Cerebral metabolic impairment in patients with obstructive sleep apnoea: an independent association of obstructive sleep apnoea with white matter change.

摘要

OBJECTIVES: To determine the relation between severity of obstructive sleep apnoea (OSA) and degree of cerebral metabolic impairment. METHODS: Fifty five patients with habitual snoring and excessive daytime sleepiness underwent standard overnight polysomnography and magnetic resonance spectroscopy separately. Proton MR spectra were measured with two dimensional chemical shift imaging (repetition time; 1500 ms, echo time; 135 ms). Severity of cerebral metabolic impairment was assessed by the N-acetylaspartate (NAA)/choline ratios for the cerebral cortex and white matter. Severity of OSA was assessed by the apnoea-hypopnoea index (AHI) and the minimum value of peripheral oxyhaemoglobin saturation. All patients were evaluated for the presence or absence of comobidities including hypertension, cardiac disease, diabetes mellitus, and hyperlipidaemia. Univariate analysis of variance (ANOVA) and mulitple linear regression analysis were used for statistical analyses. RESULTS: Univariate ANOVA disclosed significant effects of AHI, age, and the presence or absence of hypertension on the NAA/choline ratio for cerebral white matter (p=0.011, p=0.028, p=0.0496, respectively). The AHI had a significant negative association with the NAA/choline ratio for cerebral white matter, independent of age and the presence or absence of cardiac disease, in the final multivariate regression model (standardised partial regression coefficient=-0.417, p<0.001). No significant relation was found between severity of OSA and the NAA/choline ratio for the cerebral cortex. Age alone had a significant effect on the NAA/choline ratio for the cerebral cortex on univariate ANOVA (p<0.001) and a significant negative association with the NAA/choline ratio for the cerebral cortex in the regression model (r=-0.552, p<0.001). CONCLUSIONS: A significant relation exists between AHI and the degree of metabolic impairment in cerebral white matter in patients with OSA.