Managing Sleep Disorders in Childhood: A Primer for Healthcare Providers

Sleep evolves from the newborn period to adulthood. Knowledge of these developmental changes is useful in evaluating sleep disorders. Newborns have no circadian rhythm, take frequent naps 24 hours a day, and spend almost 50% of their total rest time in rapid eye movement (REM) sleep.1

The alignment of a baby’s circadian rhythm with the solar day occurs during the first months of infancy, so that a day-night rhythm is well established by 6 months of age. Daytime sleep is consolidated into 1 or 2 well-defined naps during childhood, and naps are gradually discontinued during the preschool period. In adolescence, approximately 25% of the total sleep period is occupied by REM sleep.

The cycle between REM and non-REM (NREM) sleep, known as ultradian rhythm, similarly changes throughout development, with 50-minute cycles in infants and 90-minute cycles in older children. By early childhood, the deeper stages of NREM sleep begin to cluster in the first half of the night.1

The recommended number of hours of sleep per day for infants, toddlers, preschool-age children, school-age children, and adolescents is 12 to 16, 11 to 14, 10 to 13, 9 to 12, and 8 to 10 hours, respectively. 2

Given these developmental changes, daytime napping in school-aged children is unusual and deserves further evaluation. NREM parasomnias (e.g., night terrors or sleepwalking) generally cluster in the first half of the night, when NREM sleep predominates. In contrast, sleep apnea symptoms related to REM sleep are likely to occur later and may go unnoticed by a parent monitoring their sleeping child early in the night.

The American Academy of Sleep Medicine proposed the International Classification of Sleep Disorders, which classifies sleep disorders into 6 main categories (Table 1).3

Within these categories, disorders can also occur as a consequence of medical factors, substance use, or psychiatric disorders. For example, opioids can cause breathing problems during sleep.

Caffeine may frequently be associated with insomnia or sleep-related movement disorders ; Caffeine is sometimes consumed unknowingly by those who are unaware of the ingredients in their favorite beverages.4

Mood disorders can variably cause hypersomnia or insomnia. Therefore, a complete clinical history is vital to investigate the etiology of the two most common complaints seen in the sleep clinic: “I can’t sleep” or “I sleep too much.”

The most commonly used sleep test to confirm clinical suspicions is polysomnography (PSG).5

This test essentially comprises several sensors to monitor sleep. Among these, electroencephalography, electrooculography, and chin electromyography (EMG) help distinguish wakefulness from REM and NREM sleep stages.

Oronasal airflow sensors, pulse oximetry, capnography, electrocardiography, and extremity EMG are useful for measuring breathing, movements, and other sleep-related motor phenomena, such as parasomnias. A variation of PSG is the continuous positive airway pressure titration study, during which noninvasive respiratory support is titrated to treat sleep apnea.

The multiple sleep latency test (PLMS) uses an abbreviated array of these sensors to quantify sleep propensity during the day. During this test, the patient receives five 20-minute nap opportunities spaced at 2-hour intervals throughout the day. The average time it takes to fall asleep across all naps is called mean sleep latency (MSL). Normative data are available to help diagnose hypersomnia disorders.

Although laboratory sleep testing is crucial for investigating many sleep disorders, other, more accessible and appropriate screening tools may be used, depending on the presenting sleep problems. Sleep records are manually entered each day into sleep-wake pattern diaries, and actigraphy uses a wristwatch-like device that measures body movements and ambient light to more objectively determine sleep patterns. sleep and wakefulness in a period of 1 to 2 weeks.

Insomnia is a sleep disorder that is diagnosed when a patient or caregiver reports one or more symptoms, such as difficulty initiating sleep, difficulty staying asleep, waking up earlier than desired, reluctance to go to bed at an appropriate time, or difficulty falling asleep . sleep without the intervention of parents or caregivers. These symptoms occur along with one or more associated symptoms, including fatigue, attention problems, irritability, daytime sleepiness, or dissatisfaction with sleep.3 These reported sleep/wake complaints cannot be explained purely by inadequate sleep opportunity and must occur at least 3 times a week for at least 3 months to be classified as chronic insomnia disorder.

For symptoms lasting less than 3 months, the diagnosis of short-term insomnia disorder is used.

