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Updated: Jan 24, 2026

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
Obstructive Sleep Apnea before Ischemic Stroke: Clinical Relevance to Infarction Volume and Neurological Recovery
Li Zhang1, Ran Meng2, Shuling Shang3
1Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China; Department of Neurology, The Third Hospital of Shijiazhuang, Shijiazhuang, China.
Background:
Obstructive sleep apnea (OSA) is a probable risk factor with speculative roles in the induction or aggravation of acute ischemic stroke (AIS).
Methods:
The association between OSA and AIS severity was retrospectively analyzed using clinical data of first-onset AIS patients, admitted to our hospital between January 2013 and September 2016. Eligible patients were categorized based on the presence of OSA prior to stroke. Stroke severity and functional outcomes were evaluated using the National Institute of Health Stroke Severity Scale (NIHSS) and the modified Rankin scale (mRS), respectively.
Results:
No significant differences were observed among OSA and non-OSA groups for infarction volume, NIHSS at admission and discharge, or mRS at discharge and at the 3-month follow-up (all P > .05). OSA prior to stroke negatively correlated with infarction volume (P = .008), NIHSS at discharge (P = .006), and the 3-month mRS (P = .015). In addition to OSA, it was also found that infarction volume significantly correlated with large artery occlusion (LAO), anterior circulation involvement, neutrophil count, and fibrinogen level; NIHSS at discharge significantly correlated with LAO, transient ischemia attack (TIA), neutrophil count, and thrombolysis; and the 3-month mRS significantly correlated with LAO, TIA, age, neutrophil count, and thrombolysis.
Conclusions:
OSA before AIS does not increase the severity of stroke. The negative association between OSA and infarction volume, stroke severity, and clinical outcomes suggests an endogenous neuroprotective effect.
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