Dementia with Lewy bodies and Alzheimer disease

Kantarci, Kejal; Avula, Ramesh; Senjem, Matthew L.; Samikoglu, Ali R.; Zhang, B.; Weigand, Stephen D.; Przybelski, Scott A.; Edmonson, Heidi A.; Vemuri, Prashanthi; Knopman, David S.; Ferman, Tanis J.; Boeve, Bradley F.; Petersen, R. C.; Jack, Clifford R.

doi:10.1212/wnl.0b013e3181e0f7cf

Cited by 196 publications

(201 citation statements)

References 39 publications

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“…Although amygdala is a medial temporal limbic structure that is involved with the NFT pathology of AD early in the disease course, the finding of a weaker association with NFT pathology in the amygdala compared with the hippocampus may occur because the amygdala is also highly vulnerable to LB-related pathology. 33 An increase in amygdalar diffusivity has been observed on diffusion tensor imaging in DLB, 34 and volume of the amygdala on MRI was associated with LB pathology. 16,18 In agreement with these previous reports, we found a trend of smaller amygdalar volumes in patients with a high likelihood of DLB compared with the control subjects; however, this finding did not reach statistical significance.…”

Section: Resultsmentioning

confidence: 99%

Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies

Kantarci¹,

Ferman²,

Boeve³

et al. 2012

Neurology

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Objective: To determine the association between the focal atrophy measures on antemortem MRI and postmortem neuropathologic classification of dementia with Lewy bodies (DLB) using the Third Report of the DLB Consortium criteria. Methods:We retrospectively identified 56 subjects who underwent antemortem MRI and had Lewy body (LB) pathology at autopsy. Subjects were pathologically classified as high (n ϭ 25), intermediate (n ϭ 22), and low likelihood DLB (n ϭ 9) according to the Third Report of the DLB Consortium criteria. We included 2 additional pathologic comparison groups without LBs: one with low likelihood Alzheimer disease (AD) (control; n ϭ 27) and one with high likelihood AD (n ϭ 33). The associations between MRI-based volumetric measurements and the pathologic classification of DLB were tested with analysis of covariance by adjusting for age, sex, and MRI-to-death interval. Dementia with Lewy bodies (DLB) is the second most common cause of neurodegenerative dementia after Alzheimer disease (AD); however, many patients with DLB also have AD pathology. [1][2][3][4][5] Imaging markers that predict the contribution of AD to the dementia syndrome in DLB would have an important role in treatment decisions and assessing responsiveness to treatments targeting disease-specific pathologies. Results:According to the Third Report of the DLB Consortium criteria, 6 the pathologic diagnosis of DLB is made by considering both AD and Lewy body (LB) pathologies. For example, patients with limbic LBs are diagnosed as high likelihood DLB if they have low likelihood AD, but diagnosed as low likelihood DLB if they have high likelihood AD. Therefore, in vivo identification of AD and LB pathology is critical for the differential diagnosis of DLB.

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Section: Resultsmentioning

confidence: 99%

Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies

Kantarci¹,

Ferman²,

Boeve³

et al. 2012

Neurology

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“…Dysfunction of the visuo-amygdaloid pathway has been implicated in the visual misidentification and visual hallucinations. 3 The inferior longitudinal fasciculus projects from the occipital lobe visual association cortex to the medial and anterior temporal lobe and carries modulatory projections back to the visual cortex from the amygdala. The inferior longitudinal fasciculus is disrupted in LBD with visual hallucinations compared to LBD without visual hallucinations as measured by diffusion tensor imaging.…”

Section: Discussionmentioning

confidence: 99%

“…The inferior longitudinal fasciculus is disrupted in LBD with visual hallucinations compared to LBD without visual hallucinations as measured by diffusion tensor imaging. 3 LBD is associated with widespread cholinergic dysfunction as demonstrated by PET using radiolabeled acetylcholine analogues MP4A and MP4P. 4 The maximum deficits are measured in the posterior cortical regions, the inferior temporal gyrus, the supramarginal gyrus, and the posterior cingulate.…”

