Prevalence of sleep disorders in pediatric patients
Sleep disorders are becoming increasingly common in children; they have repercussions on all aspects of a child’s health (cognition and behavior, growth and development, ability to concentrate) as well as on the quality of life of their families (disturbances in parents’ and siblings’ sleep, alterations in relations among the child, parents, and family, etc.).
Few studies have analyzed the prevalence of sleep disorders in children and adolescents in Spain or worldwide. The prevalence of sleep disorders varies depending on the definitions used and the type of problem studied.
A review of different studies shows that between 13% and 27% of parents of children aged from 4 to 12 years report that their children have difficulties sleeping, with problems such as reluctance to go to bed, anxiety on going to bed, delayed onset of sleep, reactive co-sleeping, snoring, enuresis, nocturnal awakening, nightmares, sleep terrors, sleepwalking, early morning awakening, and excessive daytime sleepiness. These problems tend to be stable throughout childhood, so a child with sleep problems at the age of 8 months will probably continue to have problems at the age of 3 years, and those with problems when they are 2 years old will continue to have problems when they are 12 years old.
In Spain, even fewer studies have been done in pediatric populations than in adult populations. One study done in the Autonomous Community of Valencia (Pin G., personal communication) found the following prevalences: insomnia (10%), restless legs syndrome (2%), sleep apnea syndrome (2%–4%), and excessive daytime sleepiness similar to in adults (15%).
The amount of sleep we need varies with age, health status, emotional status, and other factors; the ideal amount is that which enables us to carry out our daily activities without difficulties.
2. Classification of sleep disorders in pediatrics
In 2014, the American Academy of Sleep Medicine published the third edition of the International Classification of Sleep Disorders (ICSD-3), dividing them into eight main categories:
- Insomnia disorders
- Sleep-related breathing disorders
- Sleep-related movement disorders
- Central disorders of hypersomnolence (daytime sleepiness)
- Circadian-rhythm sleep-wake disorders
- Isolated symptoms and normal variants
- Other sleep disorders
a. Pediatric insomnia (behavioral or due to poor sleep hygiene)
Insomnia is the most common pediatric sleep disorder; it can affect infants from the age of 6 months and children up to the age of 5 years old. The incidence is estimated at between 20% and 30% in newborns and remains at 14% in five-year-olds. Insomnia is defined as the lack of sleepiness at bedtime or difficulty in sleeping through the night with frequent awakening for variable lengths of time. However, in this section, the term behavioral insomnia or due to poor sleep hygiene–as the most common causes of insomnia in childhood and adolescence–refers to insomnia derived from inadequate acquisition of appropriate sleep habits or an inappropriate attitude on the parents’ part in establishing good sleep hygiene. From the clinical point of view, the parents explain that the child has “never” slept well and that they wake up very often during the night .
This disorder originates in deficient acquisition of the sleep habit; in other words, the child creates distorted associations between sleep and multiple inappropriate routines that his or her parents establish to try to ensure that the child falls asleep (going to bed with TV, inducing sleep with a bottle, rocking, strolling, etc.) [5-7].
When evaluating sleep disturbances in children, we must always take the following elements into account:
- It is essential to take a very accurate history of the symptoms to detect psychological or organic precipitating factors and to determine the elements that are maintaining the problem.
- The sleep disorder should be seen within a 24-hour time frame, because it is very likely that different daytime activities have a clear influence on sleep.
- From the start, it is important to rule out the most common organic processes that can disturb sleep: colic, gastroesophageal reflux, lactose intolerance, upper respiratory tract infections, otitis media, atopy, obstructive sleep apnea syndrome, periodic limb movements, etc.
The final goal of treatment is to enable the child to learn to fall asleep alone without the need for parents to be present. To achieve this goal, we need to start by modifying the child’s sleep habits and creating a ritual related to going to bed. This routine (sleep habits) should take place over a 5- to 10-minute period in which parents and child have a pleasant time together; this requires peaceful contact that puts the child in a mood that favors sleep. It is very important for the parents to instill this routine at the same time every night (regularity in the routine)[5-8].
