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Modulating the activity of midbrain structures in humans has proven a successful therapy for chronic neuropathic pain and movement disorders. Electrical stimulation of these neurocircuitries is recently shown to change cardiovascular parameters in humans 1, indicating that these circuitries may also be of importance in autonomic reflex control of the cardiovascular system. This study aimed to test the hypothesis that midbrain structures can affect cardiovascular outcome by modulating baroreflex restraint of central sympathetic outflow. Direct recordings of multiunit efferent postganglionic muscle sympathetic nerve activity (MSNA) was obtained in patients undergoing deep brain stimulation of the periaqueductal gray (PAG) and subthalamic nucleus (STN) for chronic neuropathic pain and Parkinson's disease, respectively. MSNA was expressed as burst frequency, burst incidence and relative median burst amplitude. Blood pressure, heart rate and respiration were monitored during the recording session and spontaneous vasomotor and cardiac baroreflex sensitivity diagrams were assessed. Our results show differentiated changes in sympathetic outflow during on/off stimulation phases of midbrain structures, which are reflected in the hemodynamic response. Evidence of a differentiated control of probability and amplitude of sympathetic bursts has been reported previously 2. While it is not known how the differentiated control of sympathetic bursts is brought about, it has been suggested that the baroreflex modulation of sympathetic outflow occurs at two CNS locations. One site is thought to determine the probability of discharge, and the other site is thought to determine the strength of that discharge 3. Our results on the effects of deep brain stimulation on the STN and PAG show differentiated changes in sympathetic outflow during on/off stimulation periods, which are reflected in a differentiated hemodynamic response. As baroreflex modulation of sympathetic nerve traffic is of vital importance for cardiovascular regulation, our results may shed light on where and how this modulation occurs in the central nervous system. [ABSTRACT FROM AUTHOR]