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Central sleep apnoea
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Dimitrios Papadopoulos, Bertien Buyse and Dries Testelmans
Clinical aspects
Contrary to OSA patients, individuals with CSA are oen not obese and present
with mild or no snoring. The constant oscillations between wakefulness and sleep
contribute to sleep fragmentation and symptoms of disturbed sleep, such as sleep
onset and maintenance insomnia, frequent awakenings, poor sleep satisfaction and
feelings of nonrestorative sleep, which are usually accompanied by daytime complaints
of fatigue and poor concentration. Complaints of paroxysmal nocturnal dyspnoea,
nocturnal angina and morning headaches can be attributed to repeated nocturnal
desaturations. Nocturia is also common, while sometimes a bed partner may report
witnessed apnoeas or abnormal breathing patterns, such as the periodic breathing of
CSR in HF or stroke patients, or ataxic breathing in opioid users. However, treatmentemergent CSA (TECSA) patients demonstrate the traditional clinical aspects of OSA,
which remain unresolved aer the initiation of PAP treatment due to the emergence
or persistence of central events during sleep.
The usually insidious onset of these symptoms, along with the fact that many of
them are also part of the clinical picture of the underlying disease (as is the case with
insomnia, fatigue, shortness of breath and orthopnoea in HF, and cognitive deficits
in opioid abuse), may lead to delays in diagnosis and treatment of CSA and to poor
overall prognosis. Moreover, subjective EDS, a hallmark of SDB, may be absent in
SDB patients with HF, despite findings of reduced alertness on objective tests. This is
probably attributed to the increased sympathetic activity and makes the screening of
HF patients for SDB in general and CSA in particular even more dicult. Finally, there
Key points
• Disturbed sleep and daytime fatigue are the most common complaints of
patients with CSA.
• The presence of CSA is associated with detrimental eects on the
cardiovascular system and worse clinical outcomes in patients with HF.
• Screening of HF patients for CSA may require the recognition of a wide range
of risk factors and should not rely solely on symptomatology.
• The impact of CSA on AF, stroke, chronic kidney disease and opioid use
outcomes is currently understudied and not fully understood.
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are no specific physical examination findings or laboratory/imaging abnormalities in
CSA that could aid in its recognition or its dierentiation from other sleep-related
breathing disorders.
Consequences
Impact of CSA and CSR on HF outcomes
Long-term consequences of CSA have been extensively studied in the HF population,
which represents the majority of CSA patients in clinical practice. The presence of
CSA/CSR has been associated with several markers of disease severity in HF, including
elevated levels of brain natriuretic peptide (BNP), lower le ventricular ejection
fraction (LVEF), higher pulmonary capillary wedge pressure, occurrence of ventricular
arrhythmias and increased sympathetic stimulation, the latter being quantified either
as muscle sympathetic nerve activity or as nocturnal urinary excretion and daytime
plasma concentrations of norepinephrine. Conversely, suppression of CSA/CSR has
been shown to decrease sympathetic drive and BNP levels and improve LVEF and
New York Heart Association (NYHA) class. Furthermore, HF patients with CSA have
increased risk for recurrent unplanned hospitalisations due to HF worsening, for
ventricular arrhythmias requiring cardioverter-defibrillator implantation and for
mortality, compared to HF patients without CSA. Importantly, quantified CSR-related
features, such as cycle length, lung-to-periphery circulation time and time to peak
flow, have been positively correlated with these adverse outcomes in CSA patients
with HF.
The pathophysiological mechanisms responsible for the detrimental eects of CSA in
the context of HF are related to the characteristic oscillations of CSR regarding tidal
volume, arterial blood gases, heart rate and BP (figure 1). The two main mechanisms
are the arousal-induced sympathetic activation and the apnoea-induced repeated
Hypoxia–
reoxygenation
Oxidative stress
Inflammation
Endothelial
dysfunction
Plaque rupture
Ischaemia
Thrombosis
Peripheral
chemoreceptor
upregulation
Tachycardia
Vasoconstriction
BP elevation
Figure 1. Pathophysiology of the detrimental eects of CSR on HF.
Impaired
contractility
Cardiac
remodelling
CSA/CSR
Arousals
Sympathetic
activation
Myocyte
hypertrophy/
necrosis
HF progression
retention
RAAS activation
Atrial/
ventricular
arrhythmias
Intrathoracic
pressure
oscillations
Changes in
transmural
pressure
Sodium
Increased
preload/
aerload
85ERS Handbook: Respiratory Sleep Medicine
Central sleep apnoea
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cycles of hypoxia–reoxygenation. Cyclical arousals aer the apnoeic events produce
equally periodic elevations in sympathetic drive, which is already increased in
HF patients during wakefulness and is a known determinant of worse prognosis.