The prevalence rate of diagnosed insomnia in children is 11%, but this prevalence rate is much higher (up to 40%) when symptoms of insomnia are considered.6,7 Two common varieties of behavioral insomnia include sleep disorder. sleep onset association disorder (SOAD) and limit-setting sleep disorder, both of which tend to occur in childhood. Psychophysiological insomnia tends to occur in adolescents.

> Sleep onset association disorder

SOAD is a form of insomnia in which a child needs the presence of a parent and/or certain activities, such as bottle feeding, rocking, or watching television, to fall asleep or return to sleep after waking up in the morning. evening.

It is important to keep developmental patterns in mind when considering this diagnosis. In babies younger than 5 to 6 months, nighttime awakenings are the norm and are primarily driven by nutritional need. However, in older infants, nocturnal awakenings requiring engagement, often referred to as problematic nocturnal awakenings, are more likely related to SOAD8 and associated with shorter, less consolidated sleep.9

To prevent and address these problematic infant night wakings and SOAD, preventive parenting education can be provided at visits during the third trimester, postpartum, and during the first 6 months of a baby’s life. This education emphasizes the importance of having established bedtime routines and consistent sleep schedules, and offers guidance on appropriate parental management during infant sleep initiation and nighttime awakenings to promote the development of independent sleep skills. 9

A common recommendation is that babies should go to bed “drowsy but awake.”

This helps babies develop independent sleep initiation skills and allows them to resume sleep without caregiver intervention when nighttime awakenings occur.

For families experiencing problematic nighttime awakenings in their children, behavioral interventions can be introduced, including modified extinction or parental fading.9 Modified extinction involves the parent placing the infant in bed awake and checking on him periodically in regular increments of time until you fall asleep.

Parental fading involves parents placing their baby in bed awake, while gradually fading their level of involvement (for example, keeping a hand on their baby as they fall asleep, then standing near the baby as they fall asleep, and then sitting a little further away from the baby as he falls asleep). This process helps gradually train the baby to fall asleep independently.9

During interventions for SOAD, it is important to anticipate a possible extinction burst that involves an escalation in the number of attempts by the child to obtain parental intervention (e.g., with longer or more intense crying in the hope that the parent finally give in).

If parents observe this escalation or burst of extinction, they may assume that their intervention is not working. However, parents should be sure that this behavior is consistent with an extinction burst into the unwanted behavior. Once the child learns that intensified crying is not effective in eliciting parental intervention, crying and resistance typically decrease. In fact, previous research has shown that, on average, babies cry for approximately 45 minutes in the first 3 to 4 days of this intervention before showing a reduction in crying.10

> Sleep disorder due to limit setting

Limit -setting sleep disorder is insomnia characterized by ineffective setting of parental limits around sleep time, which can result in stagnation and refusal at bedtime. To address these factors, caregivers should first encourage the use of consistent sleep routines, which have been shown to reduce children’s bedtime resistance and other sleep problems.11

During bedtime routines, firm limits on screen time and arousal activities should be used, consistent with other general sleep hygiene recommendations (Table 2). Interactive visual schedules to represent the step-by-step bedtime routine can help a child stay on target and maintain consistency in implementing the routine across nights, caregivers, and homes, as needed. 12

The Bedtime Pass Program is also helpful in placing limits on a child’s attempts to call or look for their parents after bedtime, which can further delay sleep onset.13 The Bedtime Pass Program involves the parent providing the child with 1 to 3 bedtime passes that the child can exchange with parents for predetermined reasons (e.g., a glass of water, a hug, a question). Once the child is out of the pass, the parent will remind the child and insist that the child stay in bed, using minimal interaction with the child.

The child can be encouraged to exchange unused passes for a reward the next morning. Other techniques to effectively set and reinforce bedtime expectations include the Good Morning Light, a nightlight programmed to change color by signaling designated sleep and wake times, and the Sleep Fairy positive reinforcement program.14 With the program Sleep Fairy , parents can inform their children that the "sleep fairy" will leave a small prize in the morning if the child follows the established sleep rules. These rules can be modified over time as the child’s sleep behavior improves and progresses.

