Parkinson Disease: Boeve B

McKeith IG, Dickson DW, Lowe J, Emre M, O'Brien JT, Feldman H, Cummings J, Duda JE, Lippa C, Perry EK, Aarsland D, Arai H, Ballard CG, Boeve B, Burn DJ, Costa D, Del Ser T, Dubois B, Galasko D, Gauthier S, Goetz CG, Gomez-Tortosa E, Halliday G, Hansen LA, Hardy J, Iwatsubo T, Kalaria RN, Kaufer D, Kenny RA, Korczyn A, Kosaka K, Lee VM, Lees A, Litvan I, Londos E, Lopez OL, Minoshima S, Mizuno Y, Molina JA, Mukaetova-Ladinska EB, Pasquier F, Perry RH, Schulz JB, Trojanowski JQ, Yamada M, Anonymous00346. · Institute for Ageing and Health, University of Newcastle upon Tyne, UK. · Neurology. · Pubmed #16237129 No free full text.

Abstract: The dementia with Lewy bodies (DLB) Consortium has revised criteria for the clinical and pathologic diagnosis of DLB incorporating new information about the core clinical features and suggesting improved methods to assess them. REM sleep behavior disorder, severe neuroleptic sensitivity, and reduced striatal dopamine transporter activity on functional neuroimaging are given greater diagnostic weighting as features suggestive of a DLB diagnosis. The 1-year rule distinguishing between DLB and Parkinson disease with dementia may be difficult to apply in clinical settings and in such cases the term most appropriate to each individual patient should be used. Generic terms such as Lewy body (LB) disease are often helpful. The authors propose a new scheme for the pathologic assessment of LBs and Lewy neurites (LN) using alpha-synuclein immunohistochemistry and semiquantitative grading of lesion density, with the pattern of regional involvement being more important than total LB count. The new criteria take into account both Lewy-related and Alzheimer disease (AD)-type pathology to allocate a probability that these are associated with the clinical DLB syndrome. Finally, the authors suggest patient management guidelines including the need for accurate diagnosis, a target symptom approach, and use of appropriate outcome measures. There is limited evidence about specific interventions but available data suggest only a partial response of motor symptoms to levodopa: severe sensitivity to typical and atypical antipsychotics in approximately 50%, and improvements in attention, visual hallucinations, and sleep disorders with cholinesterase inhibitors.

Gjerstad MD, Boeve B, Wentzel-Larsen T, Aarsland D, Larsen JP. · The Norwegian Centre for Movement Disorders, Stavanger, Norway, PB 8100, N-4068 Stavanger, Norway. · J Neurol Neurosurg Psychiatry. · Pubmed #17557796 No free full text.

Abstract: OBJECTIVE: To examine the occurrence and clinical and demographic correlates of REM sleep behaviour disorder (RBD) in patients with Parkinson's disease (PD) in a community-based cohort over 8 years. METHODS: 231 patients with PD were included in a population-based prevalence study in 1993. Patients were then followed prospectively and reexamined after 4 and 8 years. Semi-structured interviews for information on clinical and demographic data were applied at all study visits. Standardised rating scales of parkinsonism, depression and cognitive impairment were used. The diagnosis of probable RBD (pRBD) was based on a sleep questionnaire. Proportional-odds ordinal logistic regression models for clustered data were used to study the relationship between pRBD and various demographic and clinical variables. RESULTS: 231 patients were evaluated for RBD in 1993 and, after 4 and 8 years, 142 and 89 patients, respectively, were available for re-evaluation. The frequency of pRBD varied from 14.6% to 27% during the study period. Probable RBD was related to male gender, higher dopaminergic treatment and less severe parkinsonism. CONCLUSION: We found that the frequency of pRBD varied over time and that it is associated with male gender, less parkinsonism and higher levodopa equivalent dose. Our findings indicate that dopaminergic therapy may contribute to the expression of RBD and that RBD is symptomatic in earlier stages of PD.

Houlden H, Rizzu P, Stevens M, de Knijff P, van Duijn CM, van Swieten JC, Heutink P, Perez-Tur J, Thomas V, Baker M, Morris H, Rossor M, Jannsen JC, Petersen RC, Dodd P, Dark F, Boeve B, Dickson D, Davies P, Pickering-Brown S, Mann D, Adamson J, Lynch T, Payami H, Hardy J. · Mayo Clinic Jacksonville, FL 32224, USA. · Neurosci Lett. · Pubmed #10076900 No free full text.

Abstract: We have assessed whether apolipoprotein E (ApoE) genotype influences the age of onset of dementia in a series of families with frontal temporal dementia with defined mutations in the tau gene. In contrast to the situation in Alzheimer's disease (AD), we could find no evidence that the age of onset of disease was influenced by the ApoE genotype.