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Sleep history
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sleep, 2) sleep disorders, 3) medical, neurological and psychiatric conditions, and
4) medications. Insucient sleep is probably the most common reason and may be self-inflicted or due to lack of time, for instance as a consequence of long work hours or social pressures. Insomnia is the most common cause of insucient sleep but oen results in fatigue rather than EDS. Many sleep disorders are typically associated with EDS, either due to reduced total sleep time or sleep fragmentation (e.g. OSA, CSA, sleep-related movement disorders) or due to their central origin (e.g. narcolepsy, Kleine–Levin syndrome, idiopathic hypersomnolence). A variety of medications can contribute to EDS, and substance abuse including alcohol, narcotics or stimulant withdrawal also requires consideration. Careful history taking is the most important tool in the evaluation of a patient with EDS.
Diculties in initiating or maintaining sleep
Diculties in initiating and/or maintaining sleep are among the most common medical complaints. For short-term problems, certain trigger mechanisms or stressors can oen be identified. Chronic insomnia is commonly linked to psychiatric or medical disorders, may coexist with other sleep disorders or be contributed to by certain medications or substance abuse (table 2). Insomnia should be clinically distinguished from sleep insuciency due to poor sleep hygiene or self-inflicted sleep restriction and habitual short sleep. A detailed interview establishing the nature and severity of the problem and identifying coexistent conditions and contributing factors will oen prevent unnecessary investigations and is the key for the initiation of appropriate treatments.
Further reading
American Academy of Sleep Medicine (AASM) (2014). International Classification of Sleep
Disorders. 3rd Edn. Darien, AASM.
Bodkin CL, et al. (2011). Oce evaluation of the ‘tired’ or ‘sleepy’ patient. Semin Neurol; 31:
42–53.
Brown J, et al. (2020). An approach to excessive daytime sleepiness in adults. BMJ; 368:
m1047.
Chervin RD (2011). Use of clinical tools and tests in sleep medicine. In: Kryger MH, et al., eds.
Principles and Practice of Sleep Medicine. 5th Edn. St Louis, Elsevier Saunders; pp. 666–679.
Chesson A Jr, et al. (2000). Practice parameters for the evaluation of chronic insomnia. An
American Academy of Sleep Medicine report. Standards of Practice Committee of the American Academy of Sleep Medicine. Sleep; 23: 237–241.
Grote L, et al. (2021). The clinical interview and clinical examination. In: Bassetti C, et al., eds.
Sleep Medicine Textbook. 2nd Edn. Regensburg, European Sleep Research Society; pp. 167–180.
Hirshkowitz M (2004). Normal human sleep: an overview. Med Clin North Am; 88: 551–565.
Merikangas KR, et al. (2014). The structured diagnostic interview for sleep patterns and
disorders: rationale and initial evaluation. Sleep Med; 15: 530–535.
Taylor DJ, et al. (2018). Reliability of the structured clinical interview for DSM-5 sleep disorders
module. J Clin Sleep Med; 14: 459–464.
Young TB (2004). Epidemiology of daytime sleepiness: definitions, symptomatology, and
prevalence. J Clin Psychiatry; 65: Suppl. 16, 12–16.
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ERS Handbook: Respiratory Sleep Medicine
Questionnaires in
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respiratory sleep medicine
Sarah Cullivan, Barry Kennedy and Brian D. Kent
Insucient sleep and sleep disorders can have profound biological and psychological implications, and sleep disorders have a bidirectional relationship with numerous comorbidities. Accurate and timely diagnosis of sleep disorders is therefore crucial, but access to appropriate diagnostics can be limited. Subjective tools such as self­reported questionnaires have an important place in the assessment of subjects with suspected SDB. These can enrich the clinical picture and facilitate subsequent triage for objective investigations. Dierent sleep questionnaires measure dierent aspects of sleep health – the degree of sleepiness, the probability of specific sleep disorders such as OSA, and subjective global sleep quality. This chapter provides an introduction to some of the questionnaires that are commonly used in clinical practice.