Sleep-inducing drugs have scant benefits in this condition, Most children will not improve at all when drugs are used to help them fall asleep . Children who have this type of insomnia are completely normal from the physical and psychological viewpoints .
b. Respiratory sleep disorders: obstructive sleep apnea-hypopnea syndrome (SAHS)
Respiratory disorders during sleep comprise a wide spectrum that encompasses many clinical presentations from habitual snorers to obstructive sleep apnea-hypopnea syndrome (SAHS). All together, these disorders have a high prevalence and impact on health. It is estimated that between 10% and 12% of preschool-age and school-age children snore habitually, and only 2% to 4% of these children clearly meet the criteria for SAHS. The maximum incidence peak occurs around the ages of 2 to 3 years, and there is a slight male predominance .
The main pathophysiological abnormality in patients with SAHS is the recurrent partial (hypopnea) or total (apnea) obstruction of the upper airway during sleep. Obstruction can cause hemoglobin desaturation, hypercapnia, arousals, or micro-arousals (resulting in fragmentation and abnormal sleep architecture in children), as well as alterations in the sympathetic and parasympathetic nervous systems .
In children, the most common cause of SAHS is anatomical obstruction from enlarged adenoids and tonsils. Associations have also been established between specific environmental and genetic factors (tobacco smoke, allergic rhinitis, and infantile and childhood asthma) and both increased incidence of adenoid and tonsillar hypertrophy and SAHS [9,12]. The alarming increase in obesity in children in developed countries has changed the classic view of SAHS toward a classification into two phenotypes. Type I is due mainly to marked adenoid and tonsillar hypertrophy, whereas Type II is due mainly to obesity. Table 1 reports the main risk factors for developing SAHS [9,12].
The most common symptom in children with respiratory alterations during sleep is snoring, an expression of upper airway resistance. These patients have “fitful” sleep, moving often and occasionally adopting peculiar postures (e.g., cervical hyperextension) to optimize the opening of the airway. Moreover, they have increased work of breathing, as evidenced by accessory muscle use and profuse sweating [9-12]. Micro-arousals due to respiratory events cause sleep fragmentation and impede restorative sleep, so children with SAHS can have increased tiredness, morning headaches, irritability, and poor performance at school.
Excessive daytime sleepiness is less common than in adults with SAHS, being reported by only 7% of parents but found in 13% to 20% of children who undergo a multiple sleep latency test in a sleep laboratory [9-12].
Patients with mild adenoid and/or tonsillar enlargement can also have nasal obstruction and breathe through their mouths at night; in severe cases, they may also breathe through their mouths during the daytime and have a nasal voice or even dysphagia. It is worth noting that the incidence of parasomnias (sleepwalking, night terrors, etc.) and bedwetting is also higher in these children .
Complications of SAHS.
- Coognitive-behavioral consequences of SAHS in children
Behavioral and neurocognitive abnormalities in childhood SAHS have been well characterized, including aggressive or oppositional-defiant behavior, attention deficit disorder with or without hyperactivity, and a wide range of learning difficulties [9,12].
- Cardiovascular consequences
The role of SAHS as a proinflammatory and atherogenic factor is well established. Intermittent hypoxia and hypercapnia have been implicated in malfunctions of arteriovenous vascularization. On the one hand, they cause autonomic dysfunction by activating the sympathetic nervous system and thereby affecting blood pressure and resulting in left ventricular hypertrophy. On the other hand, these episodes of hypoxia and hypercapnia increase pulmonary vascular resistance, resulting in pulmonary hypertension and right ventricular hypertrophy [9,12].
- Developmental delays.
