Evolution of Sleep from Birth to Adolescence and Sleep Disorders in Children

Fig. 52.1
Obstructive apnea during REM sleep (60 s PSG epoch). The event is characterized by cessation of nasal/oral (N/O) and nasal pressure (NPRE) airflow with preserved respiratory effort (THOR and ABD). Obstruction is associated with transient desaturation of SpO2 from baseline. Note that cessation of flow on the capnogram is delayed compared to other measures of flow due to cannula transit time


Fig. 52.2
Obstructive hypopnea (60 s PSG epoch). The event is characterized by diminished nasal pressure airflow (NPRE) and nasal–oral thermistor flow (N/O) associated with arousal and 3 % desaturation of SpO2 from baseline

Over time, it was discovered that children with SDB often exhibit non-apneic respiratory disturbances during sleep, and it is currently thought that prolonged partial airway obstruction may represent the predominant form of respiratory disturbance for many children as opposed to discrete events such as apneas and hypopneas (Fig. 52.3) [42, 43]. Obstructive hypoventilation is characterized by prolonged partial obstruction resulting in diminished pulmonary ventilation causing hypercapnia and/or hypoxemia [44]. Upper airway resistance syndrome (UARS) represents a form of prolonged partial airway obstruction in which increased work of breathing disrupts the quality or continuity of sleep even in the absence of gas exchange abnormalities [45].


Fig. 52.3
Prolonged partial airway obstruction during stage N3 sleep (60 s epoch). Continuous snoring and excessively negative esophageal pressure fluctuations (measured peak-to-trough on ExPES with normal being 0 to −10 cm of water) indicate prolonged partial airway obstruction. Note normal oxygen saturation (SpO2) and end-tidal CO2 levels (CAPN) despite increased work of breathing

These varieties of sleep-related airway obstruction are not mutually exclusive, and it is common for children with obstructive SDB to exhibit elements of both chronic partial obstruction and “classic” OSA during PSG.

Sleep-disordered breathing in the absence of upper airway obstruction is substantially less common than obstructive SDB in children. Non-obstructive hypoventilation during sleep usually occurs in the context of diminished respiratory drive, weakness of the respiratory muscles, intrinsic lung disease, or a combination of these factors. Ventilation or gas exchange during sleep becomes insufficient to meet the body’s needs, resulting in hypercapnia and/or hypoxemia. Predisposing conditions include disorders of the brainstem and cranial nerves (e.g., Chiari I malformation), cervical spinal cord injuries, neuromuscular disorders (e.g., Duchenne muscular dystrophy, myotonic dystrophy), and restrictive lung disease (e.g., severe scoliosis).

Congenital central hypoventilation syndrome (CCHS) is a distinct variety of non-obstructive hypoventilation that is usually present—but not always recognized—at birth. Affected children exhibit impaired ventilatory responses to hypercapnia and occasionally to hypoxemia [46]. As a result, ventilation during wakefulness may be normal or only modestly impaired, whereas ventilation during sleep is characterized by hypoventilation of a degree that may be life-threatening if the condition is not promptly identified and treated. Mutations of the PHOX2B gene have been identified in the majority of cases studied, and CCHS may be associated with Hirschsprung disease, neural crest tumors, and disturbances of cardiac autonomic regulation [47, 48]. Central hypoventilation syndromes are thought to be clinically and genetically heterogeneous, and late-onset forms with hypothalamic dysfunction have been described [4951].

Central sleep apnea affecting children is identified most frequently in the context of primary central sleep apnea of infancy, formerly called apnea of prematurity. This condition is characterized by prolonged central apneas exceeding 20 s in duration or the presence of periodic breathing for greater than 5 % of total sleep time [52]. The central apneas that characterize this condition are sometimes accompanied by obstructive or mixed respiratory patterns as well. Primary sleep apnea in small or premature infants is thought to result primarily from dysmaturity of respiratory control mechanisms and usually improves with maturation. Apnea in infants may also occur as an associated manifestation of gastroesophageal reflux, infection, metabolic disturbance, upper airway obstruction, seizure, or other serious illness.

