412 lines
30 KiB
Markdown
412 lines
30 KiB
Markdown
---
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title: "Dementia With Lewy Bodies"
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docid: "e8e46d1d-46d2-4e5a-880f-f025a84c5871"
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authors:
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- key: "1fa14dfd-71ea-4960-908e-e720313bc63a"
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value: "Santhosh Gaddikeri, MD"
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- key: "a25c450b-3d34-4f64-bba3-cc0834813df6"
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value: "Miral D. Jhaveri, MD, MBA"
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breadcrumbs:
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-
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name: "Brain"
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slug: "brain"
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treeNodeId: "6d8829f1-14d7-45af-8675-255189aa526a"
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-
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name: "Diagnosis"
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slug: "diagnosis"
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treeNodeId: "51c00394-446e-4a38-94af-d3b1d14d34e8"
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-
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name: "Pathology-Based Diagnoses"
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slug: "pathology-based-diagnoses"
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treeNodeId: "d9d3a8ed-f21b-4831-8c77-591a3500ef77"
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-
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name: "Acquired Toxic/Metabolic/Degenerative Disorders"
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slug: "acquired-toxicmetabolicdegenerativ-"
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treeNodeId: "ba3cfeaf-64d9-4117-91e8-d2ce58783fc5"
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-
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name: "Dementias and Degenerative Disorders"
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slug: "dementias-and-degenerative-disorde-"
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treeNodeId: "6381104d-7a4c-4be5-bb19-3cd90837d547"
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-
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name: "Dementia With Lewy Bodies"
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slug: "dementia-with-lewy-bodies"
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treeNodeId: null
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category: "Brain"
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cmeTopicId: "3a0ceb4e-585c-4343-b8c3-30199a551c37"
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documentVersionId: "8e3dd335-218e-43f3-9635-d2a11eb0a445"
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imageCount: 8
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lastUpdated: "08/10/20"
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pageDescription: "Dementia With Lewy Bodies"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Acquired Toxic/Metabolic/Degenerative Disorders, Dementias and Degenerative Disorders, Dementia With Lewy Bodies"
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pageTitle: "Dementia With Lewy Bodies | STATdx"
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enhancedTitle: "Dementia With Lewy Bodies"
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type: "DX"
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references: true
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breadcrumbs:
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- "Brain"
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- "Diagnosis"
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- "Pathology-Based Diagnoses"
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- "Acquired Toxic/Metabolic/Degenerative Disorders"
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- "Dementias and Degenerative Disorders"
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- "Dementia With Lewy Bodies"
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---
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# KEY FACTS
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- ## Terminology
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- Progressive neurodegenerative dementia
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- Parkinsonism, visual hallucinations prominent
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- Caused by abnormal accumulation of α-synuclein protein
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- ## Imaging
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- MR may differentiate Alzheimer disease (AD) from dementia with Lewy bodies (DLB)
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- PET, SPECT most useful for DLB diagnosis
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- Voxel-based morphometry
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- Relatively preserved hippocampal/medial temporal lobe volume in DLB vs. AD
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- ↓ volume of hypothalamus, substantia innominata, & putamen in DLB vs. AD
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- FDG PET
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- ↓ in glucose metabolism in occipital cortex, especially primary visual cortex
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- F-18 fluorodopa-PET: ↓ striatal dopamine uptake in DLB vs. AD
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- SPECT: Occipital lobe hypoperfusion, especially visual cortex
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- 123 FP-CIT SPECT: ↓ uptake in striatum in DLB vs. AD
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- ## Top Differential Diagnoses
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- Parkinson disease-associated dementia (PDD)
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- Similar clinical, pathological, imaging features with DLB
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- AD
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- Frontotemporal lobar degeneration (FTLD)
