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This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta-analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co-morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate- to high-quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders), in treatment-resistant insomnia, for professional at-risk populations and when substantial sleep state misperception is suspected (strong recommendation, high-quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (strong recommendation, high-quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short-term treatment of insomnia (≤4 weeks; weak recommendation, moderate-quality evidence). Antihistamines, antipsychotics, melatonin and phytotherapeutics are not recommended for insomnia treatment (strong to weak recommendations, low- to very-low-quality evidence). Light therapy and exercise need to be further evaluated to judge their usefulness in the treatment of insomnia (weak recommendation, low-quality evidence). Complementary and alternative treatments (e.g. homeopathy, acupuncture) are not recommended for insomnia treatment (weak recommendation, very-low-quality evidence).
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European guideline for the diagnosis and treatment of insomnia
DIETER RIEMANN
1
, CHIARA BAGLIONI
1
, CLAUDIO BASSETTI
2
,
BJØRN BJORVATN
3
, LEJA DOLENC GROSELJ
4
,JASONG.ELLIS
5
,
COLIN A. ESPIE
6
, DIEGO GARCIA-BORREGUERO
7
, MICHAELA GJERSTAD
8
,
MARTA GONC
ßALVES
9
, ELISABETH HERTENSTEIN
1
,
MARKUS JANSSON-FR
OJ M A R K
10
, POUL J. JENNUM
11
, DAMIEN LEGER
12
,
CHRISTOPH NISSEN
1,2,13
, LIBORIO PARRINO
14
, TIINA PAUNIO
15
,
DIRK PEVERNAGIE
16
, JOHAN VERBRAECKEN
17
, HANS-G
UNTER WEEß
18
,
ADAM WICHNIAK
19
, IRINA ZAVALKO
20
, ERNA S. ARNARDOTTIR
21,
,
OANA-CLAUDIA DELEANU
22,
, BARBARA STRAZISAR
23,
, MARIELLE
ZOETMULDER
24,
and KAI SPIEGELHALDER
1
1
Department of Psychiatry and Psychotherapy, Medical Center University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg,
Germany;
2
University Hospital for Neurology, Inselspital Bern, Bern, Switzerland;
3
Department of Global Public Health and Primary Care,
University of Bergen, Bergen, Norway;
4
Institute of Clinical Neurophysiology, University Medical Center Ljubljana, Ljubljana, Slovenia;
5
Northumbria Sleep Research Laboratory, Northumbria University, Newcastle, UK;
6
Sleep and Circadian Neuroscience Institute, Nufeld
Department of Clinical Neuroscience at the University of Oxford, Oxford, UK;
7
Sleep Research Institute Madrid, Madrid, Spain;
8
Stavanger
University Hospital, Stavanger, Norway;
9
Centro de Medicina de Sono, Hospital Cuf, Porto, Portugal;
10
Department of Clinical Neuroscience,
Karolinska Institute, Stockholm, Sweden;
11
Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark;
12
Centre du
Sommeil et de la Vigilance et EA 7330 VIFASOM, Universit
eParis Descartes, Clinic Hotel-Dieu, Sorbonne Paris Cit
e, APHP, HUPC,
Hotel Dieu de Paris, Paris, France;
13
University Hospital of Psychiatry, Bern, Switzerland;
14
Department of Medicine and Surgery,
University of Parma, Parma, Italy;
15
National Institute for Health and Welfare Helsinki, Helsinki, Finland;
16
Sleep Medicine Centre,
Kempenhaeghe Foundation, Heeze, The Netherlands;
17
Multidisciplinary Sleep Disorders Centre, Antwerp University Hospital and University of
Antwerp, Edegem-Wilrijk, Belgium;
18
Sleep Center Pfalzklinikum, Klingenm
unster, Germany;
19
Sleep Medicine Center and Third Department
of Psychiatry, Institute of Psychiatry and Neurology, Warsaw, Poland;
20
Burnasyan Federal Medical Biophysical Center of the Federal Medical
Biological Agency, Moscow, Russia;
21
Sleep Measurements, National University Hospital of Iceland, Reykjavik, Iceland;
22
Institute for
Pneumology, Medical Faculty, University of Bucharest, Bucharest, Romania;
23
Centre for Sleep Disorders in Children and Adolescents, General
Hospital Celje, Ljubljana, Slovenia;
24
Department of Neurology, Bispebjerg and Frederiksberg Hospital, Copenhagen, Denmark
Keywords
evidence-based medicine, CBT-I, hypnotics
Correspondence
Dieter Riemann, Department of Clinical
Psychology and Psychophysiology, Centre for
Mental Disorders, Medical Centre University of
Freiburg, Faculty of Medicine, University of
Freiburg, Hauptstr. 5, D-79104 Freiburg,
Germany.
Tel.: ++49-761-270-69190;
fax: ++49-761-270-65230;
e-mail: dieter.riemann@uniklinik-freiburg.de
Endorsed by further representatives of the
Assembly of National Sleep Societies
Accepted in revised form 18 July 2017; received
6 June 2017
DOI: 10.1111/jsr.12594
SUMMARY
This European guideline for the diagnosis and treatment of insomnia was
developed by a task force of the European Sleep Research Society, with
the aim of providing clinical recommendations for the management of
adult patients with insomnia. The guideline is based on a systematic
review of relevant meta-analyses published till June 2016. The target
audience for this guideline includes all clinicians involved in the
management of insomnia, and the target patient population includes
adults with chronic insomnia disorder. The GRADE (Grading of Recom-
mendations Assessment, Development and Evaluation) system was
used to grade the evidence and guide recommendations. The diagnostic
procedure for insomnia, and its co-morbidities, should include a clinical
interview consisting of a sleep history (sleep habits, sleep environment,
work schedules, circadian factors), the use of sleep questionnaires and
sleep diaries, questions about somatic and mental health, a physical
examination and additional measures if indicated (i.e. blood tests,
electrocardiogram, electroencephalogram; strong recommendation,
moderate- to high-quality evidence). Polysomnography can be used to
evaluate other sleep disorders if suspected (i.e. periodic limb movement
disorder, sleep-related breathing disorders), in treatment-resistant insom-
nia, for professional at-risk populations and when substantial sleep state
ª2017 European Sleep Research Society 675
J Sleep Res. (2017) 26, 675–700 European insomnia guideline
misperception is suspected (strong recommendation, high-quality evi-
dence). Cognitive behavioural therapy for insomnia is recommended as
the rst-line treatment for chronic insomnia in adults of any age (strong
recommendation, high-quality evidence). A pharmacological intervention
can be offered if cognitive behavioural therapy for insomnia is not
sufciently effective or not available. Benzodiazepines, benzodiazepine
receptor agonists and some antidepressants are effective in the short-
term treatment of insomnia (4 weeks; weak recommendation, moder-
ate-quality evidence). Antihistamines, antipsychotics, melatonin and
phytotherapeutics are not recommended for insomnia treatment (strong
to weak recommendations, low- to very-low-quality evidence). Light
therapy and exercise need to be further evaluated to judge their
usefulness in the treatment of insomnia (weak recommendation, low-
quality evidence). Complementary and alternative treatments (e.g.
homeopathy, acupuncture) are not recommended for insomnia treatment
(weak recommendation, very-low-quality evidence).
GUIDELINE REPORT AND METHODS
This European guideline for the diagnosis and treatment of
insomnia was developed on the basis of the guideline for
insomnia by the German Sleep Society (Riemann et al.,
2017), and has been modied and extended through the
involvement of experts from various European countries and
the European Insomnia Network under the umbrella of the
European Sleep Research Society (ESRS). A more detailed
version of this guidelines report can be found in the
supplemental material.
The guideline focuses on insomnia, dened as difculties
initiating or maintaining sleep, or early morning awakening
associated with impaired daytime functioning, for example,
reduced cognitive performance, fatigue or mood distur-
bances. Thus, the target population of this guideline com-
prises patients suffering from insomnia as dened by ICD-10/
ICSD-3. This includes all subtypes of insomnia, for example,
non-organic insomnia and insomnia co-morbid with somatic
or mental disorders. The guideline addresses adult patients
(18 years). The literature on insomnia in children and
adolescents was not reviewed. This guideline reviews the
available literature with a special focus on the situation in
Europe. The guideline is meant for physicians and clinical
psychologists/psychotherapists who diagnose and treat
patients with insomnia.
Computer-based searches using PubMed (www.ncbi.nlm.
nih.gov/pubmed/) and the Cochrane Library (www.cochrane
library.com) were conducted with the following keywords:
(psychotherapy OR sleep hygiene OR relaxation OR mind-
fulness OR behaviour therapy OR cognitive therapy OR
cognitive behavioural therapy OR stimulus control OR sleep
restriction OR placebo OR benzodiazepine OR benzodi-
azepine receptor agonist OR sedating antidepressant OR
antipsychotic OR neuroleptic OR antihistamine OR herbal
therapy OR phytotherapy OR melatonin OR complementary
alternative therapy OR homeopathy) AND insomnia (search
lter set to meta-analysis). Furthermore, all issues of the
journal Sleep Medicine Reviews(until June 2016) were
screened for additional relevant publications, and the search
was expanded through identifying further publications from
references in the screened full-texts. The search included
studies conducted from January 1966 to June 2016. Studies
were required to be written in English to be included. The rst
author conducted the literature search, screened titles and
abstracts, and examined the full texts with the help of the third
and last authors. Concerning the translation of effect sizes
(Cohensd) into text form, effect sizes <0.4 were dened as a
small effect; effect sizes >0.40.8 as a good effect; effect
sizes >0.8 as a very good effect.
The GRADE (Grading of Recommendations Assessment,
Development and Evaluation; Atkins et al., 2004; Guyatt
et al., 2008) system was used to grade the evidence and
inform recommendations. The published evidence was rated
as high quality if the examined meta-analyses suggested it to
be very unlikely that further research would change our
condence in the estimate of an observed effect. In contrast,
the verdict low quality was given when the examined meta-
analyses suggested that any estimate of effect is uncertain.
Table S1 shows the classication system for the quality of
evidence according to Guyatt et al. (2008) in detail. Two
grades of recommendations were used: strongand weak.
The transformation of levels of evidence into grades of
recommendation was based on a consensus being reached
between the authors.
INSOMNIA
Aetiology and pathophysiology
This guideline primarily targets insomnia as an independent
disorder, and not as an isolated symptom or a syndrome
closely related to, or even directly caused by, other somatic
or mental disorders. The type of insomnia addressed here
closely resembles the concept of psychophysiological
insomnia as conceptualized decades ago (Hauri and Fisher,
ª2017 European Sleep Research Society
676 D. Riemann et al.
1986). Given recent developments in the DSM-5 (2013) and
ICSD-3 (2014), we will use the terms insomnia and
insomnia disorder interchangeably throughout this guideline.
Instead of the previously used dichotomy primary versus
secondary insomnia, we will follow the concept of co-
morbidity.
Several research groups have suggested aetiological and
pathophysiological models of insomnia (Espie, 2002; Espie
et al., 2006; Harvey, 2002; Levenson et al., 2015; Morin,
1993; Riemann et al., 2012, 2015). Most of these are
explicitly or implicitly based on the so-called 3Pmodel of
insomnia by Spielman et al. (1987), which postulates that
predisposing, precipitating and perpetuating factors are
involved in the aetiology of insomnia. For example, genetic
inuences (Palagini et al., 2014) or personality characteris-
tics like neuroticism or maladaptive perfectionism are seen as
predisposing factors.
Acute stressors, for example, stress at work or interper-
sonal conicts, usually trigger acute insomnia. Acute insom-
nia is very common and often a transient phenomenon, which
is relieved after cessation of the stressor (Ellis et al., 2012a;
Espie, 2002). Chronic stress exposure may also be seen as
an underlying cause for chronic insomnia. In many cases,
perpetuating factors have to come into play during the
transition from acute to chronic insomnia. Spielman et al.
(1987) suggested that maladaptive coping strategies are
perpetuating factors, for example, prolonged time in bed or
napping in order to catch up on lost sleep. While these
behaviours may appear reasonable, they can reduce sleep
pressure and may lead to chronic insomnia in the long run.
Additionally, Espie et al. (2006) have emphasized the devel-
opment of a maladaptive focus upon sleep in patients with
insomnia, whereby sleep-related attentional biases and direct
attempts to control sleep disturb the two-process bioregula-
tion of sleep (Borb
ely, 1982; Borb
ely and Achermann, 1999),
interfering with the expected default recovery to normal
sleep, following episodic stress.
