ArticlePDF Available


Sleep disturbances-particularly insomnia - are highly prevalent in anxiety disorders and complaints such as insomnia or nightmares have even been incorporated in some anxiety disorder definitions, such as generalized anxiety disorder and posttraumatic stress disorder. In the first part of this review, the relationship between sleep and anxiety is discussed in terms of adaptive response to stress. Recent studies suggested that the corticotropin-releasing hormone system and the locus ceruleus-autonomic nervous system may play major roles in the arousal response to stress. It has been suggested that these systems may be particularly vulnerable to prolonged or repeated stress, further leading to a dysfunctional arousal state and pathological anxiety states, Polysomnographic studies documented limited alteration of sleep in anxiety disorders. There is some indication for alteration in sleep maintenance in generalized anxiety disorder and for both sleep initiation and maintenance in panic disorder; no clear picture emerges for obsessive-compulsive disorder or posttraumatic stress disorder. Finally, an unequivocal sleep architecture profile that could specifically relate to a particular anxiety disorder could not be evidenced; in contrast, conflicting results are often found for the same disorder. Discrepancies between studies could have been related to illness severity, diagnostic comorbidity, and duration of illness. A brief treatment approach for each anxiety disorder is also suggested with a special focus on sleep.
nxiety is an experience of everyday life. It typ-
ically functions as an internal alarm bell that warns of
potential danger and, in mild degrees, anxiety is service-
able to the individual. In anxiety disorders, however,the
individual is submitted to false alarms that may be
intense, frequent, or even continuous. These false alarms
may lead to a state of dysfunctional arousal that often
leads to persistent sleep–wake difficulties. Indeed, popu-
lation surveys indicate that the prevalence of anxiety dis-
order is about 24% to 36% in subjects with insomnia
complaints and about 27% to 42% for those with hyper-
somnia.1,2 Another point further underpinning the rela-
tionship between anxiety and sleep is that sleep distur-
bance is a diagnostic symptom for some anxiety disorders,
such as generalized anxiety disorder (GAD) and post-
traumatic stress disorder (PTSD).
Anxiety states may be focused upon some particular sit-
uation or may be generalized. Usually, there is a combi-
nation and most people suffering from severe phobic dis-
order will have some degree of generalized anxiety.
Likewise, patients with generalized anxiety often experi-
Clinical research
Sleep and anxiety disorders
Luc Staner, MD
sleep; insomnia; anxiety disorder; sleep–wake regulation; panic
disorder; generalized anxiety disorder; obsessive-compulsive disorder; posttrau-
matic stress disorder
Author affiliations: Sleep Laboratory, FORENAP, Rouffach, France
Address for correspondence: Sleep Laboratory, FORENAP, Institute for
Research in Neuroscience and Neuropsychiatry, BP29, 68250 Rouffach, France
Sleep disturbances—particularly insomnia—are highly prevalent in anxiety disorders and complaints such as insomnia
or nightmares have even been incorporated in some anxiety disorder definitions, such as generalized anxiety disorder
and posttraumatic stress disorder. In the first part of this review, the relationship between sleep and anxiety is discussed
in terms of adaptive response to stress. Recent studies suggested that the corticotropin-releasing hormone system and
the locus ceruleus–autonomic nervous system may play major roles in the arousal response to stress. It has been sug-
gested that these systems may be particularly vulnerable to prolonged or repeated stress, further leading to a dys-
functional arousal state and pathological anxiety states. Polysomnographic studies documented limited alteration of
sleep in anxiety disorders. There is some indication for alteration in sleep maintenance in generalized anxiety disorder
and for both sleep initiation and maintenance in panic disorder; no clear picture emerges for obsessive-compulsive dis-
order or posttraumatic stress disorder. Finally, an unequivocal sleep architecture profile that could specifically relate to a
particular anxiety disorder could not be evidenced; in contrast, conflicting results are often found for the same disorder.
Discrepancies between studies could have been related to illness severity, diagnostic comorbidity, and duration of illness.
A brief treatment approach for each anxiety disorder is also suggested with a special focus on sleep.
© 2003, LLS SAS Dialogues Clin Neurosci. 2003;5:249-258.
Copyright © 2003 LLS SAS. All rights reserved
ence increase in anxiety in certain situations. Moreover,
the various anxiety disorders share many biological and
clinical similarities, and are highly comorbid. Therefore,
in this article, we will first discuss common features of the
neurobiological basis of anxiety and its relationships with
sleep physiology. Next, sleep disturbances and its treat-
ment will be discussed; for clinical convenience, each of
the different anxiety disorders will be discussed sepa-
rately. Indeed, the treatment of the anxiety disorder sig-
nificantly improves sleep; however,when the sleep dis-
turbance predominates, its treatment may improve the
management of the anxiety disorder.
A brief survey of sleep physiology
Human sleep consists of two qualitatively different brain
states,non–rapid eye movement (NREM) and rapid eye
movement (REM) sleep. NREM sleep is further subdi-
vided into stages 1 through 4, with stage 1 being the light-
est and stage 4 being the deepest sleep. Since slow “delta”
waves distinguish stages 3 and 4, the stages are often
defined as delta sleep or slow-wave sleep (SWS). REM
sleep is also called paradoxical sleep because of the close
resemblance with the electroencephalogram (EEG) of
active wakefulness combined with a “paradoxical”active
inhibition of major muscle groups that seems to reflect a
heavy sleep. Normal sleep is characterized electrograph-
ically as recurrent cycles of NREM and REM sleep of
about 90 min. In the successive cycles during the night,
the duration of stages 3 and 4 decrease, and the propor-
tion of the cycle occupied by REM sleep tends to
increase with REM episodes occurring late in the night
having more eye movement bursts than REM episodes
occurring early in the night.3
Most models of sleep regulation have implicated the
monoaminergic and cholinergic systems and the impor-
tance of inhibitory GABAergic (GABA, γ-aminobutyric
acid) mechanisms in sleep regulation is well established.4
Since dysfunction of these neurotransmitter systems have
been implicated in anxiety disorders,5it is no wonder that
one of the chief complaints of anxiety disorder patients
relates to sleep alteration.
Sleep–wake regulation is classically viewed as resulting
from the interaction of two regulating processes (circa-
dian [C] and homeostatic [S]).6The propensity to sleep
or be awake at any given time is a consequence of a sleep
debt (process S), and its interaction with signals coming
from the circadian clock located in the suprachiasmatic
nucleus (process C). Process S is supposed to reflect the
activity of a somnogenic substance that progressively
accumulates with prolonged wakefulness,with adenosine
being one of the most cited candidates.7Both homeosta-
tic and circadian mechanisms are thought to influence
the opposite action of neurons promoting wakefulness
and neurons promoting sleep.Wake-active neurons are
cholinergic (located in the basal forebrain and in the
tegmentum) and monoaminergic (noradrenergic in the
locus ceruleus, serotonergic in the dorsal raphe, and his-
taminergic in the tuberomammillary nucleus), whereas
sleep-active neurons are GABAergic and located in the
preoptic area of the hypothalamus.4
The discovery of the hypocretin (also called orexin) sys-
tem has brought new inroads into understanding the
sleep-regulatory neural circuit.8Hypocretin neurons are
located in the lateral hypothalamus and have dense exci-
tatory projections to all monoaminergic and cholinergic
cell groups. Recent studies suggested that monoaminer-
gic and hypocretin neurons play a different and comple-
mentary role in wakefulness maintenance.4For example,
the dual effects of hypocretins on arousal and food intake
(orexin from “appetite-stimulating”) suggest a more
important role for hypocretins in the control of arousal
maintenance related to energy homeostasis.8In the same
way, data summarized in the following section suggest a
role for the norepinephrine (NE)–containing neurons of
the locus ceruleus (LC) in stress-induced arousal and
concomitant anxiety.
Clinical research
Selected abbreviations and acronyms
ACTH adrenocorticotropic hormone
AN autonomic nervous (system)
BZD benzodiazepine
CNA central nucleus of the amygdala
CRH corticotropin-releasing hormone
GAD generalized anxiety disorder
HPA hypothalamic-pituitary-adrenal (axis)
LC locus ceruleus
NE norepinephrine
NREM non–rapid eye movement
OCD obsessive-compulsive disorder
PTSD posttraumatic stress disorder
PVN paraventricular nucleus
REM rapid eye movement
SSRI selective serotonin reuptake inhibitor
SWS slow-wave sleep
TCA tricyclic antidepressant
Interactions between stress,
anxiety, and sleep
Anxiety and stress
Anxiety is a universal emotion and it would at times be
maladaptive not to experience it; it is a necessary part of
the response of the organism to a stress,ie,a threat to the
psychological or the physiological integrity of an indi-
vidual. Anxiety may be polarized between a state and a
trait. It may supervene at some point in the course of life,
in which case anxiety is referred as a state.Anxiety trait
is a long-term feature of a person’s experience, present
throughout life and considered to be a key feature of the
avoidant or anxious personality disorder. It probably
reflects a lifetime maladaptive response to stress due to
individual differences in biogenetic background, devel-
opmental influences, and early life experiences.There is
no hard and fast distinction between anxiety that may be
considered as a normal, acceptable accompaniment of
stress and the pathological state that warrants classifica-
tion as a psychiatric disorder. In the latter, the nature of
the stress is not always clearly discernible. In other words,
pathological anxiety could be characterized by a sense of
fear, but it is differentiated from fear in that the threat is
not immediate or always obvious. Whether normal or
pathological, the constituent features of anxiety always
comprise indices of increased arousal or alertness that
could lead to sleep–wake alterations. Indeed, anxiety is
only one part of the arousal response to stress, whether
the stress is real, implied, or overvalued.