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- Vascular dementia
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- ## Pathology
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- Pathologic aggregation of α-synuclein protein in neurites (LB)
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- ## Diagnostic Checklist
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- Unlike AD, medial temporal lobe atrophy not prominent feature
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# TERMINOLOGY
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- ## Abbreviations
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- Dementia with Lewy bodies (DLB)
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- ## Definitions
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- Neurodegenerative dementia characterized by cognitive fluctuations, visual hallucinations, & motor parkinsonism
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- Caused by pathologic aggregation of α-synuclein protein in neurites (LB)
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- MR may differentiate Alzheimer disease (AD) from DLB
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- PET, SPECT most useful for DLB diagnosis
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- ## Imaging Recommendations
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- ### Best imaging tool
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- PET or SPECT
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- ## MR Findings
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- ### T1WI
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- Mild generalized atrophy
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- ### T2WI
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- Nonspecific white matter (WM) hyperintensities
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- ### MRS
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- ↓ WM NAA/Cr in DLB vs. healthy controls (HC)
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- ↑ Cho/Cr ratios in DLB vs. HC
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- Normal levels of NAA/Cr & myoinositol in DLB vs. AD
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- Voxel-based morphometry
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- Relatively preserved hippocampal/medial temporal lobe volume in DLB vs. AD
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- ↓ volume of hypothalamus, substantia innominata, & putamen in DLB vs. AD
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- ↓ gray matter in temporal, parietal, & occipital regions vs. HC
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- DTI
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- ↑ mean diffusivity in amygdala
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- ↓ fractional anisotropy in pons & left thalamus vs. AD
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- ↓ fractional anisotropy in inferior longitudinal fasciculus & inferior occipitofrontal fasciculi vs. HC
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- ## Nuclear Medicine Findings
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- ### PET
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- FDG PET: ↓ glucose metabolism in occipital cortex & visual association cortex with relative preservation of posterior cingulate
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- F-18 fluorodopa-PET: ↓ striatal dopamine uptake in DLB vs. AD
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- ### MIBG scintigraphy
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- ↓ myocardial uptake in DLB due to ↓ postganglionic sympathetic cardiac innervation
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- SPECT
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- Occipital lobe hypoperfusion, especially visual cortex
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- 123 FP-CIT SPECT: Visualize DAT (dopamine transporter) loss
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- ↓ uptake in striatum in DLB
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# DIFFERENTIAL DIAGNOSIS
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- [Parkinson Disease-Associated Dementia](/document/parkinson-disease/0bc3188a-935b-416d-b1a0-25b2d52c6399)
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- Dementia typically develops at least 12 months after onset of initial parkinsonian symptoms
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- Similar clinical, pathologic, imaging features to DLB
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- Less pronounced atrophy in temporal, occipital, & parietal lobes vs. DLB
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- [Alzheimer Disease](/document/alzheimer-disease/f71f5cf5-b1af-4c6d-b145-b4c10eec7b58)
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- Parietal/temporal cortical atrophy
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- Disproportionate hippocampal volume loss
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- Amyloid uptake of cerebral cortex in PiB-PET
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- More severe, faster rate of progression than DLB
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- [Frontotemporal Lobar Degeneration](/document/frontotemporal-lobar-degeneration/49510d0e-acf7-45cb-9eb1-53f8193b0b6d)
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- Asymmetric frontal, anterior temporal lobar atrophy
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- Behavioral variant: Both frontal lobes atrophic
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- Semantic variant: Asymmetric anterior temporal lobe atrophy
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- [Vascular Dementia](/document/vascular-dementia/f59dab57-c511-4369-8fcc-592421a4b8d1)
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- 2nd most common dementia (15-30%)
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- WM & deep gray lacunae
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- Infarcts of different ages
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- Hyperintense lesions on T2WI, hypodense areas on CT, & focal atrophy suggestive of chronic infarcts
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- Accumulation of α-synuclein protein (LB)
