**3. Risk factors**

OSAS is a complex and multifactorial syndrome, and it is believed that some specific genes may play a crucial role in its pathogenesis, particularly involved in the expression of the CLOCK gene [7], IL-10 polymorphisms [8], and insulin variable number of tandem repeat (INS VNTR) sequence regulation [9].

In general, there are some conditions that may predispose to OSAS, such as alterations of craniofacial structures, obesity with fat deposition on side walls of the pharynx, endocrine changes, alcohol intake, and cigarette smoking [10] both in adults and in children.

In pediatric population, the main risk factor is adenotonsillar hypertrophy [11, 12], but others are rhinitis [13], nasal structure alteration [14, 15], cleft palate, velopharyngeal flap surgery, pharyngeal masses, craniofacial malformations [16], genetic syndrome (i.e. Down syndrome, Crouzon syndrome, and Apert syndrome), genetic hypoplasia mandibular (Pierre Robin syndrome, Treacher Collins syndrome, Shy-Drager syndrome, and Cornelia De Lange syndrome) [17, 18], craniofacial traumas [19, 20], chronic or seasonal rhinitis [13],

**159**

*Neuropsychological Alterations in Children Affected by Obstructive Sleep Apnea Syndrome*

(Arnold-Chiari malformation and Joubert syndrome) [24], achondroplasia [25],

On the other hand, worldwide pediatric obesity tends to be prevalent in children with respiratory disorders during sleep; however, it does not represent the main risk factor unlike the adult and is even a complication of OSAS especially after the

In OSAS, due to a reduction in the size of the upper airways and a reduction in the activity of the pharynx dilator muscles, there are an increase in critical pressure (transmural pressure value at which the area of the pharyngeal section is equal to

The obstructive events will therefore lead to the appearance of hypoxemia and hypercapnia, which will first cause an increase in respiratory effort, and then a wake-up, of a few seconds, which will serve to restore the patency of the upper airways; all these will repeat cyclically during sleep, causing an alteration of the

In the adult, there is a reduction in nonrapid eye movement (NREM) sleep and rapid eye movement (REM) sleep, and consequently, the major symptom is daytime sleepiness; in children, on the other hand, intermittent hypoxia has a role in the appearance of neocognitive deficits, which are the most common signs and symp-

Behavioral awakenings in the child with OSAS are less frequent than in adults, and this on the one hand allows the child to retain the benefits of sleep, and on the other hand, it can cause long periods of hypoventilation. Moreover, in children, the desaturation of O2 can also be achieved during short apnea due to the reduced functional lung capacity and the most frequent respiratory rate in pediatric age [29].

In OSAS, there is also a state of chronic systemic inflammation, mainly linked to intermittent hypoxia, which promotes the activation of some factors responsible for inflammation such as C-reactive protein (PCR) and IL-6 and is therefore respon-

Oxidative stress and increased production of oxygen-free radicals represent the pathophysiological substrate of the onset of cardiovascular, cerebrovascular, and

Clinical signs of OSAS appear to be different in pediatric age with respect to adulthood, and therefore, the diagnostic and therapeutic management overlapping

In adults with OSAS, the most common presentation is excessive daytime sleepiness (EDS) that results from sleep fragmentation and from the frequent nocturnal intermittent hypoxic episodes [33], while in nonobese children, EDS is a rare complain. Conversely, children with OSAS tend to be not drowsy but rather hyperkinetic during the day, and often, these children are misdiagnosed with attentiondeficit/hyperactivity disorder (ADHD) and treated with methylphenidate. This common diagnostic mistake is derived from the lack of evaluation of sleep habits in children presenting with suspected hyperactivity behavior

zero) and an enormous reduction in the pharyngeal lumen [29].

toms in the case of OSAS in the developmental age [29].

sible for a state of oxidative stress [30].

may be considered a severe clinical mistake.

metabolic complications [31, 32].

**5. Clinical signs**

asthma [21, 22], neuromuscular syndromes [23], brainstem pathologies

*DOI: http://dx.doi.org/10.5772/intechopen.91818*

and mucopolysaccharidosis [26].

adenotonsillectomy [27, 28].

**4. Pathophysiology**

structure.

*Neuropsychological Alterations in Children Affected by Obstructive Sleep Apnea Syndrome DOI: http://dx.doi.org/10.5772/intechopen.91818*

asthma [21, 22], neuromuscular syndromes [23], brainstem pathologies (Arnold-Chiari malformation and Joubert syndrome) [24], achondroplasia [25], and mucopolysaccharidosis [26].

On the other hand, worldwide pediatric obesity tends to be prevalent in children with respiratory disorders during sleep; however, it does not represent the main risk factor unlike the adult and is even a complication of OSAS especially after the adenotonsillectomy [27, 28].