Arousal and stress
Response to stress implicates two systems that both play
a key role in physiological responses to stressful situation
by promoting arousal, the corticotropin-releasing hor-
mone (CRH) system and the LC–autonomic nervous
(AN) system. This topic has recently been reviewed by
several authors9-11 and will be only briefly described here.
Before going further, it should be emphasized that pro-
moting arousal is essential for identifying a given situa-
tion as important, as well as for maintaining the central
nervous system (CNS) in states that most favor survival
during stressful situations. Arousal response to stress
comprises three components (hormonal, behavioral,and
autonomic) in which CRH and LC-AN systems have
been diversely implicated (Figure 1). Different stressors
activate different components of the stress system, eg,the
LC-AN system will be more implicated in the response
to physiological stressors such as hypoxia, while the CRH
system will be recruited for more complex environmen-
tal dangers such as emotional stress. However, there are
several connections between the two systems which are
continuously in close interaction (see next section).
The stress system
During these last years, a series of studies in rodents
established the role of CRH as a key neurotransmitter in
the stress response, beside its stimulating effect on the
hypothalamic-pituitary-adrenal (HPA) axis.9,11 It has been
shown that hypothalamic CRH neurons activate the LC-
AN system and inhibit a variety of neurovegetative func-
tions, such as food intake, sexual activity, growth, and
reproduction. CRH-containing neurons located in the
central nucleus of the amygdala (CNA) play a key role
by activating fear-related behavior, while inhibiting
exploration behavior. Like the CRH system,the NE-con-
taining neurons of the LC promote arousal, inhibit the
parasympathetic system as well as several vegetative
functions such as feeding and sleep, and contribute to
HPA axis stimulation.12 It has been shown that stress
increases NE turnover in many terminal projections of
the LC and that the activity of LC neurons is monoton-
ically related to increased arousal.9
There is also evidence that NE stimulates the release of
CRH in the paraventricular nucleus (PVN) of the hypo-
thalamus and in the CNA.9These NE-CRH influences
suggest a potential feed-forward system between the
Sleep and anxiety disorders - Staner Dialogues in Clinical Neuroscience - Vol 5 .No. 3 .2003
Figure 1. Arousal response to stress. CRH, corticotropin-releasing hor-
mone; PVN, paraventricular nucleus; CNA, central nucleus of
the amygdala; LC-AN, locus ceruleus–autonomic nervous; NE,
LC-AN system
CRH system Hormonal
Hypothalamus (PVN)
Amygdala (CNA)
LC-AN system and the CRH system, and both systems
have stimulating properties on its counterpart. It has
been suggested that such a feed-forward mechanism may
be particularly vulnerable to dysfunction during which
the arousal reaction is maintained despite the removal of
the stressful situation.9,10 The same authors have proposed
that, if prolonged,such dysfunctional arousal state could
lead to anxiety and depressive disorder.
Stress and sleep–wake regulation
Animal and human studies showed that both acute and
chronic stress have pronounced effects on sleep that are
mediated through the activation of the HPA axis and the
sympathetic system.13 For instance, in rats, effects of acute
stress on sleep are primarily manifested by changes in
REM sleep.These alterations seem to involve CRH-medi-
ated mechanisms: CRH acts as a neurotransmitter in the
LC to increase activity of the NE neurons, which leads to
an increase in REM sleep.14 Rats exposed to various mod-
els of chronic stress have shown sleep disruption, increase
in REM sleep, and decrease in SWS.15,16 There are also indi-
cations that CRH could contribute to the regulation of
spontaneous waking even in the absence of stressors.17
In humans,there is a close temporal relationship between
HPA activity and sleep structure.The HPA axis is subject
to a pronounced inhibition during the early phase of noc-
turnal sleep, during which SWS predominates. In contrast,
during late sleep, when REM sleep predominates, HPA
activity increases to reach a diurnal maximum shortly after
morning awakening. During SWS, sympathetic activity is
reduced and there is positive correlation among the
amount of REM sleep and activities of the HPA axis and
the sympathetic system.18,19 More generally, a close coupling
has been shown between adrenocorticotropic, autonomic,
and EEG indices of arousal during the sleep–wake cycle.20-
22 Exogenous administration of CRH, adrenocorticotropic
hormone (ACTH), or cortisol produces either prolonged
sleep onset, reduced SWS, and increased sleep fragmenta-
tion.13 Accordingly, patients with complaints of insomnia
show electrophysiological and psychomotor evidence of
increased daytime arousal,23-25 as well as indications of
increased HPA activity26 and increased sympathetic tone.27
Sleep complaints and anxiety disorder
Anxiety disorders are considered as the most frequently
occurring category of mental disorder in the general
population. Estimates of the lifetime prevalence of anxi-
ety disorders have ranged between 10% and 25%.28
Epidemiological studies have also demonstrated the high
prevalence of sleep complaints.As much as one third of
the adult population reports difficulty sleeping29-31 and
sleep disturbance is considered as the second most com-
mon symptom of mental distress.32 Some epidemiological
studies investigated the relationship between the occur-
rence of sleep disturbances and anxiety disorder in the
general population.1,2,33 In a longitudinal study of young
adults, Breslau et al2found that lifetime prevalence was
16.6% for insomnia alone, 8.2% for hypersomnia alone,
and 8% for insomnia plus hypersomnia. Odds ratios for
various anxiety disorder diagnoses associated with life-
time sleep disturbance varied from 1.2 to 13.1. Table I
shows that the odds ratios associated with insomnia alone
varied little from those associated with hypersomnia
alone.The three highest odds ratios were those for obses-
sive-compulsive disorder (OCD) and for panic disorder
associated with both insomnia and hypersomnia, and that
for GAD associated with insomnia alone.
These findings were replicated for chronic insomnia in a
recent study,33 which further showed that insomnia
appeared before the anxiety disorder in 18% of cases,
anxiety and insomnia appeared about in the same time
in 38.6% of cases,and anxiety appeared before insomnia
in 43.5% of cases.These authors concluded that psychi-
atric history, including anxiety disorder,is closely related
to the severity and chronicity of current insomnia.
Panic disorder and agoraphobia
The essential features of panic disorder are recurrent
attacks of severe anxiety (panic attacks), which are not
restricted to any particular situation or set of circum-
stances and are therefore unpredictable.According to
Clinical research
Table I. Odds ratios for specific anxiety disorders associated with lifetime
sleep disturbances (adapted from Breslau et al2). GAD, general-
ized anxiety disorder; OCD, obsessive-compulsive disorder.
Insomnia Hypersomnia Both
alone alone
GAD 7.0 (2.817.2) 4.5 (1.515.3) 4.8 (1.515.2)
Panic disorder 5.3 (2.013.6) 4.3 (1.314.8) 8.5 (3.123.5)
OCD 5.4 (2.014.8) 1.2 (0.19.7) 13.1 (4.835.7)
Phobic disorder 1.5 (1.02.3) 2.9 (1.84.8) 4.0 (2.56.5)
Any anxiety 2.4 (1.63.5) 3.3 (2.05.4) 4.5 (2.87.3)
the Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition (DSM-IV)34 criteria of panic disorder,
unexpected panic attacks have to be followed by at least
1 month of persistent concern about having another
panic attack. The dominant symptoms of a panic attack
vary from individual to individual. Typically, it includes
autonomic symptoms with marked psychic anxiety. The
most prominent autonomic symptoms are palpitations,
sweating, trembling, shortness of breath, dizziness,chest
pain, nausea, and paresthesias.There is almost always a
secondary fear of dying, losing control, or going mad.
Most individual attacks last only for a few minutes, but
a common complication is the development of anticipa-
tory fear of helplessness or loss of control during a panic
attack, so that the individual may progressively develop
avoidant behavior leading to agoraphobia or specific
phobias. In this respect, most, if not all, patients with
agoraphobia also have a current diagnosis (or history)
of panic disorder.34 Accordingly, sleep disturbances of
panic disorder and agoraphobia are discussed in the
same section.
Subjective sleep
Sleep disturbances, predominantly insomnia, are
extremely common in panic disorder. Sheehan et al35
reported a prevalence of 68% for difficulties in falling
asleep and of 77% for restless and disturbed sleep. In a
self-report sleep survey, Mellman and Uhde36 found that,
compared with healthy subjects, patients with panic dis-
order reported more complaints of middle night insom-
nia (67% versus 23%) and late night insomnia (67%
versus 31%); the two groups did not differ with regard
to early night insomnia. Many patients with panic disor-
der experience occasional sleep panic attacks, but only
about 20% to 45% of patients with panic disorder have
repeated nocturnal panic attacks.37-39 Some evidence sug-
gests that patients experiencing regular nocturnal panic
attacks represent a specific version of panic disorder
characterized by fearful associations with sleep and
sleep-like states.40 Therefore, nocturnal panic attacks will
be discussed in a separate section.
