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Sleep Apnea

Sleep Apnea

Sleep apnea is a condition where breathing stops intermittently during sleep, often leading to significant health issues. Each episode can last from 10 to 20 seconds or more and is frequently accompanied by a brief arousal from sleep. This disturbance, largely unnoticed by the individual, can lead to severe daytime fatigue. Commonly, individuals seek help after being informed by their partners about loud snoring and noticeable breathing pauses during sleep.
The condition is more prevalent among...

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Related Experiment Video

Updated: Jun 7, 2026

Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea

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: brain structural changes and neurocognitive function before and after treatment.

Nicola Canessa¹, Vincenza Castronovo, Stefano F Cappa

¹Center for Cognitive Neuroscience, Vita-Salute San Raffaele University, Milan, Italy.

American Journal of Respiratory and Critical Care Medicine

|November 2, 2010

Summary

Obstructive sleep apnea (OSA) causes cognitive deficits linked to brain structure changes. Treatment improved cognitive function and brain gray matter volume, highlighting the need for early diagnosis and intervention.

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Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea

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Published on: September 22, 2020

Area of Science:

Neuroscience
Sleep Medicine
Radiology

Background:

Obstructive sleep apnea (OSA) is linked to neurocognitive impairments.
Brain structure abnormalities underlying OSA-related cognitive deficits remain unclear.
Understanding these changes is crucial for effective treatment and recovery.

Purpose of the Study:

Investigate cognitive deficits in OSA patients.
Identify associated brain morphology changes using voxel-based morphometry.
Assess cognitive and structural modifications after OSA treatment.

Main Methods:

17 treatment-naive OSA patients and 15 controls underwent sleep studies, cognitive tests, and MRI.
Voxel-based morphometry analyzed brain gray matter volume.
Data collected pre- and post-treatment (3 months) to evaluate efficacy.

Main Results:

Pretreatment OSA patients showed cognitive, mood, and sleepiness impairments.
Gray matter reductions were observed in the hippocampus, parietal cortex, and frontal gyrus.
Treatment led to improved memory, attention, and executive function, with increased gray matter volume.

Conclusions:

Cognitive and structural deficits in OSA may stem from sleep deprivation and intermittent hypoxemia.
Effective OSA treatment can reverse these negative effects.
Early diagnosis and successful treatment are vital for managing OSA-related impairments.