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title: "Vascular Dementia"
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docid: "f59dab57-c511-4369-8fcc-592421a4b8d1"
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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: "Vascular Dementia"
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slug: "vascular-dementia"
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treeNodeId: null
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category: "Brain"
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||||
cmeTopicId: "a7dd2d05-d82a-4ed2-87b6-9525d7f4a6a4"
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documentVersionId: "f043b936-64b6-4a76-92f4-a926111caa85"
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imageCount: 24
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lastUpdated: "10/08/20"
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pageDescription: "Vascular Dementia"
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pageKeywords: "Brain, Diagnosis, Pathology-Based Diagnoses, Acquired Toxic/Metabolic/Degenerative Disorders, Dementias and Degenerative Disorders, Vascular Dementia"
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pageTitle: "Vascular Dementia | STATdx"
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enhancedTitle: "Vascular Dementia"
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type: "DX"
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references: true
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breadcrumbs:
|
||||
- "Brain"
|
||||
- "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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- "Vascular Dementia"
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---
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# KEY FACTS
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- ## Terminology
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- Vascular dementia (VaD), multiinfarct dementia (MID), vascular cognitive impairment (VCI)
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- Stepwise progressive ↓ in cognitive function
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- Heterogeneous group of disorders with varying etiologies, pathologic subtypes
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- VaD often mixed etiology
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- Can occur alone or in association with Alzheimer disease
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- MID secondary to repeated cerebral infarctions
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- VaD: Dementia caused by cerebrovascular disease or ↓ cerebral blood flow
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- VCI: Cognitive impairment caused by or associated with vascular factors
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- Can occur alone or in association with Alzheimer disease (AD)
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- ## Imaging
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- General features
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- Multifocal infarcts [cortical gray matter (GM), subcortical white matter (WM)]
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- Basal ganglia (BG), pons
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- Territorial as well as lacunar lesions
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- Coexisting microvascular WM disease common
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- Multiple remote microhemorrhages
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- CT
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- Multifocal infarcts
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- Single or multiple, lacunar to territorial
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- WM hypointensities (discrete to confluent)
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- FDG PET
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- Multifocal regions ↓ metabolism in cortex, WM
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- ## Top Differential Diagnoses
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- AD
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- Frontotemporal lobar degeneration
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- CADASIL
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- Dementia with Lewy bodies
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- ## Clinical Issues
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- 2nd most common dementia (after AD)
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- Mood & behavioral changes more typical than memory loss
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- ## Diagnostic Checklist
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- Report strategically placed infarcts
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- Look for hemorrhage, DWI abnormalities
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# TERMINOLOGY
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- ## Abbreviations
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- Vascular dementia (VaD)
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- ## Synonyms
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- Multiinfarct dementia (MID)
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- Vascular cognitive disorder (VCD)
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- Vascular cognitive impairment (VCI)
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- Subcortical ischemic VaD
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- Poststroke dementia
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- ## Definitions
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- Dementia caused by cerebrovascular disease or ↓ cerebral blood flow (CBF)
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- VCI: Cognitive impairment caused by or associated with vascular factors
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- Secondary to repeated cerebral infarctions
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- Can occur alone or in association with Alzheimer disease (AD)
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- 2nd most common cause of dementia next to AD
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# IMAGING
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- ## General Features
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- ### Best diagnostic clue
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- Multifocal infarcts
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- Cortical gray matter (GM), subcortical white matter (WM)
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- Basal ganglia (BG), pons
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- Territorial as well as lacunar infarcts
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- Changes of microvascular WM ischemia common
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- ### Location
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- Typically involves cerebral hemispheres & BG
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- Usually bilateral but may be unilateral
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- ### Size