Sleep EEG recording
Most polysomnographic studies indicate that patients
with panic disorder have impaired sleep initiation and
maintenance characterized by increased sleep latency
and increased time awake after sleep onset resulting in a
reduced sleep efficiency (the ratio between total sleep
time and time in bed),41-47 but there are also negative
reports showing no difference compared with controls in
these variables.48,49 Concerning sleep architecture, NREM
sleep was found differently affected across studies; some
reported a decreased in stage 2 sleep duration42,43 with a
concomitant increase in SWS.47 Time spent in SWS was
found reduced by Arriaga et al46 and Stein et al,49 but
unchanged by other authors.36,42,45 Controversial results
were also obtained regarding REM sleep.Although most
studies agreed on the fact that REM sleep time is
unchanged in panic disorder, some authors found a short-
ening of REM sleep latency,36,48 while others did not.41,44
To summarize, most studies suggest that the subjective
sleep continuity disturbances reported by patients with
panic disorder could be objectively demonstrated by
polysomnographic recordings. Findings regarding sleep
architecture are more controversial (although REM
sleep seems to be preserved). These discrepancies could
relate to sampling differences (some studies having
included patients with a comorbid depressive disorder)
and to the influence of nocturnal panic attack during the
sleep EEG recording.
Sleep disturbances linked to panic disorder respond to a
number of antipanic pharmacological agents including
selective serotonin reuptake inhibitors (SSRIs), tricyclic
antidepressants (TCAs), benzodiazepines (BZDs),and
monoamine oxidase inhibitors (MAOIs). Some patients
could have an initial increased anxiety or insomnia in
response to antidepressant medications, which should
alert the clinician to the need to increase the dosage quite
slowly. A BZD can also be used to reduce anxiety and aid
sleep in the early phases of treatment.
Nocturnal panic
The majority of patients with panic disorder experience
nocturnal panic attacks. However, in a subgroup of
patients,sleep-related panic is the predominant symptom,38
with up to 18% of all panic attacks occurring during
sleep.50 Nocturnal panic refers to waking from sleep in a
state of panic and should be distinguished from nighttime
arousal induced by nightmares or environmental stimuli
(such as unexpected noise). It has often been mistaken for
Sleep and anxiety disorders - Staner Dialogues in Clinical Neuroscience - Vol 5 .No. 3 .2003
sleep apnea, sleep terrors, and nocturnal epilepsy.
Nocturnal panic generally occurs during late stage 2 to
early stage 3 sleep, and can therefore be distinguished
from sleep terrors,which mostly occur during stage 4 sleep,
and from nightmares, which mostly occur during REM
sleep.51 Moreover,nocturnal panic could be differentiated
from nocturnal seizures by the fact that no EEG abnor-
mality was demonstrated during nocturnal panic attacks
and from sleep apnea because sleep apnea occurs mostly
during stages 1 and 2, as well as during REM sleep, and is
more repetitive than nocturnal panic.40
There are limited indications that subjects with frequent
sleep panic attacks have a severe form of panic disor-
der.37,38,52 More recent studies suggest that there are only
few differences on measures of psychopathology and on
sleep EEG between panic-disordered patients with and
without sleep-related panic attacks.40,53 However, differ-
ences may be more subtle and evidenced by techniques
such as measurement of the autonomic nervous system
(ANS) activity. For instance, Sloan et al54 used a lactate
infusion panicogenic challenge and heart rate variability as
a measurement of ANS activity to demonstrate that ANS
dysregulation during sleep is more pronounced in noctur-
nal panic patients than in daytime panic patients.This sug-
gests a more increased arousal level in nocturnal panic.
On the basis of several observations,38,40,51 it has been pro-
posed that nocturnal panic is characterized by height-
ened distress to situations that involve loss of vigilance,
such as sleep and relaxation, and that it may represent
one particular version of panic disorder that responds
just as well as other forms of panic disorder to usual
antipanic treatment.40 In this regard, the adjunction of
cognitive-behavioral therapy to pharmacological agents
will be particularly beneficial in patients with nocturnal
panic, since some patients can develop a conditioned fear
or even an avoidance of sleep, which may cause further
sleep deprivation and thus aggravate the condition.
Generalized anxiety disorder
A persistent state of anxiety, ie, lasting for at least 6
months, characterizes GAD. Anxiety and apprehensive
expectation (“worry”) need to relate to a certain number
of events and to be accompanied by additional symptoms
belonging to a motor tension cluster (muscle tension;
restlessness; and easy fatigability) or to a vigilance and
scanning cluster (difficulty falling or staying asleep; rest-
less, unsatisfying sleep; difficulty concentrating; and irri-
tability). According to DSM-IV,34 the diagnosis is not
made if the symptoms exclusively relate to another Axis I
disorder.As sleep disturbances are part of the diagnosis
requirement, a high prevalence of these symptoms is
expected in GAD. For instance, in mental health epi-
demiological surveys, Ohayon et al55 found that, among
subjects complaining of insomnia and having a primary
diagnosis of mental disorder, GAD was the most preva-
lent diagnosis. It has been estimated that about 60% to
70% of patients with GAD have insomnia complaint,
whose severity parallels that of the anxiety disorder,56,57
suggesting that insomnia could represent one of the core
symptoms of GAD.
Sleep EEG recording
Monti and Monti58 have extensively reviewed six selected
studies investigating polysomnographic recording of
patients with GAD.The sleep EEG recordings following
an adaptation night of 130 patients were compared to
those of 147 normal controls in the age range 20 to 65
years (mean 37 years). Regarding sleep continuity, the
results indicate that GAD is mostly associated with sleep
maintenance insomnia, and to a lesser extent with sleep
initiation difficulties. Five studies found a significant
decrease in total sleep time, four an increase of waking
after sleep onset, while only two studies showed a signif-
icant prolongation of sleep onset latency. As regards
NREM and REM sleep structures, results are inconsis-
tent. Stage 4 was significantly decreased in three studies,
all six studies showed nonsignificant decrease in REM
sleep, and one study a significant shortening of REM
GAD is often responsive to BZDs, buspirone, and anti-
depressants.Anxiolytic BZDs provide a prompt relief of
the GAD symptoms belonging to the motor and the vig-
ilance-scanning clusters. However, psychic symptoms
such as worry and ruminations are less affected by these
compounds and respond better to antidepressants such
as TCAs, SSRIs, or norepinephrine and serotonin selec-
tive antidepressant (NaSSA), such as venlafaxine.58
Adjunctive psychotherapy with a cognitive focus can be
beneficial. In this regard, studies have shown that cog-
nitive-behavioral techniques are better than control con-
ditions or to either cognitive or behavior therapy alone.58
Clinical research
The alleviation of the sleep disturbance can often greatly
improve the condition: therefore a low-dose, intermedi-
ate-acting BZD at bedtime may be temporarily indicated
early in the treatment. Sedative antidepressant could also
help improve sleep.
Obsessive-compulsive disorder
According to DSM-IV,34 the essential features of the OCD
are recurrent obsessions or compulsions that are suffi-
ciently severe to cause a signification disruption of a per-
son’s daily routine. The most common obsessional
thoughts are fears of contamination, of being aggressive,
and of a sexual nature; the most common compulsions
relate to checking, cleaning, and counting. The sufferer
knows that it is his or her own thought (or act), that it
arises from within him- or herself, and that it is subject to
the sufferer’s own will.Anxiety is provoked by the fear of
what may happen if the compulsive rituals are disturbed,
the need to both perform the action and preserve social
acceptability, or the fearful nature of the obsessional
thoughts themselves.The person usually functions satis-
factorily in other areas of life not contaminated by the
obsessional thoughts, but as the obsessions become more
severe there is increasing social incapacity.
Patients often complain of disrupted sleep and sleep
delay due to compulsive behaviors. In one epidemiolog-
ical survey,55 insomnia related to OCD had a prevalence
of 0.2% (ie, insomnia complaints sufficiently severe to
warrant an Axis I diagnosis in addition to OCD), while
the prevalence of OCD with insomnia (not sufficiently
severe to warrant a separate diagnosis) was 1.2%.These
data should be compared with the 2.5% of OCD preva-
lence in the general population.34
Sleep EEG recording
Studies comparing polysomnographic sleep EEG record-
ings from OCD patients with those of normal volunteers
are scanty and bring divergent results.Most of these stud-
ies contained a large number of patients with a comorbid
mood disorder, leaving doubt about the specificity of
their findings.59-61 The three studies found various degrees
of sleep continuity disturbances, mainly regarding sleep
maintenance. REM latency was found shortened in two
out of the three studies. Robinson et al62 investigated a
group of OCD patients free of major depression and
could not evidence any significant difference in sleep
continuity and architecture variables between patients
and healthy controls. However, slight negative correla-
tions were found between severity of obsessive-compul-
sive symptoms and total sleep time or sleep efficiency. In
summary, except for sleep maintenance disturbances,
there is at yet no clear pattern of polysomnographic find-
ings in OCD.
Treatment is generally a combination of pharmacotherapy
with serotonin-potentiating agents and behavioral therapy.
