Gray matter atrophy in Parkinson disease with dementia and dementia with Lewy bodies

Neurology ◽  
2007 ◽  
Vol 69 (8) ◽  
pp. 747-754 ◽  
Author(s):  
M. K. Beyer ◽  
J. P. Larsen ◽  
D. Aarsland
2009 ◽  
Vol 15 ◽  
pp. S37
Author(s):  
B.C. Kim ◽  
S.M. Choi ◽  
T.S. Nam ◽  
J.T. Kim ◽  
M.S. Park ◽  
...  

2018 ◽  
Vol 71 ◽  
pp. 171-178 ◽  
Author(s):  
Jessica J. van der Zande ◽  
Martijn D. Steenwijk ◽  
Mara ten Kate ◽  
Mike P. Wattjes ◽  
Philip Scheltens ◽  
...  

2011 ◽  
Vol 24 (4) ◽  
pp. 532-540 ◽  
Author(s):  
Rosie Watson ◽  
John T. O'Brien ◽  
Robert Barber ◽  
Andrew M. Blamire

ABSTRACTBackground: Dementia with Lewy bodies (DLB) is a common form of dementia characterized by visual hallucinations, cognitive fluctuation and parkinsonism. We aimed to compare the patterns of gray matter atrophy in DLB with those in Alzheimer's disease (AD) and normal aging, and to investigate the relationship between atrophy and cognitive measures.Methods: We used voxel-based morphometry (VBM) to investigate gray matter (GM) loss in DLB (n = 35; mean age = 78.4; MMSE = 20.3), AD (n = 36; mean age = 78.3; MMSE = 19.5) and similar aged controls (n = 35; mean age = 76.7; MMSE = 29.1). T1 weighted MRI scans were acquired at 3 Tesla from all subjects and analyzed using VBM-DARTEL in SPM8. Cognitive function was assessed using the Cambridge Cognitive Examination (CAMCOG).Results: We found reduced gray matter in temporal, parietal, occipital, and subcortical structures in DLB when compared to normal controls. The degree of atrophy was less than that observed in AD. There was significantly more medial temporal lobe atrophy in the AD group when compared with DLB. We did not find a correlation between total CAMCOG score and atrophy, but the CAMCOG memory subscale score correlated with temporal lobe atrophy in both the DLB and combined DLB/AD group.Conclusions: DLB is associated with less gray matter atrophy and relative preservation of the medial temporal lobe when compared to AD. Degree of medial temporal atrophy may be a useful imaging biomarker and our results provide support for its inclusion in the revised consensus criteria for DLB.


2019 ◽  
Vol 10 (2) ◽  
pp. 156-161
Author(s):  
Pierpaolo Turcano ◽  
Cole D. Stang ◽  
James H. Bower ◽  
J. Eric Ahlskog ◽  
Bradley F. Boeve ◽  
...  

ObjectiveTo investigate the frequency of levodopa-induced dyskinesia in dementia with Lewy bodies (DLBs) and Parkinson disease with dementia (PDD) and compare these frequencies with patients with incident Parkinson disease (PD) through a population-based cohort study.MethodsWe identified all patients with DLB, PDD, and PD without dementia in a 1991–2010 population-based parkinsonism-incident cohort, in Olmsted County, Minnesota. We abstracted information about levodopa-induced dyskinesia. We compared patients with DLB and PDD with dyskinesia with patients with PD from the same cohort.ResultsLevodopa use and dyskinesia data were available for 141/143 (98.6%) patients with a diagnosis of either DLB or PDD; 87 (61.7%), treated with levodopa. Dyskinesia was documented in 12.6% (8 DLB and 3 PDD) of levodopa-treated patients. Among these patients, median parkinsonism diagnosis age was 74 years (range: 64–80 years); 63.6%, male. The median interval from levodopa initiation to dyskinesia onset was 2 years (range: 3 months–4 years); the median daily levodopa dosage was 600 mg (range: 50–1,600 mg). Dyskinesia severity led to levodopa adjustments in 5 patients, and all improved. Patients with dyskinesia were diagnosed with parkinsonism at a significantly younger age compared with patients without dyskinesia (p < 0.001). Levodopa dosage was unrelated to increased risk of dyskinesias among DLB and PDD. In contrast, 30.1% of levodopa-treated patients with PD developed dyskinesia. In age-, sex-, and levodopa dosage–adjusted models, Patients with DLB and PDD each had lower odds of developing dyskinesia than patients with PD (odds ratio = 0.42, 95% CI 0.21–0.88; p = 0.02).ConclusionsThe dyskinesia risk for levodopa-treated patients with DLB or PDD was substantially less than for levodopa-treated patients with PD.


2009 ◽  
Vol 24 (12) ◽  
pp. 1740-1746 ◽  
Author(s):  
Cristina Sanchez-Castaneda ◽  
Ramon Rene ◽  
Blanca Ramirez-Ruiz ◽  
Jaume Campdelacreu ◽  
Jordi Gascon ◽  
...  

2019 ◽  
Vol 29 (6) ◽  
pp. 633-638 ◽  
Author(s):  
Hirokazu Doi ◽  
Ryuji Sakakibara ◽  
Masayuki Masuda ◽  
Fuyuki Tateno ◽  
Yosuke Aiba ◽  
...  

2008 ◽  
Vol 22 (10) ◽  
pp. 911-916 ◽  
Author(s):  
Soichiro Shimizu ◽  
Haruo Hanyu ◽  
Kentaro Hirao ◽  
Tomohiko Sato ◽  
Toshihiko Iwamoto ◽  
...  

Author(s):  
Bradley R. Groveman ◽  
Christina D. Orrù ◽  
Andrew G. Hughson ◽  
Lynne D. Raymond ◽  
Gianluigi Zanusso ◽  
...  

Abstract The diagnosis and treatment of synucleinopathies such as Parkinson disease and dementia with Lewy bodies would be aided by the availability of assays for the pathogenic disease-associated forms of α-synuclein (αSynD) that are sufficiently sensitive, specific, and practical for analysis of accessible diagnostic specimens. Two recent αSynD seed amplification tests have provided the first prototypes for ultrasensitive and specific detection of αSynD in patients’ cerebrospinal fluid. These prototypic assays require 5–13 days to perform. Here, we describe an improved α-synuclein real time quaking-induced conversion (αSyn RT-QuIC) assay that has similar sensitivity and specificity to the prior assays, but can be performed in 1–2 days with quantitation. Blinded analysis of cerebrospinal fluid from 29 synucleinopathy cases [12 Parkinson’s and 17 dementia with Lewy bodies] and 31 non-synucleinopathy controls, including 16 Alzheimer’s cases, yielded 93% diagnostic sensitivity and 100% specificity for this test so far. End-point dilution analyses allowed quantitation of relative amounts of αSynD seeding activity in cerebrospinal fluid samples, and detection in as little as 0.2 μL. These results confirm that αSynD seeding activity is present in cerebrospinal fluid. We also demonstrate that it can be rapidly detected, and quantitated, even in early symptomatic stages of synucleinopathy.


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