Developmental delays are a recognized consequence of childhood SAHS, so SAHS should be ruled out in children studied for failure to thrive. Multiple factors are involved in deficient growth in SAHS, and some have yet to be elucidated. Children with SAHS expend more energy during sleep, and the amount is clearly reduced after tonsillectomy. Other factors implicated in failure to thrive in SAHS include decreased growth hormone production secondary to changes in sleep architecture and/or increased peripheral resistance to growth factors .
Diagnosis of SAHS
The diagnosis of SAHS is based on thorough history taking and physical examination. Nocturnal polysomnography is the gold standard for diagnostic confirmation, since it can record neurophysiological and electroencephalographic variables that enable us to evaluate the stages and architecture of sleep as well as cardiorespiratory variables that enable us to evaluate the work of breathing and gas exchange. In 2007, the American Academy of Sleep Medicine published the current diagnostic criteria for identifying and classifying respiratory events in children: apneas, hypopneas, limited airflow, nocturnal hypoventilation, and periodic respiration [9,12]
Treatment for SAHS
In patients with enlarged adenoids and/or tonsils who have mild SAHS (apnea/hypopnea index (AHI) 1-4 events/hour of sleep), drug therapy is the treatment of choice [8, 11, 13, 14]. Anti-inflammatory drugs such as topical nasal corticosteroids and antileukotrienes have proven efficacious in decreasing airway resistance by decongesting nasal passages and the pharynx (by reducing the size of the adenoids and tonsils). Surgical treatment is reserved for patients with moderate-severe SAHS (AHI≥4) [8, 11,14].
Noninvasive ventilation is indicated in children with residual SAHS after surgery as well as in those in whom surgery is contraindicated, and the technique of choice is continuous positive airway pressure (CPAP). In patients who have no access to CPAP or cannot tolerate it, bilevel positive airway pressure (BiPAP) is indicated. Patients with concomitant obesity should be encouraged to lose weight [8, 11,12].
c. Parasomnias: disorders of arousal from non-REM sleep
Parasomnias are undesirable experiences that occur during sleep. They usually occur during transitions from one phase to another, so they are classified according to when they occur:
Predominantly on awakening
During non-REM sleep
During REM sleep
- Arousal disorders during non-REM sleep
These disorders are a fundamental group of parasomnias in children, and they should be considered as a continuum of overlapping phenomena. These phenomena usually occur in the transition to slow-wave (deep) sleep, although they can also during N2; these experiences usually consist of automatic behavior with altered environmental perception that is normally forgotten afterward [1-3]. They usually occur in the first third of the night (2–3 hours after the onset of sleep). The mechanisms through which they occur are unknown, but it has been suggested that they might be related with a dysfunction in the normal progression of sleep. Many factors can influence the occurrence of these phenomena: sleep deprivation, infectious processes, stress, drugs (neuroleptics, hypnotics, psychostimulants, and antihistamines), periodic limb movements, and SAHS. There may also be a degree of family predisposition toward the development of this type of parasomnias.
- Night terrors
Night terrors are abrupt awakenings from slow-wave sleep; they are very intense and dramatic. They occur in 3% to 15% of children aged 4 to 12 years; their occurrence peaks between the ages of 5 and 7 years, although they can also occur before the age of 2 years. They typically resolve in the preadolescent period. In a night terror, the child wakes up suddenly, screaming and crying with fear. Night terrors can be associated with autonomic activation with mydriasis, diaphoresis, and tachycardia. Children may relate that they are being attacked (by monsters, spiders, snakes) and try to defend themselves from these attacks. The child does not respond to external stimuli, acts confused and disoriented, and normally does not recall the event later on [1,16].
- Confusional arousals
This disorder is very common in children less than five years old. A typical episode consists of a partial awakening in which the child is disoriented in time and space. Seeming confused, the child may have open or closed eyes and display inappropriate behavior. Efforts to wake the child are unproductive and the child rebuffs the parents’ efforts to provide consolation. Episodes usually last from 5 to 15 minutes (sometimes more), ending when the child falls asleep again. Intervening in the event can prolong it or even worsen it [1,16].
