This systematic review synthesizes evidence on the bidirectional interaction between OSA and ICP, with emphasis on pathophysiological mechanisms, condition-specific effects, and therapeutic implications in idiopathic intracranial hypertension (IIH), traumatic brain injury (TBI), and hydrocephalus.

Obstructive sleep apnea (OSA) is a prevalent sleep-related breathing disorder characterized by recurrent upper airway obstruction, resulting in intermittent hypoxia, hypercapnia, and intrathoracic pressure fluctuations. These disturbances influence cerebral hemodynamics and may alter intracranial pressure (ICP), particularly in patients with coexisting neurological disorders.

A systematic search (PubMed, Scopus, Web of Science, Google Scholar) was performed per PRISMA guidelines. 35 studies met inclusion criteria. Data were extracted on population, ICP measurement modality (lumbar puncture, overnight ICP monitoring, cerebrospinal fluid [CSF] dynamics), OSA assessment (polysomnography, questionnaires, oxygen desaturation index), and CPAP intervention protocols.

Across 35 studies, transient ICP elevations of up to 15 mmHg were reported during apneic events, with a mean temporal delay of 3.6 seconds between apnea onset and ICP rise. In IIH cohorts (n = 5), OSA prevalence ranged from 33.3% to 50%, particularly in obese patients, though papilledema severity and opening pressure were not consistently different between OSA and non-OSA subgroups. In hydrocephalus and mixed ICP monitoring cohorts (n = 3), CPAP reduced transient ICP spikes by 37% but did not uniformly lower mean ICP.