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Restless legs syndrome
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Further reading
• Allen RP, et al. (2013). Thalamic glutamate/glutamine in restless legs syndrome: increased
and related to disturbed sleep. Neurology; 80: 2028–2034.
• Allen RP, et al. (2014). Restless legs syndrome/Willis–Ekbom disease diagnostic criteria:
updated International Restless Legs Syndrome Study Group (IRLSSG) consensus criteria –
history, rationale, description, and significance. Sleep Med; 15: 860–873.
• Allen RP, et al. (2018). Evidence-based and consensus clinical practice guidelines for the iron
treatment of restless legs syndrome/Willis–Ekbom disease in adults and children: an IRLSSG
task force report. Sleep Med; 41: 27–44.
• Beliveau V, et al. (2022). Revisiting brain iron deficiency in restless legs syndrome using
magnetic resonance imaging. Neuroimage Clin; 34: 103024.
• Chiaro G, et al. (2019). Restless legs syndrome, periodic limb movements during sleep and
cardiovascular risk. Auton Neurosci; 220: 102554.
• Frauscher B, et al. (2014). Motor events during healthy sleep: a quantitative polysomnographic
study. Sleep; 37: 763–773.
• Garcia-Borreguero D, et al. (2016). Guidelines for the first-line treatment of restless legs
syndrome/Willis–Ekbom disease, prevention and treatment of dopaminergic augmentation:
a combined task force of the IRLSSG, EURLSSG, and the RLS-foundation. Sleep Med; 21: 1–11.
• Khachatryan SG, et al. (2022). Restless legs syndrome: over 50 years of European contribution.
J Sleep Res; 31: e13632.
• Manconi M, et al. (2021). Restless legs syndrome. Nat Rev Dis Primers; 7: 80.
• Pennestri M-H, et al. (2006). PLMS and PLMW in healthy subjects as a function of age:
prevalence and interval distribution. Sleep; 29: 1183–1187.
• Picchietti DL, et al. (2015). Consensus clinical practice guidelines for the diagnosis and
treatment of restless legs syndrome/Willis–Ekbom disease during pregnancy and lactation.
Sleep Med Rev; 22: 64–77.
• Salminen AV, et al. (2014). Peripheral hypoxia in restless legs syndrome (Willis–Ekbom
disease). Neurology; 82: 1856–1861.
• Schormair B, et al. (2017). Identification of novel risk loci for restless legs syndrome in
genome-wide association studies in individuals of European ancestry: a meta-analysis. Lancet
Neurol; 16: 898–907.
• Trenkwalder C, et al. (2016). Restless legs syndrome associated with major diseases:
a systematic review and new concept. Neurology; 86: 1336–1343.
• Wipper B, et al. (2021). The long-term psychiatric and cardiovascular morbidity and mortality
of restless legs syndrome and periodic limb movements of sleep. Sleep Med Clin; 16: 279–288.
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Narcolepsy and idiopathic
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hypersomnia
Ulf Kallweit and Ambra Stefani
Narcolepsy and idiopathic hypersomnia (IH) are classified as central disorders of
hypersomnolence. All are rare neurological disorders. Narcolepsy is classified into
types 1 and 2. Type 1 refers to the presence of cataplexy and orexin deficiency. In very
rare cases, narcolepsy may be symptomatic of/secondary to other central nervous
system disorders.
Clinical presentation
Narcolepsy and IH share EDS as a key symptom. Although they are not exclusive,
some dierences in the phenotypes of these disorders do exist.
Narcoleptic patients oen describe the inability to stay awake and sleep attacks. Short
napping (<30 min) oen is described as refreshing and leading to wakefulness for some
hours. Nocturnal sleep is oen fragmented and intensive dreaming is present. Cataplexy
is a specific feature of narcolepsy (type 1). Other symptoms such as sleep-related
hallucinations or sleep paralysis oen occur in narcolepsy but can also be present in IH.
In IH, an extensive need for sleep (>10 h per night) is a key symptom. Sleep eciency
is usually high (>90%) and nocturnal sleep is only rarely disturbed. Furthermore,
patients oen have severe diculties in waking up in the morning. During the
daytime, a ‘low’ level of wakefulness is frequently described. Daytime sleep duration
is oen also long (>90 min) and not reported to improve wakefulness aerwards.