This common phenomenon is seen mostly in children; its incidence peaks between the ages of 4 and 8 years. Sleepwalking consists of the instauration of complex behaviors that start during slow-wave sleep and progress through actual walking. Sleepwalkers are normally calm and do not express fear. The transcendence of the episode is determined by the degree of mobility: from a few steps to attempts to leave the building, putting the child at risk for trauma and even hypothermia. Sleepwalking episodes usually end spontaneously with the sleepwalker returning to normal sleep. If awoken during an episode, sleepwalkers are usually confused for a few minutes .
- Parasomnias associated with REM sleep
Nightmares are usually long, very realistic and complicated dreams in which the feeling of terror or even death increases progressively. These dreams normally awaken the dreamer, who retains the sensation of having suffered. Nightmares appear from about the age of 3 years; about 30% of children have nightmares, and there is a degree of genetic predisposition. Nightmare can be triggered by trauma or real-life experiences, and children with frequent nightmares are more than three times more likely to develop psychiatric disorders[1,16].
The diagnosis of parasomnias requires clinical assessment. Children hardly ever remember events, so physicians need to question parents about the characteristics of the events, the time of night when they occur, and the behaviors they observed. It is also important to ask whether these events are rhythmic and stereotyped and whether they occur at different times doing the night, which is important for the differential diagnosis with nocturnal epileptic seizures) [1-3].Treatment
Treatment should aim mainly to ease parents’ concerns by explaining that arousal disorders are common during childhood and can be effectively managed. Proper sleep hygiene, maintaining regular bedtime hours and routines, is crucial. All drinks containing caffeine should be eliminated. Safety measures are important, especially for sleepwalkers. Physicians should explain that parents should not try to interact with or awaken the child because doing so can prolong the event. When the phenomenon occurs predictably at a specific time during the night, scheduled awakenings before the event occurs can be helpful. Drug therapy should be reserved for patients with very frequent episodes involving risk of bodily harm that are not associated to other sleep disorders. In these extreme situations, low doses of clonazepam are usually efficacious [1-3].
d. Sleep-related movement disorders
Restless legs syndrome (with or without periodic limb movements) and rhythmic movement disorder are among the most important sleep disorders in children; sometimes going unnoticed, these disorders are a common reason for consulting a sleep unit.
- Restless legs syndromeThis chronic sensory-motor neurological disorder affects between 5% and 10% of adults. Restless legs syndrome is underdiagnosed in children and adolescents, and its estimated prevalence varies widely (about 2%). It is characterized by the irresistible urge to move the legs when at rest, which is usually associated with an unpleasant sensation. These symptoms worsen at the end of the day and are alleviated by movement [17,18].Restless legs syndrome is diagnosed clinically. It does not need to be confirmed by polysomnography, but polysomnography is recommended in children, especially to rule our periodic limb movements, the symptoms of which overlap with those of restless leg syndrome (80%–90% of children with restless legs syndrome have periodic limb movements). Periodic limb movements are brief muscular contractions that can be associated with micro-arousals, tachycardia, transient increases in blood pressure, and sleep fragmentation. When periodic limb movements worsen the quality and/or quantity of sleep as evidenced by daytime symptoms, the condition is called periodic limb movements disorder [17,18].PathophysiologyIn most cases, the cause of restless legs syndrome is unknown. In about half of all cases, there is a family history of the disease, which suggests a genetic type of the disorder. Individuals with the hereditary type syndrome tend to be younger when the symptoms begin and to have slower progression of disease. In other cases, restless legs syndrome seems to be related to a series of conditions, although the actual etiopathogenic mechanisms involved remain to be elucidated [1,18]:
- Individuals with low concentrations of ferritin and/or iron or those with anemia can be more prone to developing restless legs syndrome. After deficiencies are corrected, the symptoms tend to improve.
- Chronic diseases such as renal insufficiency, diabetes, and peripheral neuropathy are associated with restless legs syndrome, and treatment of the underlying disease often improves symptoms.
