| Popis: |
Sleep disorders in general, and more specifically those related to obstructive sleep apnea syndrome (OSAS) in children, are associated with cognitive and behavioural dysfunctions. Both restriction and fragmentation of sleep as well as intermittent hypoxia are involved in the pathophysiological alterations triggered by this neurobiological comorbidity. The mechanisms that eventually give rise to these neurobehavioural disorders appear to involve a number of biological pathways, particularly oxidative stress and systemic inflammation.The role played by inter-individual susceptibility, together with the environmental conditions and lifestyle, may account for the larger part of the variance in the phenotype. Moreover, the usual clinical prototype of the patient referred to a children's sleep unit due to snoring has evolved a lot in the past 15 years. We have gone from the patient who presents adenotonsillar hypertrophy with no associated obesity (as was the case in the early nineties) to the prototype of a patient who visits our sleep unit with a slight or moderate adenotonsillar hypertrophy, and with an obese biotype that is very similar to that of the adult patient with OSAS. For this reason we therefore propose the use of the terms type I and type II OSAS in children, and their different manifestations and clinical course are discussed. |