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- LB, neuronal loss in substantia nigra → dopamine depletion
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- Loss of cholinergic neurons in nucleus basalis of Meynert
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- → cognitive impairment, visual hallucinations
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- ### Genetics
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- Majority of DLB is sporadic; some are familial
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- α-synuclein gene mutation on chromosome 4 (*A53T*, *E46K* mutation)
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- Similar inheritance, similar genetic risk for PD
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- Other genes associated with DLB include *SNCA*, *APP*, *PSEN1*/*PSEN2*, *MAPT*, *GBA*, & *APOE*
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- ## Staging, Grading, & Classification
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- 3 major forms: Brainstem dominant, limbic/transitional, diffuse neocortical
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- ## Gross Pathologic & Surgical Features
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- Nonspecific & overlap with other neurodegenerative dementias
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- Cortical atrophy is less than AD
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- Atrophy affects frontal, temporal, & parietal lobes, relative sparing of occipital lobes
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- Amygdala & cingulate gyri can show severe atrophy
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- ## Microscopic Features
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- LB in substantia nigra, neocortex, limbic system
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- α-synuclein protein aggregates: Pale eosinophilic inclusions
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- α-synuclein
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- Physiologic function: Synaptic transmission, neuroprotective effect
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- Predominantly expressed in neurons
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- Lewy neurites in hippocampus, amygdala, brainstem nuclei
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- Neuronal loss in substantia nigra, locus ceruleus, nucleus basalis of Meynert, dorsal raphe nuclei
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- Relative preservation of cortical neurons
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- Superficial microvacuolation of cerebral cortex, especially temporal cortex in severe cases
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- 80% have associated AD-like pathology
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- Neuritic/diffuse plaques or neurofibrillary tangles
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Cognitive fluctuations, visual hallucinations, parkinsonism
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- Dysautonomia & sleep disorders
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- Clinical criteria for DLB diagnosis
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- Core clinical features
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- Fluctuating cognition with pronounced variations in attention & alertness
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- Recurrent visual hallucinations (typically well formed & detailed)
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- REM sleep behavior disorder (May precede cognitive decline)
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- 1 or more spontaneous cardinal features of parkinsonism (bradykinesia, rest tremor, rigidity)
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- Supportive clinical features
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- Severe sensitivity to antipsychotic agents
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- Postural instability, repeated falls
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- Syncope or other transient episodes of unresponsiveness
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- Severe autonomic dysfunction (constipation, orthostatic hypotension, urinary incontinence)
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- Hypersomnia, hyposmia, hallucinations in other modalities, systematized delusions
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- Apathy, anxiety, & depression
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- Indicative biomarkers
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- ↓ dopamine transporter uptake in basal ganglia by SPECT or PET
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- Abnormal (low-uptake) I-123-MIBG myocardial scintigraphy
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- Polysomnographic confirmation of REM sleep without atonia
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- Supportive biomarkers
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- Relative preservation of medial temporal lobe structures on CT/MR
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- Generalized low uptake on SPECT/PET perfusion/metabolism scan with ↓ occipital activity ± cingulate island sign on FDG PET imaging
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- Prominent posterior slow-wave activity on EEG with periodic fluctuations in pre-alpha/theta range
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- Probable DLB
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- ≥ 2 core clinical features of DLB with or without indicative biomarkers; **or**
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- Only 1 core clinical feature but with ≥ 1 indicative biomarkers
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- Probable DLB should not be diagnosed on basis of biomarkers alone
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- Possible DLB
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- Only 1 core clinical feature of DLB with no indicative biomarker evidence; **or**
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- ≥ 1 indicative biomarkers but no core clinical features
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- DLB is less likely