Clinically significant central sleep apnea is otherwise uncommon in children and has received scant scientific study. Brief central apneas are frequently observed during REM sleep or following arousals in otherwise healthy children, but seldom are accompanied by significant oxygen desaturation. Central apneas may also occur in the context of periodic breathing—recurring cycles of regular respiration interrupted by pauses lasting several seconds (Fig. 52.4). This stereotyped respiratory pattern is frequently observed in young infants, where it can be benign, and is occasionally seen in older children during sleep–wake transitions.


Fig. 52.4
Periodic respiration during stage N2 sleep (60 s epoch). Repetitive, stereotyped central apneas separated by several breaths (NPRE and N/O) are accompanied by cyclical desaturation of SpO2 from baseline

Primary snoring in children is defined as snoring which does not disrupt sleep, cause gas exchange abnormalities, or result in pathologic daytime symptoms [53]. Although this condition by definition should not be associated with any secondary symptoms, subtle deficits in mood, behavior, and cognitive function have been reported in children with primary snoring compared to non-snoring controls [5456]. It is thought that primary snoring may sometimes progress to more serious varieties of SDB. In one small series of children with PSG-documented primary snoring, 10 % were found to have developed OSA when reassessed 1–3 years later [57]. In a larger cohort, 37 % of school-age children with primary snoring had developed OSA at 4-year follow-up [58].

Epidemiology of Childhood SDB

Estimated prevalence rates for SDB in children remain imprecise because universally accepted diagnostic criteria for these conditions were only recently established and because large population-based studies using PSG have not been undertaken. It is estimated that between 5 and 12 % of children snore habitually, with some reports suggesting an increased risk of children exposed to tobacco smoke [5963]. The prevalence of OSA in children is generally estimated to be 1–3 % [6467].

Data are not available regarding the prevalence of UARS, central sleep apnea, and hypoventilation in children. CCHS is a rare disorder conservatively estimated to affect at least 300 children worldwide [46]. Prevalence for primary sleep apnea of infancy varies with size and gestational age. Symptomatic apnea of infancy affects 84 % of newborns weighing less than 1000 g, 25 % of newborns weighing less than 2500 g, and less than 0.5 % of term infants [52].

Clinical Features of Childhood SDB

The clinical manifestations of SDB in children (see also Chap. 32) differ from those exhibited by adults, as summarized in Table 52.1. Children with obstructive SDB tend to be noisy breathers during sleep, but severity may range from heroic snoring or stridor to only minimally loud respiration. Snoring may be continuous, intermittent, or vary with body position. Snoring often worsens during upper respiratory infections or with exacerbations of allergic rhinitis and sometimes improves during treatment with decongestants or nasal steroids. Snoring in children with obstructive SDB is often accompanied by prominent mouth breathing and unusual sleeping positions such as neck hyperextension or excessive propping upon pillows, which represent compensatory mechanisms that may improve airway patency.

Table 52.1
Sleep-disordered breathing in children compared to adults



Physical characteristics


Younger children: sexes equally affected

Adolescents: males > females

Primarily males

Peak age

2–8 years

Middle age and older

Body weight

Usually normal, occasionally obese

Most often obese

Upper airway

Adenotonsillar enlargement frequent

Redundant soft tissue occasional

Adenotonsillar enlargement occasional

Redundant soft tissue frequent

Symptoms during sleep


Frequent, often continuous

Frequent, often interrupted by pauses

Witnessed apnea



PSG characteristics


Prolonged partial obstruction >  intermittent

Cyclical intermittent obstruction

Sleep architecture

Normal > fragmented

Frequent arousals with sleep fragmentation

Secondary symptoms

Daytime sleepiness

Most often absent or intermittent



Inattention, hyperkinesis, disturbed behavior

Cognitive slowing


Hypertension, cor pulmonale

Hypertension, cor pulmonale, stroke

Witnessed apneas are only occasionally reported for children with obstructive SDB. This observation is consistent with the premise that prolonged partial airway obstruction during sleep is more common in children than the recurring episodes of brief obstruction followed by arousal that characterize typical adult OSA. When an obstructive apnea is witnessed in a child, parents may report paradoxical chest wall motion or the presence of snorting or gasping noises as respiration resumes.