In contrast to other anxiety disorder, only drugs inhibiting
serotonin reuptake have proven their efficacy in OCD.63
According to a recent meta-analysis, clomipramine has
been demonstrated to be superior to the other drugs,64 but
poor tolerance and the lethal risk of overdose can limit
their utilization. Accordingly, SSRIs are now considered
to be first-line treatment for OCD.65 Placebo-controlled
studies have shown the efficacy of paroxetine, fluoxetine,
fluvoxamine, citalopram, and sertraline.66 Since SSRIs can
act as stimulants, especially at the doses required to treat
OCD, and induce insomnia, the concurrent use of tra-
zodone or a low-dose sedative TCA is often prescribed,
particularly for patients with a history of sleep complaints
prior pharmacotherapy.
Posttraumatic stress disorder
Neuropsychological problems following experience of a
traumatic event characterize patients suffering from
PTSD.The stressful event must have been exceptionally
threatening or catastrophic in nature, such as a natural
disaster, combat,serious accident, witnessing the violent
death of someone, or being the victim of torture or rape.
The typical features of PTSD are commonly grouped
into three catergories34: (i) reexperiencing the traumatic
event (comprising preoccupation of reliving the trauma,
intrusive memories or flashbacks,and vivid nightmares);
(ii) persistent avoidance of stimuli associated with the
trauma and numbing of general responsiveness; and (iii)
signs of increased arousal, such as hypervigilance, insom-
nia, and difficulty concentrating.Patients with PTSD may
become socially isolated and, at times, may resort the use
of drugs or alcohol to suppress the traumatic memories
and tormented wakefulness.The lifetime prevalence of
the disorder is between 1% and 9%.67 Sleep disturbances
in terms of nightmares and insomnia are a very promi-
Sleep and anxiety disorders - Staner Dialogues in Clinical Neuroscience - Vol 5 .No. 3 .2003
nent complaint of subjects who have undergone trauma;
for instance, it has been estimated that 96% of Holocaust
survivors complained of insomnia and 83% reported
recurrent nightmares.68 Pillar et al67 reported that patients
with PTSD frequently described very prolonged sleep
latencies (ie, more than 2 h), and estimate being awake
more than half of the time in bed during the night (ie, a
subjective sleep efficiency of less than 50%). More gen-
erally, it must be underlined that recurrent distressing
dreams of a traumatic event are pathognomonic of
PTSD,in the sense that they are not observed in other
disorders, contrary to complaints such as insomnia.
Sleep EEG recording
Results of studies investigating polysomnographic
recordings of patients with PTSD have been previously
reviewed67 and contrast somewhat with the prevalence of
subjective sleep complaints. Pillar et al67 concluded that
PTSD itself does not dramatically adversely affect objec-
tive sleep. Some studies found longer sleep latencies,
reduced total sleep time, and lower efficiencies among
patients with PTSD,but numerous other studies failed to
replicate this finding. SWS did not seem to be affected
during PTSD, while inconsistent results have been
reported for REM sleep: both shortening and prolonga-
tion of REM latency and lower and higher time spent in
REM were reported in PTSD.Most relevant studies in
PTSD reported on increased REM density, ie,more rapid
eye movements per REM time, a finding that could
relate to the hostile and threatening characteristics of a
dream. Some of the positive findings could be related to
comorbid psychiatric illness, such as major depression.67
Patients with PTSD generally benefit from some form of
individual or group psychotherapy, especially early in the
course of the disorder.With regard to pharmacotherapy,
SSRIs appear to be the treatment of choice and their effi-
cacy and safety have been demonstrated by meta-analysis,
while TCAs have a more modest effect on PTSD symp-
toms.66 Early in treatment, for severe cases, sedative anti-
depressant could bring relief to night terror activity. BZDs
may be helpful, but tolerance may develop because of the
chronicity of the disorder and it should be kept in mind that
the risk of associated dependence is high in these patients.
Although sleep disturbances, and particularly severe
insomnia complaints, are often encountered in patients
with anxiety disorders, polysomnographic studies docu-
mented limited alteration of sleep continuity, ie,sleep ini-
tiation and sleep maintenance. Regarding sleep architec-
ture, no clear picture emerges for specific anxiety
disorders.Discrepancies between studies could have been
related to illness severity, diagnostic comorbidity, and
duration of illness. It should be stressed that anxiety in
itself is present in many psychiatric disorders and that
therefore the assessment of anxiety as a single influence
on sleep is quite difficult. Our current preclinical under-
standing of arousal responses to aversive stress and some
confirmation that similar mechanisms may play a role in
human stress,should open the way to the development of
more specific therapeutic tools in sleep medicine, partic-
ularly for anxiety-induced sleep alterations.
Clinical research
1. Ford DE, Kamerow DB. Epidemiological study of sleep disturbances and
psychiatric disorders: an opportunity for prevention? JAMA. 1989;162:1479-
2. Breslau N, Roth T, Rosenthal L, Andreski P. Sleep disturbance and psy-
chiatric disorders: a longitudinal epidmiological study of young adults. Biol
Psychiatry. 1996;39:411-418.
3. Lesch DR, Spire JP. Clinical electroencephalography. In: Thorpy MJ, ed.
Handbook of Sleep Disorders. New York, NY: Marcel Dekker Inc; 1990:1-31.
4. Mignot E, Taheri S, Hishino S. Sleeping with the hypothalamus: emerg-
ing therapeutics targets for sleep disorders. Nat Neurosci. 2002;5:1071-1075.
5. Kent JM, Mathew SJ, Gorman JM. Molecular targets in the treatment of
anxiety. Biol Psychiatry. 2002;52:108-130.
6. Dijk DJ, Czeisler CA. Paradoxical timing of the circadian rhythm of sleep
propensity serves to consolidate sleep and wakefulness in humans. Neurosci
Lett. 1994;166:63-68.
7. Porkka-Heiskanen T, Strecker RE, Thakkar M, Bjorkum AA, Greene RW,
McCarley RW. Adenosine: a mediator of the sleep-inducing effects of pro-
longed wakefulness. Science. 1997;276:1265-1268.
8. Beuckmann CT, Yanagisawa M. Orexins: from neuropeptides to energy
homeostatis and sleep/wake regulation. J Mol Med. 2002;80:329-342.
9. Koob GF. Corticotropin-releasing factor, norepinephrine and stress. Biol
Psychiatry. 1999;46:1167-1180.
10. McEwen BS. Allostasis and allostatic load: implications for neuropsy-
chopharmacology. Neuropsychopharmacology. 2000;22:108-124.
11. Gold PW, Chroussos GP. Organisation of the stress system and its dys-
regulation in melancholic and atypical depression: high vs low CRH/NE
states. Mol Psychiatry. 2002;7:254-275.
12. Aston-Jones G, Rajkowski J, Kubiak P, Valentino R, Shipley M. Role of the
locus coeruleus in emotional activation. Prog Brain Res. 1996;107:379-402.
13. Van Reeth O, Weibel L, Spiegel K, Leproult R, Dugovic C, Maccari S.
Interactions between stress and sleep: from basic resaerch to clinical situ-
ations. Sleep Med Rev. 2000;4:201-219.
Sleep and anxiety disorders - Staner Dialogues in Clinical Neuroscience - Vol 5 .No. 3 .2003
14. Gonzales MM, Valatx JL. Effects of intracerebroventricular administration of
alpha-helical CRH (9-41) on sleep/waking cycle in rats under normal conditions
or after subjection to an acute stressful stimulus. J Sleep Res. 1997;6:164-170.
15. Cheeta S, Ruigt G, van Prosdij J, Willner P. Changes in sleep architec-
ture after mild chronic stress. Biol Psychiatry. 1997;41:419-427.
16. Marinesco S, Bonnet C, Cespuglio R. Influence of stress duration on the
sleep rebound induced by immobilisation in the rat: a possible role for cor-
ticosterone. Neuroscience. 1999;62:921-933.
17. Chang FC, Opp MR. Corticotropin-releasing hormone (CRH) as a regu-
lator of waking. Neurosci Biobehav Rev. 2001;25:445-453.
18. Somers VK, Dyken ME, Mark Al, Abboud FM. Sympathetic-nerve activ-
ity during sleep in normal subjects. N Engl J Med. 1993;328:303-307.
19. Vgontzas AN, Bixler EO, Papanicolaou DA, et al. Rapid eye movement
sleep correlates with the overall activities of the hypothalamic-pituitary-
adrenal axis and sympathetic system in healthy humans. J Clin Endocrinol
Metab. 1997;82:3278-3280.
Sueño y trastornos de ansiedad
Los trastornos del sueño particularmente el insom-
nio son altamente prevalentes en los trastornos de
ansiedad, e incluso molestias como el insomnio o
las pesadillas han sido incorporadas en las defini-
ciones de algunos trastornos de ansiedad, como el
trastorno de ansiedad generalizada y el trastorno
por estrés postraumático. En la primera parte de
esta revisión se discute la relación entre el sueño y
la ansiedad en términos de una respuesta de adap-
tación al estrés. Estudios recientes sugieren que el
sistema que implica la hormona liberadora de cor-
ticotrofina y el sistema que implica el locus ceruleus
y el sistema nervioso autónomo pueden jugar un
papel importante en la respuesta de alerta al estrés.
