مؤسسة الشرق الأوسط للنشر العلمي
عادةً ما يتم الرد في غضون خمس دقائق
Obstructive sleep apnoea-hypopnoea syndrome (OSAHS) disrupts the normal architecture of sleep by fragmenting sleep-wake cycles and inducing repeated intermittent hypoxia. However, sleep plays a central role in the consolidation of memory traces: deep slow-wave sleep orchestrates hippocampal-cortical reactivation of declarative memories via slow-wave–spindle–ripple oscillatory coupling, whilst REM sleep ensures the stabilisation of procedural and emotional memories. OSA, by disrupting these processes, differentially compromises each long-term memory system. This narrative review analyses the neuropsychological mechanisms through which OSA impairs sleep-dependent memory consolidation. It successively examines the normal architecture of sleep and its memory functions, the two central pathophysiologies of OSA (fragmentation and hypoxia), their differential impact on the declarative, procedural and emotional systems, and then the neuroanatomical correlates observed in neuroimaging. The clinical implications, notably the effects of continuous positive airway pressure (CPAP) treatment on the recovery of memory capacity, are also discussed. This review highlights a hierarchical vulnerability of memory systems and advocates for systematic neuropsychological assessment in the management of OSA.