- Some drugs such as antiemetics (prochlorperazine or metoclopramide), anticonvulsives (phenytoin), antipsychotics (haloperidol or phenothiazine derivatives), and some antivirals or antihistamines worsen the symptoms.
- Caffeine, alcohol, and tobacco can cause or exacerbate the symptoms in patients who are predisposed to developing restless legs syndrome. Some studies have found that eliminating or reducing the intake of these substances can alleviate the symptoms.
The American Academy of Sleep Medicine’s clinical guidelines contain no specific recommendations for the treatment of restless legs syndrome or periodic limb movements disorder in children. Scant information is available about the use of dopaminergic medication (first choice in adults) in children. Likewise, second-line treatments for adults such as benzodiazepines, some anticonvulsives, alpha-adrenergics, and opioids are also not normally used in children [1, 2, 17,18].
Some children with periodic limb movements disorder have low concentrations of iron and/or ferritin in serum; when serum ferritin is less than 50 µg/L, oral iron treatment for 3 months can bring about improvement [1, 2, 17,18].
Restless legs syndrome is generally lifelong. Symptoms may gradually worsen with age, although more slowly in idiopathic cases than in those associated with a concomitant medical condition.
- Rhythmic movement disordersRhythmic movement disorders (including body rolling, head rolling, body rocking, and head banging) are characterized by repetitive stereotypic rhythmic movements that occur predominantly when infants and children are falling asleep, but can also appear during the N1, N2, and N3 phases of non-REM sleep and during REM sleep. The prevalence is high during the first year of life (59%), but decreases progressively to 5% at the age of 5 years. In children with delayed psychomotor development or autistic spectrum disorder, they may persist beyond the age of 5 years. When they occur beyond this age in children without these problems, they must be investigated in a sleep medicine unit. The most prevalent rhythmic movement disorders are head rolling and body rolling, and they are equally common among boys and girls [1, 3,19].The most widely accepted theory to explain the pathophysiology of rhythmic movement disorders is that the repeated movements are maintained by the perceptual reinforcement caused by the chronic reiterative generation of the stereotypical behavior . Stepanova et al.  reported a strong association between ADHD and the persistence of rhythmic movement disorders, although this finding has not been confirmed in other studies.Treatment
Although the medical literature on the treatment of rhythmic movement disorder is scant, behavioral therapy is recommended as the first-line treatment. Behavioral treatment consists basically of applying a negative stimulus when the child starts the movements so that removing the stimulus is experienced as positive and pleasant [1,19].
The drug most often used is clonazepam, which is effective from the first night. Nevertheless, the rate of relapse after withdrawing the medication is high, and behavioral treatment is preferable [1,19].
e. Hypersomnias of central origin
- Narcolepsy Type I and Type IINarcolepsy is an uncommon chronic neurologic disease, with a prevalence of 1 in 2000 in the general population. Narcolepsy is a genetically determined disease, and patients usually have a family history of the disease. Narcolepsy is caused by the brain’s inability to regulate sleep-wake cycles. The main brain areas involved are the midbrain and brainstem. The onset of narcolepsy usually occurs during adolescence or early adulthood, and the disease persists until death .Narcolepsy is characterized by a combination of:- Excessive daytime sleepiness
– Cataplexy or sudden, reversible loss of muscle tone
– Vivid hallucinations on falling asleep or awakening (hypnagogic and/or hypnopompic)
– Short periods of paralysis at the beginning or end of sleep
Excessive daytime sleepiness is usually the first symptom; it is the only sign seen in about 46% of patients. Only 10% of patients have all four of the characteristics listed above, and up to 60% have only one of the four [1,3]. A narcoleptic patient can suffer one or several sleep crises per day, with each crisis lasting less than an hour; usually, the patient falls asleep in inopportune situations, and this can cause important problems in their lives at school and work as well as in their social lives. Cataplexy is a momentary paralysis without loss of consciousness; it occurs in response to sudden emotional reactions such as feelings of anger, fear, joy, pleasure, or surprise. It is experienced as a weakness in the limbs in which objects held in the hands can be dropped or the subject might even fall. Cataplexy is a pathognomonic sign of narcolepsy, but it is often not present until years after onset; it is the first symptom in less than 10% of patients, and it can be mistaken for atonic epileptic seizures . Episodes of paralysis occur on falling asleep or immediately after waking up. During these episodes, the patient wants to move but is incapable of doing so, and this generates terror .