Sympathetic stimulation and catecholamine release lead to tachycardia, peripheral
vasoconstriction, sodium retention and activation of the renin–angiotensin–
aldosterone (RAAS) system. The resulting increase in BP, blood volume and myocardial
oxygen demand may then lead to plaque rupture, myocardial ischaemia and elevated
preload and aerload, which will impose further stress on a failing heart. Moreover,
increased sympathoexcitation contributes to cardiac myocyte hypertrophy, apoptosis
and necrosis, leading to adverse cardiac remodelling and, together with hypoxia, exerts
arrhythmogenic eects, increasing ventricular irritability. Neurohormonal activation
and ischaemia increase the sensitivity of peripheral and central chemoreceptors,
causing further breathing instability during sleep, which triggers CSA and sustains
this vicious cycle.
The eect of chronic intermittent hypoxia (CIH) on the cardiovascular system has
been thoroughly studied in OSA and it is safe to assume that these findings can be
extrapolated to CSA patients. CIH activates oxidative stress through the production
of reactive oxygen species during reoxygenation, which could then impair myocardial
contractility, induce cardiac remodelling by molecular signalling pathways, and
aect endothelial function by interfering with nitric oxide metabolism. Furthermore,
reactive oxygen species stimulate the release of pro-inflammatory cytokines and the
resulting systemic inflammation contributes to le ventricular dysfunction, cardiac
remodelling and pulmonary congestion. Both oxidative stress and inflammation cause
endothelial dysfunction that leads to thrombosis and ventricular hypertrophy due to
heightened vasoconstriction, platelet aggregation and smooth muscle proliferation.
Studies on OSA patients have demonstrated that PAP therapy is successful
in improving oxidative stress, reducing systemic inflammation, and reversing
endothelial dysfunction. CIH may also contribute to peripheral chemoreceptor
hypersensitivity in HF, which further enhances sympathetic drive both directly and
indirectly via suppression of the baroreflex. Since the chemoreceptor upregulation
in HF is the main factor leading to breathing instability during sleep, this increased
sympathetic–respiratory coupling represents a constant feedback loop that links CSA
progression to HF progression.
Another possible pathway to adverse HF outcomes could be the increased negative
intrathoracic pressure swings during the hyperventilating phase of CSR, which are
required to overcome decreased lung compliance due to chronic pulmonary congestion
and oedema. Although not as pronounced as in OSA, these pressure swings could be
transported to the cardiac chambers, increasing right and le ventricular aerload and
inducing atrial arrhythmias, and they could raise the pulmonary capillary hydrostatic
pressure. This could lead to further worsening of the pulmonary oedema. Finally,
impaired sleep architecture and reduction of time spent in slow-wave sleep may lead
to neurocognitive sequelae and increased fatigue, which lower the quality of life and
could have an impact on physical activity and exercise tolerance.
In line with these observations, one would expect that suppression of CSR would
result in decreased mortality in HF patients. However, this was not the case in two
randomised controlled trials that evaluated the eect of two dierent modes of PAP
on mortality in HF patients with CSA: the CANPAP trial (Canadian trial of CPAP for
patients with CSA and HF) and the SERVE-HF trial (treatment of SDB with predominant
CSA by ASV in patients with HF). These results have fuelled a debate about whether
periodic breathing and CSR are just a compensatory mechanism in HF and should
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possibly not be suppressed. This notion is pathophysiologically supported by some
short-term beneficial eects of either the hyperventilating phase or the apnoeic
phase of CSR. During the hyperventilating phase, vagal stimulation and attenuation
of sympathetic hyperactivity, increased end-expiratory lung volume, and development
of PAP that augments stroke volume could be found. During the apnoeic phase, a
decreased work of breathing and, consequently, reduced respiratory muscle fatigue
was demonstrated. It is worth saying that all these benefits are likely to be reversed
when the patient enters the opposite CSR phase, while increases in lung volumes
and augmentations in PAP could result in reduced venous return and increased
pulmonary vascular resistance, which can be translated into lower cardiac output and
lower right ventricular function. If indeed the hyperpnoea of CSR was compensatory,
the application of extrinsic PAP during sleep should produce the same benefits to all
patients. However, a post hoc analysis from the CANPAP trial showed that only the
subgroup of patients in whom the AHI fell under 15 events·h−1 during PAP treatment
had significantly reduced mortality compared to control patients. We have to assume
that suppression of CSR provided this eect, instead of just the initiation of PAP. Both
trials have been criticised for methodological shortcomings and low adherence to
allocated treatments; well-designed future trials are expected to shed more light on
these issues.
