Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the Consortium on DLB International Workshop

2006 ◽  
Vol 9 (s3) ◽  
pp. 417-423 ◽  
Author(s):  
Ian G. McKeith
1996 ◽  
Vol 17 (4) ◽  
pp. S159
Author(s):  
I.G. McKeith ◽  
R.H. Perry ◽  
E.K. Perry ◽  
P.G. Ince

Author(s):  
Hiroyuki Arai ◽  
Makoto Higuchi ◽  
Nobuyuki Okamura ◽  
Xia Sheng Hu ◽  
Toshifumi Matsui ◽  
...  

2016 ◽  
Vol 23 (8) ◽  
pp. 1322-1328 ◽  
Author(s):  
S. Favaretto ◽  
U. Walter ◽  
C. Baracchini ◽  
S. Pompanin ◽  
C. Bussè ◽  
...  

Neurology ◽  
1998 ◽  
Vol 51 (2) ◽  
pp. 357-362 ◽  
Author(s):  
M. Hashimoto ◽  
H. Kitagaki ◽  
T. Imamura ◽  
N. Hirono ◽  
T. Shimomura ◽  
...  

Objective: Dementia with Lewy bodies (DLB) is emerging as a common cause of degenerative dementia. A recent pathologic study has indicated that the medial temporal lobe in patients with DLB was less atrophic than that in patients with AD. The purpose of this study was to examine whether medial temporal MRI volumetry was useful to differentiate DLB from AD clinically.Methods: We compared the volumes of the hippocampal formation, amygdaloid complex, and whole brain in 27 patients with probable DLB (based on the criteria of the Consortium on DLB International Workshop), 27 patients with probable AD(based on criteria of the National Institute of Neurological Disease and Stroke/Alzheimer's Disease and Related Disorders Association), and 27 normal elderly subjects using an MRI-based volumetric technique. The three groups were matched for age and sex. Severity of cognitive disturbances represented by their Mini-Mental State Examination score was comparable between the DLB and AD groups.Results: Hippocampal volume (normalized to intracranial volume) in the DLB group was significantly larger than that in the AD group, but significantly smaller than that in the normal control group. There were no significant differences in the amygdala and whole-brain volume between the DLB group and the AD group, but the atrophies of the amygdala and whole brain were more severe in the DLB group than those in the control group.Conclusions: These findings indicate the usefulness of MRI hippocampal volumetry in clinically discriminating patients with DLB from patients with AD.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Radoslaw Magierski ◽  
Tomasz Sobow

Dementia with Lewy bodies (DLB) is considered to be the second most frequent primary degenerative dementing illness after Alzheimer’s disease (AD). DLB, together with Parkinson’s disease (PD), Parkinson’s disease with dementia (PDD) belong toα-synucleinopathies—a group of neurodegenerative diseases associated with pathological accumulation of theα-synuclein protein. Dementia due to PD and DLB shares clinical symptoms and neuropsychological profiles. Moreover, the core features and additional clinical signs and symptoms for these two very similar diseases are largely the same. Neuroimaging seems to be a promising method in differential diagnosis of dementia studies. The development of imaging methods or other objective measures to supplement clinical criteria for DLB is needed and a method which would accurately facilitate diagnosis of DLB prior to death is still being searched. Proton magnetic resonance spectroscopy (1H-MRS) provides a noninvasive method of assessing anin vivobiochemistry of brain tissue. This review summarizes the main results obtained from the application of neuroimaging techniques in DLB cases focusing on1H-MRS.


2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Barbara E. Spencer ◽  
Robin G. Jennings ◽  
Chun C. Fan ◽  
James B. Brewer

Abstract In the clinical diagnosis of dementia with Lewy bodies, distinction from Alzheimer’s disease is suboptimal and complicated by shared genetic risk factors and frequent co-pathology. In the present study we tested the ability of polygenic scores for Alzheimer’s disease, dementia with Lewy bodies, and Parkinson’s disease to differentiate individuals in a 2713-participant, pathologically defined sample. A dementia with Lewy bodies polygenic score that excluded apolipoprotein E due to its overlap with Alzheimer’s disease risk was specifically associated with at least limbic (transitional) Lewy-related pathology and a pathological diagnosis of dementia with Lewy bodies. An Alzheimer’s disease polygenic score was associated with neuritic plaques and neurofibrillary tangles but not Lewy-related pathology, and was most strongly associated with an Alzheimer’s pathological diagnosis. Our results indicate that an assessment of genetic risk may be useful to clinically distinguish between Alzheimer’s disease and dementia with Lewy bodies. Notably, we found no association with a Parkinson’s disease polygenic score, which aligns with evidence that dementia with Lewy bodies has a distinct genetic signature that can be exploited to improve clinical diagnoses.


Medicina ◽  
2012 ◽  
Vol 48 (1) ◽  
pp. 1 ◽  
Author(s):  
Jūratė Macijauskienė ◽  
Vita Lesauskaitė

Dementia with Lewy bodies was first recognized as a separate entity about 30 years ago. The prevalence varies from 0% to 5% in the general population, and this disease accounts for 0% to 30.5% of all dementia cases. Dementia with Lewy bodies is considered the second most common cause of degenerative dementia after Alzheimer’s disease. The disease is characterized by alpha-synuclein immunoreactive protein deposits in both neurons and glial cells. The protein deposits are especially prominent in dopaminergic neurons, where they can be detected using conventional histological stains, such as hematoxylin and eosin, and are commonly referred to as Lewy bodies. The diagnosis of dementia with Lewy bodies is based on the presence of dementia as well as 2 of the following 3 core diagnostic features: 1) fluctuating cognition, 2) visual hallucinations, and 3) movement disorder. Diagnostic tests include laboratory data, structural and functional imaging, and electroencephalography. Differential diagnosis of dementia with Lewy bodies focuses on other later life dementia syndromes, other parkinsonian diseases (Parkinson’s disease, progressive supranuclear palsy, corticobasal degeneration), and primary psychiatric illnesses. There is type 1b evidence to support treatment with cholinesterase inhibitors. Glutamatergic and dopaminergic therapies are used as well. Standard neuroleptics are contraindicated, and atypical agents should be used cautiously. Nonpharmacologic measures – therapeutic environment, psychological and social support, physical activity, behavioral management strategies, caregivers’ education and support, and different services – could be suggested.


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