Yrsa Sverrisdottir

I gained my PhD in Autonomic Neurophysiology at the Institute of Neuroscience, Department of Clinical Neurophysiology, Sahlgrenska University Hospital in Gothenburg, Sweden, where I specialized in clinical microneurography. The technique was developed in Uppsala Sweden in the early 1960’s by my supervisor, Professor Gunnar Wallin, the pioneer in sympathetic research in humans, and enables direct recordings of sympathetic action potentials in awake human subjects in health and disease. Following my PhD I was awarded a two year post-doctoral fellowship which took me to Sydney, Australia where I worked both at the Prince of Wales Medical Research Institute, University of New South Wales, in Professor Vaughan Macefield's laboratory and at the Department of Physiology, University of Sydney, in Professor Roger Dampney's laboratory. I have been in the field for 20 years and worked in some of the most prestigious autonomic neuroscience labs around the world. I have successfully collaborated to establish the technique in Brazil, Portugal, Denmark and the United Kingdom (Oxford, Brighton, Cardiff, Glasgow).

I have been engaged in research at the University of Oxford since 2010, when I joined the cardiac-neural programme to combine autonomic neuroscience to the existing combination of cardiovascular science and functional neurosurgery. I have held a BHF research fellowship and am currently a NIHR RCF senior research fellow. Since my arrival in Oxford I have set up a unique high performing microneurography laboratory at the Clinical Cardiovascular Research Facility at the John Radcliffe Hospital. Through my work with Oxford Functional Neurosurgery, we successfully used sympathetic microneurography to elucidate the underlying mechanisms for the cardiovascular effects of deep brain stimulation of specific midbrain circuitries in patients with Parkinson’s disease and chronic neuropathic pain. Our findings indicate that regulation of sympathetic outflow occurs in the subthalamic nucleus (STN) and periaqueductal gray (PAG), increasing our understanding of where in the brain abnormal sympathetic discharge in cardiovascular disease is generated and may provide an opportunity for therapeutic targeting (Sverrisdóttir Y. B. et al Hypertension 2014). Considering the possible association between depression and hypertension, our results indicate a plausible role for deep midbrain structures in linking major depressive disorder with clinical cardiovascular events. This study has now prompted an industry partner, St Jude Medical to collaborate and fund further research projects on the effect of dorsal root ganglion and spinal cord stimulation on sympathetic outflow in humans – a recognition of the translation of our research.