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James FitzGerald studied Physics at Oxford University, graduating in 1992, then switched to medicine, also at Oxford, graduating in 1998. He trained in Neurosurgery in Nottingham and Cambridge.  After obtaining a PhD in neuroelectronic interfacing at Cambridge University he returned to Oxford to take up a Consultant position in 2012.

James FitzGerald

Associate Professor of Neurosurgery


I work on implanted electronic devices that interface directly with parts of the nervous system.

At present my main research focus is on the development of a novel type of interface capable of recording signals from motor axons in severed peripheral nerves after amputation, with the aim of using these signals to control sophisticated prosthetic limbs.

This requires advances in several areas including polymer microfabrication techniques, implantable electrophysiological recording systems, microsurgical implantation methods, and the development of multichannel signal processing and pattern recognition algorithms. A further problem is that like virtually all surgical implants, interfaces evoke a foreign body response that leads to the deposition of scar tissue on their surfaces, which leads to gradual electrical failure of the device. A major strand of my work at present concerns the development of techniques for long term scar suppression, and I have recently shown that drug elution is a very promising approach to this (see Journal of Neural Engineering 2016;13:026006 for further details).

I am also one of the three academic consultants in Oxford Functional Neurosurgery, which has the UK's largest clinical practice in deep brain stimulation, spinal cord and dorsal root ganglion stimulation and peripheral nerve stimulation, for the treatment of movement disorders and neuropathic pain.  Alongside and closely intertwined with this clinical work we run a research programme investigating the mechanisms by which neuromodulation treatments work and how they can be improved and their use expanded to new indications.

A new theory of the mechanism of pallidal deep brain stimulation in Parkinson's disease. Retrograde stimulation of the axons of striatal medium spiny neurons causes widespread activation of inhibitory collaterals in the striatum, an effect called striatal damping. See J Neurosci 2015;35:13043-13052 for further details.