Diagnosis
Diagnostic criteria include clinical features (chronic EDS, cataplexy for narcolepsy
type 1), sleep laboratory examinations (PSG, MSLT, actigraphy) and optional laboratory
Key points
• Narcolepsy is a disorder of sleep–wake instability and presents with EDS, the
inability to stay awake, disturbed nocturnal sleep and other REM-associated
phenomena.
• Excessive quantity of sleep, daytime sleepiness and sleep inertia are key
features of IH.
• Management of narcolepsy and IH includes nonpharmacological therapies
and treatment with stimulants, wake-promoting agents and oxybates.
325ERS Handbook: Respiratory Sleep Medicine
Narcolepsy and idiopathic hypersomnia
https://t.me/medicina_free
examinations (orexin measurement in cerebrospinal fluid (CSF) for narcolepsy type 1).
For narcolepsy, apart from chronic EDS (and cataplexy for type 1), key diagnostic
measures include the appearance of more than one sleep-onset REM (SOREM) episode
during the MSLT or PSG. Orexin deficiency in CSF clearly points to type 1 narcolepsy.
For IH, chronic EDS and either (or both) mean sleep latency (MSL) on MSLT of ≤8 min
and/or an objective measurement of long sleep (>11 h) by PSG and/or actigraphy is
mandatory. In IH, no SOREM episodes occur. For diagnosis of narcolepsy and IH, it is
very important to exclude sleep deprivation and also other sleep disorders (e.g. OSA).
Aetiology and pathogenesis
Narcolepsy is suggested to be the result of an (auto)immune process occurring in
genetically predisposed individuals (HLA-DQB1*0602 haplotype) upon triggering by
environmental factors (e.g. H1N1 influenza infection) that would lead to a selective
Table 1. Frequently used medicines for narcolepsy in adults
Drug name Maximum dosage
per day
Half-life
(h)
European Medicines
Agency-approved
therapeutic indications
(ocial text)
Modafinil 400 mg 15 Treatment of excessive
sleepiness associated with
narcolepsy with or without
cataplexy in adults
Pitolisant (Wakix) 36 mg 10–12 Treatment of narcolepsy
with or without cataplexy
in adults
Sodium oxybate
(e.g. Xyrem)
9 g 3–4 Treatment of narcolepsy
with cataplexy in adult
patients
Solriamfetol
(Sunosi)
150 mg 7.1 To improve wakefulness
and reduce EDS in adult
patients with narcolepsy
(with or without cataplexy)
Venlafaxine# (SSRI
antidepressant)
For cataplexy
usually not higher
15 O-label
than 150 mg
Clomipramine¶
(tricyclic
antidepressant)
Methylphenidate 60 mg 3
Usually not higher
than 50 mg for
cataplexy
21 O-label
§
O-label (only in a few
European countries f for
EDS in narcolepsy)
Dexamphetamine+
(as an example
of amphetamine
derivatives)
#
: details for other selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine
reuptake inhibitors (SNRIs) must be checked individually; ¶: details for other tricyclics must be
checked individually; +: details for other amphetamines must be checked individually; §: depends on
whether immediate-release or extended-release; f: only approved in a few countries, but also not
available in all countries. Data from Bassetti et al. (2021).
60 mg (in the
morning and/or
at noon, or on
demand)
11 O-label
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Narcolepsy and idiopathic hypersomnia
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loss of orexin-producing neurons in the lateral hypothalamus of the brain. Orexin is
of major importance for state (i.e. wakefulness, REM sleep, NREM sleep) boundary
control (sleep–wake stability) and sustained wakefulness in particular. For IH, some
data indicate a potential genetic component, but the details are not yet known.
Management
Treatment of narcolepsy includes counselling, self-care, behavioural strategies,
psychological treatment and pharmacological therapies. For behavioural strategies,
the strongest recommendations are made for scheduled napping during the daytime.
A regular sleep–wake rhythm is also recommended. Some data additionally indicate
an improvement of EDS with a low-carbohydrate diet and by regular physical exercise.
European guidelines for the pharmacological management of narcolepsy are shown in
table 1. Future treatment will address the orexin system (e.g. orexin receptor agonists).
The management of IH is dicult, due to the lack of approved medications. Usually,
stimulants such as modafinil are prescribed. Other therapies include oxybates,
pitolisant and some antidepressants.
Further reading
• Bassetti C, et al. (1997). Idiopathic hypersomnia. A series of 42 patients. Brain; 120: 1423–
1435.
