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For the Consortium on Dementia with Lewy Bodies; *See pages 1122 and 1123 for the Consortium of Dementia with Lewy Bodies participants.
Presented at the Proceedings of the First International Workshop of the Consortium on DLB, Newcastle upon Tyne, UK, October 1995.
Supported by Parke Davis and Company, The French Foundation for Alzheimer Research, Janssen-Cilag Ltd, Sandoz Pharma Ltd, Bayer AG, F Hoffmann-La Roche AG, The Wellcome Trust, Eli Lilly and Company, Astra Arcus AB, Lederle Laboratories, Merck Sharp & Dohme Ltd, Institute for the Health of the Elderly, University of Newcastle upon Tyne, Medical Research Council (UK), Newcastle upon Tyne City Health NHS Trust, Royal Victoria Infirmary and Associated Hospitals NHS Trust.
Received April 1, 1996. Accepted in final form May 16, 1996.
Address correspondence and reprint requests to Dr McKeith, MD, BS, FRCPsych, Department of Old Age Psychiatry, Institute for the Health of the Elderly, Newcastle General Hospital, Westgate Road, Newcastle upon Tyne NE4 6BE, U.K.
Recent neuropathologic autopsy studies found that 15 to 25% of elderly demented patients have Lewy bodies (LB) in their brainstem and cortex, and in hospital series this may constitute the most common pathologic subgroup after pure Alzheimer's disease (AD).The Consortium on Dementia with Lewy bodies met to establish consensus guidelines for the clinical diagnosis of dementia with Lewy bodies (DLB) and to establish a common framework for the assessment and characterization of pathologic lesions at autopsy. The importance of accurate antemortem diagnosis of DLB includes a characteristic and often rapidly progressive clinical syndrome, a need for particular caution with neuroleptic medication, and the possibility that DLB patients may be particularly responsive to cholinesterase inhibitors. We identified progressive disabling mental impairment progressing to dementia as the central feature of DLB. Attentional impairments and disproportionate problem solving and visuospatial difficulties are often early and prominent. Fluctuation in cognitive function, persistent well-formed visual hallucinations, and spontaneous motor features of parkinsonism are core features with diagnostic significance in discriminating DLB from AD and other dementias. Appropriate clinical methods for eliciting these key symptoms are described. Brainstem or cortical LB are the only features considered essential for a pathologic diagnosis of DLB, although Lewy-related neurites, Alzheimer pathology, and spongiform change may also be seen. We identified optimal staining methods for each of these and devised a protocol for the evaluation of cortical LB frequency based on a brain sampling procedure consistent with CERAD. This allows cases to be classified into brainstem predominant, limbic (transitional), and neocortical subtypes, using a simple scoring system based on the relative distribution of semiquantitative LB counts. Alzheimer pathology is also frequently present in DLB, usually as diffuse or neuritic plaques, neocortical neurofibrillary tangles being much less common. The precise nosological relationship between DLB and AD remains uncertain, as does that between DLB and patients with Parkinson's disease who subsequently develop neuropsychiatric features. Finally, we recommend procedures for the selective sampling and storage of frozen tissue for a variety of neurochemical assays, which together with developments in molecular genetics, should assist future refinements of diagnosis and classification.
