Effect of Deep Brain Stimulation on Sympathetic outflow in humans

      Background: Electric deep brain stimulation (DBS) in midbrain nuclei in humans alters cardiovascular parameters, presumably by modulating autonomic and baroreflex function. Baroreflex modulation of sympathetic outflow is crucial for cardiovascular regulation and is hypothesized to occur at two distinct brain locations. Aim: This study aimed to evaluate sympathetic outflow in humans with DBS electrodes during ON and OFF stimulation of specific midbrain nuclei known to regulate cardiovascular function. Methods: Muscle sympathetic nerve activity (MSNA) was recorded during DBS ON and OFF in patients with chronic neuropathic pain (n = 7) and Parkinson’s disease (n = 10). Arterial blood pressure (ABP), heart rate and respiration were monitored during the recording session and spontaneous vasomotor and cardiac baroreflex sensitivity (BRS) were assessed. Head-up tilt testing was performed separately in the Parkinson’s patients post-operatively. Results: Stimulation of the dorsal most part of the subthalamic nucleus (STN) and ventrolateral periaqueductal gray (PAG) resulted in improved vasomotor BRS, decreased MSNA burst frequency and ABP, unchanged burst amplitude distribution and a reduced fall in ABP after tilt. Stimulation of the dorsolateral PAG resulted in a shift in burst amplitude distribution towards larger amplitudes, decreased spontaneous BP variability and unchanged burst frequency, BRS and ABP. Conclusions: Baroreflex regulation of sympathetic outflow occurs in the STN and PAG. Our results may have implications in understanding abnormal sympathetic discharge in cardiovascular disease and provide an opportunity for therapeutic targeting.
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