• Bassetti CLA, et al. (2021). European guideline and expert statements on the management of
narcolepsy in adults and children. Eur J Neurol; 28: 2815–2830.
• Han F, et al. (2011). Narcolepsy onset is seasonal and increased following the 2009 H1N1
pandemic in China. Ann Neurol; 70: 410–417.
• Lammers GJ, et al. (2020). Diagnosis of central disorders of hypersomnolence: a reappraisal by
European experts. Sleep Med Rev; 52: 101306.
• Latorre D, et al. (2018). T cells in patients with narcolepsy target self-antigens of hypocretin
neurons. Nature; 562: 63–68.
• Latorre D, et al. (2022). Narcolepsy: a model interaction between immune system, nervous
system, and sleep-wake regulation. Semin Immunopathol; 44: 611–623.
• Maski K, et al. (2021). Treatment of central disorders of hypersomnolence: an American
Academy of Sleep Medicine systematic review, meta-analysis, and GRADE assessment. J Clin
Sleep Med; 17: 1895–1945.
• Nevsimalova S, et al. (2021). Idiopathic hypersomnia: a homogeneous or heterogeneous
disease? Sleep Med; 80: 86–91.
• Ohayon MM, et al. (2002). Prevalence of narcolepsy symptomatology and diagnosis in the
European general population. Neurology; 58: 1826–1833.
• Tai M, et al. (2014). DQB1 locus alone explains most of the risk and protection in narcolepsy
with cataplexy in Europe. Sleep; 37: 19–25.
• Thannickal TC, et al. (2000). Reduced number of hypocretin neurons in human narcolepsy.
Neuron; 27: 469–474.
327ERS Handbook: Respiratory Sleep Medicine
Parasomnia and associated
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conditions
Anna Heidbreder
Parasomnias include NREM parasomnias and REM parasomnias, depending on
the sleep stage in which they occur. The ICSD also distinguishes between other
parasomnias, which describe phenomena that can aect both sleep stages or occur
during the sleep–wake transition.
NREM parasomnias
Various forms are distinguished among the NREM parasomnias, including confusional
arousal (sudden startling from deep sleep, oen accompanied by sitting up and looking
around), night terrors (sudden startling accompanied by vegetative symptoms such as
palpitations and tachypnoea) and sleepwalking (complex actions involving leaving the
bed). As the name suggests, NREM parasomnias involve incomplete awakening from
NREM sleep, generally from sleep stage N3 and more rarely from sleep stage N2. These
events, which are also known as arousal disorders, predominantly occur during the
first half of the night, which is also the time when most deep sleep is physiologically
observed. Children are frequently aected by NREM parasomnias (>15%), but NREM
parasomnias also occur in adults in up to 3% of the population. Transition between
the dierent events (confused awakening, night terrors, sleepwalking) can oen be
fluid and they do not occur as one or the other.
Pathophysiologically, NREM parasomnia is dissociated sleep, meaning that areas of
the brain are asleep while others are in a waking state. Video PSG is not mandatory
for diagnosis, but it is useful to exclude dierential diagnoses (e.g. epileptic seizures).
Key points
• Parasomnias include NREM parasomnias and REM parasomnias, depending
on the sleep stage in which they occur.
• NREM parasomnias predominantly occur during the first half of the night,
which is also the time when most deep sleep is physiologically observed.
• REM behaviour disorders as a potential prodromal stage of neurodegenerative
diseases (α-synucleinopathies) is an area of particular important in sleep
medicine.
• Other parasomnias are rare, and include exploding head syndrome, sleeprelated hallucinations, sleep-related enuresis, and parasomnias associated
with other conditions or substance use/ingestion.
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Parasomnia and associated conditions
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NREM parasomnia is usually a benign condition, but there may be an increased risk of injury
due to the accompanying nocturnal behavioural abnormalities. It is important to educate
patients and their bed partners. Aected persons should be reassured during an episode and
guided back to bed if possible. Relaxation methods, sleep hygiene measures, hypnosis or
premeditation are also used for treatment. Drug therapy is used in patients whose nocturnal
behaviour poses a risk to themselves or their bed partner. Large-scale randomised studies
are lacking in this area; benzodiazepines are currently the main drugs used.
REM parasomnias
REM sleep behaviour disorder
Isolated REM sleep behaviour disorder (iRBD), as a potential prodromal stage of
neuro degenerative diseases (α-synucleinopathies), is of particular importance in
sleep medicine. Epidemiological studies have suggested that ∼0.28–1.15% of the
population is aected by iRBD and long-term studies have shown that >80% of
people with iRBD develop α-synucleinopathy within 10–15 years.
