Insular cortex metabolite changes in obstructive sleep apnea.
OBJECTIVE
Adults with obstructive sleep apnea (OSA) show significant autonomic and neuropsychologic deficits, which may derive from damage to insular regions that serve those functions. The aim was to assess glial and neuronal status from anterior insular metabolites in OSA versus controls, using proton magnetic resonance spectroscopy (PMRS), and thus to provide insights for neuroprotection against tissue changes, and to reduce injury consequences.


METHODS
Cross-sectional study.


METHODS
University-based medical center.


METHODS
Thirty-six patients with OSA, 53 controls.


METHODS
None.


RESULTS
We performed PMRS in bilateral anterior insulae using a 3.0-Tesla magnetic resonance imaging scanner, calculated N-acetylaspartate/creatine (NAA/Cr), choline/creatine (Cho/Cr), myo-inositol/creatine (MI/Cr), and MI/NAA metabolite ratios, and examined daytime sleepiness (Epworth Sleepiness Scale, ESS), sleep quality (Pittsburgh Sleep Quality Index, PSQI), and neuropsychologic status (Beck Depression Inventory II [BDI-II] and Beck Anxiety Inventory [BAI]). Body mass index, BAI, BDI-II, PSQI, and ESS significantly differed between groups. NAA/ Cr ratios were significantly reduced bilaterally, and left-sided MI/Cr and MI/NAA ratios were increased in OSA over controls. Significant positive correlations emerged between left insular MI/Cr ratios and apnea-hypopnea index values, right insular Cho/Cr ratios and BDI-II and BAI scores, and negative correlations appeared between left insular NAA/Cr ratios and PSQI scores and between right-side MI/Cr ratios and baseline and nadir change in O2 saturation.


CONCLUSIONS
Adults with obstructive sleep apnea showed bilaterally reduced N-acetylaspartate and left-side increased myo-inositol anterior insular metabolites, indicating neuronal damage and increased glial activation, respectively, which may contribute to abnormal autonomic and neuropsychologic functions in the condition. The activated glial status likely indicates increased inflammatory action that may induce more neuronal injury, and suggests separate approaches for glial and neuronal protection.
Department of Anesthesiology, David Geffen School of Medicine at UCLA.
Santosh K
SK
Yadav
Department of Anesthesiology, David Geffen School of Medicine at UCLA ; Department of Radiological Sciences, David Geffen School of Medicine at UCLA ; the Brain Research Institute, University of California at Los Angeles, Los Angeles, CA.
Rajesh
R
Kumar
UCLA School of Nursing, University of California at Los Angeles, Los Angeles, CA ; the Brain Research Institute, University of California at Los Angeles, Los Angeles, CA.
Paul M
PM
Macey
UCLA School of Nursing, University of California at Los Angeles, Los Angeles, CA.
Mary A
MA
Woo
Department of Neurology, David Geffen School of Medicine at UCLA.
Frisca L
FL
Yan-Go
the Brain Research Institute, University of California at Los Angeles, Los Angeles, CA ; Department of Neurobiology, David Geffen School of Medicine at UCLA.
Ronald M
RM
Harper
D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007294:Inositol / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D020181:Sleep Apnea, Obstructive / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
D001224:Aspartic Acid; D007294:Inositol; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline
N-acetylaspartate; anxiety; autonomic; choline; creatine; depression; magnetic resonance spectroscopy; myo-inositol