Se ha sugerido que estos sistemas pueden ser par-
ticularmente vulnerables al estrés prolongado o
repetido, lo que conduciría a un estado de alerta
disfuncional y estados de ansiedad patológica. Los
estudios polisomnográficos han documentado
pocas alteraciones del sueño en los trastornos de
ansiedad. Hay ciertos elementos a favor de una
alteración del sueño en el trastorno de ansiedad
generalizada, y del inicio y en el mantenimiento del
sueño en el trastorno de pánico; en cambio, los
datos son contradictorios en el trastorno obsesivo
compulsivo o en el trastorno por estrés postraumá-
tico. Finalmente, no se ha podido determinar que
alguna anormalidad del sueño se relacione de
manera específica con algún trastorno ansioso, y a
la inversa, se han encontrado resultados contradic-
torios para el mismo trastorno. Las discrepancias
entre los estudios pudieran deberse a la severidad
de la enfermedad, la comorbilidad diagnóstica o la
duración de la enfermedad. Además se sugiere una
breve aproximación terapéutica para cada tras-
torno ansioso con especial atención sobre el sueño.
Sommeil et troubles anxieux
Les perturbations du sommeil, et en particulier l’in-
somnie, sont très fréquentes dans les troubles
anxieux, et les plaintes comme l’insomnie et les cau-
chemars font même partie de la définition de cer-
tains troubles anxieux, comme le trouble anxieux
généralisé et l’état de stress posttraumatique. Dans
la première partie de cette revue de la littérature,
les relations entre sommeil et anxiété sont présen-
tées dans un contexte de réaction d'adaptation au
stress. Des études récentes suggèrent que le sys-
tème impliquant la corticolibérine et le système
impliquant le locus ceruleus et le système nerveux
autonome joueraient un rôle majeur dans la réac-
tion d'activation suite à un stress. Ces systèmes
pourraient être particulièrement vulnérables à des
stress prolongés ou répétés, ce qui serait à l’origine
d’un état d'activation dysfonctionnel et d’états
anxieux pathologiques. Les études polysomnogra-
phiques n’identifient que peu d’anomalies du som-
meil dans les troubles anxieux. Certains éléments
sont en faveur d’une perturbation du maintien du
sommeil dans le trouble anxieux généralisé et d’une
perturbation de l’endormissement et du maintien
du sommeil dans le trouble panique ; les données
sont contradictoires pour le trouble obsessionnel-
compulsif et l’état de stress posttraumatique. Enfin,
les études n’ont pu mettre en évidence des ano-
malies de l’architecture du sommeil spécifiques d’un
trouble anxieux particulier et, inversement, des
résultats contradictoires ont été rapportés pour un
même trouble anxieux. Ces discordances entre les
études proviennent probablement des différents
niveaux de sévérité de la maladie, de la comorbi-
dité psychiatrique et de la durée de la maladie. Une
brève approche thérapeutique est également pro-
posée pour chaque trouble anxieux avec une atten-
tion particulière au sommeil.
20. Dodt C, Breckling U, Derad I, Fehm HL, Born J. Plasma epinephrine and
norepinephrine concentrations of healthy humans associated with night-
time sleep and morning arousal. Hypertension. 1997;30:71-76.
21. Chapotot F, Gronfrier C, Jouny C, Muzet A, Brandenberger G. Cortisol
secretion is related to electroencephalographic alertness in humans sub-
jects during daytime wakefulness. J Clin Endocr Metab. 1998;83:4263-
22. Gronfrier C, Simon C, Piquard F, Ehrhart J, Brandenberger G.
Neuroendocrine processes underlying ultradian sleep regulation in man. J
Clin Endocr Metab. 1999;84:2686-2690.
23. Schneider-Helmert D. Twenty-four hour sleepwake function and per-
sonality pattern in chronic insomniacs and healthy controls. Sleep.
24. Stepanski E, Zorick F, Roehrs T, Young D, Roth T. Daytime alertness in
patients with chronic insomnia compared with asymptomatic control sub-
jects. Sleep. 1988;11:54-60.
25. Regenstein QH, Dambrosia J, Hallett M, Murawski B, Paine M. Daytime
alertness in patients with primary insomnia. Am J Psychiatry. 1993;150:1529-
26. Vgontzas AN, Bixler EO, Lin HM, et al. Chronic insomnia is associated
with nyctohemeral activation of the hypothalamic-pituitary-adrenal axis:
clinical implications. J Clin Endocr Metab. 2001;86:3787-3794.
27. Bonnet MH, Arand DL. Heart rate variability in insomniacs and matched
normal sleepers. Psychosom Med. 1998;60:610-615.
28. Wittchen HU, Essau CA. Epidemiology of anxiety disorders. In: Michels
R, ed. Psychiatry. Philadelphia, Pa: Lippincott; 1983;1:1-25.
29. Bixler EO, Kales A, Soldatos CR, Kales JD, Healy S. Prevalence of sleep
disorders in the Los Angeles metropolitan area. Am J Psychiatry.
30. Mellinger GD, Balter MB, Uhlenhut EH. Insomnia and its treatment.
Prevalence and correlates. Arch Gen Psychiatry. 1985;42;225-232.
31. Ohayon MM. Epidemiological study on insomnia in a general popula-
tion. Sleep. 1996:S7-S15.
32. National Centre for Health Statistics. Selected Symptoms of Psychological
Distress. US Public Health Service Publication 1000, Series 11, Number 37.
Washington, DC: US Department of Health, Education and Welfare; 1970.
33. Ohayon MM, Roth T. Place of chronic insomnia in the course of depres-
sive and anxiety disorders. J Psychiatric Res. 2003;37:9-15.
34. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
35. Sheehan DV, Ballenger J, Jacobsen G. Treatment of endogenous anxi-
ety with phobic, hysterical and hypochondriacal symptoms. Arch Gen
Psychiatry. 1980;37:51-59.
36. Mellman TA, Uhde TW. Sleep in panic and generalised anxiety disor-
der. In: Ballanger J, ed. Neurobiology of Panic Disorder. New York, NY: Alan
R. Liss; 1990:365-376.
37. Craske MG, Barlow DH. Nocturnal panic. J Nerv Ment Dis. 1989;177:160-167.
38. Mellman T, Uhde T. Sleep panic attacks: new clinical findings and the-
oretical implications. Am J Psychiatry. 1989;146:1024-1027.
39. Stein MB, Chartier M, Walker JR. Sleep in nondepressed patients with
panic disorder: 1. Systematic assesment of subjective sleep quality and sleep
disturbances. Sleep. 1993;16:724-726.
40. Craske MG, Lang AJ, Mystkowski JL, Zucker BG, Bystritsky A, Yan-Go F.
Does nocturnal panic represent a more severe form of panic disorder? J
Nerv Ment Dis. 2002;190:611-618.
41. Dube S, Jones DA, Bell J, Davies A, Ross E, Sitaram N. Interface of panic
and depression: clinical and sleep EEG correlates. Psychiatry Res.
42. Hauri PJ, Friedman M, Ravaris CL. Sleep in patients with spontaneous
panic attacks. Sleep. 1989;12:323-337.
43. Lydiard RB, Zealberg J, Laraia MT, et al. Electroencephalography dur-
ing sleep of patients with panic disorder. J Neuropsychiatry Clin Neurosci.
44. Pecknold JC, Luthe L. Sleep studies and neurochemical correlates in
panic disorder and agoraphobia. Progr Neuropsychopharmacol Biol Psychiatry.
45. Lauer CJ, Krieg JC, Garcia-Borreguero D, Ozdaglar A, Holsboer F. Panic
disorder and major depression: a comparative electroencephalographic
sleep study. Psychiatry Res. 1992;44:41-54.
46. Arriaga F, Paiva T, Matos-Pires A, Cavaglia F, Lara E, Bastos L. The sleep
of non-depressed patients with panic disorder: a comparison with normal
controls. Acta Psychiatr Scand. 1996;93:191-194.
47. Saletu-Zylharz GM, Anderer P, Berger P, Gruber G, Oberndorfer S, Saletu
B. Nonorganic insomnia in panic disorder: comparative sleep laboratory
studies with normal controls and placebo-controlled trials with alprazo-
lam. Hum Psychopharmacol Clin Exp. 2000;15:241-254.
48. Uhde TW, Roy-Byrne P, Gillin JC, et al. The sleep of patients with panic
disorder. A preliminary report. Psychiatry Res. 1984;12:251-259.
49. Stein MB, Enns MW, Kryger MH. Sleep in nondepressed patients with
panic disorder: II. Polysomnographic assessment of sleep architecture and
sleep continuity. J Affect Disord. 1993;28:1-6.
50. Taylor CB, Sheikh J, Agras WS, et al. Ambulatory heart rate changes in
patients with panic attacks. Am J Psychiatry. 1986;143:478-482.
51. Craske MG, Rowe MK. Nocturnal panic. Clin Psychol Sci Pract. 1997;4:153-
52. Labbate LA, Pollack MH, Otto MW, Langenauer S, Rosenbaum JF. Sleep
panic attacks: an association with childhood anxiety and adult psy-
chopathology. Biol Psychiatry. 1994;36:57-60.
53. Landry P, Marchand L, Mainguy N, Marchand A, Montplaisir J.
Electroencephalography during sleep of patients with nocturnal panic dis-
order. J Nerv Ment Dis. 2002;190:559-562.
54. Sloan EP, Natarajan M, Baker B, et al. Nocturnal and daytime panic
attacks. Comparison of sleep architecture, heart rate variability and
response to sodium lactate challenge. Biol Psychiatry. 1999;45:1313-1320.
