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Sleep Architecture Linked to Airway Obstruction and Intracranial Hypertension in Children with Syndromic
Bart Spruijt1,2, Irene M J Mathijssen1,2, Hansje H Bredero-Boelhouwer1,2
1Rotterdam, The Netherlands; London, United Kingdom; and Boston, Mass.
Insights
Children with syndromic craniosynostosis generally have normal sleep architecture. However, moderate to severe obstructive sleep apnea significantly disrupts sleep patterns, impacting sleep efficiency and REM sleep.
Area of Science:
- Pediatric Neurology
- Sleep Medicine
- Craniofacial Surgery
Background:
- Syndromic craniosynostosis is associated with obstructive sleep apnea (OSA) and intracranial hypertension (ICH).
- Understanding the impact of OSA and ICH on sleep architecture in these children is crucial.
- Evaluating the effectiveness of surgical treatment on sleep patterns is important.
Purpose of the Study:
- To assess sleep architecture in children with syndromic craniosynostosis.
- To determine if OSA and/or ICH influence sleep architecture.
- To evaluate the impact of treatment on sleep architecture.
Main Methods:
- Included 39 patients with syndromic craniosynostosis.
- Assessed obstructive sleep apnea via polysomnography (categorized as none, mild, moderate, or severe).
- Identified intracranial hypertension using funduscopy, OCT, and ICP monitoring; analyzed sleep architecture (REM/NREM sleep, arousal index, sleep efficiency).
Main Results:
- Patients without moderate/severe OSA or ICH had normal sleep architecture compared to controls.
- Moderate/severe OSA was linked to increased respiratory effort-related arousals, reduced sleep efficiency, and less REM sleep.
- Monobloc surgery improved sleep architecture in a small subset of patients.
Conclusions:
- Children with syndromic craniosynostosis typically exhibit normal sleep architecture.
- Moderate to severe obstructive sleep apnea significantly disturbs sleep architecture.
- Findings support a unifying theory linking OSA, ICH, and sleep disturbances.
Background:
Children with syndromic craniosynostosis often have obstructive sleep apnea and intracranial hypertension. The authors aimed to evaluate (1) sleep architecture, and determine whether this is influenced by the presence of obstructive sleep apnea and/or intracranial hypertension; and (2) the effect of treatment on sleep architecture.
Methods:
This study included patients with syndromic craniosynostosis treated at a national referral center, undergoing screening for obstructive sleep apnea and intracranial hypertension. Obstructive sleep apnea was identified by polysomnography, and categorized into no, mild, moderate, or severe. Intracranial hypertension was identified by the presence of papilledema on funduscopy, supplemented by optical coherence tomography and/or intracranial pressure monitoring. Regarding sleep architecture, sleep was divided into rapid eye movement or non-rapid eye movement sleep; respiratory effort-related arousals and sleep efficiency were scored.
Results:
The authors included 39 patients (median age, 5.9 years): 19 with neither obstructive sleep apnea nor intracranial hypertension, 11 with obstructive sleep apnea (four moderate/severe), six with intracranial hypertension, and three with obstructive sleep apnea and intracranial hypertension. Patients with syndromic craniosynostosis, independent of the presence of mild obstructive sleep apnea and/or intracranial hypertension, have normal sleep architecture compared with age-matched controls. Patients with moderate/severe obstructive sleep apnea have a higher respiratory effort-related arousal index (p < 0.01), lower sleep efficiency (p = 0.01), and less rapid eye movement sleep (p = 0.04). An improvement in sleep architecture was observed following monobloc surgery (n = 5; rapid eye movement sleep, 5.3 percent; p = 0.04).
Conclusions:
Children with syndromic craniosynostosis have in principle normal sleep architecture. However, moderate/severe obstructive sleep apnea does lead to disturbed sleep architecture, which fits within a framework of a unifying theory for obstructive sleep apnea, intracranial hypertension, and sleep.
Clinical Question/Level Of Evidence:
Risk, II.
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