M
Mark J. Edwards
Researcher at St George's, University of London
Publications - 398
Citations - 20432
Mark J. Edwards is an academic researcher from St George's, University of London. The author has contributed to research in topics: Dystonia & Psychogenic disease. The author has an hindex of 63, co-authored 365 publications receiving 16293 citations. Previous affiliations of Mark J. Edwards include St George’s University Hospitals NHS Foundation Trust & University College London.
Papers
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Journal ArticleDOI
Linking differences in action perception with differences in action execution
TL;DR: It is demonstrated that subjects’ sensitivity to observed movement speeds is dependent upon how quickly they themselves executed the observed action, suggesting that failures in non-verbal social interactions between individuals may in part result from differences in how those individuals move.
Journal ArticleDOI
Event related desynchronisation predicts functional propriospinal myoclonus
Anne Marthe Meppelink,Anne Marthe Meppelink,Simon Little,Ashwini Oswal,Roberto Erro,Roberto Erro,James M. Kilner,Marina A. J. Tijssen,Peter Brown,C. Cordovari,Mark J. Edwards +10 more
TL;DR: ERD in high-beta may be a useful new test for positive diagnosis of functional myoclonus, and sensitivity and specificity for both techniques are calculated.
Journal ArticleDOI
Temporal discrimination of two passive movements in humans: a new psychophysical approach to assessing kinaesthesia
Michele Tinazzi,Clementina Stanzani,Mirta Fiorio,Nicola Smania,Giuseppe Moretto,Antonio Fiaschi,Mark J. Edwards,Kailash P. Bhatia,John C. Rothwell +8 more
TL;DR: The results suggest that muscle, and in part cutaneous, afferents contribute to temporal discrimination of a dual movement and the technique may provide a useful way of measuring temporaldiscrimination of kinaesthetic inputs in humans.
Book ChapterDOI
Chapter 42 – Parkinson’s disease
John C. Rothwell,Mark J. Edwards +1 more
TL;DR: Data is emerging about the possible role of cortical plasticity in compensating for gradual loss of dopaminergic function prior to onset of clinical symptoms, and the more consistent reduction in SICI is now viewed as a superimposed excitation rather than a primary deficit in a GABAergic mechanism.