55. Ohayon MM. Prevalence of DSM-IV diagnostic criteria for insomnia: dis-
tinguishing insomnia related to mental disorders from sleep disorders. J
Psychiatry Res. 1997;31:333-346.
56. Anderson DJ, Noyes R, Crowe RR. A comparison of panic disorder and
generalized anxiety disorder. Am J Psychiatry. 1984;141:572-575.
57. Hoehn-Saric R, McLeod DR. Generalised anxiety disorder in adulthood.
In: Hersen M, Last CG, eds. Handbook of Child and Adult Psychopathology: A
Longitudinal Perspective. New York, NY: Pergamon Press; 1990:247-260.
58. Monti JM, Monti D. Sleep disturbance in generalised anxiety disorder
and its treatment. Sleep Med Rev. 2000;4:263-276.
59. Rapoport J, Elkins R, Langer DH, et al. Childhood obsessive-compulsive
disorder. Arch Gen Psychiatry. 1981;138:1545-1554.
60. Insel TR, Gillin JC, Moore A, Mendelson WB, Loewenstein RJ, Murphy
DL. The sleep of patients with obsessive-compulsive disorder. Arch Gen
Psychiatry. 1982;39:1372-1377.
61. Hohagen F, Lis S, Krieger S, et al. Sleep EEG of patients with obsessive-
compulsive disorder. Eur Arch Psychiatr Clin Neurosci. 1994;243:273-278.
62. Robinson D, Walsleben J, Pollack S, Lerner G. Nocturnal polysomnog-
raphy in obsessive-compulsive disorder. Psychiatry Res. 1998;80:257-263.
63. Ellingrod VL. Pharmacotherapy of primary obsessive-compulsive disor-
der: review of the literature. Pharmacotherapy. 1998;18:936-960.
64. Ackerman DL, Greenland S. Multivariate meta-analysis of controlled
drug studies for obsessive-compulsive disorder. J Clin Psychopharmacol.
65. Goodman WK. Obsessive-compulsive disorder diagnosis and treatment.
J Clin Psychiatry. 1999;60(suppl 6):16-20.
66. Bourin M, Lambert O. Pharmacotherapy of anxious disorders. Hum
Psychopharmacol Clin Exp. 2002;17:383-400.
67. Pillar G, Malhotra A, Lavie P. Post-truamatic stress disorder and sleep
what a nightmare! Sleep Med Rev. 2000;4:183-200.
68. Kuch K, Cox BJ. Symptoms of PTSD in 124 survivors of the Holocaust.
Am J Psychiatry. 1992;149:337-340.
Clinical research
... En parallèle, s'opère la commutation de classe qui permet la modification de la conformation de Hz allant de 30 min à 4h (Bouwens et al., 2012;Golbach et al., 2015). Les études menées chez des adultes professionnellement exposés ont montré soit une augmentation du nombre de cellules NK (exposition à 50 Hz 8h/j de 1 à 5 ans) (Bonhomme-Faivre et al., 1998, 2003Tuschl et al., 2000), soit une diminution (exposition de 50 Hz, 40 à 120 V.m-1, 20h par semaine) (Boscolo et al., 2001;Del Signore et al., 2000;Di Giampaolo et al., 2006). Gobba a montré en 2009 un nombre constant de cellules NK après exposition aux EBF (3j, 8h/j), avec toutefois une diminution de l'activité lytique de ces cellules. ...
... L'anxiété observée chez nos animaux peut être un élément en lien avec une perturbation du sommeil. Effectivement, les personnes souffrant d'anxiété peuvent présenter une augmentation de la latence d'endormissement et une qualité subjective de sommeil insuffisante, voire souffrir d'insomnie (Staner, 2003 Les animaux qui avaient été exposés au bruit présentaient pendant la période nocturne une modification du ratio NREM/REM sans que la durée totale de sommeil ne soit modifiée. ...
Avec le développement des nouvelles technologies, l'exposition aux champs électromagnétiques est de plus en plus importante. En marge de ce développement, nos sociétés ont vu émerger des personnes présentant des symptômes qu'ils attribuent à une exposition aux champs électromagnétiques. Les résultats des études expérimentales antérieurs restant à controverse, l'objectif de ce travail est de voir si une exposition conjointe entre les champs électromagnétiques et le bruit conduit à une apparition ou une exacerbation des symptômes des champs électromagnétiques. Cette étude s'est portée sur différentes fonctions physiologiques chez une population juvénile : le sommeil, le système immunitaire, la prise alimentaire, la respiration et le comportement. Nos résultats montrent un comportement anxieux, une diminution de la locomotion ainsi qu'une augmentation du poids des animaux, associé à des variations dans le pattern alimentaire. Le sommeil et la respiration sont peu modifiés chez les animaux exposés aux champs électromagnétiques. Le système immunitaire des animaux exposés aux champs électromagnétiques présente des altérations au niveau du système immunitaire acquis avec une redistribution des sous-populations lymphocytaires en faveur d'une activation des cellules et de l'immunité humorale, mais sans variation du système immunitaire inné. L'altération de ce dernier système est observée lors de la co-exposition mais est différente de celle d'une exposition au bruit. Ce travail de thèse a permis de mettre en évidence différents effets des CEM, notamment un comportement anxieux et des variations immunitaire
... Studies have shown that anxiety is considered a natural psychological reaction to ongoing stress among those who care for cancer patients; it triggers a slew of other psychological problems such as sleep disturbances, especially insomnia, which are common in anxiety disorders (Staner, 2003). (Vanderwerker et al., 2005). ...
Full-text available
Carnatic raga-Bilahari based intervention is a music therapy technique that enhances relaxation and positivity by reducing anxiety. As the detrimental impacts of cancer affect the caregiver’s mental health, the present study intends to find out the effectiveness of music therapy on reducing anxiety, sleep disturbances, and somatic symptoms among the caregivers of cancer patients. A single group pre-post research design was adopted. General Health Questionnaire (GHQ-28) was used as a screening tool to select participants, and 30 participants were chosen using the purposive sampling. These individuals received instruction in listening to Carnatic music (raga-Bilahari), 5 days a week. The vocal and instrumental recordings were given on alternative days with each session lasting 15–30 min over a month of standard care. The findings show a significant difference in anxiety, sleep disturbances, somatic symptoms, and general health scores between pre-test and post-test scores. The t value obtained for general health, anxiety, sleep quality, and somatic symptoms are 8.47 (p < 0.001), 11.47 (p < 0.001), 17.38 (p < 0.001) and 10.95 (p < 0.001), respectively. The present study result thus indicates that Carnatic raga-Bilahari-based music intervention is effective among caregivers of cancer patients to reduce anxiety, sleep disturbances, somatic symptoms presentation, and their distress level.
... Thus, it becomes very difficult to associate sleep with anxiety as the sole cause directly. [53] For example, during childhood, sleep can be caused by environmental factors, parental upbringing, traumas, etc. It is known that it is easily affected, and if not treated, this condition becomes chronic. ...
Full-text available
Sleep is one of the essential requirements for maintaining human mental and cognitive function. It is not merely a condition of rest, as was previously believed. Instead, it is composed of several stages and active processes. As new sleep processes are discovered, these factors have increased concern regarding the connection between sleep and diseases. As a consequence of the research concluded, it has become known that sleep, as it comprises standard processes, has a significant role in internal and psychological disorders. It has been demonstrated to be a prognostic, diagnostic, or predictive factor in Alzheimer's disease (AD), significant depression, and anxiety disorders. Major depression also displayed a higher level of specificity than other psychiatric disorders. It has been demonstrated to play a role in other mental conditions such as schizophrenia, attention deficit hyperactivity disorder (ADHD), and autism spectrum disorder (ASD). However, research is still ongoing to elucidate its precise role in these conditions. In this review, relationship between sleep disturbance and schizophrenia, ADHD, AD, ASD, anxiety, and major depressive disorder were discussed.
... Age and sex were included as between-person level control variables. Finally, in line with studies finding that anxiety and depression may impact both HRV and sleep [26][27][28], the depression (α = 0.86) and anxiety (α = 0.65) subscales from the Depression Anxiety Stress Scale [29] were also included as control variables on the betweenperson level. ...
Full-text available
Sleep plays an essential role in maintaining employees’ health and well-being. However, stressors, such as conflict at work, may interfere with employees’ sleep. Drawing on previous literature on the relationship between conflict at work and sleep outcomes, we proposed a negative relationship between daily conflict at work and physiological changes during early sleep, particularly nocturnal heart rate variability (HRV). Furthermore, building on the perseverative cognition hypothesis, we proposed that daily work-related rumination mediates the relationship between conflict at work and nocturnal HRV. Ninety-three healthcare employees participated in a daily diary study for five workdays, resulting in 419 observations. Multilevel analysis revealed a significant relationship between daily conflict at work and nocturnal HRV, specifically high-frequency (HF) power. Daily conflict at work was found to predict rumination; however, rumination did not significantly predict nocturnal HRV. Our results suggest that daily conflict at work increases rumination during the off-job time and may directly alter nocturnal HRV, specifically parasympathetic function in early sleep.
... Prospective deep phenotyping of children who carry neuropsychiatric risk variants provides a unique opportunity to investigate how psychiatric symptoms emerge during development transdiagnostically, and to identify early endophenotypes. Indeed, sleep functioning has been identi ed as a potential endophenotype for depression (Hasler et al., 2004), and increased sleep problems have been reported in individuals with autism(Souders et al., 2009), ADHD (Corkum et al., 1998) and anxiety (Staner, 2003). There is preliminary evidence from research on 22q11.2 ...