Questionnaires assessing sleepiness
EDS is a common and important consequence of sleep disorders. It is characterised by the urge to fall asleep during the wake phase of the sleep–wake cycle, when one is expected to be alert. EDS can be objectively quantified using in-laboratory investigations, such as the MSLT and the maintenance of wakefulness test (MWT), but these investigations are time and labour intensive, and not widely available. Questionnaires such as the ESS and the Stanford Sleepiness Scale (SSS) measure subjective sleepiness in dierent situations. This can facilitate triage of referrals to the sleep clinic and provide a metric by which to measure treatment response. However, it must be understood that not all patients with sleep disorders will report EDS, and therefore these questionnaires should not be used to exclude sleep pathology.
Key points
• The ESS exhibits a variable association with objectively measured EDS and the presence or severity of sleep disorders.
• The STOP-Bang Questionnaire has a high sensitivity for predicting moderate­to-severe and severe OSAS.
• Sleep quality can be evaluated using the PSQI and the FOSQ.
• Validated questionnaires have an important role in the assessment of subjects with suspected SDB, when accompanied by specialist consultation and access to objective diagnostics.
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Table 1. Situations assessed by the ESS
Sitting and reading Watching TV Sitting inactive in a public place As a passenger in a car for an hour without a break Lying down to rest in the aernoon when circumstances permit Sitting and talking to someone Sitting quietly aer a lunch without alcohol In a car, while stopped for a few minutes in trac
Each situation is scored from 0 to 3, with 0 representing no chance of dozing, and 3 a high likelihood of dozing. The upper limit of normal of the sum of the scores is generally considered to be 10. Reproduced and modified from Johns (1991) with permission.
The ESS
The ESS was first published by Johns in 1991 and has since become one of the most widely used measurements of sleepiness in clinical practice (table 1). Subjects score their propensity to fall asleep in eight dierent situations using a 4-point Likert scale. A score of 0 indicates a low likelihood of falling asleep, while a score of 3 indicates a high chance of dozing. A total score of 10 is indicative of EDS.
Studies evaluating the correlation of the ESS with objective measurements of sleepiness, such as the MSLT, have shown diverging results; caution should therefore be exercised when interpreting the ESS score as a marker of absolute sleepiness. Furthermore, a normal ESS score does not exclude significant sleep pathology, and the ESS does not correlate strongly with objective measures of disease severity, such as the AHI. Consequently, a normal ESS does not exclude the presence of underlying OSA or the presence of severe disease.
The SSS
The SSS consists of a one-item questionnaire that measures the current level of alertness, using a 7-point scale. A higher score is indicative of greater subjective sleepiness, and a score of 7 describes severe sleepiness: ‘No longer fighting sleep, sleep onset soon, having dream-like thoughts’.
The SSS is quick and easy to use and can measure symptom variability throughout the day, creating a dynamic picture of symptomatology. Patients can be followed longitudinally in clinical and research contexts to measure the impact of therapeutic interventions. However, the SSS cannot dierentiate EDS that is caused by simple sleep deprivation from EDS that is caused by a sleep disorder and therefore, it should not be used in isolation to diagnose sleep pathology.
Screening questionnaires for OSA
OSA is a highly prevalent condition that is associated with considerable morbidity if le untreated. This includes cardiovascular and metabolic complications, neurocognitive deficits and an elevated risk of road trac accidents and of perioperative adverse events. Clinical history and examination are inadequate screening tools to reliably identify OSA, as the absence of the typical clinical phenotype does not exclude the diagnosis. This prompted the development and validation of a number of screening tools for OSA which are the focus of this section. These include the Berlin questionnaire, the STOP and STOP-Bang questionnaires, OSA50 and the Lausanne NoSAS (Neck circumference, obesity, Snoring, Age, Sex) score.
