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Clinical diagnosis of Lewy body dementia
- Ajenthan Surendranathan, Joseph P. M. Kane, Allison Bentley, Sally A. H. Barker, John-Paul Taylor, Alan J. Thomas, Louise M. Allan, Richard J. McNally, Peter W. James, Ian G. McKeith, David J. Burn, John T. O'Brien
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- Journal:
- BJPsych Open / Volume 6 / Issue 4 / July 2020
- Published online by Cambridge University Press:
- 16 June 2020, e61
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Background
Lewy body dementia, consisting of both dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), is considerably under-recognised clinically compared with its frequency in autopsy series.
AimsThis study investigated the clinical diagnostic pathways of patients with Lewy body dementia to assess if difficulties in diagnosis may be contributing to these differences.
MethodWe reviewed the medical notes of 74 people with DLB and 72 with non-DLB dementia matched for age, gender and cognitive performance, together with 38 people with PDD and 35 with Parkinson's disease, matched for age and gender, from two geographically distinct UK regions.
ResultsThe cases of individuals with DLB took longer to reach a final diagnosis (1.2 v. 0.6 years, P = 0.017), underwent more scans (1.7 v. 1.2, P = 0.002) and had more alternative prior diagnoses (0.8 v. 0.4, P = 0.002), than the cases of those with non-DLB dementia. Individuals diagnosed in one region of the UK had significantly more core features (2.1 v. 1.5, P = 0.007) than those in the other region, and were less likely to have dopamine transporter imaging (P < 0.001). For patients with PDD, more than 1.4 years prior to receiving a dementia diagnosis: 46% (12 of 26) had documented impaired activities of daily living because of cognitive impairment, 57% (16 of 28) had cognitive impairment in multiple domains, with 38% (6 of 16) having both, and 39% (9 of 23) already receiving anti-dementia drugs.
ConclusionsOur results show the pathway to diagnosis of DLB is longer and more complex than for non-DLB dementia. There were also marked differences between regions in the thresholds clinicians adopt for diagnosing DLB and also in the use of dopamine transporter imaging. For PDD, a diagnosis of dementia was delayed well beyond symptom onset and even treatment.
Non-pharmacological interventions for Lewy body dementia: a systematic review
- Michael H. Connors, Lena Quinto, Ian McKeith, Henry Brodaty, Louise Allan, Claire Bamford, Alan Thomas, John-Paul Taylor, John T. O'Brien
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- Journal:
- Psychological Medicine / Volume 48 / Issue 11 / August 2018
- Published online by Cambridge University Press:
- 16 November 2017, pp. 1749-1758
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- Article
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Lewy body dementia (consisting of dementia with Lewy bodies and Parkinson's disease dementia) is a common neurodegenerative disease characterised by visual hallucinations, fluctuating attention, motor disturbances, falls, and sensitivity to antipsychotics. This combination of features presents challenges for pharmacological management. Given this, we sought to review evidence for non-pharmacological interventions with patients with Lewy body dementia and their carers. Bibliographic databases were searched using a wide range of search terms and no restrictions were placed on study design, language, or clinical setting. Two reviewers independently assessed papers for inclusion, rated study quality, and extracted data. The search identified 21 studies including two randomised controlled trials with available subgroup data, seven case series, and 12 case studies. Most studies reported beneficial effects of the interventions used, though the only sizeable study was on dysphagia, showing a benefit of honey-thickened liquids. Given the heterogeneity of interventions and poor quality of the studies overall, no quantitative synthesis was possible. Overall, identified studies suggested possible benefits of non-pharmacological interventions in Lewy body dementia, but the small sample sizes and low quality of studies mean no definite recommendations can be offered. Our findings underscore the clear and urgent need for future research on this topic.