> Psychophysiological insomnia

Psychophysiological insomnia is characterized by increased arousal and conditioned difficulty sleeping, resulting in an inability to initiate and/or maintain sleep and decreased functioning during wakefulness.3 Commonly seen in adolescents , this form of insomnia can be effectively treated. through cognitive behavioral therapy for insomnia (CBT-I).15 In fact, CBT-I has been established as the recommended first-line treatment for insomnia in adults.16

CBT-I typically includes promotion of healthy sleep habits, teaching stimulus control, sleep restriction therapy, relaxation skills training, and cognitive modification of thoughts.15,16

Some patients may benefit from self-administered CBT-I tools, including phone-based apps such as CBT-I Coach, SHUT-I, or SLEEPIO.17,18 These resources are easily accessible, low-cost, and effective.19 If If additional intervention is considered necessary, referral to a behavioral sleep medicine specialist may be indicated.

> Pharmacological management of insomnia

Behavioral interventions are the first-line treatment for insomnia, although a combined psychological and pharmacological approach may be useful for certain populations (for example, those with neurodevelopmental disorders, pervasive developmental disorders, chronic medical conditions, and psychiatric disorders). twenty

Although no medication is formally approved by the U.S. Food and Drug Administration (FDA) for the treatment of pediatric insomnia, there is expert consensus that medications can be beneficial if used rationally and judiciously.20 Drugs commonly Prescription medications include melatonin, hydroxyzine, trazodone, and clonidine.

Circadian sleep-wake rhythm disorders involve misalignment of biorhythms with the external environment (Table 1).

Commonly seen in adolescents with a prevalence of 7% to 16%, delayed sleep-wake phase disorder (DFSRD) presents as a chronic, recurrent delay in sleep onset with inability to fall asleep or wake up on time. desired.3,21

Actigraphy or accurate sleep recordings are very helpful in diagnosis. Behavioral treatment for TFSVR first involves promoting healthy sleep habits (Table 2). Additional treatment for TFSVR depends on the severity of the disorder, but usually involves sleep-wake progression or chronotherapy.

To advance the sleep-wake phase and address the delayed secretion of endogenous melatonin that individuals with TFSVR typically experience,22 exogenous melatonin can be administered prior to the onset of endogenous melatonin secretion with decreasing ambient light, and can be administered bright light therapy upon awakening.23,24 In humans with a typical day-night circadian rhythm, melatonin levels are low during the day and begin to increase when ambient light is dimmed (i.e., melatonin onset with light dimming).

In general, the onset of sleep occurs a couple of hours after the start of melatonin secretion.22

Although identifying the onset of endogenous melatonin secretion with light dimming can be challenging (e.g., requiring plasma, saliva, or urine analysis), research has established that it tends to occur between 7 PM and 7 PM. 9 PM in children ages 6 to 12, and approximately 30 minutes later as children get older.22

Research on the optimal dose of melatonin for chronobiological effects is still in its early stages, but based on current knowledge, clinicians can recommend 0.5 to 3.0 mg of melatonin approximately 3 hours before the onset of endogenous melatonin with the dimming of the light. This would result in the administration of melatonin approximately 5 hours before the usual onset of sleep.22

For bright light therapy, a broad-spectrum lamp can be used, which emits 1000 lux light for 30 minutes upon awakening.2 As you successfully progress through the sleep-wake phase, with the patient going to bed and waking up earlier, the time of bright light therapy should also be gradually brought forward, corresponding to the time of getting up each morning.

This phase advancement may be sufficient for TFSVR cases that are less severe, where only a few hours of advancement are needed. However, in more severe cases, chronotherapy may be necessary. Chronotherapy involves gradually moving the patient’s sleep schedule around the 24-hour clock until the desired sleep-wake time is reached and then maintaining this sleep-wake time using sleep hygiene, melatonin, and bright light.25

Pediatric sleep-related breathing disorders can be categorized as conditions with airway obstruction (obstructive sleep apnea syndrome [OSAS]), abnormal control of breathing (central sleep apnea syndrome), and ineffective gas exchange (hypoventilation). ). Of these, OSA is the most common.