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Table 2. The Berlin Questionnaire
Questions Answers Scoring
Category 1 Items 1, 4, 8, 10 Category 1
1) Do you snore?
2) If yes, how loud is it?
3) How oen do you snore?
4) Has your snoring ever
bothered other people?
5) Has anyone noticed you stop
breathing during your sleep?
Category 2
6) How oen do you feel tired
or fatigued aer your sleep?
7) During your waking time, do
you feel tired, fatigued or not up to par?
8) Have you ever nodded o or
fallen asleep while driving a vehicle?
9) If yes, how oen does this
occur?
Category 3
10) Do you have a high BP?
High risk of OSAS: 2 positive categories; low risk of OSAS: <2 positive categories. Data from Netzer et al. (1999).
Yes (1), no or don’t
know (0)
Item 2 Category 2
Slightly louder than
breathing (0) As loud as talking (0) Louder than talking (1) Can be heard in
adjacent room (1)
Items 5, 6, 7, 9
3–4 times per week (1) 1–2 times per week (0) 1–2 times per month (0) Never (0)
Positive if total score
≥2 points
Positive if total score
2 points
Category 3
Positive if answer to
item 10 is yes, or if
2
The Berlin Questionnaire
The Berlin Questionnaire was developed to identify patients at risk of OSA in a primary care setting. Subjects respond to questions from three categories, which address snoring severity, EDS, and hypertension or obesity history (table 2). An answer key is provided to score responses, which takes 10–15 min to complete. Subjects indicating persistent and frequent symptoms in two or more categories are considered to be at high risk of OSA.
The characteristics of the questionnaire vary depending on the population tested and it appears to be more sensitive than specific for detecting OSA. In a systematic review and meta-analysis of the diagnostic accuracy of screening questionnaires for OSA, the pooled sensitivity of the Berlin Questionnaire for an AHI of 30 events·h−1 was 89%, and the specificity was 33%.
The STOP and STOP-Bang questionnaires
The STOP Questionnaire was developed to screen perioperative patients for OSA. It consists of four dichotomous questions regarding the presence or absence of snoring, daytime somnolence, observed apnoeas and history of hypertension. A score of 2 indicates a high risk of OSA.
The STOP-Bang Questionnaire is an expansion of the STOP Questionnaire and incorporates four additional questions. These relate to objective factors including BMI, age, neck circumference and sex (table 3). In the initial validation of the STOP-Bang Questionnaire, a score of 3 out of a total of 8 was suggestive of OSA, with a sensitivity
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Table 3. The STOP-Bang questionnaire
1) Do you snore loudly?
2) Do you oen feel tired, fatigued or sleepy during the daytime?
3) Has anyone observed you stop breathing while you sleep?
4) Do you have or are you being treated for high BP?
5) BMI ≥35 kg·m−2?
6) Age ≥50 years?
7) Neck circumference ≥40 cm?
8) Male sex?
High risk of OSAS: answering yes to 3 items; low risk of OSAS: answering yes to <3 items. Reproduced and modified from Chung et al. (2016) with permission.
of 93% for detecting moderate OSA (AHI >15 events·h−1) and 100% for detecting severe OSA (AHI >30 events·h−1). A subsequent meta-analysis of studies examining its usage in the sleep clinic and in perioperative assessment confirmed it be a sensitive screening tool for OSA, particularly for severe disease. The negative predictive value of the STOP-Bang questionnaire increases with increasing OSA severity. It is therefore a valuable questionnaire for identifying patients at a low risk of significant OSA and can facilitate risk stratification and triage for subsequent investigations. However, this high degree of sensitivity is at the cost of specificity, and even patients with very high scores require confirmatory sleep studies. The STOP-Bang Questionnaire has the advantage of being easily applicable and quickly completed.
OSA50
The OSA50 questionnaire was developed to identify patients at high risk of OSA in the primary care setting. It is comprised of four weighted questions regarding the presence of obesity, snoring, apnoeas and age. A score of 5 out of a maximum of 10 is predictive of moderate-to-severe OSA. When followed by subsequent oximetry, this two-stage diagnostic model has a reported sensitivity of 88% and a specificity of 82% in a validation group.