Hypnagogic hallucinations (on falling asleep) and/or hypnopompic hallucinations (on awakening) are visual or auditory illusions similar to those that occur in normal dreams, but they are more intense and sometimes distort reality .
The diagnosis of narcolepsy is based on the clinical history, sleep diaries and questionnaires, nocturnal polysomnography, the Multiple Sleep Latency Test (MSLT), and hypocretin levels in cerebrospinal fluid. For the diagnosis of narcolepsy without cataplexy (Type II), a three-month history of excessive daytime sleepiness, pathologic polysomnography, and pathologic MSLT are sufficient. The diagnosis of narcolepsy with cataplexy (Type I) requires a 3-month history of excessive daytime sleepiness, pathologic polysomnography, pathologic MSLT, and hypocretin levels below 110 pg/ml. Furthermore, determinations of HLA (DRB1-15 and DQB1-0602) can help orient the diagnosis and predict the severity of disease, but cannot confirm it [1,3].
The treatment of narcolepsy must include hygienic and pharmacological measures. It is important for patients to take short naps during the day, keep to the correct sleep schedule, and ensure that their rooms have an appropriate and quiet atmosphere. Psychological support and support groups should also be considered. The drugs recommended by the Food and Drug Administration (FDA) of the United States are methamphetamines, amphetamines, dextroamphetamines, methylphenidates, and sodium oxybate.
The only drug recommended by the FDA for cataplexy is sodium oxybate, although other drugs are also used, including selegiline, serotonin-norepinephrine uptake inhibitors, serotonin-uptake inhibitors, and tricyclic antidepressants [1,3].
e. Circadian rhythm disorders (CRDS)
The third edition of the International Classification of Sleep Disorders (ICSD-3) includes nine types of circadian rhythm sleep-wake disorders, which are classified into three categories: primary disorders (delayed sleep-wake phase, advanced sleep-wake phase, irregular sleep-wake rhythm, non-24 h sleep-wake rhythm); secondary disorders (jetlag, circadian disorders secondary to shift work, circadian disorders secondary to other diseases, circadian disorders secondary to medication or drug abuse), and others .
Of all the circadian rhythm disorders listed above, we will focus on the one that is seen most often in pediatric patients (usually in adolescents or young adults): delayed sleep phase syndrome.
Delayed sleep phase syndrome .
Also called delayed sleep phase disorder, this syndrome is characterized by going to sleep and waking up at least two hours later than is conventional or socially acceptable. It is found in 7% to 16% of the population (especially in adolescents and young adults).
- Delayed setting of circadian pacemaker with respect to the solar cycle.
- Genetic causes (PER3 polymorphism).
- Excessive exposure to light at night (videogames, electronic tablets, cell phones, TV).
- Insufficient exposure to morning sunlight.
- Sleep hygiene
- Chronotherapy, delaying sleep until the desired time and setting strong zeitgebers (external markers: light, routines, mealtimes, physical exercise…).
- Exposure to 30 min to 2 h of light at the desired wakening time.
- Avoiding bright light before going to sleep (exposure to electronic devices with blue/white light, which inhibits natural melatonin secretion).
Administration of melatonin .
The effects of melatonin on the circadian system depend on the formulation and dose of melatonin as well as on the phase when it is administered.