Obstructive breathing during sleep comprises a spectrum of conditions, ranging from mild snoring to recurrent obstructive sleep apneas (OSA) in severe cases. OSA is characterized by intermittent prolonged partial or complete obstruction of the upper airways that disrupts normal ventilation during sleep and normal sleep patterns.3

Snoring is reported in approximately 10% of children, while OSA is reported in 1% to 4% of children, with a peak prevalence between 2 and 6 years of age.26,27,28

A higher prevalence of OSA is reported in children with obesity (10%-25%), craniofacial malformations (e.g., 50% in achondroplasia), and Down syndrome (60%).3,26,28 Additionally, a positive family history of OSA increase the risk of OSA in the child.27

Predisposing factors include airway narrowing, high level of airway collapse, and abnormal control of breathing. The most common cause of OSA in children is an anatomical obstruction due to large tonsils and adenoids. Increased collapsibility of the airways contributes in children with obesity or neuromuscular disorders.29

The presenting symptoms of OSA can be grouped into nocturnal and daytime symptoms (Table 3). All children should be screened for snoring, according to the American Academy of Pediatrics (AAP).30

Suspicion for OSA is high if snoring occurs 3 or more nights per week, is loud, and is associated with restless sleep, daytime sleepiness, or daytime behavioral problems. The physical examination should include evaluation of general appearance, craniofacial features, nasal anatomy, airway patency, and tonsil size. However, these clinical characteristics, including tonsil size, cannot reliably identify OSA.31,32

Untreated pediatric OSA has been shown to cause neurocognitive, metabolic, and cardiac morbidity.26

These effects could be mediated by intermittent hypoxemia, sympathetic activation, and sleep fragmentation as a result of recurrent airway obstruction. OSA can be associated with daytime attention problems, hyperactivity, and cognitive deficits, and these tend to improve with treatment.33 Additionally, abnormal blood pressure control, left ventricular hypertrophy, and left ventricular dysfunction have been reported.34,35 Metabolic effects include a higher incidence of insulin resistance and fatty liver disease in obese children with OSA.36,37,38

> Diagnosis of OSA

A PSG provides an objective measure of the frequency of respiratory events and ventilatory impairment during sleep and is the gold standard for the diagnosis of OSA.26,27,39 Events are classified as obstructive apneas or hypopneas depending on the degree of airflow limitation.39 The apnea-hypopnea index (AHI) is calculated as the number of apnea events plus hypopnea events per hour of sleep. In children, OSA is defined as an AHI greater than 1.26

Experts classify the severity of OSA based on AHI scores, with scores of 1 to 5, ≥ 5 to 10, and ≥ 10 considered mild, moderate, and severe OSA, respectively.39 Hypoventilation (carbon dioxide >50 mm Hg for >25% of sleep time) may be a key finding of obstructive breathing in children with obesity, Down syndrome, and neuromuscular disorders.40

Alternative testing modalities, such as home sleep studies and overnight pulse oximetry, show promise due to increased patient acceptance, reduced cost, and improved access, but are not currently recommended for diagnosing diabetes. Pediatric OSA due to the high rate of false negatives.41,42

> Treatment of OSA

Children with suspected OSA should be referred to a sleep medicine specialist or otolaryngologist39 or should directly undergo nocturnal PSG.26,39,40 It is important to note that the guidelines of the American Academy of Otolaryngology–Head and Neck Surgery recommend PSG only for children younger than 2 years, or if they have comorbidities (e.g., obesity, Down syndrome, craniofacial anomalies, neuromuscular disorders, sickle cell disease, or mucopolysaccharidosis), or when examination findings are not consistent with symptoms.43

Treatment of OSA is indicated for an AHI greater than 5, regardless of comorbidities associated with OSA, as well as for an AHI of 1 to 5 in the presence of comorbidities associated with OSA.40 Adenotonsillectomy is generally considered the first-line treatment. line for OSA in healthy children aged 2 to 18 years with adenotonsillar hypertrophy.26

Adenotonsillectomy is usually performed in the outpatient setting unless there is an increased risk of postoperative respiratory compromise due to young age (<2 years), severe OSA, obesity, or cardiac disease and craniofacial anomalies .

