Cortical Autonomic Network Grey 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 (CAN) 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 grey matter thickness in subjects without and with OSA; 2) determine if oxygen desaturation index (ODI) relates to cortical thickness; and 3) determine if cortical thickness or volume in these regions predicts muscle sympathetic nerve (MSNA) burst incidence (BI). Overnight polysomnography, anatomical MRI and MSNA data were acquired in 41 subjects with no or mild OSA (n=19; 59±2 yrs [Mean±SE]; 6 female; apnea-hypopnea index [AHI] 7±1 events/hour) or moderate to severe OSA (n=22; 59±2 yrs; 5 female; AHI 31±4 events/hour). Between group CTA analyses identified cortical thinning within the left dorsal posterior insula (LdpIC) and thickening within the left mid-cingulate (LMCC) cortex, while VBM identified thickening within bilateral thalami (all, (P<0.05)). CTA revealed inverse relationships between ODI and bilateral dpIC and left posterior cingulate (LPCC)/precuneus thickness. Positive correlations between BI and LMCC grey matter thickness/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.