The hyperarousal model of insomnia postulates that
increased arousal levels in the cognitive, emotional and
physiological domains represent both predisposing and
perpetuating factors (Perlis et al., 1997; Riemann et al.,
2010, 2015). Central to this model are results showing that
patients with insomnia have increased power in fast elec-
troencephalographic (EEG) frequencies during non-rapid eye
movement sleep. This might also be reected by an
increased cyclic alternating pattern rate (Chouvarda et al.,
2012). An increased frequency of microarousals during rapid
eye movement (REM) sleep, which contributes to the
perception of parts of REM sleep as wakefulness, has also
been observed in patients with insomnia, relative to normal
sleepers (Feige et al., 2013; Riemann et al., 2012). Neuro-
biologically, hyperarousal may be driven by a dominance of
arousal-generating brain areas relative to sleep-inducing
brain areas (Saper et al., 2005).
Cognitive models of insomnia stress the relevance of worry
and rumination in the development and maintenance of
insomnia (Harvey, 2002). Moreover, Baglioni et al. (2010)
have emphasized that patients with insomnia have an
increased emotional reactivity, which may also be of aetio-
logical relevance.
Circadian factors are important in a subgroup of individu-
als, for example in those who undertake shift work or in blind
patients, where desynchronization of the sleepwake pattern
and the circadian phase contributes to sleep initiation and
sleep maintenance difculties. This also applies to some
cases of sleep-onset insomnia in adolescents/young adults,
whereby a circadian phase delay may be the underlying
factor, and to elderly patients with early awakening, whereby
a phase advance may play a role (Abbott et al., 2016).
Denition of insomnia diagnostic classication
systems
In most European countries, use of the International Classi-
cation of Diseases (ICD-10, 1992) is mandatory for physi-
cians and clinical psychologists/psychotherapists in order to
get reimbursed through health insurance. For the diagnosis
of insomnia, the diagnostic categories Non-organic insom-
nia(F51.0) and Disorders of initiating and maintaining sleep
(insomnias)(G47.0) are relevant. The denition for non-
organic insomnia is presented in Table 1.
The diagnosis of non-organic insomnia, according to ICD-
10, is based solely on the subjective experience of aficted
individuals. No quantitative criteria for sleep-onset latency,
sleep duration, or the frequency, or duration, of nocturnal
awakenings is required. The term non-organic insomnia
refers to the fact that this sleep disorder does not have a
specic recognizable somatic disorder at its core. However,
the use of this term has been discussed critically over the last
few years in light of documented neurobiological alterations
in patients with insomnia.
DSM-5 (2013) has removed the distinction between
primary and secondary insomnia. This distinction was aimed
at differentiating pureindependent insomnia from sec-
ondaryinsomnia, i.e. insomnia being related to or even
hypothetically being caused by another somatic/mental
disorder. Instead, the new umbrella category insomnia
disorderwas introduced, which is also used in the third
Table 1 Diagnostic criteria for non-organic insomnia
(F51.0) according to ICD-10
Disturbance of sleep onset or sleep maintenance,
or poor sleep quality.
Sleep disturbances occur at least three times a week
over a period of 1 month.
The aficted individuals focus extremely on their sleep
disorder (especially during the night) and worry
about the negative consequences of insomnia.
The insufcient sleep duration and quality is coupled
with a high degree of suffering or impairs daily
activities.
ª2017 European Sleep Research Society
European guideline for the diagnosis and treatment of insomnia 677
version of the International Classication of Sleep Disorders
(ICSD-3; AASM, 2014). The decision to remove the distinc-
tion between primary and secondary insomnia was based on
an NIH conference on insomnia in 2005 (National Institutes of
Health, 2005), with the lack of evidence that treating the
primary disorder would relieve insomnia accordingly, for
example in cases of insomnia associated with depression,
being the main reason for this change.
The denition of insomnia within the ICSD-3 largely follows
that of the DSM-5. Table 2 shows the diagnostic criteria for
insomnia according to the ICSD-3. In order to receive the
diagnosis, there must be a disturbance of nocturnal sleep
(criterion A) and related daytime impairment (criterion B).
Furthermore, the sleep disorder has to occur at least 3 nights
a week for a period of 3 months to be diagnosed as a
clinically relevant disorder. If diagnostic criteria are fullled
co-morbid with a mental or somatic disorder, both disorders
are diagnosed.
As already mentioned, acute insomnia is very common and
does not need a specic treatment in all cases (Ellis et al.,
2012b). Chronic insomnia, instead, needs to be treated. The
denitions for chronicity are, however, varying. ICD-10
requires a minimum duration of 1 month, whereas the
ICSD-3 species 3 months. The authors of this guideline
endorse the use of ICSD-3 for diagnostic purposes, and
expect the development of ICD-11 will most likely follow the
conceptual innovations of ICSD-3.
Diagnostic procedure
The recommended procedure for the diagnostic management
of insomnia disorder, and its co-morbidities, is shown in
Table 3.
A medical and psychiatric/psychological anamnesis is
mandatory, and has to be tailored to the clinical picture of
the patient and his/her symptomatology. With respect to the
assessment of medical disorders, it needs to be borne in
mind that some somatic causes of insomnia can be specif-
ically treated, for example hyperthyroidism. However, even in
the case of a clear somatic cause, many patients with
insomnia develop a psychophysiological vicious cycle of
insomnia, which includes rumination, worry about the con-
sequences of poor sleep and increased physiological ten-
sion. These processes can be successfully treated in these
co-morbid cases of insomnia.
Similar considerations should be made for substance use
(e.g. alcohol/caffeine), which is important to evaluate in
patients with insomnia. In particular, alcohol consumption is a
common maladaptive self-treatment strategy in patients with
insomnia, and can contribute to sleep-maintenance difcul-
ties. Thus, alcohol consumption should be actively evaluated
and considered during treatment planning. Furthermore,
many medications can interfere with sleep. Therefore, the
use, dosage and timing of medication should also be
evaluated.
Mental disorders, especially depression, bipolar disorder or
psychosis are also frequently accompanied by sleep-onset or
sleep-maintenance difculties or early morning awakening. A
recent meta-analysis (Baglioni et al., 2016) showed that
disturbances of sleep continuity (prolonged sleep latency,
increased frequency of nocturnal awakenings, prolonged
periods of wakefulness after sleep onset) occur transdiag-
nostically in almost all mental disorders. Patients with chronic
insomnia often suffer from a co-morbid mental disorder,
which they do not spontaneously report. This may be due to
the fact that it is easier for some patients to talk about sleep
than to talk about emotional distress. Thus, the presence of
mental disorders should also be actively examined. Tired-
ness/fatigue also occurs in many mental or neurodegenera-
tive disorders. Sleepiness (presumably experienced as a
consequence of sleep loss) is usually not a symptom of
insomnia per se, but may be due to an accumulation of sleep
loss in these patients. As such, tiredness/fatigue and sleepi-
ness should also be assessed.
Table 2 Diagnostic criteria for chronic insomnia disorder
according to ICSD-3
A The patient reports, or the patients parent or
caregiver observes, one or more of the following:
1. Difculty initiating sleep.
2. Difculty maintaining sleep.
3. Waking up earlier than desired.
4. Resistance to going to bed on appropriate
schedule.
5. Difculty sleeping without parent or caregiver
intervention.
B The patient reports, or the patients parent or
caregiver observes, one or more of the following
related to the nighttime sleep difculty:
1. Fatigue/malaise.
2. Attention, concentration or memory impairment.
3. Impaired social, family, occupational or academic
performance.
4. Mood disturbance/irritability.
5. Daytime sleepiness.
6. Behavioural problems (e.g. hyperactivity,
impulsivity, aggression).
7. Reduced motivation/energy/initiative.
8. Proneness for errors/accidents.
9. Concerns about or dissatisfaction with sleep.
C The reported sleep/wake complaints cannot be
explained purely by inadequate opportunity
(i.e. enough time is allotted for sleep) or inadequate
circumstances (i.e. the environment is safe, dark,
quiet and comfortable) for sleep.
D The sleep disturbance and associated daytime
symptoms occur at least three times per week.
E The sleep disturbance and associated daytime
symptoms have been present for at
least 3 months.
F The sleep/wake difculty is not better explained
by another sleep disorder.
ª2017 European Sleep Research Society
678 D. Riemann et al.
Table 4 summarizes the major somatic and mental co-
morbidities of insomnia.
The diagnostic procedure should also include a clinical
interview consisting of a thorough sleep history (to assess
sleep hygiene behaviour, sleep habits, sleep environment
including co-sleeping arrangements, work schedules, circa-
dian factors and indications of other sleep disorders, e.g.
restless legs syndrome, sleep apnea, circadian sleepwake
disorder, etc.). The consensus sleep diary (Carney et al.,
2012), for 714 days, is also strongly recommended. More-
over, the Pittsburgh Sleep Quality Index (PSQI) can be used
to assess subjective sleep during the previous month
(Buysse et al., 1989). The PSQI, however, is not a specic
instrument for diagnosing insomnia and should not be used
for that purpose. The Insomnia Severity Index (ISI) has been
developed to assess the severity of the disorder, and has
also been shown to be a reliable and valid instrument to
detect patients with insomnia (Bastien et al., 2001). In
addition, the Bergen Insomnia Scale (Pallesen et al., 2008)
and the Sleep Condition Indicator (Espie et al., 2012) have
promising psychometric properties. An overview of the
available scales for assessing sleep, and sleep disorders,
is provided by Shahid et al. (2012). Furthermore, if indicated,
actigraphy or polysomnography should be considered.
A meta-analysis of polysomnographic studies showed that
patients with insomnia have a signicantly reduced total sleep
time, signicantly prolonged sleep-onset latencies, and an
increased number of nocturnal awakenings and amount of
time awake during the night (Baglioni et al., 2014). Further-
more, slow-wave sleep and REM sleep percentages are
reduced compared with good sleepers. However, the differ-
ences were not very pronounced, for example, total sleep time
was reduced by about 25 min. In contrast, subjective total
sleep time is reduced by about 2 h in patients with insomnia
compared with good sleepers (Feige et al., 2008). This has led
to the use of the terms pseudoinsomnia,sleep state
misperceptionor paradoxical insomnia. Many experts argue
that polysomnography is not helpful in the assessment of
insomnia because it does not correlate with the subjective
perceptions of patients. However, we suggest polysomnogra-
phy may have an additional diagnostic value becauseit does
not correlate with subjective measures and thus may deliver
information not inherent in the subjective patient report. In
addition, objective measures are mandatory to diagnose
potential co-morbid disorders (e.g. PLMD =Periodic Leg
Movement Disorder, sleep apnea), which are common. Sleep
apnea may have a complex relationship with insomnia, thus
being more than a mere co-morbidity (Sweetman et al., 2017).
Several studies suggest that the polysomnographically deter-
mined microstructure of sleep is altered in insomnia, with
increases in fast frequency power and in the number of
microarousals. These phenomena are partly independent of
the subjective experience of sleep (Riemann et al., 2015), and
may become relevant for treatment decisions in the future (see
Table 3 Diagnostic management of insomnia and its
co-morbidities
1. Medical history and examination (strong
recommendation)
The anamnesis should include caregivers if
necessary
Former and present somatic disorders (including
pain)
Substance use (medication, alcohol, caffeine,
nicotine, illegal drugs)
Physical examination
Additional measures (if indicated):
laboratory testing including, e.g. blood
count, thyroid, hepatic and renal parameters,
CRP, haemoglobin, ferritin and
vitamin B12
ECG, EEG, CT/MRT
Circadian markers (melatonin, core
body temperature)
2. Psychiatric/psychological history (strong
recommendation)
Former and present mental disorders
Personality factors
Work and partnership situation
Interpersonal conicts
3. Sleep history (strong recommendation)
History of the sleep disorder, including triggering
factors
Information from bed partner (periodic limb
movements during sleep, pauses in breathing)
Work time/circadian factors (shift- and night-work,
phase advance, delay)
Sleepwake pattern, including daytime sleep (sleep
diary, sleep questionnaires)
4. Actigraphy
In case of clinical suspicion of irregular sleepwake
schedules or circadian rhythm disorders (strong
recommendation)
To assess quantitative sleep parameters (weak
recommendation)
5. Polysomnography
In case of clinical suspicion of other sleep
disorders like periodic limb movement disorder,
sleep apnea or narcolepsy
(strong recommendation)
Treatment-resistant insomnia (strong
recommendation)
Insomnia in occupational at-risk groups,
e.g. professional drivers (strong recommendation)
In case of clinical suspicion of large discrepancy
between subjectively experienced and polysomno-
graphically measured sleep (strong
recommendation)
CRP, C-reactive protein; CT, Computed Tomography; ECG,
electrocardiogram; EEG, electroencephalogram; MRT, Magnetic
Resonance Tomography.
ª2017 European Sleep Research Society
European guideline for the diagnosis and treatment of insomnia 679
Outlook for the future). Another recent discovery concerns
differences between insomnia with, and without, an objective
short sleep duration (Fernandez-Mendoza, 2017; Vgontzas
et al., 2013). It is hypothesized that insomnia with polysomno-
graphically documented short sleep duration has primarily
biological roots and would thus respond better to biological
treatments. If this hypothesis turns out to be true, polysomnog-
raphy may become even more important in the diagnostic
procedure for insomnia.