The success rate of adenotonsillectomy in otherwise healthy children aged 2 to 18 years is approximately 80%.33 Risk factors for persistent OSA after adenotonsillectomy include obesity, severe OSA, and craniofacial abnormalities.33 Weight loss improves OSA in overweight children and can be used in combination with other treatments for moderate to severe OSA or as the only treatment for mild OSA.44,45

Administration of continuous positive airway pressure (PAP) through a mask or through bilevel pressures distends/opens the airway during sleep and has been shown to improve OSA and its sequelae in children.46 The rate of Adherence to PAP in children is approximately 50%, with a higher compliance rate among children aged 6 to 12 years.46,47 PAP therapy, when tolerated, is very effective for OSA in children, especially in those with Down syndrome.48 PAP adherence can improve with proper mask fit and behavioral intervention from a psychologist.

Supplemental oxygen can be used to correct oxygen desaturations during sleep in children with severe OSA who are not candidates for surgical treatment and do not tolerate PAP therapy. It can also be used as a bridge to definitive therapy. Of note, hypercapnia can occur with oxygen supplementation and should be ruled out before prescribing home oxygen.

Dental procedures ( eg, rapid maxillary expansion) may benefit children who have OSA and a narrow palate. Mandibular advancement devices are an option in selected patients.40 Recently, hypoglossal nerve stimulator implants have shown promise in adolescents with Down syndrome and severe OSA despite adenotonsillectomy.49

Alternative treatment options for mild OSA include corticosteroid nasal spray or watchful waiting for 6 months.50 Resolution of PSG-confirmed OSA has been demonstrated in up to 50% of school-age children with mild to moderate OSA without intervention. specific.33

Current management paradigms for OSA commonly use an abnormal PSG as a criterion for initiation of treatment. However, improvement in behavioral outcomes after adenotonsillectomy has been demonstrated, even in children who snore and do not meet PSG criteria for OSA.33 Results from the Pediatric Adenotonsillectomy for Snoring Trial are awaited to guide treatment of children. with mild or subclinical obstructive sleep-disordered breathing in the future.51

Excessive daytime sleepiness ( EDS) is defined as “the inability to remain awake and alert during the main waking episodes of the day, resulting in periods of uncontrollable need to sleep or involuntary lapses of drowsiness or sleep.”3 Pediatric EDS It has a prevalence of approximately 30% and can also manifest as emotional lability, inattention and hyperactivity behaviors, or deterioration in school performance.3,52,53

The modified Epworth Sleepiness Scale and other screening questionnaires can help distinguish EDS from lack of energy or fatigue.54,55 In clinical practice, EDS is most often due to lack of sleep or poor sleeping habits. sleep hygiene, including nighttime alert activities, such as sports or work, caffeine use, or media consumption.56

Outside of these lifestyle factors, EDS in a school-aged child should be taken seriously, and a number of interacting etiologies should be considered (Table 4). Central disorders of hypersomnolence include narcolepsy, idiopathic hypersomnia, and Kleine-Levin syndrome (KLS).3 These central disorders are a distinct category of disorders in which EDS cannot be attributed to other untreated sleep or circadian rhythm disorders. .3

> Narcolepsy

Narcolepsy comprises a tetrad of symptoms, including EDS for more than 3 months, cataplexy, sleep paralysis, and hypnagogic hallucinations, with a prevalence of 1 in 2,000 in the United States.57 Although onset is typically in the second decade , Classic symptoms may not appear all at once, and diagnosis is often delayed by 15 years or more.58,59

By definition, SDE is seen in 100% of narcolepsy cases, with daily periods of irrepressible sleep, unexpected "sleep attacks," or extreme "sleep inertia" (i.e., propensity to continue sleeping), with confusion or even aggression upon forced awakening.3,54 Daytime naps are generally refreshing, while nighttime sleep may be interrupted by frequent awakenings.3

Sleep paralysis ( awakening from sleep unable to move), and visual or auditory hallucinations at sleep-wake transitions may be reported in 33% to 80% of patients.3 Cataplexy manifests as a sudden loss, brief (usually <2 minutes), symmetrical, bilateral skeletal muscle tone precipitated by strong emotions (e.g., laughter). Consciousness is preserved, but deep tendon reflexes are temporarily suppressed. The suddenness of the spell may mimic syncope or seizures.60 Mild cataplexy may present with facial drooping, ocular ptosis, jaw drooping, tongue protrusion, or unsteady gait.3 Childhood narcolepsy may coincide with the onset of obesity or puberty. precocious.61

PSG followed by PLMS the next day is indicated when narcolepsy is suspected. The PSG night serves to eliminate alternative causes of EDS (e.g., OSA) and adequately document total sleep time. The PLMS assesses sleep propensity during the day. Any REM period of sleep onset (PREMIS) is observed, defined as REM sleep that occurs within 15 minutes of sleep onset.

