters have been found as yet. Therefore, two ques-
tions arise. First, what is the utility of psychiatric sleep
research in a clinical setting and can it contribute to diag-
nostic classification, assessment of the course and predic-
tion of the outcome? Second, can this research offer an
insight into biological mechanisms of mental disorders?
Many data confirm that the clinical state, and the under-
lying pathology as well, can be mirrored in sleep variables.
Disturbed sleep-wake patterns parallel cognitive decline in
patients with possible or probable Alzheimer’s disease (38).
The amount of slow wave sleep appears to be inversely cor-
related with the presence of negative symptoms of schizo-
phrenia (41). Slow wave sleep loss corresponds with cere-
bral atrophy in abstinent alcoholics (39).
Longitudinal follow-up and family studies suggest that
sleep disturbances in depression are trait-like. Sleep of de-
pressed patients in remission is still disturbed: delta sleep is
decreased and REM latency is shortened. Shorter REM
latency is associated with an increased risk for relapse (42).
Polysomnographic studies in high risk probands showed
that short REM latency and slow wave deficits are familial,
and polysomnographic abnormalities may precede the clin-
ical expression of depression (43). Relapsing primary alco-
holics show significantly shorter REM latency and more
REM percent compared with abstainers. Polysomnograph-
ic measures at time of hospital admission appeared to be a
better predictor of relapse within 3 months than any other
clinical or demographic variables (44).
Sleep disturbances may be of value in predicting suicide.
A prospective study conducted in the general population
demonstrated that the frequency of reported nightmares
was related to the risk of suicide (45). Insomnia, hypersom-
nia and subjective sleep quality based on PSQI are related
to suicidal behavior (46). Major depressive patients with
nightmares at least twice a week have higher suicide scale
scores (47). Suicide attempters have longer sleep latency,
fewer late-night delta counts, and longer REM time (48).
Sleep data may also help in prediction of the PTSD
course. Koren et al (49) reported that sleep complaints
from 1 month after the trauma are significant in predicting
PTSD after 1 year. Mellman et al (50) demonstrated that
more fragmented REM pattern within a month of injury is
associated with PTSD development.
THE NEUROPSYCHOBIOLOGICAL SUBSTRATE
OF DISTURBED SLEEP
Considerable advances have been made in the elucida-
tion of mechanisms underlying sleep disorders. Hyper-
arousal has been identified as the cardinal feature of insom-
nia (51). Chronic insomnia is associated with an around-
the-clock activation of both major components of the stress
system, the hypothalamic-pituitary-adrenal axis and the
sympathetic system. The 24-h urinary free cortisol and cat-
echolamine metabolites are significantly higher in insomni-
acs and correlate with objective sleep disturbances (52).
Many additional measures suggest arousal due to augment-
ed activity of the sympathetic nervous system: worse sleep
maintenance, increased basal metabolic rates, altered heart
rate variability, increased body temperature (for a review see
53). It has been proposed that the chronic activation of the
stress system plays a significant role in the poor mental and
physical health associated with persistent insomnia (31,52).
In the stress-diathesis model of mood and anxiety disor-
ders, abnormal corticotropin releasing factor (CRF) regula-
tion is responsible for such behavioral responses as arous-
al, restlessness and insomnia (54). Richardson and Roth
(53) indicated that primary insomnia has an extensive
overlap with major depressive disorder, suggesting com-
monality in pathophysiology. This has led to the hypothe-
sis that increased activity of CRF neurons is responsible for
primary insomnia. However, the CRF-producing neurons
of the hypothalamus are only the final integrator which
transforms the stress response into the endocrine response.
It has been proposed that stressors requiring interpretation
and modulation by previous experience may be relayed to
paraventricular nucleus through multisynaptic limbic-fore-
brain circuits (55).
Many issues remain to be addressed in the field of sleep
disorders. The incorporation of sleep medicine into the cur-
ricula of medical schools and residency programs is badly
needed. Most studies concentrate on sleep disturbances in
depressive disorder and non-organic insomnia. Interest in
studies on sleep in schizophrenia is waning; yet, sleep distur-
bances in this disorder are well documented. Fewer studies
focus on altered sleep in anxiety disorders. There are also
unmapped territories. For instance, daytime complaints of
impaired functioning are a precondition for the diagnosis of
insomnia, but performance decrements in insomniacs remain
a subject of controversy. Relatively little is known about the
safety and efficacy of chronic hypnotic use. There is a strong
evidence that insomniacs are at higher risk for depressive dis-
order, but whether early treatment of insomnia prevents the
onset of depression, a question posed in the Ford and
Kamerow (2) seminal study, still remains unknown.
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