Epidemiology
Approximately 6% of the adults in industrialized countries
suffer from chronic insomnia as a disorder (for overview, see
Ohayon, 2002), with a clear-cut preponderance of females
compared with males (Zhang and Wing, 2006) and an age-
related increase in prevalence rates. More recent data (e.g.
from Norway, the UK and Germany) indicate an increase in
the prevalence of insomnia, to about 10% of the population,
in recent years (Calem et al., 2012; Marschall et al., 2017;
Pallesen et al., 2014). Moreover, it appears that the use of
hypnotic agents has also increased signicantly over a 10-
year period (e.g. from 7% to 11% in Norway; Pallesen et al.,
2001, 2014). Table 5 shows epidemiological data on the
prevalence of insomnia, as a disorder, in 10 European
countries (no such data are available for insomnia, on the
disorder level, for the other European countries).
Table 5 demonstrates that the prevalence of insomnia
varies largely from one European country to the other. This
may be, in part, due to differences in methodological quality
between studies. At present the prevalence of insomnia, as
a disorder, in Europe, seems to vary from a minimum of
5.7% in Germany to a maximum of 19% in France. There is
only one comprehensive epidemiological study (Van de
Straat and Bracke, 2015) that employed a cross-national
approach and studied sleep problems across 16 European
countries, but only in older adults. This study did not
specically include questions to derive insomnia diagnoses,
just a single item measure of sleep problems. This study
showed that the prevalence rate for this type of sleep
problem varies from a minimum of 16.6% in Denmark to a
maximum of 31.2% in Poland. Our literature search and the
study by van de Straat and Bracke suggest an urgent need
for Pan-European cross-sectional studies to better under-
stand the size of the problem in Europe, also with respect to
co-morbidities.
Studies in general practice or medical specialty settings
deliver substantially higher prevalence rates: data from
general practice in Germany (Wittchen et al., 2001) indicate
that one-fth of the patients consulting a GP suffer from
insomnia; whereas in Norway more than 50% of GP patients
have insomnia (Bjorvatn et al., 2017).
In terms of the persistence of insomnia, there is very little
information from Europe. However, Morin et al. (2009a)
provided data on the natural course of insomnia in Canada,
and showed that approximately 70% of the patients show
persistent symptoms over the course of 1 year. In this study,
Table 4 Major co-morbidities of insomnia
Psychiatric Medical Neurological
Substance
use/dependence
Depressive disorders Chronic obstructive pulmonary
diseases
Neurodegenerative diseases Alcohol
Bipolar disorders Diabetes mellitus Fatal familial insomnia Nicotine
Generalized anxiety disorder Chronic kidney diseases Cerebrovascular diseases Caffeine
Panic disorder Human immunodeciency
virus infection
Multiple sclerosis Marijuana
Posttraumatic stress disorder Malignancy
Rheumatic disorders
Traumatic brain injury Opioids
Schizophrenia Chronic pain RLS Designer drugs
Sleep apnea Cocaine
Amphetamine
RLS, Restless Legs Syndrome.
Table 5 Prevalence of insomnia disorder in different European
countries
Country Author (year)
Sample
size
% Insomnia
diagnosis
England Calem et al. (2012) 20 503 5.8%
Finland Ohayon and
Partinen (2002)
982 11.7%
France L
eger et al. (2000) 12 778 19%
Germany Schlack et al. (2013) 7988 5.7%
Hungary Novak et al. (2004) 12 643 9%
Italy Ohayon and
Smirne (2002)
3970 7%
Norway Pallesen et al.
(2001, 2014)
2000 15.5%
Romania Voinescu and
Szent
agotai (2013)
588 15.8%
Spain Ohayon and
Sagales (2010)
4065 6.4%
Sweden Mallon et al. (2014) 1550 10.5%
ª2017 European Sleep Research Society
680 D. Riemann et al.
46% of those suffering from insomnia showed persistent
symptoms over the course of 3 years.
The prevalence of hypnotic usage, i.e. usage of benzodi-
azepines (BZ) and benzodiazepine receptor agonists
(BZRAs), varies largely from one European country to the
other. A UK study reported an increase in hypnotic usage
from 0.4% to 0.8% in the general population from 1993 to
2000 the data remained stable from 2000 to 2007 (Calem
et al., 2012). A German study described the prevalence of
having taken a hypnotic, at least once, increased from 4.7%
to 9.2% from 2009 to 2016 (Marschall et al., 2017). In
general, it is not clear how many patients with insomnia in
Europe regularly take hypnotics further research is neces-
sary to determine the exact scale of this issue.
Health risks
Several meta-analyses show that insomnia is a signicant
risk factor for cardiovascular diseases (Li et al., 2014; Meng
et al., 2013; Soet al., 2014). Specically, insomnia is a risk
factor for arterial hypertension, myocardial infarction and
chronic heart failure (Laugsand et al., 2011, 2014a; Palagini
et al., 2013). In addition, Anothaisintawee et al. (2015)
showed that insomnia is a risk factor for type 2 diabetes.
Besides insomnia itself, there is evidence suggesting that
short sleep duration (sleeping less than 6 h on average) is a
risk factor for obesity, type 2 diabetes, hypertension and
cardiovascular diseases (Bayon et al., 2014; Buxton and
Marcelli, 2010; Cappuccio et al., 2010; Faraut et al., 2012;
Patel and Hu, 2008). Consequently, short sleep duration also
increases mortality (Liu et al., 2017). However, the associa-
tion between a short sleep duration and insomnia is not yet
fully understood.
Neurological disorders are frequently co-morbid with
insomnia (Mayer et al., 2011), and insomnia may play a role
in the development of cognitive impairment (Yaffe et al.,
2014). In addition, one cross-sectional study suggests a
relationship between impaired sleep quality and cortical
atrophy in older adults (Sexton et al., 2014). More recent
work points to a general involvement of insomnia in the
development of neurodegenerative disease, especially
dementia (Osorio et al., 2011). Bassetti et al. (2015) stress
the bi-directional nature of the relationship between insomnia
and brain disorders.
Signicant evidence has been gathered with respect to the
relationship between insomnia and mental disorders (Rie-
mann and Voderholzer, 2003). In a meta-analysis, Baglioni
et al. (2011) showed that people with insomnia have an
increased risk for the development of major depressive
disorder (odds ratio 2.1), which may also lead to early
retirement (Paunio et al., 2015). Similar relationships have
been documented for insomnia complaints and suicide
ideation, suicide attempts and completed suicides (Malik
et al., 2014; Pigeon et al., 2012).
Large epidemiological studies have also demonstrated that
insomnia is a risk factor for sick leave, an increased number
of accidents in the work place (Laugsand et al., 2014b;
Sivertsen et al., 2009a,b) and motor-vehicle accidents (L
eger
et al., 2014).
Costs of insomnia
The question of the direct and indirect costs of insomnia has
been dealt with in several large, well-designed, studies (Daley
et al., 2009; L
eger and Bayon, 2010; Ozminkowski et al.,
2007). Of particular relevance to Europe, the costs of several
brain disorders in Europe were compared in 2010 (Gustavsson
et al., 2011). This study ranked sleep disorders ninth among all
neuropsychiatric disorders with respect to direct and indirect
costs. An average total sum (costs) of 790 per year, per
patient, was calculated. These overall costs were based on
individual costs calculated against the estimated prevalence of
insomnia, ranging from 6% to 12%, in the European population
(Wittchen et al., 2011). Concerning so-called DALYs (disabil-
ity-adjusted life-years), a gure of 10.3/10 000 individuals was
given for females, and 8.4/10 000 individuals for males
ranking ninth among all neuropsychiatric disorders studied.
According to WHO data, insomnia ranked 11th in the list of
most important brain disorders with respect to global burden
(Collins et al., 2011). Thus, it can be concluded that insomnia
represents a high nancial burden to European healthcare
systems, either through direct costs, i.e. costs for medication or
psychotherapeutic treatment, or indirect costs, for example,
due to sick leave or early retirement.
Treatment of insomnia
In the presence of co-morbidities, clinical judgement should
decide whether the insomnia or the co-morbid condition is
treated rst, or whether both are treated at the same time. Of
note, the grading and recommendations of all the treatment
options outlined in this section are collectively summarized in
Table 15.
Cognitive behavioural therapy for insomnia (CBT-I) and other
psychotherapeutic approaches
Cognitive behavioural therapy for insomnia usually consists
of psychoeducation/sleep hygiene, relaxation training, stim-
ulus control therapy, sleep restriction therapy and cognitive
therapy (Riemann and Perlis, 2009). Usually, CBT-I is
applied face to face (either on an individual basis or in a
group format) by a trained clinician in four-eight sessions. A
number of manuals have been published in different lan-
guages (Dutch: Verbeek and van de Laar, 2014; English:
Morin and Espie, 2004; Perlis et al., 2005; French: Goulet
et al., 2013; German: Hertenstein et al., 2015; Spiegelhalder
et al., 2011; Italian: Devoto and Violani, 2009; Norwegian:
Bjorvatn, 2013; Portuguese: Paiva, 2008; and Slovakian:
Backhaus and Riemann, 2003).
Psychoeducation/sleep hygiene. In the context of CBT-I,
psychoeducation typically includes the so-called sleep
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European guideline for the diagnosis and treatment of insomnia 681
hygiene rulesabout health practices (e.g. clockwatching,
physical exercise, substance use) and environmental factors
(e.g. light, noise, temperature) that may promote or disrupt
sleep (Hauri, 1991). Furthermore, psychoeducation includes
basic information about normal sleep and age-related
changes in sleep patterns.
Relaxation therapy. Relaxation therapy includes clinical
procedures aimed at reducing somatic tension (e.g. progres-
sive muscle relaxation, autogenic training) or intrusive
thoughts at bedtime (e.g. imagery training, meditation).
Behavioural strategies (sleep restriction, stimulus control).
Sleep restriction therapy is a method designed to curtail the
time in bed to the actual amount of sleep being achieved
(Spielman et al., 1987). For example, if a patient with
insomnia reports sleeping 6.5 h per night on average, the
initial recommended sleep window (the time from lights out
to nal arising time) would be restricted to 6.5 h (with a
minimum sleep window of 46 h being advised, even when
the average sleep time is lower; Kyle et al., 2015). On a
weekly basis, adjustments to this sleep window are made.
Time in bed is either increased by 1530 min (when sleep
efciency is >8590%), kept stable or decreased by 15
30 min (when sleep efciency is <80%), until an optimal
sleep duration is reached. It is strongly recommended that
sleep diaries be used to estimate sleep time, both before
starting sleep restriction therapy and also during follow-ups.
Stimulus control therapy is a set of behavioural instructions
designed to re-associate the bed/bedroom with sleep and to
re-establish a consistent sleepwake schedule (Bootzin,
1972): (1) go to bed only when sleepy; (2) get out of bed
when unable to sleep; (3) use the bed/bedroom only for
sleep and sex (e.g. no reading, no watching TV); (4) arise
at the same time every morning; (5) do not nap during the
day.
Cognitive therapy. Cognitive strategies are psychological
methods designed to identify, challenge and change mis-
conceptions about sleep and faulty beliefs about insomnia
and its perceived daytime consequences (Morin and Espie,
2004). These strategies include methods aimed at reducing
or preventing excessive monitoring of, and worrying about,
insomnia and its correlates or consequences.
Other psychotherapeutic approaches. Other psychothera-
peutic approaches that have been empirically investigated
include mindfulness-based treatments and hypnotherapy.
Mindfulness-based treatments are rooted in Buddhist philos-
ophy, and include stress reduction techniques and cognitive
elements (Crane et al., 2017). Hypnotherapy is also con-
ceived as a mindbody intervention bearing similarities to
meditation techniques. Hypnotherapy consists of verbal
suggestions by the therapist, which are supposed to elicit
subconscious changes (Facco, 2017; Terhune et al., 2017).
Grading of the evidence. There are 15 published meta-
analyses on the efcacy of CBT-I (Table 6). These comprise
meta-analyses of CBT-I for primaryinsomnia as well as
meta-analyses of CBT-I for co-morbid insomnia. In the latter,
it was shown that CBT-I has a positive impact on both
insomnia complaints and co-morbid symptoms.
The rst ve meta-analyses (Irwin et al., 2006; Mont-
gomery and Dennis, 2004; Morin et al., 1994; Murtagh and
Greenwood, 1995; Pallesen et al., 1998) and the meta-
analysis provided by Trauer et al. (2015) dealt with the
efcacy of CBT-I, or its components, in patients with primary
insomnia. All these meta-analyses demonstrated good ef-
cacy for CBT-I (according to our translated denition of effect
sizes) on sleep-related outcome parameters, and a good
stability of the results at follow-up assessments.