Children with obstructive SDB demonstrate greater degrees of restlessness, enuresis, and perspiration during sleep than healthy controls [68]. Several reports additionally suggest that obstructive SDB may be associated with increased risk of parasomnias [69, 70].

In contrast to the prominent snoring and restlessness exhibited during the sleep of children with obstructive SDB, children with non-obstructive SDB tend to be quiet sleepers who only occasionally exhibit obvious respiratory symptoms at night. The lack of easily recognizable nighttime symptoms may lead to delays in diagnosis and treatment, particularly if sleepiness or other daytime symptoms are misattributed to other causes.

Children with obstructive SDB frequently exhibit sore throat, dry mouth, headache, or grogginess upon morning waking, although these symptoms are often transient and self-limited. Daytime mouth breathing is frequently seen in children with obstructive SDB, particularly when adenotonsillar hypertrophy is present [68]. Somnolence as a daytime symptom is seldom prominent in younger children unless their underlying SDB is severe [71]. When excessive somnolence is present, it is more often subtle or intermittent and sometimes evident only during sedentary activities such as riding in an automobile.

Neurobehavioral deficits represent the most common and most variable daytime symptoms of childhood SDB. Early reports of childhood OSA, documenting relatively severe cases, identified a high prevalence of school problems, behavioral disturbances, and hyperactivity among affected children [41, 72, 73]. More recent reports have suggested that even less severe varieties of childhood SDB may be associated with the same daytime symptoms. Children with SDB have been reported to have higher rates of parentally reported behavior problems, lower scores on tests of sustained attention, and lower scores on neuropsychometric assessments of executive function [7477]. Subtle neurocognitive deficits have also been reported for children with primary snoring [54, 76, 77, 78].

There is also compelling evidence that SDB is overrepresented in children with ADHD and learning problems. Snoring was reported to be three times as frequent among children with attention-deficit/hyperactivity disorder (ADHD) compared to non-ADHD controls drawn from general pediatric and child psychiatry clinics, with higher snoring scores being associated with greater levels of inattention and hyperactivity [79]. Among 297 first-grade children performing poorly in school, 54 (18 %) were found to have evidence of nocturnal hypoxemia or hypercapnia during limited, home-based sleep studies [80].

Physical Features Associated with Childhood SDB

The physical examination may be entirely normal in children with SDB, but predisposing anatomic features are often identified in affected children. Adenotonsillar enlargement, which is most common between 2 and 8 years of age, is associated with several physical findings [81]. In addition to visible tonsillar hypertrophy, “adenoid facies”—visible mouth breathing, pinched nose, and elongated facial appearance—is often observed. Narrow and high-arched hard palate, maxillary or mandibular hypoplasia, and macroglossia represent additional physical features which may predispose to SDB.

Obesity represents a risk factor for obstructive SDB in children, but this association is less robust in prepubertal children and more common during adolescence. In a group of 22 obese adolescents without sleep complaints, 10 (46 %) were reported to have abnormal PSGs [82]. Daytime sleepiness and AHI for this group both correlated with degree of obesity.

Some children with SDB—particularly infants and young children with severe airway obstruction—may present with decreased growth, low body weight, or failure-to-thrive [83, 84]. Treatment of these children may result in improved growth parameters and insulin-like growth factor 1 levels [8587].

A variety of medical, genetic, and craniofacial conditions are associated with increased risk for SDB during childhood (Table 52.2). Detailed epidemiologic data are not available for most of these conditions; however, it is estimated that over 30 % of children with Down syndrome may exhibit SDB [8891].

