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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

Other relevant positions: Phase 1 Lead; Year 2 Lead; Chair of AWERB 


Andrew Dilley is Professor in Neuroanatomy 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, and he currently leads Phase 1 of the BM BS programme. His external roles include Board member of the International Federation of Associations of Anatomists (IFAA) Federative International Programme on Anatomical Research, where he is the lead for Neuroscience Research. 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 and complex regional pain syndrome.

Laboratory studies focus on models of peripheral neuroinflammation. He uses a range of electrophysiological techniques, combined with behavioural and immunohistochemical procedures, to study the responses of 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. 

Human studies employ a range of imaging techniques (MRI and ultrasound) to identify peripheral neuroinflammation, and other neuropathology, in patients with chronic musculoskeletal pain. These studies allow a two-pronged approach to try and fully understand the involvement of in pain production. Ultimately, Andrew’s studies aim to reveal novel potential therapeutic targets for the treatment of chronic 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 is the Phase 1 (Years 1 and 2) lead for the BM BS medical programme and is also the Year 2 Lead. As such, he plays a significant role in curriculum development and the assessment process for the programme. 

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 is always keen to engage the public in science, and frequently receives invitations to speak at both national and international public events.

Selected publications

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. 

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

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. 

Pulman KGT, Smith M, Mengozzi M, Ghezzi P, Dilley A. The erythropoietin-derived peptide ARA290 reverses mechanical allodynia in the neuritis model. Neuroscience. 2013; 233: 174-83. doi: 10.1016/j.neuroscience.2012.12.022. 

Richards N, Batty T, Dilley A. CCL2 has similar excitatory effects to TNF-α in a subgroup of inflamed C-fiber axons. J Neurophysiol. 2011; 106: 2838-2848. doi: 10.1152/jn.00183.2011. 

Dilley A, Bove GM. Disruption of axoplasmic transport induces mechanical sensitivity in intact rat C-fibre nociceptor axons. J Physiol. 2008; 586: 593-604. doi: 10.1113/jphysiol.2007.144105.

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