Belleville et al. (2011) showed that CBT-I has a small to
moderate effect on anxiety levels in patients with or without
clinically relevant co-morbid anxiety. Miller et al. (2014)
investigated one component of CBT-I, i.e. sleep restriction
therapy. This meta-analysis was based on only four studies,
but showed good efcacy for sleep restriction therapy. Group
CBT-I was investigated by Koffel et al. (2015). This meta-
analysis demonstrated a good efcacy for group format;
however, only eight original studies could be included. The
most recent meta-analyses addressed CBT-I for co-morbid
insomnia, i.e. insomnia in the context of mental or somatic
disorders. Geiger-Brown et al. (2015) and Wu et al. (2015a,
b) dealt with a variety of co-morbid conditions, whereas Ho
et al. (2016), Johnson et al. (2016) and Tang et al. (2015)
specically investigated insomnia in the context of posttrau-
matic stress disorder, cancer and chronic pain. These meta-
analyses showed that co-morbid insomnia also responds well
to CBT-I. Of particular importance, CBT-I, though focusing
exclusively on sleep, also had good effects on the co-morbid
conditions.
There is also evidence supporting the efcacy of brief
versions of CBT-I, for example, using two face-to-face
sessions and two telephone calls (Buysse et al., 2011) or
just one session for acute insomnia (Ellis et al., 2015). There
are also other forms of application, for example, group CBT-I
courses delivered by nurses (Espie et al., 2007).
Table 7 shows meta-analyses on the efcacy of self-help
and internet-based CBT-I. These six meta-analyses focus on
self-help CBT-I approaches (Ho et al., 2015; Van Straten and
Cuijpers, 2009), or internet-based CBT-I, for example, the
programmes sleep healthy using the internet(SHUTi;
Ritterband et al., 2009) or SLEEPIO (Espie et al., 2012).
The four meta-analyses on internet-based CBT-I showed
good treatment efcacy; however, the efcacy was lower
than for face-to-face CBT-I. One of these meta-analyses
investigated the effects of internet-based CBT-I on anxiety
and depression levels, and showed small to moderate effects
(Ye et al., 2015). A recent large randomized controlled trial
also suggested that internet-based CBT-I reduced subclinical
depression levels and may thus be used for the prevention of
depression (Christensen et al., 2016). Moreover, Thiart et al.
(2016) investigated the health economic effects of comput-
erized CBT-I (cCBT-I), concluding that it was associated with
an 87% probability of being more effective than treatment as
usual.
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682 D. Riemann et al.
Table 6 Meta-analyses on the efcacy of CBT-I
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints Effects on study endpoints
Morin et al.
(1994)
Insomnia 59/2102 CBT-I and single
components
SOL, WASO,
NOA, TST a)Good effects of CBT-I on
all parameters
b)Good follow-up results
Murtagh and
Greenwood
(1995)
Insomnia 66/2007 CBT-I and single
components
SOL, NOA,
TST, SQ a)Good effects of CBT-I on
all parameters
b)Good follow-up results
Pallesen
et al. (1998)
Insomnia,
age >50 years
13/388 CBT-I and single
components
SOL, NOA,
WASO, TST a)Good effects of CBT-I on
all parameters
b)Good follow-up results
Montgomery and
Dennis (2004)
Primary insomnia,
age >60 years
7/322 CBT-I, bright
light and
physical
exercise
SOL, TST,
SE, WASO a)Good effects of CBT-I on
sleep maintenance
b)Almost no effects of bright
light and physical exercise
Irwin
et al. (2006)
Insomnia,
age >55 years
versus younger
patients
23/NA CBT-I and single
components
SQ, SOL, TST,
SE, WASO
Medium to strong effects in
older patients
Belleville
et al. (2011)
Insomnia
with/without
co-morbid anxiety
50/2690 CBT-I Anxiety scales Moderate effects on anxiety
Okajima
et al. (2011)
Primary insomnia 14/927 CBT-I SOL, WASO, EMA,
SE, PSG, ACT
a)Good effects of CBT-I on
all parameters
b)Good follow-up results
Miller
et al. (2014)
Primary insomnia 4/192 Sleep restriction
therapy
SOL, WASO, TST,
NOA, SE, SQ
Sleep restriction alone is effective
Koffel
et al. (2015)
Insomnia 8/659 Group CBT-I SOL, WASO, SE,
SQ, TST, pain,
depression
Group CBT-I is effective
Trauer
et al. (2015)
Chronic insomnia 20/1162 CBT-I SOL, WASO,
TST, SE
Clinically relevant efcacy without
undesired side-effects
Geiger-Brown
et al. (2015)
Co-morbid
insomnia
(somatic/mental)
23/1379 CBT-I SOL, WASO,
TST, SE,
ISI, PSQI
Good efcacy; long-term effects
at 18 months
Wu et al.
(2015a)
Co-morbid
insomnia
(somatic/mental)
37/2189 CBT-I SOL, WASO,
SQ, TST,
remission,
co-morbid symptoms
Good efcacy; smaller effects on
co-morbid symptoms; better
effects for mental outcomes
Ho et al. (2016) Insomnia +PTSD 11/593 CBT-I SOL, WASO,
SE, TST,
PTSD symptoms
Good sleep effects, good effects
on PTSD symptoms
Johnson
et al. (2016)
Insomnia +cancer 8/752 CBT-I SE, WASO,
ISI, cancer
symptoms
Good sleep effects, good effects
on cancer symptoms
Tang
et al. (2015)
Insomnia +pain 11/1066 CBT-I SQ, fatigue, pain Good sleep effects, good effects
on co-morbid symptoms
ACT, actigraphy; CBT-I, cognitive behavioural therapy for insomnia; EMA, early morning awakening; ISI, insomnia severity index; NOA,
number of awakenings; PSG, polysomnography; PSQI, Pittsburgh Sleep Quality Index; PTSD, posttraumatic stress disorder; SE, sleep
efciency; SOL, sleep-onset latency; SQ, sleep quality; TST, total sleep time; WASO, wake time after sleep onset.
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European guideline for the diagnosis and treatment of insomnia 683
Two meta-analyses have been published comparing CBT-I
with pharmacotherapy. Smith et al. (2002) compared phar-
macological studies using BZ or BZRAs with psychothera-
peutic studies, and concluded that both options are
comparably effective in the short term. Mitchell et al. (2012)
analysed studies that directly compared CBT-I with pharma-
cotherapy; only ve studies fullled the inclusion criteria.
Based on this evidence, the authors concluded that CBT-I
and hypnotics have comparable efcacy in the short term,
and that CBT-I is superior in the long term.
An interesting question is whether a combination of CBT-I
with medication has synergistic effects. Two randomized
controlled trials addressed this issue using CBT-I with
temazepam or zolpidem (Morin et al., 1999, 2009b). In the
acute treatment phase, the combination of CBT-I and
pharmacotherapy appears to be slightly superior compared
with either treatment alone. However, during maintenance
treatment, discontinuation of pharmacotherapy appears to be
more favourable (Morin et al., 2009b). The authors also
present their data in terms of response/remission criteria.
According to this data evaluation, CBT-I alone led to a
positive treatment response in 60% and remission in 40% of
cases. These outcomes were stable at follow-ups or even
improved (remission at 6 months follow-up: 67.8%).
With respect to mindfulness-based treatments and hyp-
notherapy, three meta-analyses have been published (Gong
et al., 2016; Kanen et al., 2015; Lam et al., 2015). The meta-
analyses on mindfulness-based treatments noted moderate
to good effects (Gong et al., 2016; Kanen et al., 2015) on
sleep parameters. Hypnotherapy had a positive impact on
sleep-onset latency; however, the overall quality of the
studies included was poor. Thus, these treatments may be
promising but the evidence is less convincing than it is for
CBT-I.
As will be discussed in more detail in the section on
hypnotics, the placebo effect needs to be noted in the context
of the efcacy of psychotherapy. In comparison with phar-
macological research, placebo-controlled studies are more
difcult to conduct in psychotherapy research, as therapists
can usually not be blinded towards shamtherapies. Thus,
due to this methodological difculty, psychotherapy studies
may overestimate treatment efcacy.
The aforementioned evidence suggests that CBT-I is
recommended as rst-line treatment for chronic insomnia in
adults of any age (strong recommendation, high-quality
evidence; see Tables 6, 7 and 15).
Table 7 Meta-analyses on the efcacy of self-help/computerized CBT-I
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints Effects on study endpoints
Van Straten and
Cuijpers (2009)
Insomnia 10/1000 Self-help
CBT-I
SOL, WASO, SE,
SQ, TST
Small to moderate effects
Cheng and
Dizon (2012)
Insomnia 6/433 cCBT-I SOL, WASO, SE,
SQ, TST
Small to moderate effects
Ho et al. (2015) Insomnia 20/2411 Self-help +
cCBT-I
SOL, WASO, SE,
SQ, TST
Self-help CBT-I is effective
and acceptable as a starter
for treatment
Ye et al. (2015) Insomnia with
co-morbid
conditions
9/776 cCBT-I Anxiety, depression Moderate effect sizes for
co-morbid symptoms
Zachariae
et al. (2017)
Insomnia 11/1460 cCBT-I ISI, SOL, WASO,
NOA, TST, SQ
Comparable to face-to-face CBT-I
Seyffert
et al. (2016)
Insomnia 15/2392 cCBT-I ISI, SOL, TST,
WASO, NOA,
SQ, PSQI
Good efcacy for sleep parameters,
good follow-up results
CBT-I, cognitive behavioural therapy for insomnia; cCBT-I, computerized cognitive behavioural therapy for insomnia; ISI, insomnia severity
index; NOA, number of awakenings; PSQI, Pittsburgh Sleep Quality Index; SE, sleep efciency; SOL, sleep-onset latency; SQ, sleep quality;
TST, total sleep time; WASO, wake time after sleep onset.
Table 8 Major drug classes used to treat insomnia in Europe
BZ Diazepam, unitrazepam, urazepam,
lormetazepam, nitrazepam, oxazepam,
temazepam, triazolam
BZRA Zaleplone, zolpidem, zopiclone
Antidepressants Agomelatine, amitriptyline, doxepin,
mianserin, mirtazapine, trazodone,
trimipramine
Antipsychotics Chlorprothixene, levomepromazine,
melperone, olanzapine, pipamperone,
prothipendyl, quetiapine
Antihistamines Diphenhydramine, doxylamine, hydroxyzine,
promethazine
Phytotherapeutics Hops, melissa, passiora, valerian
Melatonin
receptor agonists
Melatonin, ramelteon, slow-release
melatonin
BZ, benzodiazepines; BZRA, benzodiazepine receptor agonists.
ª2017 European Sleep Research Society
684 D. Riemann et al.
Pharmacotherapy
Several overviews of hypnotics for insomnia have been
published (Riemann and Nissen, 2012). Available sub-
stances include BZ and BZRAs, antidepressants, antipsy-
chotics, antihistamines, phytotherapeutic substances and
melatonin (Table 8).
Before summarizing the efcacy of these different phar-
macological substances, we present four meta-analyses on
the placebo effects in this condition (Table 9). The three
newest of these meta-analyses concluded that there are
signicant placebo effects in clinical trials of pharmacological
treatments for insomnia. Most notably, Winkler and Rief
(2015) analysed 32 studies with 3969 participants, and found
that more than 60% of the response to medication (in most
studies BZ and BZRAs) was also observed with placebo.
This nding held true for both subjectively and polysomno-
graphically measured sleep parameters.
Grading of the evidence. Table 10 summarizes the meta-
analyses on the efcacy of BZ and BZRAs in the treatment of
insomnia. These meta-analyses clearly show that BZ and
BZRAs are effective in the short-term treatment (4 weeks)
of insomnia. Pillai et al. (2017) analysed data from one
randomized controlled trial with BZRAs according to deni-
tions of treatment response/remission, and observed positive
treatment responses in 76.7% of cases and remissions in
47.7% of participants.
Table 11 (upper panel) summarizes the meta-analyses on
the efcacy of antidepressants in the treatment of insomnia. It
should be noted that dosages for antidepressants to treat
insomnia are usually much lower than the recommended
doses for depression. Only a few randomized controlled trials
have evaluated the efcacy of these mostly sedating antide-
pressants. The authors of the rst two meta-analyses
concluded that the efcacy of sedating antidepressants is
weaker than that for BZ/BZRAs. However, McCleery et al.
(2014) described positive effects of trazodone for sleep
disorders co-morbid with Alzheimers disease. The meta-
analysis by Yeung et al. (2015) dealt exclusively with low-
dose doxepin, and showed that there are signicant effects
on subjective and polysomnographic parameters in the short
term.
There are no meta-analyses on the efcacy of antihistami-
nes in insomnia, but one systematic review concluded that
antihistamines have only a small to moderate efcacy in the
treatment of insomnia and that tolerance to these substances
develops quickly (Vande Griend and Anderson, 2012). Of
note, many sedating antidepressants (Table 11, upper panel)
probably exert their hypnotic effect through the histaminergic
system.