Table 52.2
Conditions associated with sleep-disordered breathing (SDB) in children

Craniofacial syndromes associated with maxillary or mandibular hypoplasia

  Apert syndrome

  Crouzon syndome

  Goldenhar syndrome (hemifacial microsomia)

  Hallermann-Streiff syndrome

  Robin sequence (Pierre Robin syndrome)

  Treacher Collins syndrome

Other syndromes with prominent craniofacial involvement


  Klippel-Feil syndrome

  Saethre-Chotzen syndrome

  Velocardiofacial syndrome (Shprintzen syndrome)

Conditions associated with macroglossia

  Beckwith-Wiedemann syndrome

  Down syndrome


  Mucopolysaccharide storage disorders (Hunter, Hurler, and Scheie syndromes)

Conditions causing congenital upper airway abnormalities

  Cleft palate

  Choanal atresia

  Fetal warfarin syndrome

  Pfeiffer syndrome

Systemic neurological disorders

  Structural lesions of the brainstem and medulla (eg, Chiari malformation)

  Cranial neuropathies (eg, Fazio-Londe disease)

  Neuromuscular disorders (eg, myasthenia gravis, Duchenne muscular dystrophy, myotonic dystrophy

Miscellaneous conditions

  Prader–Willi syndrome

Secondary Sequelae of Childhood SDB

The long-term effects of childhood SDB are not well understood apart from limited data regarding cardiovascular effects. Reversible cor pulmonale and congestive heart failure have been reported in children with severe SDB [9294]. In addition, electrocardiographic evidence of heart strain was reported for 3.3 % of 92 children referred for adenotonsillectomy [95]. The frequency with which hypertension affects children with SDB remains uncertain, but obesity and respiratory disturbance index (RDI) were found to be independently associated with increased blood pressure in a large cohort of 6- to 11-year-old children [96].

The public health impact of childhood SDB has also received little scrutiny. The extent to which affected children’s neurobehavioral symptoms limit their long-term academic achievement and adult socioeconomic status has not been studied, although the effect is suspected to be substantial for at least some children with SDB. Perhaps the most dramatic evidence illustrating the public health impact of childhood SDB is data reporting substantially higher health care utilization for children with OSA compared to controls, including higher rates for hospitalization, medication use, and emergency department visits [97]. Treatment of OSA children with adenotonsillectomy resulted in a reduction of total annual health care costs by one-third, compared to no change for controls and untreated OSA children [98].

Clinical and Laboratory Assessment of Children with SDB

The assessment of a child with suspected SDB should begin with a detailed history and physical exam as outlined in Table 52.3. The sleep history must thoroughly screen for the symptoms of SDB already discussed, but also should also include limited assessment for other sleep disorders whose clinical manifestations may mimic those of SDB. The medical history and physical examination should also include screening for other conditions that might cause or predispose toward SDB.

Table 52.3
Clinical assessment of the child with suspected sleep-disordered breathing (SDB)

Sleep history

Snoring: volume, frequency, character, changes over time

Mouth breathing

Unusual sleeping positions (eg, neck hyperextension, propping on pillows)

Restlessness, limb movements

Excessive perspiration

Night waking: frequency, duration, and patterns


Symptoms upon waking: grogginess, headache, sore throat, dry mouth

Sleep schedule

Family history of SDB or other sleep disorders

Daytime symptoms

Mouth breathing


Behavior: irritability, distractibility, hyperkinesis, temperamental behavior

School: attention, academic performance, decline in grades

Sleepiness, especially in sedentary situations (e.g., automobile rides)

Medical history

ENT: adenotonsillar disease, allergic rhinitis, congenital anatomic abnormalities

Endocrine: obesity, growth, thyroid disease

Cardiovascular: hypertension, congenital heart disease

Pulmonary: asthma, other intrinsic lung disease

Neurologic: disorders affecting brainstem and cranial nerves or causing muscle weakness

Development: developmental delay, infant failure-to-thrive

Other: craniofacial disorders, genetic syndromes (eg, Prader–Willi Syndrome, Down Syndrome)