Implications for screening HF patients for CSA
Several studies demonstrate that the presence of CSA/CSR is detrimental for HF
patients in the long term and has an impact on their prognosis. Therefore, it is of
the utmost importance to diagnose CSA quickly and accurately to enable targeted
treatment. In-laboratory PSG remains the gold standard for diagnosing CSA, especially
in HF patients who generally have low sleep eciency. This is a major reason why an
ambulatory type 3 sleep study in this setting may underestimate apnoea severity.
Screening tools currently being used for OSA have not been validated for CSA, not
to mention the fact that their performance for OSA screening in the HF population
is suboptimal, especially regarding questionnaires for EDS assessment. Relying
solely on symptoms reported by the patient may be impractical, since most of the
time these symptoms have an insidious onset and slow progression, are frequently
underestimated, or are being attributed to the underlying HF. This acknowledgement
is reflected in the proposed diagnostic criteria for CSA with CSR by the American
Academy of Sleep Medicine, where, with the occurrence of HF, presence of sleep
apnoea symptoms is not prerequisite for the diagnosis.
Identification of predictors for CSA/CSR in HF patients can be based on a combination
of epidemiological, pathogenetic and clinical data. Older age, male sex, higher BMI and
greater neck circumference have been correlated with increased AHI in HF patients
with CSA. Parameters reflecting the severity of HF, including NYHA class, LVEF, BNP or
C-reactive protein levels, could equally predict CSA severity. It should be kept in mind
that CSA is also prevalent in HF patients with preserved ejection fraction. Indicators
of increased loop gain, such as hypoxaemia and hypocapnia on arterial blood gas
measurements and decreased FRC and diusion capacity on pulmonary function
testing, may identify HF patients with an increased propensity for periodic breathing
during sleep. Recognition of a periodic breathing pattern at rest or during exercise
in HF patients has been associated with very high sensitivity and specificity for the
presence of CSA. Finally, possible consequences of SDB, like atrial fibrillation (AF)
or other arrhythmias, increased heart rate variability or other measures of elevated
sympathetic activity, low physical capacity and poor quality of life, may be present and
guide referral for further investigation.
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Impact of CSA on other underlying medical conditions
AF
In studies in OSA patients, SDB has been associated with incident AF, recurrent AF,
and decreased ecacy of anti-arrhythmic drugs, catheter-based therapies or electrical
cardioversion. No such evidence exists for the impact of CSA on AF outcomes and
projecting data from OSA on the CSA population with AF might be risky. The reason is
the larger arrhythmogenic eect exerted by the much higher intrathoracic pressures
produced during obstructive apnoeic events compared to the ones during CSA/CSR.
Moreover, prospective studies have shown that central respiratory events during sleep
significantly decrease aer successful restoration of sinus rhythm aer electrical
cardioversion of AF. This implies that haemodynamic instability and subsequent
fluid retention and overnight rostral shi causing pulmonary congestion might be a
decisive mechanism triggering CSA in AF patients. These observations highlight the
need for timely treatment of the arrhythmia rather than focusing on the treatment
of CSA.
Stroke
Aer a major cerebrovascular event, the occurrence of SDB has been recognised as a
risk factor for worse functional and cognitive outcomes, recurrent stroke, and mortality.
Vascular impairment as a result of sympathetic activation and oxidative stress, poor
cerebral oxygenation and plasticity due to CIH, and altered daytime functioning owing
to sleep fragmentation have been postulated as underlying mechanisms. Most of
these also apply in the case of CSA; however, there are no cohort studies evaluating the
eect of predominant CSA on stroke outcomes. Central respiratory events during sleep
are common in the acute phase aer ischaemic stroke, but are significantly reduced
in the chronic phase. These temporal variations also have implications for screening,
which is generally recommended to be performed at the earliest opportunity, even
before the patient exits the stroke unit, using portable testing devices.
Chronic kidney disease
SDB has been associated with incident chronic kidney disease and accelerated decline
in kidney function through the damaging eects of CIH and glomerular hypertension/
hyperfiltration on renal tissues, caused by the elevated sympathetic drive. The
occurrence of CSA has been found to be a predictor of all-cause mortality in chronic
kidney disease patients. However, no study has tested whether treating CSA leads to
a possible survival benefit in these patients.
