Cortical autonomic network gray matter and sympathetic nerve activity in obstructive sleep apnea.

The sympathetic excitation elicited acutely by obstructive apnea during sleep (OSA) carries over into wakefulness. We hypothesized that OSA induces structural changes in the insula and cingulate, key central autonomic network elements with projections to brainstem sympathetic premotor regions. The aims of this study were to (1) apply two distinct but complementary methods (cortical thickness analysis [CTA] and voxel-based morphometry [VBM]) to compare insula and cingulate gray matter thickness in participants without and with OSA; (2) determine whether oxygen desaturation index (ODI) relates to cortical thickness; and (3) determine whether cortical thickness or volume in these regions predicts muscle sympathetic nerve activity (MSNA) burst incidence (BI). Overnight polysomnography, anatomical magnetic resonance imaging, and MSNA data were acquired in 41 participants with no or mild OSA (n = 19; 59 ± 2 years [Mean ± SE]; six females; apnea-hypopnea index [AHI] 7 ± 1 events per hour) or moderate-to-severe OSA (n = 22; 59 ± 2 years; five females; AHI 31 ± 4 events per hour). Between-group CTA analyses identified cortical thinning within the left dorsal posterior insula and thickening within the left mid-cingulate cortex (LMCC), whereas VBM identified thickening within bilateral thalami (all [p < .05]). CTA revealed inverse relationships between ODI and bilateral dpIC and left posterior cingulate cortex (LPCC) or precuneus thickness. Positive correlations between BI and LMCC gray matter thickness or volume were evident with both methods and between BI and left posterior thalamus volume using VBM. In OSA, the magnitude of insular thinning, although a function of hypoxia severity, does not influence MSNA, whereas cingulate and thalamic thickening relate directly to the intensity of sympathetic discharge during wakefulness.