Physical examination

Vital signs: weight, height, body mass index, blood pressure, percentile ranks

Oropharynx: tonsillar size, airway patency, palate, dentition, occlusion, tongue

Nasopharynx: polyps, septal deviation, airflow, “pinched-nose” appearance

Craniofacial: micrognathia, maxillary hypoplasia, occlusion, cleft palate, or other craniofacial syndrome

Neck: thyroid, masses, circumference

Thorax: cardiac exam, lung auscultation, evidence of scoliosis

Neurologic: cranial nerve palsies, evidence of muscular weakness or neuropathy

Behavior: attention, hyperkinesis, evidence of irritability or sleepiness

Other: mouth breathing, noisy respiration, “adenoid facies”

The history and physical examination are often supplemented by other assessment tools that are less expensive and more easily administered than PSG. A variety of standardized questionnaires have been developed with the goal of predicting whether sleepiness or SDB is likely to be present based on the presence and severity of specific symptoms. Questionnaires such as the Epworth Sleepiness Scale and Stanford Sleepiness scale are of limited usefulness in the assessment of children with suspected SDB due to limited validation data for this age-group and because the symptom that these measures assess—sleepiness—is often not obvious in affected children [99, 100]. Several questionnaires have been developed specifically for use in children, and limited validation data have been obtained regarding the use of the Pediatric Sleep Questionnaire and OSA-18 as screening tools for childhood SDB in clinical and research populations, [101103]. The sensitivity of these tools for detection of SDB in clinical populations may be limited, however [104].

Although audio recordings of a child’s snoring have long been recommended as a “$5.00 sleep study,” this technique did not reliably distinguish primary snoring from SDB (AHI ≥ 5) in a blinded study assessing 29 snoring children [105]. Although home video recordings of a child’s sleep are an easy and usually inexpensive supplement to the clinical history during evaluation of a child with suspected SDB, the sensitivity and specificity of this technique have not been rigorously assessed.

Overnight oximetry is not recommended for primary assessment of children with suspected SDB [106]. Although the technique is unobtrusive, inexpensive, and well tolerated by most children, it reliably detects SDB only when arterial oxygen desaturation is prominent and does not identify those children whose SDB is characterized primarily by hypercapnia or obstruction without desaturation. Among 210 children with PSG-documented OSA (AHI ≥ 1), 120 (57 %) had normal or inconclusive nocturnal oximetry, confirming that normal oximetry cannot be used to rule out SDB in children [107].

Other non-PSG diagnostic tests are used on selective basis for children with suspected SDB, primarily in children with predisposing conditions and children presenting with severe symptoms. Anatomic obstruction of the upper airway is often demonstrable on radiographic or endoscopic assessment [108, 109]. Children suspected to have severe SDB or concurrent cardiorespiratory problems sometimes require chest X-rays, electrocardiogram (ECG), echocardiogram, and formal pulmonary function testing for complete assessment. Children with prominent learning or behavioral problems usually benefit from neuropsychometric testing and age-appropriate behavioral assessment and intervention, even when such symptoms are secondary to SDB.

Polysomnography in Childhood SDB

Laboratory-based PSG represents the most sensitive and reliable tool presently available for the detection and classification of SDB in children. It is also a test that can be easily customized based on the clinical presentation of each patient. For example, 16-lead EEG can be added to standard PSG to provide increased sensitivity for the detection of interictal discharges or nocturnal seizures. Similarly, esophageal pressure monitoring (Pes) is sometimes performed for children felt to be at risk of UARS and other obstructive SDBs associated with prolonged partial airway obstruction.

PSG also has several limitations when used in children. The test itself is lengthy, expensive, and potentially stressful for both children and their parents. Laboratories having substantial experience in performing and interpreting PSG for children are limited in number and sometimes have lengthy waiting lists. Finally, routine PSG is not always sensitive for the detection of prolonged partial airway obstruction (e.g., UARS), but tools such as Pes make the study more invasive and are not available in all pediatric sleep laboratories.