Melatonin has the opposite effects of light on the circadian system. Administering immediate-release melatonin between 5 and 2 hours before bedtime advances the phase of sleep, whereas administering it in the morning delays the phase (chronobiotic effects). Slow-release melatonin is more efficacious than immediate-release melatonin in sleep-maintenance insomnia but not in sleep-onset insomnia. Regarding the dose, significant chronobiotic effects are obtained with 0.3 mg to 3 mg. Larger doses can act in both the phase advancement and phase delay zones, with antagonizing chronobiotic effects.
There is very little evidence from primary studies about the efficacy and safety of melatonin for its role in changing circadian rhythms. As a treatment for pediatric delayed sleep phase syndrome, one review including three studies in which only a minority of the patients were adolescents or young adults concluded that, compared to a placebo, melatonin decreased the latency of sleep onset, but had no effect on the total time spent sleeping or subjective status during daytime wakefulness. The review also concluded that the dosing and optimum time for administration are yet to be established, because the studies administered doses ranging from 0.3 mg to 3 mg or 5 mg between 1.5 and 6 hours before bedtime.
A later meta-analysis included primary studies in adults as well as studies in children aged between 6 years and adolescence, where the dose of melatonin ranged from 0.3 mg to 6 mg administered 3 to 4 hours before bedtime for an average of 4 weeks. The authors concluded that administering exogenous melatonin for pediatric delayed sleep phase syndrome is efficacious because it advances the dim light melatonin onset phase and the onset of sleep, decreases latency, and increases the duration of sleep; however, no significant improvement in awakening was observed.
Physical exercise or intense mental activity advances or delays sleep phase differently at different times of day, similar, although less potent, than the effects of light.
Approximately 30% of children and adolescents have some type of sleep disorder, from isolated difficulties in falling asleep or sleeping through the night to more serious problems such as sleep apnea-hypopnea syndrome.
Sleep disorders have clear, easily identifiable clinical manifestations at night: snoring, noisy and difficult breathing, respiratory pauses, breathing through the mouth, abnormal postures, profuse sweating, or bedwetting. Nevertheless, daytime symptoms must also be taken into consideration, given their impact on the quality of life of patients and their families: motor restlessness, sleepiness, poor performance at school, behavior problems, aggressiveness, and accidents. For diagnosis, it can be useful to administer both structured questionnaires that facilitate initial screening and other, complementary tests such as nocturnal polysomnography.
The main cause of sleep disorders in preschool and school-aged children is inappropriate habits, especially in relation to television. Using television to bring on asleep and prolonged exposure to television (more than 2 hours/day) reduce the efficient time of sleep, increase nocturnal arousals, and generate problems at bedtime. Furthermore, these habits are likely to persist through adolescence and adulthood, with consequent repercussions on social life and work. Nowadays, easy access to videogame consoles and internet-connected devices isalso problematic.
At puberty, the physiological onset of sleep is delayed, but the total sleep requirements are not reduced during adolescence. School schedules require specific times to start the day that can result in adolescents not getting enough sleep, which can affect learning. Appropriate sleep hygiene in this stage of life includes avoiding television, videogames, mobile phones, and stimulating drinks such as coffee, cola, alcohol, and other drugs. It is also advisable to maintain school-day schedules during weekends and to ensure that the adolescent gets adequate exercise. Exposure to natural light in the morning favors good sleep physiology at night. It is also necessary to treat concomitant diseases (e.g., asthma, obesity, and others than can affect sleep) appropriately.
Primary care professionals play a fundamental role in the early detection, diagnosis, treatment, and follow-up of these patients; they also provide key support for patients’ families. Professionals must encourage good sleep hygiene and recognize the need to refer patients to a sleep specialist when necessary. Good relations with specialists will enable their patients to obtain access to more complex complementary tests such as polysomnography and specific treatment for their disorders.
In conclusion, sleep is a physiological necessity, and insufficient quantity or quality of sleep will have important repercussions on both current and future physical, cognitive, and psychosocial health. Sleep disorders also generate stress and problems in the family. Many problems that can be easily resolved in the first weeks of life with behavioral measures can persist for years if not appropriately redressed.
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