NEUROLOGY 1996;47: 1113-1124
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D. Galasko, D. Salmon, A. Gamst, J. Olichney, L. J. Thal, L. Silbert, J. Kaye, P. Brooks, R. Adonay, U.-K Craig, et al. Prevalence of dementia in Chamorros on Guam: Relationship to age, gender, education, and APOE Neurology, May 22, 2007; 68(21): 1772 - 1781. [Abstract] [Full Text] [PDF] |
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C. C. Rowe, S. Ng, U. Ackermann, S. J. Gong, K. Pike, G. Savage, T. F. Cowie, K. L. Dickinson, P. Maruff, D. Darby, et al. Imaging {beta}-amyloid burden in aging and dementia Neurology, May 15, 2007; 68(20): 1718 - 1725. [Abstract] [Full Text] [PDF] |
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K. Ishii, T. Soma, A. K. Kono, K. Sofue, N. Miyamoto, T. Yoshikawa, E. Mori, and K. Murase Comparison of Regional Brain Volume and Glucose Metabolism Between Patients with Mild Dementia with Lewy Bodies and Those with Mild Alzheimer's Disease J. Nucl. Med., May 1, 2007; 48(5): 704 - 711. [Abstract] [Full Text] [PDF] |
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B. M. Dufty, L. R. Warner, S. T. Hou, S. X. Jiang, T. Gomez-Isla, K. M. Leenhouts, J. T. Oxford, M. B. Feany, E. Masliah, and T. T. Rohn Calpain-Cleavage of {alpha}-Synuclein: Connecting Proteolytic Processing to Disease-Linked Aggregation Am. J. Pathol., May 1, 2007; 170(5): 1725 - 1738. [Abstract] [Full Text] [PDF] |
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C. F. Lippa, J. E. Duda, M. Grossman, H. I. Hurtig, D. Aarsland, B. F. Boeve, D. J. Brooks, D. W. Dickson, B. Dubois, M. Emre, et al. DLB and PDD boundary issues: Diagnosis, treatment, molecular pathology, and biomarkers Neurology, March 13, 2007; 68(11): 812 - 819. [Abstract] [Full Text] [PDF] |
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M. S. Forman, E. J. Mufson, S. Leurgans, D. Pratico, S. Joyce, S. Leight, V. M.-Y. Lee, and J. Q. Trojanowski Cortical biochemistry in MCI and Alzheimer disease: Lack of correlation with clinical diagnosis Neurology, March 6, 2007; 68(10): 757 - 763. [Abstract] [Full Text] [PDF] |
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M. K Beyer, C. C Janvin, J. P Larsen, and D. Aarsland A magnetic resonance imaging study of patients with Parkinson's disease with mild cognitive impairment and dementia using voxel-based morphometry J. Neurol. Neurosurg. Psychiatry, March 1, 2007; 78(3): 254 - 259. [Abstract] [Full Text] [PDF] |
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B. R. Reed, D. M. Mungas, J. H. Kramer, W. Ellis, H. V. Vinters, C. Zarow, W. J. Jagust, and H. C. Chui Profiles of neuropsychological impairment in autopsy-defined Alzheimer's disease and cerebrovascular disease Brain, March 1, 2007; 130(3): 731 - 739. [Abstract] [Full Text] [PDF] |
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A. Lannuzel, G. U. Hoglinger, S. Verhaeghe, L. Gire, S. Belson, M. Escobar-Khondiker, P. Poullain, W. H. Oertel, E. C. Hirsch, B. Dubois, et al. Atypical parkinsonism in Guadeloupe: a common risk factor for two closely related phenotypes? Brain, March 1, 2007; 130(3): 816 - 827. [Abstract] [Full Text] [PDF] |
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M. L. Kramer and W. J. Schulz-Schaeffer Presynaptic {alpha}-Synuclein Aggregates, Not Lewy Bodies, Cause Neurodegeneration in Dementia with Lewy Bodies J. Neurosci., February 7, 2007; 27(6): 1405 - 1410. [Abstract] [Full Text] [PDF] |
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L. Rozzini, B. V. Chilovi, E. Bertoletti, M. Conti, I. Delrio, M. Trabucchi, and A. Padovani Cognitive and Psychopathologic Response to Rivastigmine in Dementia With Lewy Bodies Compared to Alzheimer's Disease: A Case Control Study American Journal of Alzheimer's Disease and Other Dementias, February 1, 2007; 22(1): 42 - 47. [Abstract] [PDF] |
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P. K. Panegyres and K. Frencham Course and Causes of Suspected Dementia in Young Adults: A Longitudinal Study American Journal of Alzheimer's Disease and Other Dementias, February 1, 2007; 22(1): 48 - 56. [Abstract] [PDF] |
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G. Gliebus and C. F. Lippa The Influence of {beta}-Blockers on Delayed Memory Function in People With Cognitive Impairment American Journal of Alzheimer's Disease and Other Dementias, February 1, 2007; 22(1): 57 - 61. [Abstract] [PDF] |
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G. K. Tofaris, T. Revesz, T. S. Jacques, S. Papacostas, and J. Chataway Adult-Onset Neurodegeneration With Brain Iron Accumulation and Cortical {alpha}-Synuclein and Tau Pathology: A Distinct Clinicopathological Entity Arch Neurol, February 1, 2007; 64(2): 280 - 282. [Abstract] [Full Text] [PDF] |
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D. E. Clarke, R. v. Reekum, M. Simard, D. L. Streiner, M. Freedman, and D. Conn Apathy in Dementia: An Examination of the Psychometric Properties of the Apathy Evaluation Scale J Neuropsychiatry Clin Neurosci, February 1, 2007; 19(1): 57 - 64. [Abstract] [Full Text] [PDF] |
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