PSG should be performed when a child’s symptoms, medical history, and physical examination suggest significant risk of clinically significant SDB. Isolated snoring—especially when it is only soft and occasional—is seldom a sufficient indication for PSG unless other symptoms or risk factors are also present. Practice guidelines that address respiratory indications for PSG in children have recently been issued by the American Academy of Sleep Medicine [106, 110]. Although it is common for otolaryngologists to perform adenotonsillectomy for suspected SDB without preoperative PSG, the safety and cost-effectiveness of this practice have been vigorously debated [111113]. In addition, this practice can potentially result in children with noisy respiration, but no clinically significant SDB having surgery for which the overall health benefit is uncertain. Until validated practice guidelines address these issues, the author’s practice is to apply the same standards presently used for adults: to obtain a baseline PSG for patients with clinically suspected SDB before decisions are made with respect to treatment.

PSG in children is performed in a manner comparable to adult studies, utilizing frontal, central, and occipital EEG channels, electrooculogram (EOG), and ECG, as well as chin and limb electromyogram (EMG). Respiratory monitoring at minimum includes oral and nasal airflow, chest and abdominal movement, arterial oxygen saturation, and measures of carbon dioxide (end-tidal and/or transcutaneous). Most laboratories use nasal pressure transducers—thought to be sensitive to flow limitation and subtle decrements in flow—to assess nasal airflow, but since many children breathe through their mouths, thermistor, or thermocouple sensors to monitor oral or oral–nasal flow remain necessary as well.

Many sleep laboratories have the capability to supplement standard recording techniques with additional modes of respiratory monitoring when clinically indicated. Pes may be added to improve the sensitivity of PSG for partial airway obstruction and increased work of breathing. Pes is minimally invasive—requiring insertion of a thin catheter through the nasopharynx into the esophagus—but the technique has negligible impact upon children’s sleep and is the most sensitive method presently available for the measurement of increased upper airway resistance [114, 115]. Several less invasive techniques for the assessment of partial airway obstruction have been investigated for use in children, including pulse transit time, peripheral arterial tonometry, respiratory cyclerelated EEG changes, and intercostal EMG monitoring, but none of these techniques are yet available for routine clinical use [116121].

Scoring of sleep stages, movements, and arousals during pediatric PSG is performed in the same manner used for adult studies. Thirty-second epochs are reviewed and scored manually using standard criteria recently revised by the American Academy of Sleep Medicine [122124]. Scoring of respiratory events for children differs slightly from that for adults. Whereas scoring of apneas, hypopneas, and respiratory effort-related arousals (RERAs) requires a minimum event duration of 10 s in adult studies, scoring of these events for pediatric studies requires only that the event last at least the duration of 2 missed breaths. This rule permits scoring of brief events in children whose baseline respiratory rate during sleep exceeds 12 breaths per minute.

Standards for interpreting the results of pediatric PSG have evolved over time. Normative PSG data for 50 healthy, asymptomatic children between 1 and 18 years of age were reported in 1992, as summarized in Table 52.4 [125]. Although these data have helped define the statistical limits of normality in healthy children, the point at which abnormal PSG parameters become associated with pathologic symptoms and outcomes has not been precisely determined. An AHI exceeding 5 events per hour is generally considered to be abnormal for adults. Although this threshold had previously been used for the diagnosis of OSA in children, the fact that children frequently demonstrate symptomatic OSA with AHIs below 5 has long suggested that a lower threshold is more appropriate for children [55, 56].

Table 52.4
Polysomnographic (PSG) parameters in 50 healthy children aged 1–18 years

PSG parameter

Mean ± SD

Apnea index (events/hour)

0.1 ± 0.5

Minimum SaO2 (%)

96 ± 2

Desaturations ≥4 % (per hour of total sleep time)

0.3 ± 0.7

Maximum ETCO2 (mm Hg)

46 ± 4

Duration of hypoventilation (ETCO2 > 45 mm Hg) (percentage of total sleep time)

7 ± 19 %

Adapted from Marcus et al. [125]

The current International Classification of Sleep Disorders, Third edition (ICSD3), criteria for the diagnosis of pediatric OSA require the presence of one or more scorable obstructive events per hour of sleep or documentation of obstructive hypoventilation in conjunction with other clinical and PSG findings as outlined in Table 52.5 [52]. These revised criteria now permit many children who previously would have been classified as having nocturnal hypoventilation or UARS to be classified as having OSA. Further outcomes-based research remains necessary to better define the thresholds at which abnormal respiratory parameters on PSG become associated with clinically significant sequelae.