In an appropriate clinical setting, a mean sleep latency (LMS) of 8 minutes or less on the PLMS and a total of 2 or more PREMIS counted between the PSG and the PLMS are diagnostic.3 This test is not valid for children under the age of 6 years. Careful pre-planning of testing is required to reduce false-positive results from medication effects or poor sleep habits. A urine drug test is recommended in adolescents.62

Narcolepsy is subclassified into type 1 (NT-1) and type 2 (NT-2).3 NT-1 most commonly results from hypothalamic hypocretin (orexin) deficiency. Most patients with NT-1 carry the human leukocyte antigen (HLA) subtype DQB1*0602 and present with cataplexy.63 However, HLA typing is not diagnostic of NT-1 because up to 38% of the general population carries this marker. The association with certain infections (e.g., H1N1 influenza) and a specific adjuvant-associated influenza vaccine suggests that the interaction of genetic and environmental factors mediates autoimmune loss of hypocretin neurons.64

NT-1 is diagnosed either by an abnormal PLMS result and cataplexy or by a low level of hypocretin-1 in the cerebrospinal fluid (<110 pg/mL).3 NT-2 is defined by an abnormal PLMS without cataplexy or hypocretin abnormalities in the cerebrospinal fluid. Only approximately half of patients with NT-2 carry HLA-DQB1*0602.63 Less commonly, narcolepsy may be associated with paraneoplastic disorders, hypothalamic lesions, myotonic dystrophy, and Prader-Willi syndrome.3,65

> Other hypersomnias

Idiopathic hypersomnia ( IH) presents with EDS for more than 3 months, long total daily sleep needs (>12-14 hours), non-restorative naps, sleep inertia, and absence of cataplexy. PSG and PLMS together show less than 2 PREMIS and can record an LMS of less than 8 minutes.3

KLS is a rare disorder presenting in adolescents, with cyclical KLS accompanied by behavioral changes (e.g., hyperphagia, anorexia, hypersexuality) and altered cognition and mood. During the sleeping phase, the patient may sleep 16 to 20 hours a day and cycles may last from 2 days to 5 weeks, with relapses usually several times a year, but at least once every 18 months. Children are normal between episodes.3 There are no confirmatory tests for KLS.66

> Treatment of hypersomnia

Narcolepsy and IH are lifelong diseases, while KLS tends to resolve over the years.3,66

Management of narcolepsy includes attention to good sleep habits, regular exercise, judiciously planned daytime naps, and specialized education.54 In older adolescents, driving safety, alcohol avoidance, and career counseling are important.56

Warning agents such as amphetamines and methylphenidate may be helpful. Modafinil is approved by the FDA for people 17 years and older with the warning of Stevens-Johnson syndrome, psychosis, and oral contraceptive failure.67 Tricyclic antidepressants or selective serotonin reuptake inhibitors (SSRIs)/norepinephrine such as venlafaxine, protriptyline or clomipramine are useful for cataplexy.56

Sodium oxybate and newer low-sodium formulations of oxybate mixed salts are FDA-approved for children 7 years and older for both SDE and cataplexy of narcolepsy. Oxybates are unique in that they are administered at night in divided doses.

Of note, the American Academy of Sleep Medicine has recently published evidence-based guidelines for patients with central hypersomnolence disorders using the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) process, with a “conditional recommendation” for modafinil and oxybate. sodium for pediatric narcolepsy, but no recommendations for SKL or HI.68

Parasomnias are defined as “undesirable physical events or experiences that occur during sleep entry, during sleep, or during awakening from sleep.”3

Human consciousness comprises 3 states: wakefulness, NREM sleep and REM sleep. Confusion of established boundaries and involuntary activation of primitive locomotor centers (central pattern generators) in the brain stem and spinal cord are thought to result in a complex amalgamation of behaviors, experiences, mental activity, and memory.69 In Generally speaking, the various parasomnias can occur in NREM or REM sleep (Table 1).