There are no meta-analyses on the efcacy of antipsy-
chotics in insomnia, but four related systematic reviews exist.
Monti and Monti (2004; Monti et al., 2017) and Cohrs (2008)
concluded that sedating antipsychotics increase total sleep
time and the amount of slow-wave sleep in patients with
schizophrenia. However, Anderson and Vande Griend (2014)
and Thompson et al. (2016) conclude that the evidence on
quetiapine is insufcient to recommend its use in the
treatment of insomnia, in the absence of psychiatric disor-
ders, particularly in light of its potential side-effects.
Table 11 (lower panel) summarizes the meta-analyses on
the efcacy of phytotherapeutics in the treatment of insomnia.
The authors of these publications came unanimously to the
conclusion that the methodological quality of the studies
included was poor and further studies are warranted. The
meta-analyses did not show a clinically relevant efcacy of
the investigated substances. A meta-analysis of studies
investigating Chinese herbal medicine (CHM) concluded that
CHM is superior to placebo with respect to its effect on
subjective sleep parameters and equally effective as BZ.
However, the authors of the meta-analysis emphasize the
poor quality of the original studies, which cannot be
independently assessed by the authors of this guideline
Table 9 Placebo effects in pharmacological studies on insomnia
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints Effects on study endpoints
Hr
objartsson and
Gøtzsche (2001)
40 clinical conditions
including insomnia
5/100 Placebo versus
active drug
Sleep parameters Almost no evidence that placebo
has strong effects
McCall et al. (2003) Insomnia 5/213 Placebo versus
active drug
SOL, TST Signicant placebo effects for
SOL +TST (subjective)
B
elanger
et al. (2007)
Primary insomnia 34/1392 Placebo/wait
list versus
active drug
SOL, TST, WASO,
NOA, SE/subjective
and objective
Signicant placebo effects in
pharmacological studies
Winkler and
Rief (2015)
Insomnia 32/3969 Placebo versus
active drug
Sleep parameters/
objective
and subjective
63.5% of drug response was
obtained with placebo
NOA, number of awakenings; SE, sleep efciency; SOL, sleep-onset latency; TST, total sleep time; WASO, wake time after sleep onset.
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European guideline for the diagnosis and treatment of insomnia 685
because all the original manuscripts were published in
Chinese.
Table 12 summarizes meta-analyses on the efcacy of
melatonin (including mainly fast-release preparations, but
also ramelteon and prolonged-release formulations) in the
treatment of insomnia. These meta-analyses do not provide
a uniform picture concerning the efcacy of melatonin and
the melatonin receptor agonist ramelteon. Buscemi et al.
(2005) and Ferracioli-Oda et al. (2013) reported that
melatonin reduces sleep-onset latency, which was also
demonstrated for ramelteon (Liu and Wang, 2012).
Kuriyama et al. (2014) also found signicant positive
effects of melatonin on sleep-onset latency and sleep
quality. However, the effects were small from a clinical
point of view. Some of the original studies also investigated
undesired side-effects and concluded that melatonin is a
safe drug.
The aforementioned evidence suggests that BZ and
BZRAs may be used in the short term if the rst-line
treatment (CBT-I) is ineffective or unavailable (high-quality
evidence). Some sedating antidepressants too may be used
for short-term treatment (moderate-quality evidence).
Further, antihistamines and antipsychotics are not recom-
mended for the treatment of insomnia (strong recommenda-
tion low- to very-low-quality evidence), and melatonin and
phytotherapy are not recommended for insomnia (weak
recommendation low-quality evidence; Tables 812 and
15).
Light therapy and exercise
Light exposure has been used as a powerful experimental
tool in animal research on sleepwake and circadian
rhythms, with clear-cut effects being observed on a variety
of biological outcome variables. In humans, light therapy
has been used as a treatment for seasonal affective
disorders and circadian rhythm disorders with supposedly
good clinical efcacy (Huck et al., 2014). Exercise doubt-
lessly has positive effects on psychological and physical
health, and many studies show that regular exercise
reduces mortality (Hupin et al., 2015). Of particular impor-
tance for the current guideline, both light therapy and
exercise have also been suggested to be efcacious in
patients with insomnia.
Table 10 Meta-analyses on the efcacy of BZ and BZRA in the treatment of insomnia
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints Effects on study endpoints
Nowell
et al. (1997)
Primary
insomnia
22/1894 BZ +zolpidem versus
placebo, short-term
treatment
SOL, NOA, TST, SQ Signicant improvement
of sleep
Holbrook
et al. (2000)
Primary
insomnia
45/2672 BZ +zopiclone versus
placebo, short-term
treatment
SOL, TST, USE a)Signicant improvement
of sleep
b)Increased risk for USE
D
undar
et al. (2004)
Insomnia 24/3909 BZ versus BZRA,
short-term treatment
SOL, TST, NOA,
WASO, SQ, USE
a)No difference between
substances
b)USE not analysed due to
poor data quality
Glass
et al. (2005)
Insomnia,
age >60 years
24/2417 BZ +BZRA versus
placebo, short-term
treatment
SQ, SOL, TST,
NOA, USE
a)Signicant improvement
of sleep
b)Increased risk for USE
Buscemi
et al. (2007)
Chronic
insomnia
105/5582 BZ +BZRA +sedating
antidepressants
SOL +secondary
outcomes, USE
BZ and BZRA are effective;
more USE with active
drugs versus placebo
Huedo-Medina
et al. (2012)
Insomnia 13/4378 BZRA (zolpidem,
zaleplone,
eszopiclone)
SOL +secondary
outcomes
Small but signicant
effects on subjective
and objective SOL
Winkler
et al. (2014)
Insomnia 31/3820 BZ, BZRA, sedating
antidepressants,
melatonin
Polysomnographic and
subjective sleep
parameters
BZ and BZRA have
signicant effects on
subjective and objective
outcomes; smaller
effects for
antidepressants
BZ, benzodiazepines; BZRA, benzodiazepine receptor agonists; NOA, number of awakenings; SOL, sleep-onset latency; SQ, sleep quality;
TST, total sleep time; USE, undesired side-effects; WASO, wake time after sleep onset.
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Grading of the evidence. Van Maanen et al. (2016) inves-
tigated the impact of light therapy on insomnia, and found
small to moderate effects of this treatment on sleep param-
eters. Kredlow et al. (2015) investigated the effects of
different exercise regimes on sleep in good and poor
sleepers. While moderately positive effects were shown on
several sleep parameters, it has to be stressed that most
original studies did not focus on clinically relevant insomnia.
Given the fact that both light therapy and exercise are
supported by extensive basic and public health research,
further studies should be devoted to delineate their effects in
patients with insomnia.
The aforementioned evidence suggests that light therapy
and/or exercise may be useful adjuvant therapies for insom-
nia (weak recommendation low-quality evidence;
Table 15).
Complementary and alternative medicine
In the area of complementary and alternative medicine,
several treatments for insomnia have been suggested,
including acupuncture, acupressure, aromatherapy, foot
reexology, homeopathy, meditative movement therapies,
moxibustion, music therapy and yoga.
Grading of the evidence. Table 13 summarizes meta-
analyses and systematic reviews on the efcacy of comple-
mentary and alternative treatments for insomnia. Overall, the
studies underlying this evidence are methodologically poor
and thus difcult to evaluate. There is some evidence
suggesting that acupuncture is effective (Cao et al., 2009;
Cheuk et al., 2012; Lan et al., 2015; Sarris and Byrne, 2011).
However, evaluation of the studies on this topic is difcult for
the authors of this guideline because most of the original
articles are published in Chinese. The authors of all of the
above-mentioned meta-analyses have stressed caution due
to the quality of the original studies. There is no evidence
supporting the efcacy of aromatherapy or homeopathy.
Three meta-analyses on music therapy (Jespersen et al.,
2015; de Niet et al., 2009; Wang et al., 2016) exist and
suggest a potential positive effect of this treatment. However,
the methodological quality of these studies is questionable. A
similar picture arises for foot reexology, moxibustion and
meditative movement therapies, including yoga. These
Table 11 Meta-analyses on the efcacy of sedating antidepressants and phytotherapeutic interventions in the treatment of insomnia
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints Effects on study endpoints
Sedating antidepressants
Buscemi
et al. (2007)
Chronic
insomnia
105/873 BZ +BZRA +sedating
antidepressants
SOL Sedating antidepressants are
less effective than BZ/BZRA
Winkler
et al. (2014)
Insomnia 31/3820 BZ +BZRA +sedating
antidepressants +
melatonin
Subjective and
objective
sleep parameters
Sedating antidepressants are
less effective than BZ/BZRA
McCleery
et al. (2014)
Insomnia
co-morbid with
M. Alzheimer
5/313 Trazodone +melatonin +
ramelteon
SOL, TST,
WASO, SE
Trazodone improves
TST and SE
Yeung
et al. (2015)
Insomnia 9/1983 Low-dose doxepin Subjective and
objective
sleep parameters
Small to moderate effects for
sleep maintenance and TST,
but no effects for SOL
Phytotherapeutic interventions
Bent
et al. (2006)
Insomnia 16/1093 Valerian versus placebo,
short-term treatment
SQ, SOL a)Slight improvement for
sleep quality
b)No improvement of other
sleep parameters
c)Poor quality of studies
Fern
andez-
San-Mart
ın
et al. (2010)
Insomnia 18/1317 Valerian versus placebo SQ No effects on quantitative
parameters, slight
effects for SQ
Leach and
Page (2015)
Insomnia 14/1602 Valerian, chamomile,
kava, wuling
SOL, SE,
TST, SQ
No signicant effects
Ni et al. (2015) Insomnia 76/7240 CHM versus placebo
versus BZ
PSQI, CGI CHM better than placebo,
but poor quality
of studies
BZ, benzodiazepines; BZRA, benzodiazepine receptor agonists; CGI, clinical global impression; CHM, Chinese herbal medicine; PSQI,
Pittsburgh Sleep Quality Index; SE, sleep efciency; SOL, sleep-onset latency; SQ, sleep quality; TST, total sleep time; WASO, wake time
after sleep onset.
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treatments may have potential; however, the poor quality of
many of the original studies (as noted by the authors of the
meta-analyses) makes it difcult to reach clear conclusions.
The aforementioned evidence suggests that complemen-
tary and alternative treatments for insomnia are not recom-
mended (weak recommendation very-low-quality evidence;
Tables 13 and 15).
Long-term treatment of insomnia with hypnotics
The pharmacological literature summarized above dealt with
the short-term treatment of insomnia (4 weeks). The
rationale for this is that the hypnotics available are exclu-
sively indicated, and approved, only for short-term treatment
in most European countries. Arguably, however, the long-
term treatment of insomnia using hypnotics is clinically
relevant because insomnia typically returns following with-
drawal. Table 14 summarizes the results of studies that
investigated the long-term use of hypnotics (for at least
12 weeks) for insomnia.
These long-term studies show that the efcacy of hyp-
notics may remain stable over longer periods of administra-
tion. However, in some studies the effects decreased over
time. Moreover, it has to be noted that some of the
investigated substances, i.e. eszopiclone, zolpidem SR,
ramelteon and suvorexant, are not available in Europe. To
circumvent the possible risks of chronic hypnotic usage,
such as dependence and rebound insomnia, some authors
have suggested intermittent use especially for BZ and
BZRAs (Parrino et al., 2008). However, there are no meta-
analyses examining the effects of intermittent use of
hypnotics on insomnia. An alternative solution, suggested
by Voshaar et al. (2006), is to employ counselling interven-
tions including, where necessary, CBT-I during discontinua-
tion. In general, hypnotic discontinuation should be based on
slowly tapering off medication, supporting patients during this
sometimes difcult period with counselling, CBT-I or, if
necessary, alternative medications (e.g. sedating antide-
pressants).
Based upon the evidence, BZ and BZRAs are not
recommended in the longer-term treatment of insomnia
(strong recommendation low-quality evidence; Tables 14
and 15).