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- Presence of any other physical illness or brain disorder, including cerebrovascular disease, sufficient to account in part or in total for clinical picture
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- If parkinsonian features are only core clinical feature & appear for 1st time at stage of severe dementia
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- ## Demographics
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- ### Age
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- 55-85 years; age is only risk factor
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- Average at presentation is 75 years
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- ### Ethnicity
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- LB formation more common in African Americans than Caucasians, but clinical diagnosis of DLB is not significantly different
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- ### Sex
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- M:F = 4:1
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- ### Epidemiology
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- 5% of general population & 30% of dementia cases
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- 2nd most common neurodegenerative dementia (after AD)
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- Incidence rate of 0.1% per year in general population & 3.2% for new dementia cases
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- ## Natural History & Prognosis
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- Average survival after diagnosis < 8 years
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- ## Treatment
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- ### Options, risks, complications
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- No disease-modifying treatments for DLB
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- Symptomatic, targeted toward specific disease manifestations
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- Cholinesterase inhibitor for cognitive features
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- DLB responds better to cholinesterase inhibitor than AD
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- Treatment against hallucination should be conservative due to neuroleptic hypersensitivity of DLB
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# DIAGNOSTIC CHECKLIST
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- ## Image Interpretation Pearls
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- No characteristic features on standard MR
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- Clinical dementia + no/relatively mild medial temporal lobe atrophy
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- Unlike AD, medial temporal lobe atrophy is not prominent
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f336b865-74c1-456e-9130-6db7efb9e7b3
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## References
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# Selected References
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1. [Colloby SJ et al: Cortical thinning in dementia with Lewy bodies and Parkinson disease dementia. Aust N Z J Psychiatry. 4867419885165, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31696728%5Bpmid%5D)
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1. [Gupta V et al: Metabolic imaging patterns in posterior cortical atrophy and Lewy body dementia. Nucl Med Commun. 40(12):1275-82, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31633646%5Bpmid%5D)
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1. [Yamada M et al: Diagnostic criteria for dementia with lewy bodies: updates and future directions. J Mov Disord. ePub, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31694357%5Bpmid%5D)
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1. [Orimo S: [Differential diagnosis of dementia with lewy bodies.] Brain Nerve. 67(4):413-25, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25846590%5Bpmid%5D)
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1. [Bertelson JA et al: Neuroimaging of dementia. Neurol Clin. 32(1):59-93, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24287385%5Bpmid%5D)
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1. [Broski SM et al: Structural and functional imaging in parkinsonian syndromes. Radiographics. 34(5):1273-92, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25208280%5Bpmid%5D)
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1. [Mak E et al: Neuroimaging characteristics of dementia with Lewy bodies. Alzheimers Res Ther. 6(2):18, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25031634%5Bpmid%5D)
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1. [Peraza LR et al: fMRI resting state networks and their association with cognitive fluctuations in dementia with Lewy bodies. Neuroimage Clin. 4:558-65, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=24818081%5Bpmid%5D)
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1. [Bhogal P et al: The common dementias: a pictorial review. Eur Radiol. 23(12):3405-17, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=24081643%5Bpmid%5D)
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1. [Mortimer AM et al: Neuroimaging in dementia: a practical guide. Pract Neurol. 13(2):92-103, 2013](http://www.ncbi.nlm.nih.gov/pubmed/?term=23468560%5Bpmid%5D)
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1. [Burton EJ et al: Medial temporal lobe atrophy on MRI differentiates Alzheimer's disease from dementia with Lewy bodies and vascular cognitive impairment: a prospective study with pathological verification of diagnosis. Brain. 132(Pt 1):195-203, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19022858%5Bpmid%5D)
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1. [Ota M et al: Degeneration of dementia with Lewy bodies measured by diffusion tensor imaging. NMR Biomed. 22(3):280-4, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19009555%5Bpmid%5D)
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1. [Watson R et al: Magnetic resonance imaging in lewy body dementias. Dement Geriatr Cogn Disord. 28(6):493-506, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19996594%5Bpmid%5D)