> NREM parasomnias

Confusional awakenings involve moaning, crying, or sitting up in bed with a confused appearance.3 Night terrors begin with a sudden piercing scream associated with profound autonomic activity, including pupillary dilation, sweating, tachypnea, and tachycardia.3 Sleepwalking usually involves getting up from sleep. bed with glassy eyes aimlessly or with partial purpose, but agitated, dangerous, violent, or uncharacteristic behavior may sometimes occur. (e.g., urinating in unusual places, leaving the house).70

NREM parasomnias are relatively common in children of both sexes. The prevalence of confusional awakenings is approximately 17.3% among children aged 3 to 13 years.3 Night terrors peak at age 1.5 years (34.4% prevalence) and sleepwalking at age 10 years (13.4% prevalence), with approximately one-third of children with night terrors going on to develop sleepwalking in late childhood.71 The prevalence of sleepwalking is highest for children who have one or both parents who had historically been sleepwalkers.71 In contrast, adults have a lower rate of sleepwalking (1.5%) and confusional awakenings (2.9%–4.2%).3,72

As a group, NREM parasomnias generally arise from deep sleep (NREM stage 3), which is usually most prominent in the first third of the night. These parasomnias often last a few minutes, but may well exceed 30 minutes.67 The eyes are usually open, but the child is difficult to awaken, resists or responds poorly to parental intervention, and has very limited memory or null of the subsequent event.3.67

Psychiatric pathology is rarely associated.70

Untreated OSA, gastroesophageal reflux disease, anxiety, and neurodevelopmental disorders (e.g., autism) may increase risk.56,73 Sleep deprivation, social stress, external or internal stimuli (e.g., phone ringing, fever , full bladder) and certain medications (e.g., sedatives) can prepare or trigger such events.3 As a differential diagnosis, certain nocturnal epilepsies can present with brief (<2 minutes), multiple (sometimes in clusters), stereotypic events, with behaviors complex motors and vocalizations.70,74

NREM parasomnias are mostly benign and do not require investigation, and children usually outgrow them. Parents should be advised not to interfere with the event and to ensure the child’s safety (e.g., installing barriers on stairs, or perimeter door alarms).75,76

Frequent, disruptive, and potentially dangerous parasomnias, high parental anxiety, or parental suspicion of comorbid sleep disorders warrant overnight PSG. Concomitant video electroencephalography is useful if suspicion of seizures is high. Treatment of any associated sleep disorders (e.g., OSA, poor sleep hygiene) may be beneficial. Clonazepam has been used to suppress NREM parasomnia in high-risk patients.56

> REM parasomnias

Nightmares are defined as “extremely dysphoric, well-remembered dreams that generally involve threats to survival, safety, or physical integrity.”3

Anxiety, fear, shame or disgust are common. (3) In contrast to NREM parasomnias, nightmares tend to occur in the second half of the night, when REM sleep is common. During nightmares, children often wake up easily with a vivid memory of the experience.

The prevalence of occasional nightmares is 60% to 75%, while recurrent nightmares occur in 20% to 30% of children and 4% of adults.76,77,78 They may be associated with post-traumatic stress, anxiety or other psychopathology, as well as certain medications.3,56 Nightmare disorder is diagnosed when recurrent nightmares result in effects such as mood disturbance, resistance to bedtime, nighttime fears, daytime fatigue, effect on education or family dysfunction.3

Peace of mind and attention to good sleep hygiene are helpful. (Table 2). Depending on the patient’s age, specific psychological interventions may include imagery rehearsal therapy, relaxation techniques, desensitization, and exposure therapy.79

REM sleep behavior disorder ( RSBD) involves “acting out of dreams” due to the loss of normal skeletal muscle atonia, which is characteristic of typical REM sleep.3 This results in complex or even violent behaviors (punching, kicking, jumping out of bed). Upon awakening, the person quickly becomes alert and coherent (in contrast to sleepwalking).3 In adults, it is frequently associated with degenerative brain disorders.3

TCSR is very rare in childhood and can sometimes be associated with brainstem lesions, narcolepsy, and SSRI use.56 Diagnostic PSG is always indicated if TCSR is suspected to confirm loss of skeletal muscle atony in the electromyography (EMG) of the extremities and to detect other sleep disorders, such as OSA, which may be associated with motor activity during sleep.3 Treatment usually involves clonazepam or melatonin and attention to any underlying precipitants.56