Video PSG is required for the diagnosis of REM sleep behaviour disorder (RBD). REM
sleep without atonia, as well as REM sleep-associated talking, twitching, and complex
behavioural abnormalities that are oen associated with vivid dreams, can be observed
videographically. Currently, the derivation of muscle activity at the upper extremity (flexor
digitorum superficialis) and the application of standardised cut-os is recommended.
Pathophysiologically, RBD involves impairment of the brainstem centres (mainly the locus
subcoeruleus, periaqueductal grey matter, pontine nuclei and reticular pontine nuclei) that
are responsible for physiological muscle tone reduction during REM sleep. RBD can also
occur in connection with other diseases, such as narcolepsy or diseases with local damage
to the above-mentioned centres (in the context of a tumour or a stroke, for example).
When awakened from an episode of RBD, patients are quickly reoriented and are able
to recall dream content.
At diagnosis, they should be informed about the potential risk of injury during RBD
episodes. The trigger for presentation to a doctor is oen self-injury or injury to others
when acting out vivid dreams, whereby kicks or blows unintentionally injure the bed
partner. Securing the bed environment or, in some cases, separating the bed partners
is sometimes recommended.
Currently, RBD can only be treated symptomatically using melatonin and benzodiazepines. Large-scale placebo-controlled studies with representative case
numbers are lacking. Neuroprotective therapy is desirable due to the potential risk
of neurodegenerative disease development; this, however, is not yet available. Largescale placebo-controlled studies with representative case numbers, conducted to
determine appropriate treatments are lacking.
Patients with iRBD may wish to be informed about the potential risk of developing a
neurodegenerative disease. Regular follow-ups (e.g. once a year) should therefore be
oered to patients in order to make specific therapy available to them as quickly as
possible in the event of conversion to a neurodegenerative disease.
Isolated sleep paralysis
Isolated sleep paralysis is another REM parasomnia. It is characterised by an inability
to perform voluntary movement with full or at least partial consciousness, and
occurs during the sleep–wake transition. The lifetime prevalence of sleep paralysis is
estimated to be ∼7%.
329ERS Handbook: Respiratory Sleep Medicine
Parasomnia and associated conditions
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Sleep paralysis can occur in isolation but also oen occurs in the context of other
psychiatric disorders (e.g., anxiety disorders, post-traumatic stress disorder) or even
sleep medical disorders (e.g. instructive sleep apnoea, insomnia, narcolepsy).
Pathophysiologically, the atonia of REM sleep persists in wakefulness. Electrophysiologically, it is represented by muscle atonia with simultaneously observed alpha
EEG. Comprehensive anamnesis is sucient for diagnosis. Further PSG examination is
indicated if sleep paralysis is suspected in the context of other diseases.
Therapeutically, it is sucient to inform the aected person about the benignity of
sleep paralysis – a specific therapy is not necessary. However, possible comorbid
diseases (e.g. narcolepsy, OSA) should be evaluated.
Nightmares
Nightmares are another form of REM parasomnia. The lifetime prevalence of
nightmares is almost 100%. They are only referred to as a ‘nightmare disorder’ when
they occur regularly and place a significant burden on then aected person’s everyday
life or sleep.
Repeated occurrences of dysphoric, well-remembered dreams are reported, which
are about fighting for one’s own safety and integrity. These dreams are experienced
as extremely stressful and lead consecutively to relevant restrictions during the day
(exhaustion, concentration restrictions) and to fear of falling asleep or returning
to sleep.
Therapeutically, imagery rehearsal therapy (IRT) is recommended for nightmare
disorder. IRT is a cognitive behavioural therapy (CBT) technique that aims to inhibit
the original nightmare and bring about cognitive change, refuting the nightmare’s
content through systematic restructuring.
Nightmares also occur in the context of other disorders, which should be treated when
present (e.g. schizophrenia, depression, post-traumatic stress disorder, alcoholism).
Other parasomnias
Other parasomnias are rare. These include exploding head syndrome, sleep-related
hallucinations, sleep-related enuresis, and parasomnias associated with other
conditions or substance use/ingestion.
Exploding head syndrome, which has a probable lifetime prevalence of ∼10%, is a
sudden and brief perception of a popping sound in the head. This form of parasomnia
is also benign. Pathophysiologically, short-term dysfunction of the brainstem neurons
during the sleep–wake transition has been considered.