Full-text available
Children with rare neurodevelopmental genetic conditions (ND-GCs) are at high risk for a range of neuropsychiatric conditions. Sleep symptomatology may represent a transdiagnostic risk indicator within this patient group. Here we present data from 629 children with ND-GCs, recruited via the United Kingdom’s National Health Service medical genetic clinics. Sibling controls (183) were also invited to take part. Detailed assessments were conducted to characterise the sleep phenotype of children with ND-GCs in comparison to controls. Latent class analysis was conducted to derive subgroups of children with a ND-GC based on sleep symptomatology. Assessment of cognition and psychopathology allowed investigation of whether sleep phenotypic subgroup was associated with neuropsychiatric outcomes. We found that children with a ND-GC, when compared to control siblings, were at elevated risk of insomnia (ND-GC = 41% vs Controls = 17%, p < 0.001) and of experiencing at least one sleep symptom (ND-GC = 66% vs Controls = 39%, p < 0.001). Insomnia was reported to have an average onset of 2.8 years in children with a ND-GC, and impacted across multiple contexts. Children in subgroups linked to high sleep symptomatology were also at high risk of psychiatric outcomes (OR ranging from 2.0 to 21.5 depending on psychiatric condition). Our findings demonstrate that children at high genetic vulnerability for neuropsychiatric outcomes exhibit high rates of insomnia and sleep symptomatology. Sleep disruption has wide-ranging impacts on psychosocial function, and indexes those children at greater neuropsychiatric risk. Insomnia was found to on average onset in early childhood, highlighting the potential for early intervention strategies for psychiatric risk informed by sleep profile.
... The rate of clinically relevant levels of anxiety (25.4%) was comparable to reports from Europe [58] and, according to our findings, could potentially be reduced by preventing sedimentary routines and excessive consumption of alcohol during the pandemic. Further, the close relationship between anxiety and quality of sleep measured in our study was in concordance with previous research that highlighted high rates of comorbidity between anxiety disorders (for example, generalized anxiety disorder) and sleep illnesses (such as insomnia) [59][60][61]. However, the coexistence of high levels of anxiety and sleep problems is not yet fully explained. ...
Full-text available
Background and Objectives: The COVID-19 pandemic has disrupted routine sleep and work patterns in the general population. We conducted an anonymous online survey among white-collar workers from various finance, IT and technology companies in Lithuania to define factors associated with worse sleep quality and diminished productivity during a COVID-19 lockdown. Materials and Methods: Employees of selected companies in Lithuania completed an anonymous questionnaire online that included the Pittsburgh Sleep Quality Index (PSQI), The Sleep Locus of Control (SLOC), the Generalized Anxiety Disorder Scale-7 (GAD-7), and the World Health Organization’s Health and Work Performance Questionnaire (WHO-HPQ). Respondents also provided information about their sleep hygiene, physical activity and alcohol use. Results: Data of 114 respondents (56, 49.1% male) were used for analysis. Among them, 49 (43.0%) suffered from poor sleep and 29 (25.4%) had clinically relevant levels of anxiety. However, there were only negligible levels of absenteeism in the sample (a median of zero hours of work lost over the past month). In a stepwise linear regression model (F(5,108) = 11.457, p < 0.001, R2adj = 0.316), high levels of anxiety, daily hours spent using the screen, use of electronic devices in the bedroom, smoking in the evening, and COVID-19-related changes in appetite were associated with worse sleep quality. Absenteeism was associated with physical activity of moderate intensity and decreased self-reported productivity during the pandemic (F(2,111) = 7.570, p = 0.001, R2adj = 0.104). However, there was no strong relationship between sleep-related variables (i.e., sleep hygiene, sleep locus of control, quality of sleep) or levels of anxiety and measures of work productivity. Conclusions: Our findings suggest that while bad sleep hygiene, anxiety, and changes in appetite are associated with worse sleep quality among white-collar workers during the pandemic, work productivity may remain high irrespective of disrupted sleep.
... One of the novel findings of this study is the role of early sleep difficulties as risk factors for persistent high levels of anxiety disorders. Sleep disturbances are highly prevalent in anxiety (Staner, 2003). Further, sleep problems in childhood associate with anxiety in adulthood (Gregory et al., 2005). ...
Full-text available
Background: Patterns of development and underlying factors explaining anxiety disorders in children and adolescents are under‐researched, despite their high prevalence, impact and associations with other mental disorders. We aimed to a] understand the pattern and persistence of specific anxiety disorders; b] examine differing trajectories of symptoms of specific anxiety disorders and; c] examine socio‐demographic and health‐related predictors of persistent anxiety disorder-specific symptoms, across middle childhood to early adolescence. Methods: The current study used data from 8122 participants in the Avon Longitudinal Study of Parents and Children birth cohort. The Development and Wellbeing Assessment questionnaire was administered to parents to capture child and adolescent anxiety total scores and DAWBA‐derived diagnoses. Separation anxiety, specific phobia, social anxiety, acute stress reaction, and generalized anxiety at 8, 10 and 13 years were selected. Further, we included the following socio‐demographic and health‐related predictors: sex, birth weight, sleep difficulties at 3.5 years, ethnicity, family adversity, maternal age at birth, maternal postnatal anxiety, maternal postnatal depression, maternal bonding, maternal socio‐economic status and maternal education. Results: Different anxiety disorders presented different prevalence and patterns of development over time. Further, latent class growth analyses yielded a trajectory characterized by individuals with persistent high levels of anxiety across childhood and adolescence; for specific phobia (high = 5.8%; moderate = 20.5%; low = 73.6%), social anxiety (high = 3.4%; moderate = 12.1%; low = 84.5%), acute stress reaction (high = 1.9%; low = 98.1%) and generalized anxiety (high = 5.4%; moderate = 21.7%; low = 72.9%). Finally, the risk factors associated with each of the persistent high levels of anxiety disorders were child sleeping difficulties and postnatal maternal depression and anxiety. Conclusions: Our findings show that a small group of children and young adolescents continue to suffer from frequent and severe anxiety. When considering treatment strategies for anxiety disorders in this group, children's sleep difficulties and postnatal maternal depression and anxiety need to be assessed as these may predict a more prolonged and severe course of illness.
Sleep deprivation may induce anxiety. On the other hand, anxiety disorders elicit main changes in the quality of sleep. Moreover, orexin and citalopram play a role in the modulation of insomnia and mood diseases. Thus, we planned preclinical research to evaluate the effect of combinations of orexin agents and citalopram on anxiety behavior in rapid eye movement (REM) sleep-deprived mice. For drug intracerebroventricular (i.c.v.) infusion, the guide cannula was surgically implanted in the left lateral ventricle of mice. REM sleep deprivation was conducted via water tank apparatus for 24 h. The anxiety behavior of mice was evaluated using the elevated plus maze (EPM). Our results revealed that REM sleep deprivation reduced the percentage of open arm time (%OAT) and the percentage of the open arm entries (%OAE) but not closed arm entries (locomotor activity) in the EPM test, presenting an anxiogenic response (P < 0.05). We found a sub-threshold dose of SB-334867, orexin-1 receptor antagonist, and orexin-1 which did not alter anxiety reaction in the REM sleep-deprived mice (P > 0.05). Intraperitoneal (i.p.) injections of citalopram (5 and 10 mg/kg) increased both %OAT and %OAE (P < 0.001) representing an anxiolytic effect, but not locomotor activity in the REM sleep-deprived mice. Interestingly, co-treatment of citalopram (1, 5 and 10 mg/kg; i.p.) and SB-334867 (0.1 µg/mouse; i.c.v.) potentiated the anxiolytic effect in the REM sleep-deprived mice. On the other hand, co-treatment of different dosages of citalopram along with a sub-threshold dose of orexin-1 did not alter %OAT, %OAE, and locomotor activity in the REM sleep-deprived mice. We found a synergistic anxiolytic effect of citalopram and SB-334867 in the REM sleep-deprived mice. These results suggested an interaction between citalopram and SB-334867 to prevent anxiogenic behavior in the REM sleep-deprived mice.
Kabuki syndrome (KS) is a rare epigenetic disorder caused by heterozygous loss of function variants in either KMT2D (90%) or KDM6A (10%), both involved in regulation of histone methylation. While sleep disturbance in other Mendelian disorders of the epigenetic machinery has been reported, no study has been conducted on sleep in KS. This study assessed sleep in 59 participants with KS using a validated sleep questionnaire. Participants ranged in age from 4 to 43 years old with 86% of participants having a pathogenic variant in KMT2D. In addition, data on adaptive function, behavior, anxiety, and quality of life were collected using their respective questionnaires. Some form of sleep issue was present in 71% of participants, with night‐waking, daytime sleepiness, and sleep onset delay being the most prevalent. Sleep dysfunction was positively correlated with maladaptive behaviors, anxiety levels, and decreasing quality of life. Sleep issues were not correlated with adaptive function. This study establishes sleep disturbance as a common feature of KS. Quantitative sleep measures may be a useful outcome measure for clinical trials in KS. Further, clinicians caring for those with KS should consider sleep dysfunction as an important feature that impacts overall health and well being in these patients.
