History and exam
Key diagnostic factors
common
presence of risk factors
Strong risk factors for obstructive sleep apnoea include craniofacial anomalies, adenotonsillar hypertrophy, macroglossia, gastro-oesophageal reflux disease, allergic rhinitis, environmental tobacco, obesity, hypotonia, medications, alcohol, and Down's syndrome.
Inconsistent parenting contributes to chronic insomnia disorder in the appropriate age group (age 5 years or younger).
Adolescents are especially prone to delayed sleep-wake phase disorder, especially with exposure to light in the evening.
snoring, gasping, choking while asleep (obstructive sleep apnoea)
While snoring is often a prominent symptom of obstructive sleep apnoea (OSA), not all children who snore have OSA. Studies have found that between 3% and 15% of children snore on a regular basis, especially between 3 and 6 years of age (13%-35%).[28]
In high-risk groups, such as children with Down's syndrome, the absence of snoring does not rule out OSA. In the presence of other signs and/or symptoms, proceeding to a sleep study should be considered.[80]
night sweats (obstructive sleep apnoea)
Often a consequence of laboured breathing.
breathing through an open mouth (obstructive sleep apnoea)
Often associated with adenoidal hypertrophy.
sleeping with hyperextended neck (obstructive sleep apnoea)
May be seen as the child attempts to maintain a clear airway during sleep.
restless sleep and periodic limb movements (obstructive sleep apnoea)
Brought about by effort during sleep to maintain a clear airway.
secondary nocturnal enuresis (obstructive sleep apnoea)
Nocturnal enuresis that reappears after a child has been dry for at least 3 months is considered secondary nocturnal enuresis, and is often seen with obstructive sleep apnoea.
hypertension (obstructive sleep apnoea)
May be seen.
inability to fall asleep (sleep association disorder)
Sleep association disorder is associated with apparent inability to sleep through the night, which does not appear to have any outward effect during the day.
cataplexy (narcolepsy)
Sudden temporary loss of muscle tone. Diagnostic for narcolepsy type 1.
hypnagogic or hypnopompic hallucinations (narcolepsy)
Represents REM intrusion into wakefulness. Hypnagogic hallucinations occur as one falls asleep. Hypnopompic hallucinations occur as one awakens.
sleep paralysis (narcolepsy)
While common in the general population, a component of narcolepsy thought to represent REM phase intrusion into wakefulness.
erratic sleep schedule (delayed sleep-wake phase disorder)
Especially if sleep is erratic between weekdays and weekends.
Other diagnostic factors
common
excessive daytime sleepiness
Can be present in many sleep disorders, and thus non-specific. Often presents with history of falling asleep in school. Can be found with insufficient sleep in adolescents, circadian rhythm disorders (especially delayed sleep-wake phase disorder), obstructive sleep apnoea (more common in older, obese children than in younger, thinner children), restless legs syndrome, periodic limb movement disorder, narcolepsy, Kleine-Levin syndrome, Smith-Magenis syndrome, secondary to medications.
difficulty awakening in the morning
Present in many sleep disorders, and thus non-specific. Can be found with insufficient sleep in adolescents, circadian rhythm disorders (especially delayed sleep-wake phase disorder), obstructive sleep apnoea, restless legs syndrome, periodic limb movement disorder, Kleine-Levin syndrome, Smith-Magenis syndrome, secondary to medications.
sleepwalking or talking (obstructive sleep apnoea)
Associated with confusional events either falling asleep or during awakening in narcolepsy.
sleep attacks (narcolepsy)
Associated with sudden sleep onset particularly brought on by emotional states.
refusal to sleep in own bedroom (chronic insomnia disorder)
Also associated with anxiety or PTSD.
Risk factors
strong
craniofacial abnormalities (obstructive sleep apnoea)
Abnormal craniofacial structure, including maxillary hypoplasia, retrognathia, micrognathia, and congenital syndromes associated with craniosynostosis all reduce the aperture of the upper airway and narrow its calibre. Examples of these conditions include Down's syndrome, along with rarer entities such as Robin's sequence and Collins, Pfeiffer, and Apert syndromes.[5][22][45][46][57][58][59]
adenotonsillar hypertrophy (obstructive sleep apnoea)
Enlargement of the tonsils and adenoids results in narrowing of the upper airway, reducing its calibre, and leading to obstruction. Removal of the tonsils and adenoids resolves obstructive sleep apnoea (OSA) in most cases, although some studies have shown recurrence of OSA with long-term follow-up.[60][61][62]
macroglossia (obstructive sleep apnoea)
An enlarged tongue as is found in Down's syndrome, Beckwith-Wiedemann syndrome, or certain storage diseases, can narrow the calibre of the upper airway, leading to obstruction.[48]
gastro-oesophageal reflux (obstructive sleep apnoea)
Can cause inflammation of the soft tissues of the upper airway, narrowing its calibre and increasing its tendency to collapse with the negative pressures exerted during inspiration.[49]
allergic rhinitis (obstructive sleep apnoea)
Can narrow the calibre of the upper airway, increasing its tendency to collapse with the negative pressures exerted during inspiration.[50]
environmental tobacco smoke exposure (obstructive sleep apnoea)
Has been shown to be an independent risk factor for developing obstructive sleep apnoea, probably through a direct inflammatory effect on the mucosa of the upper airway.[51]
obesity (obstructive sleep apnoea)
hypotonia (obstructive sleep apnoea)
Low baseline muscle tone and/or central hypotonia all reduce upper airway calibre and predispose to obstructive sleep apnoea.[53]
alcohol (obstructive sleep apnoea)
Obstructive sleep apnoea is worsened in response to alcohol.[54]
medications (obstructive sleep apnoea)
Obstructive sleep apnoea is made worse by certain medications such as benzodiazepines and baclofen.[55]
Down's syndrome (obstructive sleep apnoea)
evening light exposure (delayed sleep-wake phase disorder)
inconsistent parenting style or unrealistic sleep expectations (chronic insomnia disorder)
Limit-setting behaviours in chronic insomnia disorder (previously behavioural insomnia of children: limit-setting type) can be caused by a child testing the limits of what parents consider acceptable. A lack of consistency in parenting styles between the parents can send mixed messages to a child and lead to an unstructured sleep environment, resulting in differing perceptions by the parents of appropriateness. Parents may also predispose children to insomnia by assigning too much time in bed or putting them to bed too early.[5]
age <6 years (chronic insomnia disorder or obstructive sleep apnoea)
adolescent age (delayed sleep-wake phase disorder)
Delayed sleep-wake phase disorder is commonly seen in adolescents.[5][11]
Without external cues to entrain their internal circadian body clock, adolescents tend to delay their sleep phase and adopt a circadian rhythm that is >24 hours.[41] It is often brought on by a combination of poor sleep hygiene and external pressures such as school work, social engagements, and sport activity. These all delay going to sleep. Insufficient sleep during the week is coupled with a tendency to sleep in late on weekends in order to catch up on lost sleep. The syndrome may also stem from a heightened sensitivity to evening light exposure, and in some cases from genetic differences in clock genes.[5][43][44]
distractions in bedroom (delayed sleep-wake phase disorder)
Lack of darkness and quiet, pets in the room, and use of a computer, television, or mobile phone may distract the child from falling asleep.
traumatic or stressful life events (chronic insomnia disorder)
Life stressors that might impact sleep in children include the development of a medical or psychiatric illness; emotional, physical, or sexual abuse; exposure to negative parental interactions or separation; death of a parent; and placement in an alternate care setting, such as foster care.[5][64]
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