Sleep-related hallucinations, also a benign disorder, oen occur in connection with
other sleep-related diseases, particularly narcolepsy. The hallucinations occur during
the sleep–wake transition (hypnagogic during falling asleep, hypnopompic during
waking) and can be visual, auditory, haptic, kinetic or olfactory. In dierential diagnosis,
narcolepsy, possible epileptic seizures, or even psychiatric diseases should be considered.
Enuresis is not a parasomnia in the true sense of the word; a distinction is made
between primary and secondary enuresis (a period of ≥6 months during which there
was no enuresis). Pathophysiologically, functional disturbances are dierentiated
into a disturbance at the level of bladder function, brain function in connection
with bladder control, or the arousal threshold. Therapeutically, behaviour-modifying
measures are carried out, and treating possible underlying diseases is recommended.
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Parasomnia and associated conditions
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Parasomnias associated with other diseases or substance use/ingestion are oen an
expression of cerebral dysfunction caused by the underlying disease (e.g. autoimmune
encephalopathy). In such cases, both REM and NREM parasomnias can occur.
Therapeutically, these can partly be influenced by the treatment of the underlying
disease. Occasionally, however, the sleep phenomenon is also the central symptom
of the disease, such as in anti-Iglon5 disease, with typical complex behavioural
abnormalities in NREM sleep combined with RBD.
Further reading
• American Academy of Sleep Medicine (2014). International Classification of Sleep Disorders.
3rd Edn. Darian, AASM.
• Castelnovo A, et al. (2018). NREM sleep parasomnias as disorders of sleep-state dissociation.
Nat Rev Neurol; 14: 470–481.
• Cesari M, et al. (2022). Video-polysomnography procedures for diagnosis of rapid eye
movement sleep behavior disorder (RBD) and the identification of its prodromal stages:
guidelines from the International RBD Study Group. Sleep; 45: zsab257.
• Frauscher B, et al. (2012). Normative EMG values during REM sleep for the diagnosis of REM
sleep behavior disorder. Sleep; 35: 835–847.
• Gaig C, et al. (2017). Clinical manifestations of the anti-IgLON5 disease. Neurology; 88:
1736–1743.
• Gieselmann A, et al. (2019). Aetiology and treatment of nightmare disorder: state of the art
and future perspectives. J Sleep Res; 28: e12820.
• Gossard TR, et al. (2023). Patient values and preferences regarding prognostic counseling in
isolated REM sleep behavior disorder. Sleep; 46: zsac244.
• Haba-Rubio J, et al. (2018). Prevalence and determinants of rapid eye movement sleep
behavior disorder in the general population. Sleep; 41; zsx197.
• Haid B, et al. (2017). Primary and secondary enuresis: pathophysiology, diagnosis, and
treatment. Eur Urol Focus; 3: 198–206.
• Högl B, et al. (2017). Rapid eye movement sleep behavior disorder and other rapid eye
movement sleep parasomnias. Continuum (Minneap Minn); 23: 1017–1034.
• Högl B, et al. (2018). Idiopathic REM sleep behaviour disorder and neurodegeneration – an
update. Nat Rev Neurol; 14: 40–55.
• Morgenthaler TI, et al. (2018). Position paper for the treatment of nightmare disorder in adults:
an American Academy of Sleep Medicine position paper. J Clin Sleep Med; 14: 1041–1055.
• Stefani A, et al. (2021). Nightmare disorder and isolated sleep paralysis. Neurotherapeutics;
18: 100–106.
• Zadra A, et al. (2013). Somnambulism: clinical aspects and pathophysiological hypotheses.
Lancet Neurol; 12: 285–294.
331ERS Handbook: Respiratory Sleep Medicine
Circadian disorders
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Anna Heidbreder
The circadian rhythm is endogenously determined and lasts ∼24 h in most living
organisms. This intrinsic rhythm is synchronised by external timers, especially light.
Information about light and darkness is transmitted via light-sensitive retinal ganglion
cells to the internal clock in the suprachiasmatic nucleus (SCN). Pulsatile melatonin
secretion from the pineal gland is controlled by the SCN and serves as the most
important biological correlate of darkness in all light-sensitive species. Melatonin
promotes sleep in diurnal species and increases activity in nocturnal species. The
circadian rhythm is a prerequisite for optimal timing of sleeping and waking. In most
humans, the genetically determined oscillation of the circadian rhythm is slightly
longer than 24 h, which is why the human rhythm is brought into harmony with
external timers every day. In addition to sleeping and waking, the circadian rhythm
also schedules other bodily functions, such as the secretion of various hormones,
body temperature and metabolism. When assessing circadian disorders, it is crucial
to consider the individual chronotype.