Objective Depression is a risk factor for cardiovascular disease (CVD), and subgroups of people with depression may be at particularly elevated CVD risk. Lower high-frequency heart rate variability (HF HRV), which reflects diminished parasympathetic activation, is a candidate mechanism underlying the depression-CVD relationship and predicts cardiovascular events. Few studies have examined whether certain depression subgroups – such as those with co-occurring affective factors – exhibit lower HF HRV. The present study sought to assess associations between co-occurring affective factors and HF HRV in people with depression. Methods Utilizing baseline data from the 216 primary care patients with depression in the eIMPACT trial, we examined cross-sectional associations of depression's co-occurring affective factors (i.e., anxiety symptoms, hostility/anger, and trait positive affect) with HF HRV. HF HRV estimates were derived by spectral analysis from electrocardiographic data obtained during a supine rest period. Results Individual regression models adjusted for demographics and depressive symptoms revealed that anxiety symptoms (standardized regression coefficient β = −0.24, p = .002) were negatively associated with HF HRV; however, hostility/anger (β = 0.02, p = .78) and trait positive affect (β = −0.05, p = .49) were not. In a model further adjusted for hypercholesterolemia, hypertension, diabetes, body mass index, current smoking, CVD prevention medication use, and antidepressant medication use, anxiety symptoms remained negatively associated with HF HRV (β = −0.19, p = .02). Conclusion Our findings suggest that, in adults with depression, those with comorbid anxiety symptoms have lower HF HRV than those without. Co-occurring anxiety may indicate a depression subgroup at elevated CVD risk on account of diminished parasympathetic activation.
Full-text available
Although insomnia is, by far, the most commonly encountered sleep disorder in medical practice, our knowledge in regard to its neurobiology and medical significance is limited. Activation of the hypothalamic-pituitary-adrenal axis leads to arousal and sleeplessness in animals and humans; however, there is a paucity of data regarding the activity of the hypothalamic-pituitary-adrenal axis in insomniacs. We hypothesized that chronic insomnia is associated with increased plasma levels of ACTH and cortisol. Eleven young insomniacs (6 men and 5 women) and 13 healthy controls (9 men and 4 women) without sleep disturbances, matched for age and body mass index, were monitored in the sleep laboratory for 4 consecutive nights, whereas serial 24-h plasma measures of ACTH and cortisol were obtained during the fourth day. Insomniacs, compared with controls, slept poorly (significantly higher sleep latency and wake during baseline nights). The 24-h ACTH and cortisol secretions were significantly higher in insomniacs, compared with normal controls (4.2 +/- 0.3 vs. 3.3 +/- 0.3 pM, P = 0.04; and 218.0 +/- 11.0 vs. 190.4 +/- 8.3 nM, P = 0.07). Within the 24-h period, the greatest elevations were observed in the evening and first half of the night. Also, insomniacs with a high degree of objective sleep disturbance (% sleep time < 70), compared with those with a low degree of sleep disturbance, secreted a higher amount of cortisol. Pulsatile analysis revealed a significantly higher number of peaks per 24 h in insomniacs than in controls (P < 0.05), whereas cosinor analysis showed no differences in the temporal pattern of ACTH or cortisol secretion between insomniacs and controls. We conclude that insomnia is associated with an overall increase of ACTH and cortisol secretion, which, however, retains a normal circadian pattern. These findings are consistent with a disorder of central nervous system hyperarousal rather than one of sleep loss, which is usually associated with no change or decrease in cortisol secretion or a circadian disturbance. Chronic activation of the hypothalamic-pituitary-adrenal axis in insomnia suggests that insomniacs are at risk not only for mental disorders, i.e. chronic anxiety and depression, but also for significant medical morbidity associated with such activation. The therapeutic goal in insomnia should be to decrease the overall level of physiologic and emotional arousal, and not just to improve the nighttime sleep.
• Data for this report come from a nationally representative probability sample survey of noninstitutionalized adults, aged 18 to 79 years. The survey, conducted in 1979, found that insomnia afflicts 35% of all adults during the course of a year; about half of these persons experience the problem as serious. Those with serious insomnia tend to be women and older, and they are more likely than others to display high levels of psychic distress and somatic anxiety, symptoms resembling major depression, and multiple health problems. During the year prior to the survey, 2.6% of adults had used a medically prescribed hypnotic. Typically, use occurred on brief occasions, one or two days at a time, or for short durations of regular use lasting less than two weeks. The survey also found a small group of hypnotic users (11% of all users; 0.3% of all adults) who reported using the medication regularly for a year or longer. If we include anxiolytics and antidepressants, 4.3% of adults had used a medically prescribed psychotherapeutic drug that was prescribed for sleep; 3.1% had used an over-the-counter sleeping pill. The majority of serious insomniacs (85%) were untreated by either prescribed or over-the-counter medications.
Both subjective and electroencephalographic arousal diminish as a function of the duration of prior wakefulness. Data reported here suggest that the major criteria for a neural sleep factor mediating the somnogenic effects of prolonged wakefulness are satisfied by adenosine, a neuromodulator whose extracellular concentration increases with brain metabolism and which, in vitro, inhibits basal forebrain cholinergic neurons. In vivo microdialysis measurements in freely behaving cats showed that adenosine extracellular concentrations in the basal forebrain cholinergic region increased during spontaneous wakefulness as contrasted with slow wave sleep; exhibited progressive increases during sustained, prolonged wakefulness; and declined slowly during recovery sleep. Furthermore, the sleep-wakefulness profile occurring after prolonged wakefulness was mimicked by increased extracellular adenosine induced by microdialysis perfusion of an adenosine transport inhibitor in the cholinergic basal forebrain but not by perfusion in a control noncholinergic region.
As part of the National Institute of Mental Health Epidemiologic Catchment Area study, 7954 respondents were questioned at baseline and 1 year later about sleep complaints and psychiatric symptoms using the Diagnostic Interview Schedule. Of this community sample, 10.2% and 3.2% noted insomnia and hypersomnia, respectively, at the first interview. Forty percent of those with insomnia and 46.5% of those with hypersomnia had a psychiatric disorder compared with 16.4% of those with no sleep complaints. The risk of developing new major depression was much higher in those who had insomnia at both interviews compared with those without insomnia (odds ratio, 39.8; 95% confidence interval, 19.8 to 80.0). The risk of developing new major depression was much less for those who had insomnia that had resolved by the second visit (odds ratio, 1.6; 95% confidence interval, 0.5 to 5.3). Further research is needed to determine if early recognition and treatment of sleep disturbances can prevent future psychiatric disorders. (JAMA. 1989;262:1479-1484)
• Fourteen patients with obsessive-compulsive disorder (OCD) were studied with all-night sleep EEG recordings. Nine of these patients reported abnormal sleep patterns before the polygraphic study. Analysis of the sleep records disclosed significantly decreased total sleep time with more awakenings, less stage 4 sleep, decreased rapid-eye-movement (REM) efficiency, and shortened REM latency compared with those of a group of age-and sex-matched normal subjects. These abnormalities generally resembled those of an age-matched group of depressed patients, although significant differences remained. These findings suggest that such sleep abnormalities as shortened REM latency may not be entirely specific for primary affective illness. They also point to a possible biological link between OCD and affective illness.
This chapter discusses recent studies of the noradrenergic locus coeruleus (LC) system to consider its possible roles in emotion. It describes the recent studies of the effects of manipulating LC neurons on electroencephalographic (EEG) activity and attentional behavior. Emotional responses are typically measured by EEG or autonomic arousal. Emotionally arousing stimuli produce activation of the cortical EEG, and parallel activation of autonomic measures such as blood pressure, heart rate, or galvanic skin response (as commonly used in lie detector tests). Recent results link the LC both to the EEG and autonomic responses that accompany emotionally arousing events LC neuronal projections, effects of NE on LC target cells, and discharge characteristics of LC neurons in unanesthetized, unconditioned animals are reviewed. More recent studies on the effects of stress on LC neurons, and on activity of LC neurons in behaving monkeys during a conditioned attentional task are also examined. The chapter reviews new findings on afferents to the LC that indicate the status of this key noradrenergic system in brain circuitry. Although the LC is not typically considered in the context of emotion, the analysis suggests that the LC system could play an important role in the process of emotional activation.
Acute stress is a fundamental adaptive response which enables an organism to cope with daily threatening environmental stimuli. If prolonged and uncontrollable, the stress response may become inadequate and ultimately result in health damage. Animal models of stress in rodents indicate that both acute and chronic stressors have pronounced effects on sleep architecture and circadian rhythms. One major physiological response elicited by stress is activation of the hypothalamo-pituitary-adrenal axis. In both animals and humans, the hypothalamo-pituitary-adrenal axis plays an important role in sleep–wake regulation and in alterations of the sleep–wake cycle secondary to exposure to acute or chronic stressors. In humans, dysfunction of the neuroendocrine regulation of sleep can lead to severe sleep disturbances. The progressive decay of the hypothalamo-pituitary-adrenal axis in elderly people, which mimics chronic exposure to stress, may contribute to fragmented and unstable sleep in ageing. Shift workers, chronic insomniacs or patients suffering from mental disorders show abnormal hypothalamo-pituitary-adrenal secretory activity and concomitant sleep disturbances. Those sleep disorders and possible underlying mechanisms are briefly reviewed.