Section: Discussionmentioning

confidence: 99%

Capgras-like visual decomposition in Lewy body dementia with therapeutic response to donepezil

et al. 2014

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D efects in visual/spatial cognition, including hallucinations and Capgras syndrome, are common in Lewy body dementia (LBD).1 In Capgras syndrome, a person holds a delusion that a friend, spouse, parent, or other close family member has been replaced by an identical-looking impostor. These visual phenomena frequently induce anxiety and agitation, and the only treatment currently available is neuroleptics. Neuroleptics have severe side effects in LBD as well as a black box warning for increased risk of death and stroke in elderly patients with dementia. We report 2 cases of LBD where visual phenomena including Capgras-like syndrome responded favorably to the use of a cholinesterase inhibitor. Case reportsCase 1 A 79-year-old man presented with a 3-year history of progressive word-finding difficulties and memory decline. His symptoms fulfilled criteria for probable LBD including cognitive impairment, fluctuating attention/concentration, and REM sleep behavior disorder. 2Neuropsychological testing was consistent with LBD (table e-1 at Neurology.org/cp). He alleged that his wife was an intruder with similar facial features. He did not recognize his wife during these periods and was uncooperative with her efforts to assist him. He was started on donepezil 5 mg, which was subsequently titrated to 10 mg daily after 4 weeks, and it was well-tolerated. These episodes became less frequent within 2 weeks of initiation of treatment parallel to improvement in cognitive function (Mini-Mental State Examination [MMSE] 19-28). He then was able to reconstruct the image of her face, starting with a unique mole on her cheek. Within a year, severe depression necessitated psychiatric admission, during which donepezil was discontinued. He developed paranoia and experienced visual hallucinations of Podcast Practical ImplicationsConsider cholinesterase inhibitors for visual hallucinations or Capgras syndrome first.

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“…Kantarci et al (2001Kantarci et al ( , 2010) used a dedicated DTI sequence based on fluid-attenuated inversion recovery (FLAIR) to suppress the CSF signal during data acquisition. Salminen et al (2016aSalminen et al ( , 2016b recomputed the MD for each region of interest (ROI) using a customized diffusion weighted imaging sequence with multiple non-zero b-values and an extended model to fit the tensor.…”

Section: Introductionmentioning

confidence: 99%

“…They could show that the decay of signal intensity was mono-exponential for b-values ≥ 680, indicating successful suppression of CSF signal after removal of b~0 data. Both approaches by Kantarci et al (2001Kantarci et al ( , 2010 and by Salminen et al (2016aSalminen et al ( , 2016b are well-grounded, but they require additional MR sequences that go beyond current clinical standards, either a FLAIR DTI sequence or a DTI sequence with more than one non-zero b-value. So far, three approaches were proposed for post-acquisition partial volume correction (PVC) of single-shell DTI as used in clinical practice.…”

Section: Introductionmentioning

confidence: 99%

[IC‐P‐161]: MEAN DIFFUSIVITY IN CORTICAL GRAY MATTER IN ALZHEIMER's DISEASE: THE IMPORTANCE OF PARTIAL VOLUME CORRECTION

Henf

Grothe

Teipel

et al. 2017

Alzheimer's & Dementia

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Mean diffusivity (MD) measured by diffusion tensor imaging can reflect microstructural alterations of the brain's gray matter (GM). Therefore, GM MD may be a sensitive marker of neurodegeneration related to Alzheimer's Disease (AD). However, due to partial volume effects (PVE), differences in MD may be overestimated because of a higher degree of brain atrophy in AD patients and in cases with mild cognitive impairment (MCI). Here, we evaluated GM MD changes in AD and MCI compared with healthy controls, and the effect of partial volume correction (PVC) on diagnostic utility of MD.We determined region of interest (ROI) and voxel-wise group differences and diagnostic accuracy of MD and volume measures between matched samples of 39 AD, 39 MCI and 39 healthy subjects before and after PVC. Additionally, we assessed whether effects of GM MD values on diagnosis were mediated by volume.ROI and voxel-wise group differences were reduced after PVC. When using these ROIs for predicting group separation in logistic models, both PVE corrected and uncorrected GM MD values yielded a poorer diagnostic accuracy in single predictor models than regional volume. For the discrimination of AD patients and healthy controls, the effect of GM MD on diagnosis was significantly mediated by volume of hippocampus and posterior cingulate ROIs.Our results suggest that GM MD measurements are strongly confounded by PVE in the presence of brain atrophy, underlining the necessity of PVC when using these measurements as specific metrics of microstructural tissue degeneration. Independently of PVC, regional MD was not superior to regional volume in separating prodromal and clinical stages of AD from healthy controls.

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Dementia with Lewy bodies and Alzheimer disease

Cited by 196 publications

References 39 publications

Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies

Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies

Capgras-like visual decomposition in Lewy body dementia with therapeutic response to donepezil

[IC‐P‐161]: MEAN DIFFUSIVITY IN CORTICAL GRAY MATTER IN ALZHEIMER's DISEASE: THE IMPORTANCE OF PARTIAL VOLUME CORRECTION

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