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- Vary from single to multiple, punctate to large/confluent
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- ### Morphology
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- Small infarcts are rounded or oval; large confluent abnormalities are ill defined
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- ## CT Findings
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- ### NECT
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- Hypodensity in periventricular WM
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- Cortical, subcortical, BG infarcts
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- Generalized atrophy with focal cortical infarcts typical
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- ## MR Findings
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- ### T1WI
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- Generally have hypointense BG lacunar infarcts
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- Atrophy with enlargement of ventricles & sulci
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- ### T2WI
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- Punctate or confluent regions of hyperintense WM
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- Central pontine infarcts
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- Large areas of volume loss with widened sulci
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- ### FLAIR
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- Hyperintense foci within BG
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- Multifocal diffuse & confluent WM hyperintensities
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- ### T2* GRE
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- Multiple blooming hypointensities in cortex & along pial surface
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- ### DWI
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- ↓ fractional anisotropy & ↑ ADC within lesions, normal-appearing WM (NAWM)
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- ↑ in mean diffusivity of NAWM correlates with disability found on tests of executive function
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- ### MRA
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- Most abnormalities in small arteries, generally not well seen on MRA
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- ### MRS
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- ↓ NAA in both cortical & WM regions
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- Frontal cortex NAA negatively correlated with volume of WM signal hyperintensity
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- ## Ultrasonographic Findings
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- Transcranial Doppler sonography: Pulsatility indices in large arteries ↑ compared to AD
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- ## Nuclear Medicine Findings
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- FDG PET
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- Multiple areas of hypometabolism without specific lobar predominance
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- Severity of MID neuropsychiatric symptoms correlates with extent of ↓ metabolism in cortex & WM
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- SPECT
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- Iodine-123-iodoamphetamine: ↓ frontal & BG CBF, which correlates with low cognitive scores
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- Tc-99m hexamethyl propyleneamine oxime: CBF heterogeneity more prominent in anterior portion of brain
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- Unlike pattern in AD, in which posterior abnormalities predominate
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- ## Imaging Recommendations
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- ### Best imaging tool
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- MR
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- PET/SPECT may also provide specificity
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- ### Protocol advice
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- Axial FLAIR to detect WM infarcts
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- Axial & coronal T2WI to assess regions of atrophy
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- T2* GRE/SWI to identify hemorrhage
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# DIFFERENTIAL DIAGNOSIS
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- [Alzheimer Disease](/document/alzheimer-disease/f71f5cf5-b1af-4c6d-b145-b4c10eec7b58)
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- Striking hippocampus & amygdala atrophy
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- PET: Bilateral temporoparietal hypoperfusion/hypometabolism (BG spared)
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- Often coexists with VaD
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- [Frontotemporal Lobar Degeneration](/document/frontotemporal-lobar-degeneration/49510d0e-acf7-45cb-9eb1-53f8193b0b6d)
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- Characterized by early onset of behavioral changes with intact visual, spatial skills
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- Frontal, temporal lobe atrophy
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- Marked atrophy → knife-like gyri
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- [Alcoholic Encephalopathy](/document/alcoholic-encephalopathy/88021852-b73d-4cdf-a719-dd4ae3231e45)
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- 3rd most common cause of dementia
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- Generalized > focal atrophy; superior vermis atrophy
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- [CADASIL](/document/cadasil/6b5a24c8-afd7-4106-bb4b-11421ed1592c)
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- Most common heritable cause of stroke, VaD in adults
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- Earlier age of onset
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- Imaging looks like small vessel disease
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- [Dementia With Lewy Bodies](/document/dementia-with-lewy-bodies/e8e46d1d-46d2-4e5a-880f-f025a84c5871)
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- Hypometabolism of entire brain
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- Without infarcts or significant atrophy
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# PATHOLOGY
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- ## General Features
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- ### Etiology
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- MID is usually due to multiple small infarctions
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- Infarcts involving entire major vessel territories are usually absent
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- Minority may be secondary to single or few large infarctions
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- ~ 75% of all MID patients exhibit small vessel disease rather than thromboembolism
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- Growing evidence exists for involvement of cholinergic system in VaD