Opioid use
Chronic use of opioids is a risk factor for cardiovascular morbidity, especially myocardial
infarction, and also all-cause mortality, which is generally attenuated with prolonged
use over 6 months. However, the presence of CSA was not found to alter the incidence
of cardiac-related admissions in chronic opioid users in a cohort of veterans in the
USA. Whether SDB and its consequences contribute to the excess mortality of opioid
users or if it is just a dose–response relationship, since higher opioid dose is linked to
more severe CSA, remains to be elucidated.
Further reading
• Baillieul S, et al. (2022). Sleep apnoea and ischaemic stroke: current knowledge and future
directions. Lancet Neurol; 21: 78–88.
• Bekfani T, et al. (2016). Current and future developments in the field of central sleep apnoea.
Europace; 18: 1123–1134.
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• Costanzo MR, et al. (2015). Mechanisms and clinical consequences of untreated central sleep
apnea in heart failure. J Am Coll Cardiol; 65: 72–84.
• Dharia SM, et al. (2017). Epidemiology of sleep-disordered breathing and heart failure: what
drives what. Curr Heart Fail Rep; 14: 351–364.
• Draganova AI, et al. (2016). Identifying predictors of central sleep apnea/Cheyne–Stokes
breathing in chronic heart failure: a pathophysiological approach. Folia Med; 58: 225–233.
• Ishikawa O, et al. (2021). Central sleep apnea. Clin Geriatr Med; 37: 469–481.
• Javed F, et al. (2020). Association of serious adverse events with Cheyne–Stokes respiration
characteristics in patients with systolic heart failure and central sleep apnoea: a SERVE-Heart
Failure substudy analysis. Respirology; 25: 305–311.
• Kwon Y, et al. (2018). Sleep, sleep apnea and atrial fibrillation: questions and answers. Sleep
Med Rev; 39: 134–142.
• Lin CH, et al. (2020). Sleep apnea and chronic kidney disease: a state-of-the-art review. Chest;
157: 673–685.
• Oldenburg O, et al. (2017). CSA is not beneficial long term in heart failure patients with
reduced ejection fraction. Int J Cardiol; 227: 474–477.
• Randerath W, et al. (2017). Definition, discrimination, diagnosis and treatment of central
breathing disturbances during sleep. Eur Respir J; 49: 1600959.
• Ratz D, et al. (2018). Correlates and consequences of central sleep apnea in a national sample
of US veterans. Sleep; 41: zsy058.
• Terziyski K, et al. (2018). Central sleep apnea with Cheyne–Stokes breathing in heart failure –
from research to clinical practice and beyond. Adv Exp Med Biol; 1067: 327–351.
• Wang D, et al. (2021). Chronic opioid use and central sleep apnea, where are we now and
where to go? A state of the art review. Anesth Analg; 132: 1244–1253.
• Xu J, et al. (2016). The eect of sleep apnea on all-cause mortality in nondialyzed chronic
kidney disease patients. Sleep Med; 27–28: 32–38.
89ERS Handbook: Respiratory Sleep Medicine
Sleep history
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Silke Ryan
A sleep history involves more than a description of a patient’s sleep and, in fact, is a
sleep–wake history with an evaluation of the entire 24-h span. This involves recording of
alertness and tiredness, work and leisure hours, in addition to details of rest and sleep.
The first step in obtaining a history is to assess the patient’s complaint or reason for
seeking attention, e.g. diculties in initiating or maintaining sleep, waking unrefreshed
and/or feeling sleepy during the day, or abnormal breathing, behaviour or movements
during sleep. Furthermore, the history should establish when the problem began and
how frequently symptoms occur. A potential relationship to external factors such
as environmental, social or medical influences also needs to be understood and
evaluated, and every history needs to include details on medication, caeine, alcohol
or illicit drug use. In addition, the interview needs to include a detailed family history,
as several sleep disorders such as OSA, insomnia, restless legs syndrome or NREM
parasomnia are genetically influenced and follow a familial aggregation.
Detailed questionnaires have been developed to cover important questions that
need to be asked and that can serve as a road map for planning the direction of the
interview. Completion of a sleep diary for 1–2 weeks may give important indications
of sleep habits, sleep hygiene and daytime symptoms, and is especially useful in
the assessment of insomnia or daytime sleepiness of unknown cause. This typically
includes the recording of bedtime, time asleep, nocturnal awakenings, rising time,
daytime naps and consumption of substances that may aect alertness.