The Lausanne NoSAS score
The Lausanne NoSAS score was developed to screen individuals at risk of SDB. It focuses on five parameters: neck circumference, obesity, snoring, age and sex. A score of 8 out of a total of 17 is highly indicative of OSA. In a validation study, a NoSAS score of 8 had a sensitivity of 89.8% and a specificity of 27.1% for detecting moderate-to-severe OSA (AHI >15 eventsh−1) in a sleep clinic cohort.
Questionnaires assessing sleep quality
Sleep quality can be dicult to define as it encompasses both the quantitative and qualitative aspects of sleep. Optimum sleep should be restful and restorative. SDB is oen associated with poor sleep quality and there are a number of questionnaires that have been developed to evaluate this, including the Pittsburgh Sleep Quality Index (PSQI) and the Functional Outcomes of Sleep Questionnaire (FOSQ).
The PSQI
The PSQI was developed in 1989 to measure sleep quality in psychiatric clinical practice and research, and has since been validated in diverse populations. It is a self-administered questionnaire that measures sleep quality and patterns of sleep during the preceding month. It consists of 19 individual items across seven domains,
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which are scored on a 4-point Likert scale. A global PSQI score of 5 is indicative of poor sleep quality, with a reported diagnostic sensitivity of 89.6% and a specificity of 86.5%. The PSQI score does not correlate significantly with objectively measured polysomnographic sleep parameters; additional diagnostic tests are therefore required to define the aetiology of poor sleep quality when present.
The FOSQ
The FOSQ was published in 1997 to quantify the impact of EDS on activities of daily living. It is a 30-item self-reported questionnaire and consists of five domains pertaining to activity levels, vigilance, intimacy and sexual relationships, productivity, and social outcomes. It can be used to evaluate the impact of EDS on normal activities and the extent to which these change with interventions. The questionnaire takes 15 min to complete and is graded using a 4-point scale, with a lower score indicating issues with sleepiness and a higher score suggesting ‘no diculty’. The FOSQ-10 is an abbreviated version of the FOSQ, comprised of 10 questions to facilitate rapid assessment.
There are many more questionnaires that measure additional components of sleep, such as the Insomnia Severity Index (ISI), the cataplexy questionnaire, and the International Restless Legs Syndrome Study Group scale. However, these are beyond the scope of this chapter.
Conclusion
Questionnaires are commonly used in clinical practice in the respiratory sleep clinic to evaluate the degree of subjective sleepiness, the probability of OSA and subjective sleep quality. Validated questionnaires have an important role in the assessment of subjects with suspected SDB, when accompanied by specialist consultation and access to appropriate objective diagnostic studies.
Further reading
Aurora RN, et al. (2011). Correlating subjective and objective sleepiness: revisiting the
association using survival analysis. Sleep; 34: 1707–1714.
Bernhardt L, et al. (2022). Diagnostic accuracy of screening questionnaires for obstructive
sleep apnoea in adults in dierent clinical cohorts: a systematic review and meta-analysis. Sleep Breath; 26: 1053–1078.
Buysse DJ, et al. (1989). The Pittsburgh Sleep Quality Index: a new instrument for psychiatric
practice and research. Psychiatry Res; 28: 193–213.
Buysse DJ, et al. (2008). Relationships between the Pittsburgh Sleep Quality Index (PSQI),
Epworth Sleepiness Scale (ESS), and clinical/polysomnographic measures in a community sample. J Clin Sleep Med; 4: 563–571.
Chai-Coetzer CL, et al. (2011). A simplified model of screening questionnaire and home
monitoring for obstructive sleep apnoea in primary care. Thorax; 66: 213–219.
Chasens ER, et al. (2009). Development of the FOSQ-10: a short version of the Functional
Outcomes of Sleep Questionnaire. Sleep; 32: 915–919.
