Muscle sympathetic nerve activity (MSNA) is increased in patients with obstructive sleep apnoea (OSA) in the awake state, leading to hypertension. By recording MSNA concurrently with functional Magnetic Resonance Imaging (fMRI) of the brain we aimed to identify the central processes responsible for the sympathoexcitation. Spontaneous fluctuations in MSNA were recorded via tungsten microelectrodes inserted into the peroneal nerve in 17 OSA patients and 15 age-matched controls while lying in a 3 T MRI scanner. Blood Oxygen Level Dependent (BOLD) contrast gradient echo, echo-planar images were continuously collected in a 4 s ON, 4 s OFF protocol. BOLD signal intensity, measured every 1 s during the 4 s OFF period, was coupled to the bursts of MSNA, measured every 1 s during the 4 s ON period. Fluctuations in BOLD signal intensity covaried with the intensity of the concurrently recorded bursts of MSNA from the preceding 4 s. MSNA-coupled BOLD signal intensity in the dorsolateral PFC, medial PFC, dorsal precuneus, anterior cingulate cortex, retrosplenial cortex and caudate nucleus was higher in OSA than in controls, while in the RVLM, dorsolateral pons and medullary raphe it was lower. All of these changes were reversed following 6 months of continuous positive airway pressure, which caused a significant fall in MSNA towards control levels. We conclude that the elevated MSNA in OSA results from functional changes within suprabulbar regions known to be directly or indirectly involved in the modulation of sympathetic outflow via the brainstem, as well as from functional changes within the brainstem.
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© 2015 Published by Elsevier Inc.