Risks and side-effects of insomnia treatment
The side-effects of CBT-I have not been thoroughly investi-
gated yet. However, Kyle et al. (2011, 2014) stress that
sleep restriction, as one component of CBT-I, leads to
transient increases in somnolence and fatigue and
Table 12 Meta-analyses on the efcacy of melatonin and melatonin receptor agonists in the treatment of insomnia
Author (year) Population
Number of
studies/number
of patients Intervention Study endpoints
Effects on study
endpoints
Brzezinski
et al. (2005)
Different populations
including insomnia
17/284 Melatonin 0.340 mg
versus placebo
SOL, TST, SE SOL ; TST ;SE
Buscemi
et al. (2005)
Primary sleep disorders 14/425 Melatonin 15mg
versus placebo
SOL, WASO, TST,
SE, SQ, USE
SOL ; best effect in
sleep phase delay
Buscemi
et al. (2006)
Secondary sleep
disorders
15/524 Melatonin 110 mg
versus placebo
SOL, USE No effect on SOL
No USE
Braam
et al. (2009)
Sleep problems with
intellectual dysfunction
9/183 Melatonin 0.59mg
versus placebo
SOL, TST, NOA SOL ; TST ; NOA
Geijlswijk
et al. (2010)
Delayed sleep
phase syndrome
9/317 Melatonin 0.35mg
versus placebo
DLMO, SOL, TST Phase advance DLMO,
improved sleep
Ferracioli-Oda
et al. (2013)
Primary sleep disorders 19/1683 Melatonin
110 mg
versus placebo
SOL, TST, SQ Moderate effects on
sleep continuity
Liu and
Wang (2012)
Chronic insomnia 8/4055 Ramelteon 432 mg
versus placebo
SOL, USE Positive effects on
subjective/objective
SOL/no USE
McCleery
et al. (2014)
Insomnia with
M. Alzheimer
5/313 Trazodon, melatonin,
ramelteon
SOL, TST, WASO, SE No evidence supporting
melatonin/ramelteon
Kuriyama
et al. (2014)
Insomnia 13/5812 Ramelteon SOL, TST, SQ SOL ;SQ; clinically
small effects
Zhang
et al. (2016)
Sleep disorders with
neurodegenerative
disorders
9/370 Melatonin PSQI Positive effects on
PSQI and RBD
DLMO, dim light melatonin onset; NOA, number of awakenings; PSQI, Pittsburgh Sleep Quality Index; RBD, rapid eye movement sleep
behaviour disorder; SE, sleep efciency; SOL, sleep-onset latency; SQ, sleep quality; TST, total sleep time; USE, undesired side-effects;
WASO, wake time after sleep onset.
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688 D. Riemann et al.
Table 13 Complementary and alternative medicine in the treatment of insomnia
Author (year) Population
Number of
studies/
number
of patients Intervention Study endpoints Effects on study endpoints
Acupuncture
Chen
et al. (2007)
Insomnia (primary
and secondary)
6/673 Auricular acupuncture TST, reduction
of insomnia
Positive effects for
acupuncture, but poor
quality of studies
Cheuk
et al. (2012)
Insomnia 33/2293 Acupuncture versus no
treatment versus pseudo-
acupuncture
PSQI Not interpretable because
of poor quality of studies
Yeung
et al. (2012)
Insomnia (primary
and secondary)
40/4115 Acupuncture, reexology,
ear acupuncture versus
school medicine/sham/sleep
hygiene/music therapy/routine
treatment
PSQI, SRSS,
effect rate,
GHQ-28, STAI,
AIS, BDI,
PFS, sleep diary
Acupuncture marginally
better than sham
treatment; ear
acupuncture versus sham
questionable; each
intervention better than
routine treatment
Lan
et al. (2015)
Poor sleepers 15/1429 Auricular acupuncture versus
sham acupuncture
versus placebo
Response
rate, PSG,
sleep diaries
positiveeffects of
acupuncture, poor quality
of studies
Lee and
Lim (2016)
Insomnia
post-stroke
13/1051 Acupuncture (TCM) versus
sham acupuncture
versus drugs
PSQI, ISI, AIS,
TCM standards
Acupuncture better than
drugs, poor quality
of studies
Aromatherapy
Hwang and
Shin (2015)
Different groups 12/704 Aromatherapy versus control Sleep disorder Highly signicant
improvement of sleep
(poor quality of studies)
Homeopathy
Cooper and
Relton (2010)
Insomnia 4/199 Individualized homeopathy
versus placebo
SOL, TST, SQ, etc. Trendsfor homeopathic
medicine, no signicant
changes of sleep,
poor quality of studies
Ernst
et al. (2011)
Insomnia 6/263 Individualized homeopathy
versus placebo
TST, SQ, etc. No effects, poor quality
of studies
Moxibustion
Sun
et al. (2016b)
Primary insomnia 22/1971 Moxibustion versus
Western medications, TCM
Clinical effective rateModerate effects,
poor quality of studies
Music therapy
Wang
et al. (2016)
Heterogenous
samples
with acute
or chronic
sleep problems
10/557 Passive music consumption RCSQ, PSG, VAS,
VSH, PSQI
Positive effects
on sleep quality
Jespersen
et al. (2015)
Insomnia 6/340 Music therapy versus no
treatment versus TAU
PSQI Increase of sleep quality,
reduction of PSQI scores
Oil
Lillehei and
Halcon (2014)
Sleep
disturbances
15/? Essential oil Different outcomes Essential oils could be
helpful with minor
sleep problems
Reex zone massage
Lee
et al. (2011)
Different target
groups
44/1860 Reex zone massage
versus control
Fatigue, pain, sleep Good effect strengths
for sleep
Yoga/Tai Chi/Chi Gong
Wang
et al. (2016)
Insomnia 17/1880 MM versus wait list PSQI, SQ Increase of sleep quality,
poor quality of studies
Wu et al.
(2015b)
Insomnia
(>60 years)
14/1225 MM versus control group PSQI Improved sleep quality,
heterogeneous quality
of studies
AIS, Athens Insomnia Scale; BDI, Beck Depression Inventory; GHQ-28, General Health Questionnaire; ISI, Insomnia Severity Index; MM,
meditative movement=yoga, Tai Chi, Chi Gong; PFS, Piper Fatigue Scale; PSG, polysomnography; PSQI, Pittsburgh Sleep Quality Index;
RCSQ, RichardsCampbell Sleep Questionnaire; SOL, sleep-onset latency; SQ, sleep quality; SRSS, Self-Rating Scale on Sleep; STAI,
State Trait Anxiety Inventory; TAU, Treatment As Usual; TCM, traditional Chinese medicine; TST, total sleep time; VAS, visual analogue
scale; VSH, Verran SnyderHalpern Sleep Scale.
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European guideline for the diagnosis and treatment of insomnia 689
objectively impaired vigilance. As such, sleep restriction
therapy can only be recommended without restrictions when
there are no safety concerns, for example, sleep restriction
may be contraindicated in professional drivers. Similar side-
effects can also be expected with stimulus control therapy. A
more detailed and critical evaluation of the undesired effects
of CBT-I is suggested.
With respect to hypnotics, a variety of side-effects have
been reported, including hangover, nocturnal confusion, falls,
rebound insomnia, tolerance and dependency (Hoffmann,
2013; Kapil et al., 2014; Uhlenhuth et al., 1999). These side-
effects are often aggravated by multi-pharmacy, especially in
older adults. It is undisputed that BZ and BZRA have the
potential for tolerance and dependency. However, there are
little data available on the number of patients who will
become dependent when taking BZ or BZRA for a certain
period of time. Hallfors and Saxe (1993) showed in one meta-
analysis that substances with short half-lives induce depen-
dency more quickly. Moreover, the acute cognitive effects of
zopiclone, zolpidem, zaleplone and eszopiclone were
Table 14 Placebo-controlled studies on the long-term intake (at least 12 weeks) of hypnotics
Author (year) Sample Substance
Duration of
treatment Tolerance
Abuse
dependency Rebound
Other
undesired
side-effects
Krystal
et al. (2003)
N=593 (ESZ)
N=195 (PLA)
3 mg eszopiclone
(39.5% dropouts)
Placebo (43.3%
dropouts)
6 months –– no (no detailed
analysis)
moderate
Perlis
et al. (2004)
N=98 (ZOLP)
N=101 (PLA)
10 mg zolpidem
(18.4% dropouts)
Placebo (20.7%
dropouts)
12 weeks –– no moderate
Roth
et al. (2005)
N=471 (ESZ) Open label ext.
ESZ: 17.8% dropouts
PLA: 22.5% dropouts
6+6 months –– not indicated moderate
Walsh
et al. (2007)
N=548 (ESZ)
N=280 (PLA)
3 mg eszopiclone
(37% dropouts)
Placebo (52%
dropouts)
6 months –– no questionable moderate
Krystal
et al. (2008)
N=669 (ZOLP)
N=349 (PLA)
12.5 mg zolpidem SR
(35.3% dropouts)
Placebo (47.6%
dropouts)
24 weeks –– no questionable moderate
Mayer
et al. (2009)
N=227 (RAM)
N=224 (PLA)
8 mg ramelteon
(30% dropouts)
Placebo (21.4%
dropouts)
6 months –– no questionable moderate
Ancoli-Israel
et al. (2010)
N=194 (ESZ)
N=194 (PLA)
2 mg eszopiclone
(24.2% dropouts)
Placebo (elderly)
(23.7% dropouts)
12 weeks –– no questionable moderate
Krystal
et al. (2010)
N=159 (DOX)
N=81 (PLA)
1/3 mg doxepin
(10% dropouts)
Placebo (14%
dropouts)
12 weeks –– no moderate
Roehrs
et al. (2011)
N=17 (ZOLP)
N=16 (PLA)
5/10 mg zolpidem
(17.6% dropouts)
Placebo (12.5%
dropouts)
12 months no dose
escalation
no indication no indication
Randall
et al. (2012)
N=60 (ZOLP)
N=65 (PLA)
10 mg zolpidem
(26.7% dropouts)
Placebo (27.6%
dropouts)
8 months –– no indication no indication
Uchimura
et al. (2012)
N=164 (ESZ)
N=161 (ESZ)
1/2/3 mg eszopiclone
(about 15% dropouts)
24 weeks –– no questionable moderate
Michelson
et al. (2014)
N=522 (SUV)
N=259 (PLA)
30/40 mg suvorexant
(38% dropouts)
Placebo (37%
dropouts)
12 months –– no but stronger
under suvorexant
moderate
cave:
hypersomnia
ª2017 European Sleep Research Society
690 D. Riemann et al.
Table 15 Recommendations
Diagnostic management of insomnia and its co-morbidities
The diagnostic procedure for insomnia should include a clinical interview consisting of a thorough evaluation of the
current sleepwake behaviour and sleep history as well as questions about somatic and mental disorders, a physical
examination, the use of sleep questionnaires and sleep diaries, and, if indicated, additional measures (blood test, ECG,
EEG, CT/MRT, circadian markers; strong recommendation, moderate- to high-quality evidence).
It is recommended to actively ask for medication and other substance use (alcohol, caffeine, nicotine, illegal drugs),
which may disturb sleep (strong recommendation, high-quality evidence).
Sleep diaries or actigraphy can be used in case of clinical suspicion of irregular sleepwake schedules or circadian
rhythm disorders (strong recommendation, high-quality evidence), and actigraphy can be used to assess quantitative
sleep parameters (weak recommendation, high-quality evidence).
Polysomnography is recommended when there is clinical suspicion of other sleep disorders, like periodic limb
movement disorder, sleep apnea or narcolepsy, treatment-resistant insomnia, insomnia in occupational at-risk
groups, or suspicion of a large discrepancy between subjectively experienced and polysomnographically
measured sleep (strong recommendation, high-quality evidence).
Treatment
In the presence of co-morbidities, clinical judgement should decide whether insomnia or the co-morbid condition is treated
rst, or whether both are treated at the same time.CBT-I
CBT-I is recommended as rst-line treatment for chronic insomnia in adults of any age (strong recommendation,
high-quality evidence).
Pharmacological interventions
A pharmacological intervention can be offered if CBT-I is not effective or not available.
BZ and BZRA
BZ and BZRA are effective in the short-term treatment of insomnia (4 weeks; high-quality evidence).
The newer BZRA are equally effective as BZ (moderate-quality evidence).
BZ/BZRA with shorter half-lives may have less side-effects concerning sedation in the morning (moderate-quality
evidence).
Long-term treatment of insomnia with BZ or BZRA is not generally recommended because of a lack of evidence and
possible side-effects/risks (strong recommendation, low-quality evidence). In patients using medication on a daily basis,
reduction to intermittent dosing is strongly recommended (strong recommendation, low-quality evidence).
Sedating antidepressants
Sedating antidepressants are effective in the short-term treatment of insomnia; contraindications have to be carefully
considered (moderate-quality evidence). Long-term treatment of insomnia with sedating antidepressants is not generally
recommended because of a lack of evidence and possible side-effects/risks (strong recommendation,
low-quality evidence).
Antihistaminics
Because of insufcient evidence, antihistaminics are not recommended for insomnia treatment (strong recommendation,
low-quality evidence).
Antipsychotics
Because of insufcient evidence and in light of their side-effects, antipsychotics are not recommended for insomnia
treatment (strong recommendation, very low-quality evidence).
Melatonin
Melatonin is not generally recommended for the treatment of insomnia because of low efcacy (weak recommendation,
low-quality evidence).
Phytotherapy
Valerian and other phytotherapeutics are not recommended for the treatment of insomnia because of poor evidence
(weak recommendation, low-quality evidence).
Light therapy and exercise
Light therapy and exercise regimes may be useful as adjunct therapies (weak recommendation, low-quality evidence).
Complementary and alternative medicine
Acupuncture, aromatherapy, foot reexology, homeopathy, meditative movement, moxibustion and yoga are not
recommended for the treatment of insomnia because of poor evidence (weak recommendation, very low-quality
evidence).