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- Cholinergic deficits well documented in VaD, independent of concomitant AD pathology
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- Cholinergic neuron loss in 70% of AD, 40% of VaD
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- ### Genetics
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- Apolipoprotein E (*APOE*)
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- Serum protein involved in lipid metabolism
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- Encoded at single gene locus on chromosome 19 by 3 alleles: ε2, ε3, ε4
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- Frequency of ε4 allele significantly higher among patients with AD & VaD compared to controls
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- Odds of developing AD or VaD are 4.4x & 3.7x higher (respectively) in presence of even single ε4 allele
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- Paraoxonase (*PON1*)
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- Component of high-density lipoproteins with antioxidative potential
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- 2 *PON1* polymorphisms (Gln192Arg associated with enzyme activity & T-107C associated with enzyme concentration) are independent risk factors for VaD, particularly in *APOE* (ε4)
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- ## Staging, Grading, & Classification
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- 8 subtypes of VaD
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- MIDs: Due to large cerebral emboli, usually readily identifiable
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- Strategically placed infarctions causing dementia
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- Multiple subcortical lacunar lesions: Develop VaD 5-25x more frequently than age-matched controls
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- Binswanger disease: Small vessel disease → widespread incomplete infarction of WM
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- Mixtures of 2 or more VaD subtypes
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- Hemorrhagic lesions causing dementia
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- Subcortical dementias due to other causes [e.g., cerebral autosomal dominant arteriopathy with subcortical infarcts & leukoencephalopathy (CADASIL)]
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- Hybrid forms of AD & VaD
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- ## Gross Pathologic & Surgical Features
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- Multifocal infarctions with atrophy
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- ## Microscopic Features
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- Arteriosclerosis & amyloid angiopathy major underlying pathologies in small vessel vascular disease
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- Vessels display atheromata, lipohyalinosis, subintimal thickening, fibrinoid necrosis
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- Infarcted tissue undergoes necrosis → gliotic wall surrounding CSF cavity
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- Myelin & axonal loss with astrocytosis
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# CLINICAL ISSUES
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- ## Presentation
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- ### Most common signs/symptoms
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- Infarcts with transient focal neurologic deficits
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- Most deficits persist
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- Mood & behavioral changes
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- Deterioration of executive function & attention, changes in personality (rather than memory loss) predominate
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- Severe depression is more common in VaD than AD
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- ### Clinical profile
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- Main risk factors
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- Advanced age, HTN, diabetes, smoking
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- Hypercholesterolemia, hypercoagulable states
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- ## Demographics
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- ### Age
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- Generally earlier age than AD
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- Incidence ↑ with age
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- ### Sex
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- M > F
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- ### Epidemiology
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- 10% of dementias
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- 2nd most common dementia (after AD)
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- ~ 25% of elderly stroke patients meet VaD criteria
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- Cerebral small vessel disease accounted for 33% of dementia risk
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- ## Natural History & Prognosis
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- Poststroke dementia: Progressive, episodic, stepwise cognitive decline following stroke
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- VaD without recent stroke: Progressive or stepwise cognitive decline without concurrent history of symptomatic stroke but with imaging evidence of clinically unrecognized cerebrovascular disease
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- Neuropsychiatric & motor signs: VaD accompanied by neuropsychiatric signs, such as depression, abulia, apathy, & psychosis with delusions or hallucinations
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- Intervals of clinical stabilization ± limited recovery
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- 5-year survival with VaD ~ 50% of age-matched controls
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- ## Treatment
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- Prevent further vascular insult
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- Control precipitating factors (e.g., HTN, diabetes)
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# DIAGNOSTIC CHECKLIST
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- ## Image Interpretation Pearls
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- Not single entity but large group of conditions with variable clinical & imaging findings
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- ## Reporting Tips
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- Report strategically placed infarcts, hemorrhagic components, DWI abnormalities, pattern of cortical volume loss if present
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6999ad9a-6bd9-47dd-8707-b571f32301e3
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## References
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# Selected References
