This document summarises the conclusions of a European Respiratory Society Task Force on the diagnosis and management of obstructive sleep disordered breathing (SDB) in childhood and refers to children aged 2-18 years. Prospective cohort studies describing the natural history of SDB or randomised, double-blind, placebo-controlled trials regarding its management are scarce. Selected evidence (362 articles) can be consolidated into seven management steps. SDB is suspected when symptoms or abnormalities related to upper airway obstruction are present (step 1). Central nervous or cardiovascular system morbidity, growth failure or enuresis and predictors of SDB persistence in the long-term are recognised (steps 2 and 3), and SDB severity is determined objectively preferably using polysomnography (step 4). Children with an apnoea-hypopnoea index (AHI) >5 episodes·h(-1), those with an AHI of 1-5 episodes·h(-1) and the presence of morbidity or factors predicting SDB persistence, and children with complex conditions (e.g. Down syndrome and Prader-Willi syndrome) all appear to benefit from treatment (step 5). Treatment interventions are usually implemented in a stepwise fashion addressing all abnormalities that predispose to SDB (step 6) with re-evaluation after each intervention to detect residual disease and to determine the need for additional treatment (step 7).

https://erj.ersjournals.com/content/erj/47/1/69.full.pdf

Obstructive sleep disordered breathing in 2- to 18-year-old children: diagnosis and management.

Sleep phenotypes in attention deficit hyperactivity disorder

Our aim is to review studies which assess the prevalence of sleep apneas in children with epilepsy and discuss possible mechanisms linking these two conditions, as well as the impact of sleep apneas on the prognosis of these children. PubMed was used as the medical database source, and articles were selected and classified according to their originality, level of evidence, and relevance to the broad scope of the review. Children with epilepsy have a higher prevalence of sleep breathing disorders in comparison to healthy children, but this prevalence varies widely depending on the methodology of each study. Major risk factors for sleep apneas in childhood epilepsy include mainly poor seizure control and antiepileptic drug polytherapy. Indeed, epilepsy can trigger sleep apneas, as abnormal electrical discharge amplifies sleep-induced breathing instability, antiepileptic drugs disturb muscle tone, and vagus nerve stimulation modulates neurotransmission to airway muscles. On the other hand, sleep apneas enhance sleep fragmentation, thus reducing the threshold for the appearance of seizures. Moreover, they have a negative effect on the neurocognitive profile of these children, as they disturb neuroplasticity mechanisms and also have a probable association with sudden unexpected death in epilepsy. The surgical treatment of sleep apneas has been found to reduce seizure frequency, and this can offer new therapeutic choices. Between sleep apneas and childhood epilepsy, there is a complex relationship with reciprocal interactions. The presence of sleep apneas should be taken into account when designing the management of these children, as it creates therapeutic opportunities and limitations.

Sleep apneas and epilepsy comorbidity in childhood: a systematic review of the literature

We describe the case of a 12-year-old boy who developed temporal lobe epilepsy (TLE) with daily complex partial seizures (CPS) and monthly generalized seizures. Moreover, he frequently snored while asleep since early childhood. Polysomnography (PSG) revealed severe obstructive sleep apnea with apnea–hypopnea index (AHI) of 37.8/h. Video-PSG with simultaneous electroencephalography (EEG) recording captured two ictal apneic episodes during sleep, without any motor manifestations. The onset of rhythmic theta activity in the midtemporal area on EEG was preceded by the onset of apnea by several seconds and disappeared soon after cessation of central apnea. One episode was accompanied by ictal bradycardia of < 48 beats/min which persisted for 50 s beyond the end of epileptic activity. After treatment with carbamazepine and tonsillectomy/adenoidectomy, the seizures were well controlled and AHI decreased to 2.5/h. Paroxysmal discharges also disappeared during this time. Uncontrolled TLE complicated by sleep apnea should be evaluated for the presence of ictal central apnea/bradycardia.

Ictal central apnea and bradycardia in temporal lobe epilepsy complicated by obstructive sleep apnea syndrome.

Introduction: The comorbidity of epilepsy and sleep apnea is not uncommon. The diagnosis and treatment of obstructive sleep apneas will improve the prognosis and the quality of life in patients with epilepsy.Areas covered: In this paper, the authors review the pathological link between sleep apnea and epilepsy and systematically analyze the current literature on the diagnosis and treatment of obstructive sleep apnea in patients with epilepsy. This review includes studies retrieved from the PubMed, Embase and Google Scholar databases.Expert commentary: A variety of treatments are available for OSA and epilepsy independently but there are no standards or guidelines for how to implement these treatments for patients who suffer from both disorders. The authors expect that alternative efficient therapies for comorbidity will be explored, which may change the current clinical practice for the management of epileptic patients.

Annamaria Mazzotta

Papers

The cooccurrence of interictal discharges and seizures in pediatric sleep-disordered breathing.