Contributors
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- By Yohance M. Allette, Christophe Altier, Charles E. Argoff, Nadine Attal, Paul J. Austin, Didier Bouhassira, Ian Carroll, Kristine M. Chapman, Stephen Coleman, Lynn Kerene Cooper, Michael R. Due, Mary-Ann Fitzcharles, Robyn Flynn, Andrea D. Furlan, Vishal Gupta, Maija Haanpää, Jennifer Hah, Steven H. Horowitz, John Hughes, Mark R. Hutchinson, Scott Jarvis, Maan Kattan, Manpreet Kaur, Bradley J. Kerr, Krishna Kumar, Yuen Hei Kwok, Wojciech Leppert, Liang Liu, Angela Mailis-Gagnon, Gila Moalem-Taylor, Dwight E. Moulin, Harsha Nagaraja, Dontese Nicholson, Lauren Nicotra, Anne Louise Oaklander, John Xavier Pereira, Syed Rizvi, Stephan A. Schug, Michael Serpell, Amanda Sherwin, Howard S. Smith, Peter A. Smith, Pam Squire, Peter A. Ste-Marie, Patrick L. Stemkowski, Nicole M. Sumracki, Cory Toth, Krista van Steeg, Jan H. Vranken, Bharati Vyawahare, Mark A. Ware, Linda R. Watkins, C. Peter N. Watson, Fletcher A. White
- Edited by Cory Toth, Dwight E. Moulin
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- Book:
- Neuropathic Pain
- Published online:
- 05 December 2013
- Print publication:
- 07 November 2013, pp vii-x
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Contributors
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- By Joanne R. Adler, David A. Alexander, Laurence Alison, Catherine C. Ayoub, Peter Banister, Anthony R. Beech, Amanda Biggs, Julian Boon, Adrian Bowers, Neil Brewer, Eric Broekaert, Paula Brough, Jennifer M. Brown, Kevin Browne, Elizabeth A. Campbell, David Canter, Michael Carlin, Shihning Chou, Martin A. Conway, Claire Cooke, David Cooke, Ilse Derluyn, Robert J. Edelmann, Vincent Egan, Tom Ellis, Marie Eyre, David P. Farrington, Seena Fazel, Daniel B. Fishman, Victoria Follette, Katarina Fritzon, Elizabeth Gilchrist, Nathan D. Gillard, Renée Gobeil, Agnieszka Golec de Zavala, Jane Goodman-Delahunty, Lynsey Gozna, Don Grubin, Gisli H. Gudjonsson, Helinä Häkkänen-Nyholm, Guy Hall, Nathan Hall, Roisin Hall, Sean Hammond, Leigh Harkins, Grant T. Harris, Camilla Herbert, Robert D. Hoge, Todd E. Hogue, Clive R. Hollin, Lorraine Hope, Miranda A. H. Horvath, Kevin Howells, Carol A. Ireland, Jane L. Ireland, Mark Kebbell, Michael King, Bruce D. Kirkcaldy, Heidi La Bash, Cara Laney, William R. Lindsay, Elizabeth F. Loftus, L. E. Marshall, W. L. Marshall, James McGuire, Neil McKeganey, T. M. McMillan, Mary McMurran, Joav Merrick, Becky Milne, Joanne M. Nadkarni, Claire Nee, M. D. O’Brien, William O’Donohue, Darragh O’Neill, Jane Palmer, Adria Pearson, Derek Perkins, Devon L. L. Polaschek, Louise E. Porter, Charlotte C. Powell, Graham E. Powell, Martine Powell, Christine Puckering, Ethel Quayle, Vernon L. Quinsey, Marnie E. Rice, Randall Richardson-Vejlgaard, Richard Rogers, Louis B Schlesinger, Carolyn Semmler, G. A. Serran, Ralph C. Serin, John L. Taylor, Max Taylor, Brian Thomas-Peter, Paul A. Tiffin, Graham Towl, Rosie Travers, Arlene Vetere, Graham Wagstaff, Helen Wakeling, Fiona Warren, Brandon C. Welsh, David Wexler, Margaret Wilson, Dan Yarmey, Susan Young
- Edited by Jennifer M. Brown, London School of Economics and Political Science, Elizabeth A. Campbell, University of Glasgow
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- Book:
- The Cambridge Handbook of Forensic Psychology
- Published online:
- 06 July 2010
- Print publication:
- 29 April 2010, pp xix-xxiii
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12 - Kin-selection Models as Evolutionary Explanations of Malaria
- Edited by Ulf Dieckmann, International Institute for Applied Systems Analysis, Austria, Johan A. J. Metz, Universiteit Leiden, Maurice W. Sabelis, Universiteit van Amsterdam, Karl Sigmund, Universität Wien, Austria
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- Book:
- Adaptive Dynamics of Infectious Diseases
- Published online:
- 15 January 2010
- Print publication:
- 11 April 2002, pp 165-178
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Summary
Introduction
Malaria, a disease caused by protozoan parasites of the genus Plasmodium, can substantially reduce host fitness in wild animals (Atkinson and Van Riper 1991; Schall 1996). In humans, the major disease syndromes – severe anemia, coma, and organ failure, as well as general pathology such as respiratory distress, aches, and nausea – cause considerable mortality and morbidity (Marsh and Snow 1997).
Biomedical research attributes malaria to red cell destruction, infected cell sequestration in vital organs, and the parasite-induced release of cytokines (Marsh and Snow 1997). But mechanistic explanations are just one type of explanation for any biological phenomenon, and, in recent years, evolutionary biologists have become interested in offering evolutionary explanations of infectious disease virulence. This is entirely appropriate (Read 1994). In the context of malaria, for example, the clinical outcome of infection has an important impact on parasite and host fitness and is – at least in part – determined by heritable variation in host and parasite factors (Greenwood et al. 1991). Yet in the recent rush to provide evolutionary explanations of disease, there has been, in our view, too little interaction between the models built by evolutionary biologists and reality. There is unlikely to be a simple, general model of virulence: the causes of disease and the fitness consequences for host and parasite are too variable. Instead, different models, and even different frameworks, will be relevant in different contexts.