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Professor Andrew Dilley

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Professor Andrew Dilley (PhD)

Professor in Neuroanatomy
T: +44 (0)1273 877094
Location: Trafford Centre, University of Sussex, Falmer, Brighton, BN1 9RY

Areas of Expertise: Neuroscience; pain physiology; neuroanatomy; imaging 

Research areas: Mechanisms of neuropathic pain; neuroinflammation; electrophysiology, imaging

Other relevant positions: Head, Department of Neuroscience; Lead, Sussex Pain Network


Andrew Dilley is Professor in Neuroanatomy and Head of the Department of Neuroscience at Brighton and Sussex Medical School. He completed a BSc in Anatomy and Development Biology at University College London (UCL) and went on to undertake a PhD in neurophysiology at Kings College London, focussing on the mechanisms underlying the peripheral neuropathy, Guillain-Barré syndrome. Following completion of his PhD, Andrew returned to UCL as a Postdoctoral Research Fellow within the Department of Physiology. At UCL, he established his interest in peripheral neuropathic pain mechanisms. Following this post, he took a position at Harvard Medical School, in Boston, as an Instructor in Anesthesia. During his time at Harvard, he continued his laboratory research into the role of peripheral neuroinflammation in chronic musculoskeletal pain. Andrew joined Brighton and Sussex Medical School in 2007 as Lecturer in Anatomy. From 2018 to 2020, Andrew was the Interim Head of Anatomy for the new Kent and Medway Medical School.


Andrew’s research encompasses both laboratory and human studies into the role of peripheral neuroinflammation in chronic musculoskeletal pain. His research is aimed at understanding the causes of pain in conditions such as repetitive motion disorders, radiculopathies, non-specific back and arm pain, whiplash-associated disorders, fibromyalgia and complex regional pain syndrome.

Human studies employ imaging techniques (MRI and ultrasound), as well as quantitative sensory testing and the examination blood and tissue samples to identify peripheral neuroinflammation, and other neuropathology, in patients with chronic musculoskeletal pain. Andrew is also developing the use of microneurography as a clinical tool to examine the physiology of sensory nerve fibres in humans. 

Laboratory studies focus on models of peripheral neuroinflammation. A range of electrophysiological techniques, combined with behavioural and immunohistochemical procedures, are used to study the responses of nociceptive (pain) axons to inflammation. His laboratory has considerable expertise in single unit extracellular recording techniques, which enable recordings from isolated nociceptive (pain) axons. Andrew’s research is specifically aimed at understanding the mechanisms that lead to increases in excitability in inflamed primary sensory neurons. An area of particular interest is the role of axonal transport disruption. 

Together, these studies provide a multifaceted approach to fully understand the mechanisms of pain in patients with complex chronic pain conditions.  In particular, they aim to determine novel targets for the treatment of pain.  Andrew has published extensively in his field and has received funding from the Versus Arthritis, NC3Rs, Pain Relief Foundation and the US Department of Defence.


Andrew’s main teaching focus is neuroanatomy, neurophysiology and musculoskeletal anatomy. He is actively involved in teaching within Phase 1 of the BM BS medical programme. Andrew uses a multifaceted approach for his teaching, whereby lectures are combined with human dissection and practical tutorials that together produce a multimodal learning experience. He has won best second year teacher for nine consecutive years, as well as two University of Sussex awards for teaching excellence.  Andrew is particularly interested in the practical use of medical imaging in anatomy and physiology education and has successfully integrated ultrasound as a tool for learning anatomy and physiology into Phase 1 teaching. 

Andrew’s teaching extends beyond the undergraduate medical course. He also teaches on a range of other programmes, which include undergraduate and postgraduate programmes at the Universities of Sussex, Brighton and Chichester, and the NHS. In addition, Andrew supervises undergraduate and postgraduate students in the laboratory. 

Andrew plays a significant role in curriculum development and the assessment process for the BM BS medical programme.

Selected publications

Ridehalgh C, Fundaun J, Bremner S, Cercignani M, Young R, Trivedy C, Novak C, Greening J, Schmid A, Dilley A. Does peripheral neuroinflammation predict chronicity following whiplash injury? Protocol for a prospective cohort study. BMJ Open. 2022; 12(12): e066021.

Fundaun J, Kolski M, Baskozos G, Dilley A, Sterling M, Schmid AB. Nerve pathology and neuropathic pain after whiplash injury: a systematic review and meta-analysis. Pain. 2022 Jul 1; 163(7): e789–e811.

Dilley A, Harris M, Barbe MF, Bove GM. Aberrant Neuronal Activity in a Model of Work-Related Upper Limb Pain and Dysfunction. J Pain 2022 May;23(5):852-863. 

Bove GM, Dilley A. A lesson from classic British literature. Lancet. 2019; 393(10178): 1297-1298. doi: 10.1016/S0140-6736(18)32533-9. 

Goodwin G, Bove GM, Dayment B, Dilley A. Characterizing the mechanical properties of ectopic axonal receptive fields in inflamed nerves and following axonal transport disruption. Neuroscience. 2019; 429: 10-22. doi: 10.1016/j.neuroscience.2019.11.042. 

Satkeviciute I, Dilley A. Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability. Mol Pain. 2018; 14: 1744806918799581. doi: 10.1177/1744806918799581. 

Greening J, Anantharaman K, Young R, Dilley A. Evidence for increased MRI signal intensity and morphological changes in the brachial plexus and median nerves of patients with chronic arm and neck pain following whiplash injury. J Orthop Sports Phys Ther. 2018; 48: 523-532. doi: 10.2519/jospt.2018.7875. 

Satkeviciute I, Goodwin G, Bove GM, Dilley A. The time course of ongoing activity during neuritis and following axonal transport disruption. J Neurophysiol. 2018; 119: 1993-2000. doi: 10.1152/jn.00882.2017. 

Richards N, Dilley A. Contribution of hyperpolarization-activated channels to heat hypersensitivity and ongoing activity in the neuritis model. Neuroscience. 2015; 284: 87-98. doi: 10.1016/j.neuroscience.2014.08.058. 

Dilley A, Richards N, Pulman KGT, Bove GM. Disruption of fast axonal transport in the rat induces behavioral changes consistent with neuropathic pain. J Pain. 2013; 14: 1437-49. doi: 10.1016/j.jpain.2013.07.005.

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