Circadian disturbances can occur due to a disturbance of the intrinsic rhythm or as
a consequence of the mismatch between the individual’s sleep–wake rhythm and
the social and physical 24-h rhythm. In the ICSD-3, circadian rhythm sleep–wake
disorders (CRSWD) are defined as being caused by:
• A change in the circadian timing system.
• The entrainment mechanism.
• A maladjustment of the endogenous circadian rhythm to the external environment.
Key points
• Circadian disturbances can occur due to a disturbance of the intrinsic rhythm
or as a consequence of the mismatch between the individual’s sleep–wake
rhythm and the social and physical 24-h rhythm.
• For the diagnosis of circadian rhythm sleep–wake disorders, in addition to a
comprehensive history of the individual’s sleep–wake behaviour, sleep diaries
and actigraphy are primarily used.
• The ICSD distinguishes delayed and advanced sleep–wake phase syndrome,
irregular sleep–wake rhythm disorder, non-24-h sleep–wake rhythm disorder,
shi work disorder and jet lag disorder.
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Circadian disorders
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Table 1. ICSD-3 circadian rhythm sleep–wake disorders
Delayed sleep–wake phase disorder
Advanced sleep–wake phase disorder
Irregular sleep–wake rhythm disorder
Non-24-h sleep–wake rhythm disorder
Shi work disorder
Jet lag disorder
Circadian sleep–wake disorder NOS
NOS: not otherwise specified. Data from American Academy of Sleep Medicine (2014).
Symptomatically, patients with a circadian disorder become conspicuous by the
occurrence of insomnia and daytime sleepiness symptoms, which is caused by the
misalignment of the biological sleep/wake propensity and social requirements. For
the diagnosis of CRSWD, in addition to a comprehensive history of the individual’s sleep–
wake behaviour, sleep diaries and actigraphy are primarily used. Questionnaires are
oen used to determine the chronotype; the determination of the dim light melatonin
onset in urine, blood or saliva can also be used. Patients with CRSWD oen complain
about insomnia and/or EDS, which massively restricts their daily life (table 1).
Delayed sleep–wake phase syndrome
Delayed sleep–wake phase syndrome (DSPS) is characterised by a relevant delay
in the main sleep phase, which deviates significantly from the desired or required
sleep time. Due to a lack of good epidemiological studies, prevalence figures vary
widely from 0.2% to 10%. This disorder is oen caused by an interaction between
genetic disposition (eveningness) and a lifestyle with very little light exposure in the
morning and lots of artificial light at night. Since those aected cannot sleep at the
desired time, DSPS patients complain about a combination of insomnia and daytime
sleepiness with severely impaired awakening in the morning. Adolescents and young
adults are more oen aected as the timing of the circadian clock shis forward by
an average of 5 h during puberty. In the treatment of this condition, melatonin can be
used as a chronotherapeutic agent together with behaviour-modifying measures (e.g.
morning light therapy, fixed or stepwise advanced bedtime).
Advanced sleep–wake phase syndrome
In advanced sleep–wake phase syndrome (ASPS) the main sleep phase of the
individual is advanced and does not correspond to the desired and necessary sleep
times. The result is premature fatigue, falling asleep in the evening, and premature
awakening in the morning. Since this disorder is oen compatible with a professional
life, suering is mainly caused by the inability to be active in the evening when social
interactions oen take place. ASPS probably occurs even less frequently than DSPS,
but representative studies for estimating the prevalence are lacking. Elderly people
are more likely to be aected because the timing of the circadian clock shis with
age. ASPS should be distinguished from aective disorders, especially depressive
disorders. Therapy should only be used if the patient suers due to the disorder; in
that case, behaviour-modifying measures (e.g. activities in the evening, light therapy
in the evening) can be implemented.
Irregular sleep–wake rhythm disorder
Irregular sleep–wake rhythm disorder (ISWRD) is characterised by total cancellation of
a recognisable recurring rhythm between sleep and waking phases. In this condition
sleep and wake bouts occur irregularly and recurrently within a 24-h rhythm.
333ERS Handbook: Respiratory Sleep Medicine
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