Abstract
Born on Merseyside, Andrew Lees qualified in medicine at the Royal London Hospital Medical College in 1970. His neurological training was at University College London Hospitals and the National Hospital for Neurology and Neurosurgery, Queen Square. He also spent time at L’Hopital Salpetriere, Paris. At the age of thirty-two he was appointed to the consultant staff at the National Hospitals, The Middlesex, and Whittington Hospitals and in 1987 was elected a Fellow of the Royal College of Physicians. He was later appointed Professor of Neurology at the National Hospital for Neurology and Neurosurgery, Queen Square and was Director of the Reta Lila Weston Institute for Neurological Studies (1998–2012). He was Clinical Director of the Queen Square Brain Bank for Neurological Disorders (1985–2012) and Director of the Sara Koe PSP Research Centre (2002–2012). He is a Visiting Professor at the University of Liverpool and has close collaborations with a number of Brazilian universities. For his contributions to Brazilian neurology he was elected an overseas member of the Academia Nacional de Medicina and the Academia Brasileira de Neurologica. He was elected as a Council member of the Academy of Medical Sciences 2012- 2015. Appointed as an Expert Adviser for the UK Government National Institute for Health and Care Excellence Centre for Guidelines (2006–2019). Andrew has achieved international recognition for his work on Parkinson’s disease and abnormal movement disorders. He is an original member of the Highly Cited Researchers ISI Database. Founder member of the international Movement Disorder Society, he was elected President (2004–2006) and co-edited the Movement Disorders Journal between 1995 and 2003. In 2006, he was awarded the Movement Disorders Research Award by the American Academy of Neurology. In recent years, he has delivered the Gowers Memorial Lecture at the National Hospital, The Inaugural Lord Brain Memorial Lecture at Barts and the Royal London Hospitals and David Marsden Memorial Lecture at the European Federation of Neurological Societies. He was the recipient of Stanley Fahn Lectureship Award, MDS Dublin 2012, and has been awarded the German Society of Neurology’s 2012 Dingebauer Prize for outstanding scientific attainment in the field of Parkinson’s disease and Neurodegenerative Disorders. In 2014, Andrew received the prestigious Jay Van Andel award for outstanding research in Parkinson’s disease. Based in Grand Rapids Michigan, the Van Andel Institute is an independent research organisation dedicated to preserving, enhancing and expanding the frontiers of medical science. In 2015, he became the recipient of the Association of British Neurologists Medal, awarded annually in recognition of outstanding contributions by British and Irish neurologists to the science and practice of neurology. Jean-Martin described ‘maladie de Parkinson’ as a nevrose, a term introduced into France by Pinel and used to describe any nervous disorder without demonstrable organic pathology. In 1917 Tretiakoff working at L’Hopital Salpetriere demonstrated that a severe loss of pigmented nerve cells in the pars compacta of the substantia nigra was invariably present giving it a ‘solidity’ denied to many other movement disorders such as dystonia and chorea and brought the disease firmly into the fold of neurology. From the earliest clinical descriptions, it has been recognised that anxiety and depression can have a profound effect on the expression and severity of the motor symptoms of Parkinson’s diseasse and that the kinesics of chronic anxiety and psychomotor retardation bear a superficial similarity to the movement disorder that characterises Parkinson’s disease. Slowness of willed movement an invariable feature of Parkinson’s disease can be seen in depression and also in a rare form of obsessional compulsive disorder. The intimate links between motion and emotion in basal ganglia disorders and the notion of Parkinson’s disease as a neuropsychiatric disorder are now widely acknowledged but the idea that severe emotional stress could cause neurodegeneration is more controversial. In a paper published in 2014 Djamshidian and I hypothesised that chronic stress might cause Parkinson’s disease in susceptible individuals and that many of the symptoms reported in the pre-diagnostic phase of the illness are identical to those seen in functional somatic syndromes (Djamshidian A, et al. J Neurol Neurosurg Psychiatry 2014;85:879–882). The clinical clues that stress might be a neglected risk factor for Parkinson’s disease will be discussed in the hope of stimulating further research.
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