Table 52.5
ICSD-3 criteria for pediatric obstructive sleep apnea

Criteria A and B must both be satisfied:

A. The presence of one or more of the following symptoms:

1. Snoring

2. Obstructed, labored, or paradoxical respiration during sleep

3. Hyperactivity, disturbed behavior, learning problems, or sleepiness

B. PSG demonstrates one or both of the following findings:

1. One or more obstructive apneas, hypopneas, or mixed apneas per hour of sleepOR

2. The presence of obstructive hypoventilation (≥25 % of total sleep time spent with PCO2 > 50 mm Hg) associated with one or more of the following findings:

a. Snoring

b. Flattening/ flow restriction of the inspiratory nasal pressure waveform

c. Paradoxical thoraco-abdominal effort

Adapted from The International Classification of Sleep Disorders, Third Edition [52]

ICSD-3 did not specify separate pediatric criteria for non-obstructive forms of hypoventilation, with the partial exception of congenital central hypoventilation syndrome, a genetically mediated condition secondary to mutations of the PHOX2B gene which typically presents during infancy [52]. Current American Academy of Sleep Medicine, PSG, scoring rules define sleep-related hypoventilation for children as consisting of PCO2 levels exceeding 50 mm Hg for greater than 25 % of total sleep time [123] (Fig. 52.5).


Fig. 52.5
Sleep-related hypoventilation (60 s epoch). Capnography (CAPN) demonstrates persistent elevations of end-tidal CO2 above 50 mm Hg during REM sleep in the absence of desaturation and scorable respiratory events. Paradoxical respiratory effort is demonstrated in the thoracic (THOR) and abdominal (ABD) effort channels

Diagnostic criteria for UARS in children were not addressed in ICSD-3, although proposed criteria have been published elsewhere [55].

Treatment of SDB in Children

Adenotonsillectomy is the most commonly administered treatment for obstructive SDB in children [126]. Although this procedure is thought to be effective in alleviating upper airway obstruction for many symptomatic children, the frequency with which adenotonsillectomy “cures” SDB in children is variable.

Early case series assessing response of childhood OSA to adenotonsillectomy reported surgical cure rates exceeding 70 %; however, these studies were limited by substantial variability in patient selection and frequent use of adult rather than pediatric PSG criteria to define OSA [127, 128].

More recent studies have reported variable and sometimes lower operative success rates. Among one group of 110 children with OSA (AHI > 1, mean AHI 22.3), complete postoperative normalization of the AHI was observed in only 27 subjects (25 %) [129]. In another large cohort of successively seen children with OSA (AHI > 1), 94 of 199 subjects (47 %) demonstrated abnormal polysomnograms postoperatively [130]. Among 397 children with OSA enrolled in a large, randomized, multicenter trial, PSG findings normalized in 79 % of children treated with adenotonsillectomy compared to 46 % of those assigned to watchful waiting and supportive care [131]. These and other studies suggest that children with high Mallampati scores, high preoperative AHI, obesity, or atypical anatomy of the upper airway may be at elevated risk of residual SDB following adenotonsillectomy.

In addition to improvements in obstructive symptoms and PSG parameters, adenotonsillectomy for children with SDB may also be associated with tangible improvements in behavior, school performance, and quality of life measures [132134]. In one large cohort of children assessed before and after clinically indicated adenotonsillectomy, half of the children having ADHD prior to surgery no longer qualified for the diagnosis when reassessed one year postoperatively [117, 118].

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Oct 7, 2017 | Posted by in NEUROLOGY | Comments Off on Evolution of Sleep from Birth to Adolescence and Sleep Disorders in Children

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