While many components of the sleep history are common to all sleep complaints,
some disorders require special questions, and the physician should be constantly
Key points
• A detailed longitudinal sleep history is the most critical part in the assessment
of subjects with sleep disorders.
• The elicitation of a collateral history is oen crucial in the assessment of a
subject with a sleep disorder.
• EDS and sleeping diculties are common symptoms and, besides occurring in
sleep disorders, are frequently associated with other psychiatric, neurological
and medical disorders and medications.
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formulating and testing hypotheses of diagnosis as the history evolves. One must also
bear in mind that there are oen multiple causes of a sleep-related problem.
Sleep-related symptoms
The patient oen has little or no awareness of sleep-related problems and, therefore,
it is highly desirable to conduct an interview with the patient’s bed partner or caregiver
or, in the case of a child, with the parent or teacher. The bed partner can provide
vital information regarding sleep behaviour, abnormal movements or breathing
problems during sleep, and can also provide valuable independent input of events
during wakefulness. Video or audio recordings from smart phones or similar devices
can also be helpful and the patient should be actively encouraged to provide such
information if applicable. However, caution is advised on the reliance on digital
technology such as smart phones, watches or activity trackers in their recordings
of sleep cycles, sleep quality or oxygen saturation. The accuracy of such recordings
is commonly not evaluated by scientific studies, particularly in subjects with sleep
disorders. Nonetheless, as technology advances, such consumer devices are likely to
become more clinically useful in the future.
It is important to establish the regularity of the sleep –wake pattern, including preferred
bed and rising times. Irregularity of this pattern, such as with varying work shis, at
weekends or during holidays, should be noted and, where relevant, compared to the
premorbid sleep cycle. Particularly in the case of insomnia, note should also be taken
of the sleep environment. Noise, temperature and brightness of the bedroom and
also comfort of the bed can frequently influence sleep quality, and the patient may be
unaware of these links. The time of sleep onset should be recorded and if sleep latency
is prolonged, potential reasons should be sought with the patient. Activities before
bed and any behaviour while awake in bed, such as reading or watching television,
should be described, as these can aect sleep onset.
Furthermore, problems with sleep maintenance need to be ascertained. These include
recording of the number of awakenings with an attempt to determine the causes
of arousals, which could include external factors such as restless partners, noise,
nightmares, or medical causes including dyspnoea, leg jerking, nocturia or anxiety.
Multiple causes of pain or discomfort can also arouse patients, including arthritis,
fibromyalgia, restless legs or angina. The length of time before returning to sleep
and an estimation of total time spent asleep should be evaluated. Moreover, events
at sleep termination are important in the overall evaluation. These include the time
of wakening, whether the awakening is spontaneous and how tired or refreshed the
patient feels.
There are several sleep-related symptoms that are more specific to certain sleep
disorders (table 1). Snoring is among the most common nocturnal symptoms and is
frequently the primary reason for a patient and partner to seek medical attention. To
help distinguish ‘simple’ snoring from snoring as part of OSA, one should ascertain
the intensity, duration and frequency of snoring, as well as the sleeping position
associated with snoring, in addition to potential association with alcohol or sedative
medication. The bed partner should be carefully interviewed about frequency and
length of apnoeas as well as the position in which they occur. Apnoeas may also be
associated with jerking movements, suggesting an associated arousal, and the patient
may report episodes of waking with a choking sensation in the throat. Nocturnal
dyspnoea can be a symptom of various respiratory or cardiac diseases and further
details such as wheeze, chest pain, palpitations, association with apnoeas or body
position when dyspnoea occurs may help to narrow the dierential diagnosis.
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Table 1. Common nocturnal and daytime symptoms encountered in sleep medicine and their
possible implications
Symptom Possible implications
Sleeping diculties See dierential diagnosis in table 2
Snoring ‘Simple’ snoring, upper airway resistance
syndrome, OSA
Nocturnal gasping/choking OSA, asthma, COPD, cardiac failure,
gastro-oesophageal reflux, panic attacks
Early morning headaches OSA, carbon dioxide retention, sleep
deprivation, insomnia
Frequent leg movements during sleep Restless legs syndrome, periodic limb
movement disorder
Loss of strength with emotion Cataplexy (narcolepsy type 1)
EDS See dierential diagnosis in table 2
Abnormal movements or behaviour during sleep occur in 15–20% of children and
4% of adults and the interviewer needs to establish from the individual and witnesses
if those are simple (such as hypnic jerks or bruxism), periodic (such as periodic
limb movement disorder) or complex (parasomnias). Obtaining video recordings
of the events is highly desirable and targeted questionnaires, e.g. the Mayo Sleep
Questionnaire, can assist in the interview with the patient. In addition to a detailed
description of the events, the time of night they occur, duration, age of onset or
patient’s awareness, the history should also focus on any potential predisposing
factors such as comorbid medical, neurological or sleep conditions, traumatic
events, stress, poor sleep hygiene or medications, family history and risk of harm to
self and others.
