nanoLAB

Staff Profile

Professor Roger Whittaker

Professor of Clinical Neurophysiology

Background

I studied medicine at Cambridge University before moving to the Institute of Molecular Medicine in Oxford on a BMA scholarship. After completing my specialist training in Clinical Neurophysiology in Newcastle and Edinburgh, I returned to Newcastle to complete a PhD in cortical network dynamics. I am now Professor of Clinical Neurophysiology, Newcastle University, and an Honorary Consultant in the Department of Clinical Neurophysiology in the Royal Victoria Infirmary. Outside work my main interests are my family and anything to do with going up or coming down mountains.

Research

My research interest is in developing novel diagnostic and therapeutic approaches to neurological diseases.  I am PI on an EPSRC funded project to develop a multi-channel electromyography system to allow electrical cross-sectional imaging of human skeletal muscles. This project uses microfabrication techniques to pattern multiple electrodes within flexible substrates such as parylene-C. These are subsequently bonded to metal needles to allow recordings to be made from within human muscles. We hope that these techniques will for the first time allow the accurate definition of normal human motor unit structure, ultimately leading to improved diagnostic techniques for a range of neuromuscular diseases such as motor neuron disease and myasthenia gravis.

I am also clinical lead on an EPSRC/Wellcome Trust funded project to develop a novel optogenetic treatment for focal epilepsy. Currently, epilepsy surgery is one treatment option for patients with focal epilepsy that does not respond to anti-epileptic medications. Surgery to remove the epileptic focus abolishes seizures in approximately 70% of patients; however this figure falls to approximately 50% after 10 years. Furthermore, many patients with epilepsy are not suitable for this approach because of the risk of unacceptable side-effects of the surgery. Our approach is to use closed-loop control of optogenetically sensitized neurons to normalise the activity of the focus rather than removing it.

Publications