Chung F, et al. (2016). STOP-Bang questionnaire: a practical approach to screen for obstructive
sleep apnea. Chest; 149: 631–638.
Hoddes E, et al. (1973). Quantification of sleepiness: a new approach. Psychophysiology; 10:
431–436.
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Johns MW (1991). A new method for measuring daytime sleepiness: the Epworth sleepiness
scale. Sleep; 14: 540–545.
Marti-Soler H, et al. (2016). The NoSAS score for screening of sleep-disordered breathing:
a derivation and validation study. Lancet Respir Med; 4: 742–748.
Nagappa M, et al. (2015). Validation of the STOP-Bang questionnaire as a screening tool for
obstructive sleep apnea among dierent populations: a systematic review and meta-analysis. PloS One; 10: e0143697.
Netzer NC, et al. (1999). Using the Berlin Questionnaire to identify patients at risk for the sleep
apnea syndrome. Ann Intern Med; 131: 485–491.
Weaver TE, et al. (1997). An instrument to measure functional status outcomes for disorders
of excessive sleepiness. Sleep; 20: 835–843.
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Clinical examination
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Louise Byrne, Brian D. Kent and Barry Kennedy
Clinical examination is an essential component of the evaluation for sleep disorders. As a minimum, the assessment should involve examination of the cardiac, pulmonary and neurological systems. Ideally, it should also include screening for secondary causes of sleep disorders as well as commonly associated comorbidities.
Obesity
Obesity is the most common modifiable risk factor for OSA and should be identified immediately. Increasing obesity is associated with increased prevalence and severity of sleep apnoea. The association between OSA and obesity arises from narrowing of the upper airway, increased pharyngeal collapsibility and reductions in lung volume that occur in obesity.
As obesity increases, there is an increase in subcutaneous fat deposition around the upper airway. The additional subcutaneous tissue exerts an extrinsic force on the upper airway causing airway narrowing. Furthermore, elevated BMI appears associated with increased pharyngeal collapsibility. Finally, as the severity of obesity increases, lung volumes reduce; this reduces caudal traction on the upper airway which further increases risk of pharyngeal collapse and severity of SDB.
The importance of adipose tissue as a mediator of the metabolic consequences of SDB is being increasingly recognised. As adipose tissue expands, alterations within
Key points
• Clinical examination can significantly inform the diagnosis and management of SDB.
• General inspection may identify important comorbidities in sleep clinic patients such as neuromuscular disease, obesity or acromegaly.
• Examination of the upper airway is strongly advised as it may identify reversible causes of SDB such as tonsillar hypertrophy.
• Tools such as Mallampati grading and Friedman classification can be useful in stratifying risk and identifying management strategies.
• Obesity is the most important modifiable risk factor in managing SDB and should be identified at initial assessment.
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Clinical examination
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its milieu of inflammatory cells ensue. This altered inflammatory phenotype leads to excess production of proinflammatory cytokines, which in turn are associated with insulin resistance and metabolic dysfunction.
Given the central role of obesity in the pathophysiology and metabolic consequences of SDB, BMI and neck circumference should always be measured. Evidence of diabetes (peripheral neuropathy and autonomic neuropathy) and hypercholesterolaemia (corneal arcus and xanthelasmas) should also be sought.
General inspection
Aside from obesity, endocrine disorders, chromosomal abnormalities and neuro­muscular disease are commonly associated with SDB and can be readily identified on general inspection. 80% of patients with acromegaly have OSA; this arises from distortion of the upper airway due to mandibular overgrowth and macroglossia. Features indicating acromegaly include enlarged hands and feet, frontal bossing and excessive sweating. Cushing disease may present with hirsutism, round face and easy bruising, while hypothyroidism is associated with elevated BMI, lassitude, dry skin and hair loss.