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1. [Edison P et al: Amyloid load in Parkinson's disease dementia and Lewy body dementia measured with [11C]PIB positron emission tomography. J Neurol Neurosurg Psychiatry. 79(12):1331-8, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18653550%5Bpmid%5D)
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1. [Perneczky R et al: Cerebral metabolic dysfunction in patients with dementia with Lewy bodies and visual hallucinations. Dement Geriatr Cogn Disord. 25(6):531-8, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18477846%5Bpmid%5D)
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1. [Schmidt SL et al: Value of combining activated brain FDG-PET and cardiac MIBG for the differential diagnosis of dementia: differentiation of dementia with Lewy bodies and Alzheimer disease when the diagnoses based on clinical and neuroimaging criteria are difficult. Clin Nucl Med. 33(6):398-401, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18496445%5Bpmid%5D)
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1. [McKeith I et al: Sensitivity and specificity of dopamine transporter imaging with 123I-FP-CIT SPECT in dementia with Lewy bodies: a phase III, multicentre study. Lancet Neurol. 6(4):305-13, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17362834%5Bpmid%5D)
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1. [Seppi K et al: Dementia with Lewy bodies and Parkinson disease with dementia: can MRI make the difference? Neurology. 69(8):717-8, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17709701%5Bpmid%5D)
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1. [Whitwell JL et al: Focal atrophy in dementia with Lewy bodies on MRI: a distinct pattern from Alzheimer's disease. Brain. 130(Pt 3):708-19, 2007](http://www.ncbi.nlm.nih.gov/pubmed/?term=17267521%5Bpmid%5D)
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1. [Burton EJ et al: Progression of white matter hyperintensities in Alzheimer disease, dementia with lewy bodies, and Parkinson disease dementia: a comparison with normal aging. Am J Geriatr Psychiatry. 14(10):842-9, 2006](http://www.ncbi.nlm.nih.gov/pubmed/?term=17001024%5Bpmid%5D)
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## Images
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### Selected Images
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Right & left medial sagittal FDG PET source & 3DSSP images of a 74-year-old man with dementia with Lewy bodies (DLB) presenting with visual hallucinations show severe ↓ metabolic activity in left visual cortex <img src='img/arrows/CO.png'/> & precuneus <img src='img/arrows/WS.png'/>. Note moderate ↓ metabolic activity in right occipital lobe <img src='img/arrows/CS.png'/> & precuneus <img src='img/arrows/WC.png'/> & relative sparing of bilateral posterior cingulate gyri <img src='img/arrows/CC.png'/>.*
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*Axial PET of the same patient shows preserved metabolism in frontal <img src='img/arrows/CS.png'/> & temporal <img src='img/arrows/CO.png'/> lobes. (Courtesy S Behnia, MD.)*
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*Axial PET of the same patient shows preserved metabolism in frontal <img src='img/arrows/CS.png'/> & temporal <img src='img/arrows/CO.png'/> lobes. (Courtesy S Behnia, MD.)*
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*Axial T2WI MR in a patient with DLB shows nonspecific diffuse cortical atrophy. Conventional MR findings are frequently nonspecific in DLB.*
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*Axial T2WI MR in a patient with DLB shows nonspecific diffuse cortical atrophy. Conventional MR findings are frequently nonspecific in DLB.*
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*123FP-CIT-SPECT, DAT imaging (dopamine transporter) shows normal symmetric uptake in the striatum <img src='img/arrows/WS.png'/> of a healthy control (HC). In DLB, there is marked ↓ update in the putamen <img src='img/arrows/WC.png'/> & mild in the caudate nuclei <img src='img/arrows/WO.png'/>. Using DAT imaging, it is not possible to distinguish DLB from atypical parkinsonian syndromes like MSA, PSP, & CBD.*
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*123FP-CIT-SPECT, DAT imaging (dopamine transporter) shows normal symmetric uptake in the striatum <img src='img/arrows/WS.png'/> of a healthy control (HC). In DLB, there is marked ↓ update in the putamen <img src='img/arrows/WC.png'/> & mild in the caudate nuclei <img src='img/arrows/WO.png'/>. Using DAT imaging, it is not possible to distinguish DLB from atypical parkinsonian syndromes like MSA, PSP, & CBD.*
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### Additional Images
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*Axial T2WI MR in a patient with cognitive decline, visual hallucination, & parkinsonism shows diffuse cortical atrophy consistent with DLB.*
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*Axial T2WI MR in a patient with cognitive decline, visual hallucination, & parkinsonism shows diffuse cortical atrophy consistent with DLB.*
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*Axial T2WI MR in the same patient exhibits mild atrophy of the medial temporal lobes.*
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*Axial T2WI MR in the same patient exhibits mild atrophy of the medial temporal lobes.*
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*Coronal T1WI MR in a patient with DLB shows prominent frontal lobe volume loss with relative sparing of hippocampal volume. (Courtesy M.J. Firbank, MD & J.T. O'Brien, MD.)*
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*Coronal T1WI MR in a patient with DLB shows prominent frontal lobe volume loss with relative sparing of hippocampal volume. (Courtesy M.J. Firbank, MD & J.T. O'Brien, MD.)*
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*Coronal T1WI MR in a patient with Alzheimer disease (AD) shows marked hippocampal volume loss <img src='img/arrows/CC.png'/> & relative sparing of frontal lobes. (Courtesy M. J. Firbank, MD & J. T. O'Brien, MD.)*
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*Coronal T1WI MR in a patient with Alzheimer disease (AD) shows marked hippocampal volume loss <img src='img/arrows/CC.png'/> & relative sparing of frontal lobes. (Courtesy M. J. Firbank, MD & J. T. O'Brien, MD.)*
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