Daytime symptoms
EDS is a very common complaint and is experienced in a number of somatic,
psychiatric and primary sleep disorders, but also occurs physiologically in the absence
of suciently restorative sleep periods. EDS should be distinguished from mental or
physical fatigue, which usually has an organic cause or may be related to insomnia.
EDS severity can be gauged by frequency of occurrence and the type of situation in
which the patient falls asleep. EDS is likely to be more severe if sleep occurs despite
stimulating circumstances, such as while talking, eating or on exertion, and if it
occurs frequently and at any time during the day. Sleepiness while driving should be
characterised in terms of the time and distance before lapses of alertness occur and
whether motor vehicle accidents or near misses have occurred as a consequence.
When evaluating patients, it is also important to ask about counteractive strategies
such as intake of caeine or energy drinks, avoiding sedentary activities or scheduling
naps. The duration and frequency of the latter should be noted, as should whether or
not they are restorative. Some daytime symptoms are more relevant to certain sleep
disorders, e.g. morning headaches, sore throat and dry mouth are commonly reported
by patients with sleep apnoea. Abnormal movements during the daytime due to
epilepsy or a primary movement disorder may be related to unusual movements
during sleep and, therefore, should be determined. Cataplexy, i.e. the sudden bilateral
loss of muscle strength due to emotion, especially laughter, is a classical symptom of
narcolepsy. Any history of transient paralysis or hallucinations may further support
this diagnosis, but it should be noted that these manifestations could also occur as
part of other conditions.
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Dierential diagnosis of EDS and diculties in initiating or
maintaining sleep
EDS
EDS is defined as inability to maintain wakefulness or alertness during the major waking
episodes of the day. As outlined already, it needs to be distinguished from fatigue,
which refers to a subjective lack of physical or mental energy. EDS is highly prevalent,
with studies reporting up to 28% of the adult population being aected. There are
numerous causes for EDS (table 2) and in many patients there is a multifactorial
origin. The causes of EDS can be crudely divided into four categories: 1) insucient
Table 2. Common conditions and additional diagnostic clues in the dierential diagnosis of EDS
and diculties in initiating or maintaining sleep
EDS
Insucient sleep Behavioural or environmentally induced
Sleep disorders
SDB Loud snoring, witnessed apnoeas,
obesity, cardiovascular comorbidities,
male predominance
Narcolepsy types 1 and 2 Irresistible and sudden sleep episodes,
±cataplexy, hypnagogic hallucinations,
sleep paralysis, young age
Idiopathic hypersomnia Prolonged but unrefreshing naps, long
sleep duration, young age
Circadian rhythm sleep–wake disorder Abnormally timed sleep–wake patterns
Sleep-related movement disorder
Neurological disorders e.g. neurodegenerative diseases, multiple
sclerosis, motor neuron disease,
traumatic brain injury
Medical disorders e.g. hypothyroidism, obesity, end-stage
renal disease
Psychiatric disorders e.g. depression, anxiety, substance abuse
Medication e.g. benzodiazepines and other sedatives,
antipsychotics, opioid analgesics
Diculties in initiating/maintaining sleep
Habitual short sleep duration Feeling refreshed during the day
Insucient sleep Behavioural or environmentally induced,
poor sleep hygiene
Circadian rhythm sleep–wake disorder Abnormally timed sleep–wake patterns
Insomnia secondary to a psychiatric
disorder
Insomnia secondary to a medical/
neurological disorder
Insomnia secondary to substance abuse Alcohol or drug abuse, stimulant
Insomnia secondary to another sleep
disorder
Chronic insomnia disorder Negative thoughts towards sleep, sleep
Acute insomnia Short duration, identifiable stressors/
e.g. depression, anxiety, panic disorder,
personality disorder
e.g. gastro-oesophageal reflux, asthma,
HF, chronic pain, trauma
medication usage
e.g. OSA, restless legs syndrome, periodic
limb movement disorder
phobia, certain psychological traits
(anxious, obsessive-compulsive)
triggers
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