The presence of Down syndrome is indicated by low-set ears, a flat nasal bridge and a flat occiput. Patients with achondroplasia are prone to airway obstruction through a combination of anatomical and physiological variations; these patients present with short stature, frontal bossing and thoracolumbar kyphosis. Finally, muscle wasting, fasciculations and paradoxical breathing indicate a neuromuscular disorder.
Head and neck examination
Craniofacial abnormalities are commonly observed in OSA due to anatomical limitations of the upper airway. Micrognathia and retrognathia contribute to airway narrowing. Macroglossia (common in Down syndrome and acromegaly) precipitates upper airway narrowing during supine sleep due to posterior displacement of the tongue. Inspection of the neck may reveal goitre, increased muscle mass or increased adiposity; increased neck circumference (>43 cm in males, >41 cm in females) is a helpful clinical indicator of OSA.
Evaluation of the upper airway
Upper airway patency depends on several factors including muscle activity, extent of so tissue swelling and bony anatomy. OSA is commonly associated with an anatomically narrow pharyngeal airway. Many causes of upper airway narrowing can be identified on clinical examination.
Inspection of the nose may reveal evidence of previous nasal trauma. Assessment of the nasal passages may show abnormalities such as polyps, swollen turbinates or deviated septum. On inspection of the mouth, crowding of the teeth may suggest micrognathia. Any macroglossia should be noted. The oropharynx may demonstrate palatal oedema, tonsillar hypertrophy or an elongated uvula.
The degree of airway compromise can be estimated by the modified Mallampati grading tool, which was initially developed to predict dicult tracheal intubation. This grading tool is applied by visually measuring the space between the base of the tongue, uvula, and the so palate to assess the degree of oropharyngeal narrowing (figure 1). A high Mallampati score increases the risk of sleep apnoea as well as predicting increased severity.
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Clinical examination
Class I Class IVClass IIIClass II
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Figure 1. Modified Mallampati grading. Class I: so palate, fauces, uvula and pillars are visible. Class II: so palate, fauces and uvula are visible. Class III: so palate, fauces and the base of uvula are visible. Class IV: so palate is not visible.
The Friedman classification tool was designed to identify those patients who may benefit from a surgical procedure such as uvulopalatopharyngoplasty or lingual tonsillectomy. It consists of assessment of the tongue position in relation to other oropharyngeal structures, grading of tonsillar size and grading of lingual tonsil hypertrophy.
Pulmonary and cardiovascular system
The lungs should be auscultated to assess for evidence of decreased air-entry or wheeze, which may indicate COPD or asthma. OSA patients with coexisting COPD have high mortality rates and have worse outcomes than those with COPD alone. The thoracic spine should be assessed for skeletal abnormalities (e.g. scoliosis or kyphosis), as these may contribute to nocturnal oxygen desaturations and hypoventilation.
Pulmonary hypertension (PH) has been reported to be present in 17–70% of OSA patients. Although PH in OSA is oen mild, it may be identified by an elevated jugular venous pressure (JVP), hepatomegaly, ankle oedema, and auscultation for tricuspid and pulmonary murmurs. The presence of cor pulmonale in OSA patients is associated with a higher burden of nocturnal hypoxia.
BP readings for hypertension should be taken as multiple studies report an association between systemic hypertension and OSA. Ankle oedema, elevated JVP, and bilateral crepitations may indicate CHF; coexisting OSA or CSA in patients with CHF increases rates of hospital re-admission and mortality. The pulse should also be assessed for atrial fibrillation (AF) which is four times more common in patients with severe OSA than those without OSA.
Neurological assessment
SDB is a common finding in patients with neuromuscular disease. Its aetiology is multifactorial. Upper airway muscle weakness, diaphragmatic weakness, impaired chemosensitivity and lung restriction can lead to OSA, CSA and nocturnal hypoventilation.
Neurological assessment should include testing for generalised muscle weakness; proximal myopathy is associated with greater risk to the respiratory muscles. Mixed upper and lower motor neuron signs as well as small muscle wasting in the hands
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