Sleep-related movements are common in young children and may occur in the transition from wakefulness to sleep, during sleep, or both.80,81,82

Restless legs syndrome (RLS) and periodic limb movement disorder (PEMD) have a prevalence of 2% to 4% in children and adolescents.83,84 Although periodic limb movements during sleep (PEMS) are common in RLS, TMPE and RLS are distinct clinical conditions with specific diagnostic criteria.3 Their pathogenesis is not well understood, but genetic factors, dopaminergic dysfunction, and iron deficiency have been implicated.84 RLS and TMPE are associated with cardiovascular, autonomic, and neurocognitive changes.83,84

General symptoms may include leg discomfort, attention deficit, and lack of restful sleep.3 A complete neurological examination is essential to rule out other causes of leg discomfort, such as postural alterations, sprains or tears of muscles/ligaments/tendons. , positional ischemia (numbness), dermatitis, peripheral neuropathy and fibromyalgia. MPES are defined by specific PSG scoring criteria and include repetitive and stereotyped movements of the extremities, with a frequency > 5 per hour considered abnormal in children.3

RLS is diagnosed clinically by a set of symptoms, including an irresistible urge to move the legs, usually accompanied by unpleasant sensations in the legs that worsen during inactivity and are partially or completely relieved by movement, and that occur predominantly due to afternoon or evening.3

A family history of RLS or MPES on PSG may be supportive of the diagnosis of RLS in the child who is too young to describe the classic set of symptoms. When abnormal MPES or restless legs symptoms cause problems in initiating or maintaining sleep (with or without daytime disturbance), and cannot be better explained by another cause, TMPE or RLS are considered diagnostic, respectively (Table 1) .3

Restless sleep disorder ( RSD) is a recently described sleep disorder characterized by large body movements and position changes during the night, with at least 5 large body movements per hour and a significant effect on daytime behaviors.85

Sleep-related rhythmic movements (e.g., head banging, body rocking) are quite common during sleep-wake transitions in normally growing infants and toddlers, but are called “rhythmic movement disorder” if they interfere with sleep. sleep, compromise daytime functioning, or cause injuries.3

Tests to evaluate iron status, including a complete blood count, serum iron level, and serum ferritin level, are indicated for RLS, TMPE, and TSI. Additional tests may be indicated if neuropathy is suspected, such as thyroid function, fasting blood glucose, insulin level, and serum levels of vitamins B6, B9, and B12.

> Management of sleep-related movement disorders

Like other sleep disorders, attention to good sleep habits is a cornerstone of IPD management (Table 2). Medications, such as SSRIs, that could aggravate IPD and TMPE, should be replaced or discontinued. Caffeine should be avoided. Rhythmic movement disorder usually requires reassurance and common sense safety measures.

Pharmacotherapy is used when lifestyle modifications are not enough. Oral iron supplemented at 3 mg elemental iron per kilogram per day for 3 months is the first-line treatment in children with RLS, TMPE, or TSI, who have low levels of serum ferritin (<50 ng/mL [<50 mg/mL). L]).85,86,87

Intravenous iron has been used in children who do not tolerate or fail oral iron therapy. Second-line treatment options for RLS and TMPE include α2δ-1 ligands such as gabapentin, pregabalin, and gabapentin enacarbil.88 Clonazepam has also been tested.89

Table 1. International Classification of Sleep Disorders, third edition (ICSD-3)

Table 2. Sleep hygiene recommendations

Table 3. Symptoms of obstructive sleep apnea in children

Table 4. Common causes of excessive daytime sleepiness

Sleep disorders cover a wide spectrum of clinical conditions, which, to a greater or lesser extent, affect the child’s health.

Difficulty falling or staying asleep, frequent awakenings, daytime sleepiness, associated respiratory disorders, among other issues, affect the patient’s daily activity.

Knowing the normal evolutionary patterns of sleep from the neonatal period to adulthood, taking a complete clinical history to investigate the etiology of sleep disorders, and carrying out an objective evaluation of the patient will allow us to arrive at a specific diagnosis.

Promoting good sleep hygiene and providing optimal targeted treatment will help improve sleep-wake periods and the quality of life of the patient and their family.