BZ, benzodiazepine; BZRA, benzodiazepine receptor agonist; CBT-I, cognitive behavioural therapy for insomnia; CT, Computed
Tomography; ECG, electrocardiogram; EEG, electroencephalogram; MRT, Magnetic Resonance Tomography.
ª2017 European Sleep Research Society
European guideline for the diagnosis and treatment of insomnia 691
examined in one meta-analysis by Stranks and Crowe
(2014). On the basis of their ndings, they suggest zolpidem
and zopiclone have signicant negative effects on next-day
cognitive performance. Other notable results with respect to
the negative impact of BZRAs include: Tom et al. (2016),
who reported that use of zolpidem was associated with
greater risk of hip fracture and traumatic brain injury than
eszopiclone; Sun et al. (2016a) who demonstrated a signif-
icant relationship between zolpidem use and suicide
attempts, as well as completed suicides; and Joya et al.
(2009) who showed an increased risk for minor infections
with the use of eszopiclone and zolpidem, compared with
placebo. In terms of cognitive effects after withdrawal from
long-term BZ use, one meta-analysis showed that negative
effects might last up to 6 months (Barker et al., 2004). In light
of the evidence, Glass et al. (2005) conclude that the
undesired side-effects outweighed the benets of BZ/BZRA
use in the elderly >60 years.
Three meta-analyses have been published on the effects
of BZ and BZRAs on driving abilities. Verster et al. (2006)
showed that BZ and zopiclone lead to impaired driving
abilities. Further, Rapoport et al. (2009) and Dassanayake
et al. (2011) showed a signicant correlation between BZ use
and accidents. A combination of alcohol use and BZ intake
further increases the risk for accidents. Of note, sedating
antidepressants also increase the risk of accidents.
It has been discussed, albeit controversially, whether BZ
and BZRA increase the risk for mortality. In terms of the
existing evidence, Palmaro et al. (2015) conducted an
analysis of two large cohort studies from France
(n=60 000 patients) and UK (n=90 000 patients). These
authors showed that the occasional intake of BZ was
associated with an increase in mortality. Moreover, data from
the American Cancer Society suggest that the combination of
insomnia with the intake of hypnotics may be associated with
an increased mortality (Kripke, 2009, 2011, 2013; Kripke
Clinical algorithm
Figure 1. Clinical algorithm for the diagnosis and treatment of insomnia. If a patient suffers from sleep onset/sleep maintenance/early morning
awakening disturbances and associated daytime impairment, he/she is a candidate for applying this guideline. If the symptoms are not severe
enough to qualify for clinically signicant impairment, psychoeducative/preventive interventions should be applied (e.g. sleep hygiene). If the
symptoms are clinically signicant, the clinician, following the diagnostic process outlined in Table 3, should check for possible circadian
underpinnings, substance intake (e.g. alcohol) and somatic and mental co-morbidities. Positive results in any of these areas should lead to
corresponding interventions (i.e. insomnia coupled with high intake of alcohol: abstinence from alcohol, etc.). The sequence of treatments
(insomnia versus its co-morbidities), i.e. consecutive versus simultaneous, is determined by the clinician. Cognitive behavioural therapy for
insomnia (CBT-I) should always be considered as rst-line treatment, medications like benzodiazepines (BZ), benzodiazepine receptor agonists
(BZRA) or sedating antidepressants are recommended only for short-term use. [Colour gure can be viewed at wileyonlinelibrary.com]
ª2017 European Sleep Research Society
692 D. Riemann et al.
et al., 1979, 2002). Further research (Frandsen et al., 2014;
Jennum et al., 2015, 2016) investigated mortality associated
with the use of BZ, antidepressants and antipsychotics in
patients with Parkinsons disease, dementia and stroke.
These studies also showed an increased mortality in those
using psychotropic agents.
RECOMMENDATIONS
Our overall recommendations for the diagnosis and therapy
of insomnia are presented in Table 15. Additionally, a clinical
algorithm for the diagnostic and therapeutic process is
summarized in Fig. 1.
Please note that these recommendations largely corre-
spond to the guidelines for insomnia treatment of the
American College of Physicians (ACP, 2016). Both guideli-
nes recommend CBT-I as rst-line treatment for insomnia.
Concerning the pharmacological treatment of insomnia, an
American Academy of Sleep Medicine guideline gave a
weakrecommendation for orexin receptor antagonists, BZ,
BZRAs, doxepine and ramelteon to treat insomnia (Sateia
et al., 2017). Substances like trazodone, tiagabine, diphen-
hydramine, melatonin, tryptophan and valerian were explicitly
not recommended in this guideline.
OUTLOOK FOR THE FUTURE
Cognitive behavioural therapy for insomnia, though being
the rst-line treatment for insomnia, is not easily available.
It is assumed that only a minority of patients with chronic
insomnia will receive this treatment in Europe. Thus, the
widespread implementation of CBT-I will be a major
challenge for the future. Apart from physicians and
clinical psychologists/psychotherapists, other health profes-
sionals (e.g. nurses) should be trained in CBT-I. Further-
more, web-based delivery of CBT-I may offer a chance to
improve the healthcare situation for patients with insomnia
in Europe.
The efcacy of the different components of CBT-I as
standalone interventions has been rarely investigated or
compared. Thus, more work is necessary to dismantle the
effects of these components in randomized controlled stud-
ies. In addition, the impact of CBT-I on daytime function in
those with insomnia has been scarcely investigated.
With respect to new psychotherapeutic approaches,
further research is needed to evaluate mindfulness-based
treatments and hypnotherapy. Furthermore, these
approaches, in addition to other techniques, should be
explored, especially in those who do not respond to
traditional CBT-I. For example, one pilot study indicated
that Acceptance and Commitment Therapy (ACT; Herten-
stein et al., 2014) might be a useful alternative for non-
responders. Another innovative approach consists of
intensive sleep retraining (Harris et al., 2012). This very
brief therapeutic approach is realized in the sleep labora-
tory, and can be utilized over a period of 25 h and is
thought to be based on a reconditioning of sleep. The
positive effects of a rst randomized controlled trial (Harris
et al., 2012) also raise questions about the potential of
sleep deprivation in the context of insomnia treatment.
With respect to the most frequently used drugs for
insomnia, BZ and BZRAs, the question of efcacy and
side-effects of long-term treatment should be addressed in
naturalistic studies. It would be especially helpful to know
before the rst prescription, which patient will abuse these
substances or become dependent on them.
Newer hypnotic drugs like ramelteon or suvorexant have
been introduced into the healthcare system of the USA, but
not in Europe. In particular, it remains an open question
whether the orexin receptor antagonists will be available on
the European market in the near future. Other drugs that are
sometimes used for the treatment of insomnia, like tiagabine
and pregabalin, have not been subjected to thorough testing
concerning their efcacy and side-effects further research is
needed here.
Light therapy and exercise may be useful treatment
approaches for insomnia, and it is unlikely that these
treatments produce severe side-effects. Light therapy has
clear effects on several biological parameters. In this context
it is also suggested that further research into circadian
underpinnings of insomnia might be helpful to gain new
insights into its pathophysiology. However, the efcacy for
those with insomnia remains to be seen. Similarly, exercise is
a well-established strategy for improving general health.
However, whether it has specic effects on insomnia remains
unclear.
Very new treatments include brain cooling and electros-
timulation. A brain-cooling device has been introduced on to
the market in the USA recently (Nofzinger and Buysse,
2011). Electrostimulation has been shown to induce slow-
wave sleep in experimental studies, and it has been tested
in good sleepers and poor sleepers with mixed effects
(Frase et al., 2016, 2017). Further research needs to be
conducted and published on the efcacy of these treat-
ments.
ACKNOWLEDGEMENTS
The authors would like to express their gratitude to the
European Sleep Research Society and its current board
members (Walter McNicholas, Tiina Paunio, Tom de Boer,
Lino Nobili, Philippe Peigneux, Hans-Peter Landolt, Pierre-
Herv
e Luppi) for their condence and the nancial support
provided (travel costs for the Frankfurt consensus meeting,
31 March, 2017), and critical feedback during the process of
developing the guideline.
ª2017 European Sleep Research Society
European guideline for the diagnosis and treatment of insomnia 693
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Payments for speaking
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consulting (ABC),
royalties (R), etc.
Financial activities
outside the topic Patents/copyrights
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payments
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SUPPORTING INFORMATION
Additional Supporting Information may be found online in the
supporting information tab for this article:
Table S1. Classication of the quality of evidence accord-
ing to the GRADE system (Guyatt et al., 2008).
Table S2. QUORUM checklist.
ª2017 European Sleep Research Society
700 D. Riemann et al.
... Insomnia is an extremely common sleep disorder that affects a large proportion of people worldwide. The prevalence of insomnia in the United States and Europe is 10-22 and 5-19% (1, 2), respectively, and is more commonly observed in women and older adults (2,3). In China, ∼15% of the population is diagnosed with insomnia (4), and 45% of the population reportedly experienced varying degrees of insomnia symptoms in a given month (5). ...
... Pharmacological treatments, such as benzodiazepines (BZDs), non-benzodiazepine receptor agonists (nBZRAs), antidepressants, antipsychotics, melatonin receptor agonists (MRAs), and orexin receptor antagonists (ORAs), are recommended if non-pharmacological therapies are ineffective (2,7,8). However, inappropriate use of these medications causes an increased risk of abuse, dependency, drug tolerance, dysmnesia, daytime sleepiness, hospitalizations, and death (9,10). ...
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Background:The inappropriate use of pharmacological treatments for insomnia may increase patients' risk of serious adverse events. However, few epidemiological studies on the use of medications for insomnia in China have been conducted to date.Objective We aimed to investigate the current pharmacological treatments for insomnia and guide the rational use of drugs.Methods The prescription data of outpatients with insomnia between 2015 and 2019 in Zhejiang province were extracted from the Hospital Prescription Analysis Cooperative Project of China and evaluated. The demographic characteristics of insomnia and the proportion and prescription trends of different drugs were analyzed along with multidrug combinations for insomnia.ResultsThe number of patients with insomnia who were prescribed medications for insomnia increased from 2,385 in 2015 to 3,919 in 2019, with an increase of 64.32%, whereas the mean age of these patients decreased from 64.07 years to 60.94 years. There were nearly 1.42 times as many female patients prescribed medications for insomnia as male patients, and female patients tended to be younger than male patients. Benzodiazepines (53.99%) were the most common type of medicine for insomnia. The incidence of benzodiazepine usage decreased significantly yearly (P < 0.01), whereas the incidences of non-benzodiazepine receptor agonist (nBZRA) and antidepressant usage increased (P < 0.05). The most common benzodiazepine, nBZRA, antidepressant, and antipsychotic were estazolam, zolpidem, trazodone, and olanzapine, respectively. A total of 13.97% of outpatients with insomnia were prescribed multiple drugs for insomnia, even though nearly half of the drug combinations had similar pharmacological mechanisms.Conclusions Benzodiazepines remained the most common medication for insomnia, but the prescription rates of nBZRAs and antidepressants increased. Attention should be paid to multidrug combinations for insomnia, which may lead to an increased risk of serious adverse effects.
... Hypnotics do produce modest, clinically-relevant reductions in sleep latency [3], but at the expense of side-effects, dependency, and risk of abuse. Consequently, cognitive behavioural therapy for insomnia (CBT-I) is increasingly recommended as a first-line treatment [4,5]. However, some recent studies suggest that combining CBT-I with managed, short-term zolpidem can increase the rate of symptom improvement [6,7]; but see [4]. ...
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Benzodiazepines and ‘Z-drugs’ (including zolpidem and zopiclone) are GABAA receptor (GABAAR) positive modulators commonly prescribed as hypnotics to treat insomnia and/or anxiety. However, alongside sedation, augmenting GABAAR function may also alter coordinated neuronal activity during sleep, thereby influencing sleep-dependent processes including memory consolidation. We used simultaneous recordings of neural population activity from the medial prelimbic cortex (PrL) and CA1 of the dorsal hippocampus (dCA1) of naturally sleeping rats to detail the effects of zolpidem on network activity during the cardinal oscillations of non-REM sleep. For comparison, we also characterized the effects of diazepam and 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP/gaboxadol), which acts predominantly at extra-synaptic GABAARs. Zolpidem and THIP significantly increased the amplitudes of slow-waves, which were attenuated by diazepam. Zolpidem increased hippocampal ripple density whereas diazepam decreased both ripple density and intrinsic frequency. While none of the drugs affected thalamocortical spindles in isolation, zolpidem augmented the temporal coordination between slow-waves and spindles. At the cellular level, analyses of spiking activity from 523 PrL and 579 dCA1 neurons revealed that zolpidem significantly enhanced synchronized pauses in cortical firing during slow-wave down states, while increasing correlated activity within and between dCA1 and PrL populations. Of the drugs compared here, zolpidem was unique in augmenting coordinated activity within and between hippocampus and neocortex during non-REM sleep. Zolpidem’s enhancement of hippocampal-prefrontal coupling may reflect the cellular basis of its potential to modulate offline memory processing.
... Because the relationship between insomnia and pain intensity has been regarded as bidirectional [7][8][9], the management of insomnia in people with LBP has the potential to improve both sleep and pain. International guidelines recommend cognitive behavioral therapy (CBT-i) as the first line of care for insomnia [10][11][12][13][14][15]. A recent systematic review conducted by our group concluded that the use of face to face CBT-i for insomnia for people with comorbid chronic LBP reduced insomnia severity (Pittsburgh Sleep Quality Index = − 3.90/21, 95% CI [− 5.65, − 2.15]) and pain intensity (visual analog scale = − 8.49/100, 95% CI [− 16.46, − 0.53] ) [16]. ...
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Background Digital cognitive behavioral therapy for insomnia (CBT-i) in people with low back pain (LBP) may be efficacious in improving both sleep and pain; and twin trial designs provide greater precision of treatment effects by accounting for genetic and early environmental factors. We aimed to determine the feasibility of a trial investigating the efficacy of a digital CBT-i program in people with comorbid symptoms of insomnia and LBP, in twins and people from the general community (singletons). Methods Thirty-two twins (16 pairs) and 66 singletons with comorbid symptoms of insomnia and LBP (> 6 weeks duration) were randomized to digital CBT-i (intervention) or educational program (control) for 6 weeks. The digital CBT-I, Sleepio (developed by Big Health Inc.), was an online interactive, automated, personalized course comprising of six sessions, once a week. The education program was six emails with general sleep information, once a week. Participants were blinded to their group allocation and offered the alternative intervention at the completion of the study. Feasibility outcomes included recruitment and follow-up rates, data collection and outcome measure completion, contamination (communication about trial interventions), acceptability (adherence), credibility, and participants’ experience of the intervention. Results Sixteen out of 722 contacted twin pairs were recruited (recruitment rate = 2.2%). Twins were recruited between September 2015 and August 2018 (35 months) and singletons between October 2017 and Aug 2018 (10 months). Follow-up rates for post-intervention and 3-month follow-up were 81% and 72% for twins and 82% and 78% for singletons respectively. Adherence rates (percentage of sessions completed out of six) for the digital CBT-i were 63% for twins and 55% for singletons. Contamination (speaking about the study to each other) was present in two twin pairs (13%). Written or verbal feedback ( n = 21) regarding the digital CBT-i intervention from participants were positive ( n = 11), neutral ( n = 5), or negative ( n = 6). Conclusions Online CBT-i was received favorably with people with comorbid symptoms of insomnia and LBP. While the online data collection was successful, strategies need to be implemented to improve adherence, follow-up, control group credibility (for digital CBT-i), and twin recruitment rates (for twin trials). Trial registration Australian New Zealand Clinical Trials Registry ( ACTRN12615000672550 ). Registered 29 June 2015
... Insomnia treatment can be psychological, pharmacological or both. Cognitive-behavioral therapies (CBT) are the first-line treatment for insomnia and focuses on the psychological, behavioral, and cognitive factors that maintain or exacerbate sleep disorders (Morin et al., 2017;Riemann et al., 2017). A recent clinical practice guideline (Buysse et al., 2017) recommended eszopiclone, zaleplon, zolpidem, triazolam, temazepam, and ramelteon for sleep-onset insomnia in adults. ...
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Over the past few decades, research has suggested that cognitive variables play a key role in sleep disorders, particularly, in insomnia. The SLOC (Sleep Locus of Control Scale) evaluates the sleep locus of control, which is associated with the degree to which an individual attributes her/his experiences of sleep to chance or internal causes. The aim of this study was to develop the first translation and adaptation of the SLOC into the European Portuguese, as well as to analyze its psychometric properties. In this study, it was recruited a sample of 2029 Portuguese Higher Education students, aged ≥ 18 years, where approximately 75% of the sample were women and 25% men. The results showed that the SLOC had acceptable internal consistency value (α = .64), considering that it is a measure with a reduced number of items. As in the original study, a principal component analysis with varimax rotation identified two components. A parallel analysis was also conducted, identifying two factors. The correlation between the two subscales “internal sleep locus of control” and “chance sleep locus of control” was positive albeit of low magnitude (r = .15). Through the analysis carried out, it was also observed that individuals with “insomnia”, relative to those without, had a more chance sleep locus of control. Overall, these findings show similarities with the original study. The SLOC seems to be a useful psychological assessment measure to be used in clinical and research settings.
Article
Objectives Significant research has shown that health is a heterogeneous concept, and one person's poor health may not be comparable with another's. Yet, little consideration has been given to whether sleep quality judgments are also heterogeneous or whether they cohere between individuals. Another possibility is that there are group differences in the ways in which sleep quality is perceived. If this is the case, it is possible known inequalities in sleep are—in part—an artifact of social position influencing how we conceive of sleep problems. The current study explores this possibility. Design Cross-sectional, using World Health Organization data from 207,608 individuals; aged between 15 and 101 years of age from 68 countries. Alongside a battery of sleep and demographic variables, data contained sleep and energy vignettes. Random effect anchoring vignette models were applied to investigate interpersonal incompatibility and whether sleep quality perceptions operate differently depending on social location, context, and function. Results While sleep quality judgments are largely comparable across individuals, findings also highlight how the relationship between education and self-reported sleep changes following adjustment for reporting heterogeneity. Estimates of threshold parameters suggest that those with more years of education have a slightly increased threshold for reporting mild sleep problems (B 0.005; s.e. 0.001) but a lower threshold for reporting sleep problems as extreme (B -0.007; s.e. 0.001). Conclusions Sleep quality judgments occupy a complex position between heterogeneity and coherence. This has implications for both epidemiological methodologies and contemporary debates about social justice, public health and sleep.
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This paper reports the preliminary findings of a cross-disciplinary research on emotions, insomnia and mental health with joint efforts from linguistic, computer science, and medical researchers. We take a computational linguistic approach to analyze a corpus of over 400 posts crawled from online psychological consultation platforms in China that complaint about insomnia problems, with annotations for the psychiatric conditions of post contributors made by professional psychiatrists. Based on results of our automatic analysis of six basic emotions in the posts and their intensity levels, logistic regression and artificial neural network models were successfully performed to predict the mental health conditions of post contributors. Relevance analysis were further run to explore the associations among emotion types and between emotions and the psychiatric disorders of depression and anxiety. Depression and anxiety were found to have divergent association patterns with the basic emotion types. Overall, the findings support the previous hypothesis that emotions modulate insomnia and psychiatric disorders, and have important linguistic and clinical implications.
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Background: Insomnia in depression is common and difficult to resolve. Unresolved depression-related sleep disturbances increase risk of relapse at high costs for individuals and society. Trials have suggested music for insomnia in various populations, but there is little research on the effectiveness of music for depression-related insomnia. Methods: We examined the efficacy of a music intervention on insomnia, depression symptoms and quality of life in adults with depression-related insomnia. A two-armed randomized controlled trial was conducted, including depression outpatients with insomnia (n = 112) in a 1:1 ratio to music intervention and waitlist control group. The intervention group listened to music at bedtime for 4 weeks. Participants received treatment as usual during 8 weeks with assessments at baseline, at 4 and 8 weeks. The primary outcome measure was Pittsburgh Sleep Quality Index (PSQI), secondary outcomes comprised Actigraphy, the Hamilton Depression Rating Scale (HAMD-17) and World Health Organisation well-being questionnaires (WHO-5, WHOQOL-BREF). Results: The music intervention group experienced significant improvements in sleep quality and well-being at 4 weeks according to global PSQI scores (effect size = -2.1, 95%CI -3.3; -0.9) and WHO-5 scores (effect size 8.4, 95%CI 2.7;14.0). At 8 weeks, i.e. 4 weeks after termination of the music intervention, the improvement in global PSQI scores had decreased (effect size = -0.1, 95%CI -1.3; 1.1). Actigraphy sleep assessments showed no changes and there was no detection of change in depression symptoms. Conclusions: Music intervention is suggested as a safe and moderately effective sleep aid in depression-related insomnia. Trial registration: Clinicaltrials.gov. ID NCT03676491.
Article
Sleep disturbances are common in pregnancy and affect sleep quality. The maternal body is going through constant physical and physiological changes to adapt to the growing fetus. Sleep disorders may manifest at any point during pregnancy; some may result in adverse maternal or fetal outcomes. A strong clinical suspicion is crucial to identify sleep disorders in pregnancy and their management should be evaluated with a multidisciplinary team approach. In this review, we provide an overview of changes in sleep during pregnancy and summarise the key features of common sleep disorders in pregnancy, including practical tips on their management. Educational aims To provide an overview of common sleep disorders in pregnancy and their management options. To highlight the impact of the physiological changes in pregnancy on sleep. To outline the type of sleep studies available to investigate sleep disorders in pregnancy.
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Hypnosis and meditation, as a whole, form a heterogeneous complex of psychosomatic techniques able to control mind and body regulation. Hypnosis has been pragmatically used for limited therapeutic targets, while Eastern meditation has much wider philosophical and existential implications, aiming for a radical liberation from all illusions, attachments, suffering and pain. The available data on the history, phenomenology, and neuropsychology of hypnosis and meditation show several common features, such as the following: (a) induction based on focused attention; (b) capability to reach an intentional control of both biologic-somatic activities and conscious-unconscious processes; (c) activation/deactivation of several brain areas and circuits (e.g., the default modality network and pain neuromatrix) with a relevant overlapping between the two. Copyright
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There has been an explosion of interest in mindfulness-based programs (MBPs) such as Mindfulness-Based Stress Reduction (MBSR) and Mindfulness-Based Cognitive Therapy. This is demonstrated in increased research, implementation of MBPs in healthcare, educational, criminal justice and workplace settings, and in mainstream interest. For the sustainable development of the field there is a need to articulate a definition of what an MBP is and what it is not. This paper provides a framework to define the essential characteristics of the family of MBPs originating from the parent program MBSR, and the processes which inform adaptations of MBPs for different populations or contexts. The framework addresses the essential characteristics of the program and of teacher. MBPs: are informed by theories and practices that draw from a confluence of contemplative traditions, science, and the major disciplines of medicine, psychology and education; underpinned by a model of human experience which addresses the causes of human distress and the pathways to relieving it; develop a new relationship with experience characterized by present moment focus, decentering and an approach orientation; catalyze the development of qualities such as joy, compassion, wisdom, equanimity and greater attentional, emotional and behavioral self-regulation, and engage participants in a sustained intensive training in mindfulness meditation practice, in an experiential inquiry-based learning process and in exercises to develop understanding. The paper's aim is to support clarity, which will in turn support the systematic development of MBP research, and the integrity of the field during the process of implementation in the mainstream.
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Introduction: The purpose of this guideline is to establish clinical practice recommendations for the pharmacologic treatment of chronic insomnia in adults, when such treatment is clinically indicated. Unlike previous meta-analyses, which focused on broad classes of drugs, this guideline focuses on individual drugscommonly used to treat insomnia. It includes drugs that are FDA-approved for the treatment of insomnia,as well as several drugs commonly used to treat insomnia without an FDA indication for this condition. This guideline should be used in conjunction with other AASM guidelines on the evaluation and treatmentof chronic insomnia in adults. Methods: The American Academy of Sleep Medicine commissioned a task force of five experts in sleep medicine. A systematic review was conducted to identify randomized controlled trials, and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) process was used to assess the evidence. The task force developed recommendations and assigned strengths based on the quality of evidence, the balance of benefits and harms, and patient values and preferences. Literature reviews are provided for those pharmacologic agents for which sufficient evidence was available to establish recommendations. The AASM Board of Directors approved the final recommendations.
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If ever a book could be called timely, this is it. Sleep disorders medicine has made rapid advances in recent years. The field has attained growing respectability, with a textbook recently published, a congressionally man­ dated National Commission on Sleep Disorders Research, and a growing public awareness of the importance of sleep disorders. However, this rapid growth has made the discrepancy among certain components of the field all the more obvious. Thus, we find that patients who complain of insom­ nia are almost never in the majority of those seen in sleep disorders centers, in spite of the well-known fact that the prevalence of such individ­ uals in our society is by far the largest. Current articles on insomnia abound, but they tend to be facile recitations of diagnosis and impractical global recommendations for treat­ ment, without providing the essential details. Indeed, the clinical profes­ sions really do not know what to do about insomnia. This is reflected in a number of observations I have made in the recent past. For example, the majority of individuals who complain of insomnia take alcohol, aspirin, over-the-counter medications, hot baths, and a host of other nostrums, but rarely seek a physician. In the unlikely event that a physician is consulted, he is likely to prescribe a sleep medication but without any particular consistency, or any clear instructions on its use.