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1. [Alber J et al: White matter hyperintensities in vascular contributions to cognitive impairment and dementia (VCID): knowledge gaps and opportunities. Alzheimers Dement (N Y). 5:107-17, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31011621%5Bpmid%5D)
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1. [Huang WQ et al: Susceptibility weighted imaging (SWI) recommended as a regular magnetic resonance diagnosis for vascular dementia to identify independent idiopathic normal pressure hydrocephalus before ventriculo-peritoneal (V-P) shunt treatment: a case study. Front Neurol. 10:262, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30984097%5Bpmid%5D)
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1. [Lim J et al: Utilization of magnetic resonance imaging by comorbidity of patients with dementia. Int J Environ Res Public Health. 16(23), 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31783540%5Bpmid%5D)
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1. [Mahalingam S et al: Neuroimaging in dementias. Semin Neurol. 39(2):188-99, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30925612%5Bpmid%5D)
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1. [Sengupta P et al: Pattern of cognitive deficits in vascular dementia. Indian J Med Res. 149(4):503-7, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=31411174%5Bpmid%5D)
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1. [Smith EE et al: Harmonizing brain magnetic resonance imaging methods for vascular contributions to neurodegeneration. Alzheimers Dement (Amst). 11:191-204, 2019](http://www.ncbi.nlm.nih.gov/pubmed/?term=30859119%5Bpmid%5D)
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1. [Shivamurthy VK et al: Brain FDG PET and the diagnosis of dementia. AJR Am J Roentgenol. 204(1):W76-85, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25539279%5Bpmid%5D)
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1. [Venkat P et al: Models and mechanisms of vascular dementia. Exp Neurol. 272:97-108, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25987538%5Bpmid%5D)
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1. [Villeneuve S et al: Imaging vascular disease and amyloid in the aging brain: implications for treatment. J Prev Alzheimers Dis. 2(1):64-70, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25844350%5Bpmid%5D)
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1. [Yamada M: Cerebral amyloid angiopathy: emerging concepts. J Stroke. 17(1):17-30, 2015](http://www.ncbi.nlm.nih.gov/pubmed/?term=25692104%5Bpmid%5D)
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1. [Ihara M et al: Understanding and preventing the development of post-stroke dementia. Expert Rev Neurother. 14(9):1067-77, 2014](http://www.ncbi.nlm.nih.gov/pubmed/?term=25105544%5Bpmid%5D)
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1. [Dufouil C et al: Severe cerebral white matter hyperintensities predict severe cognitive decline in patients with cerebrovascular disease history. Stroke. 40(6):2219-21, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19390070%5Bpmid%5D)
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1. [Targosz-Gajniak M et al: Cerebral white matter lesions in patients with dementia - from MCI to severe Alzheimer's disease. J Neurol Sci. 283(1-2):79-82, 2009](http://www.ncbi.nlm.nih.gov/pubmed/?term=19268974%5Bpmid%5D)
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1. [Jellinger KA: Morphologic diagnosis of "vascular dementia" - a critical update. J Neurol Sci. 270(1-2):1-12, 2008](http://www.ncbi.nlm.nih.gov/pubmed/?term=18455191%5Bpmid%5D)
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1. [O'Sullivan M et al: DTI MRI correlates with executive dysfunction in patients with ischaemic leukoaraiosis. J Neurol Neurosurg Psychiatry. 75(3):441-7, 2004](http://www.ncbi.nlm.nih.gov/pubmed/?term=14966162%5Bpmid%5D)
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1. [Yoshikawa T et al: Heterogeneity of cerebral blood flow in Alzheimer disease and vascular dementia. AJNR Am J Neuroradiol. 24(7):1341-7, 2003](http://www.ncbi.nlm.nih.gov/pubmed/?term=12917125%5Bpmid%5D)
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## Images
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### Selected Images
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*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
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*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
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*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
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*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
|
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|
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|
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*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
*Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts <img src='img/arrows/CS.png'/>, an acute left occipital lobe infarct <img src='img/arrows/CO.png'/>, and small lacunar infarcts in the basal ganglia/thalami <img src='img/arrows/CC.png'/>.*
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*Axial T2 MR in a 72-year-old man with VaD demonstrates multiple remote lacunar infarcts in bilateral deep gray nuclei <img src='img/arrows/CS.png'/> and extensive white matter (WM) hyperintensity <img src='img/arrows/CO.png'/> due to chronic WM ischemic changes. Also note prominent cortical sulci <img src='img/arrows/CC.png'/> due to cerebral atrophy.*
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|
||||
*Axial T2 MR in a 72-year-old man with VaD demonstrates multiple remote lacunar infarcts in bilateral deep gray nuclei <img src='img/arrows/CS.png'/> and extensive white matter (WM) hyperintensity <img src='img/arrows/CO.png'/> due to chronic WM ischemic changes. Also note prominent cortical sulci <img src='img/arrows/CC.png'/> due to cerebral atrophy.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in an 80-year-old man with VaD demonstrates extensive confluent hyperintense signal in bilateral cerebral hemispheric WM <img src='img/arrows/CS.png'/> due to chronic ischemic changes and a remote lacunar infarct in right coronal radiata <img src='img/arrows/CO.png'/>. Note the prominent cortical sulci <img src='img/arrows/CC.png'/> due to diffuse parenchymal volume loss.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in an 80-year-old man with VaD demonstrates extensive confluent hyperintense signal in bilateral cerebral hemispheric WM <img src='img/arrows/CS.png'/> due to chronic ischemic changes and a remote lacunar infarct in right coronal radiata <img src='img/arrows/CO.png'/>. Note the prominent cortical sulci <img src='img/arrows/CC.png'/> due to diffuse parenchymal volume loss.*
|
||||
|
||||
|
||||
*Axial SWI MR in the same patient demonstrates multiple scattered remote microhemorrhagic foci <img src='img/arrows/CS.png'/> bilaterally in both central and peripheral distribution.*
|
||||
|
||||
|
||||
*Axial SWI MR in the same patient demonstrates multiple scattered remote microhemorrhagic foci <img src='img/arrows/CS.png'/> bilaterally in both central and peripheral distribution.*
|
||||
|
||||
|
||||
*Sagittal (top row), axial (bottom left) and coronal (bottom right) reformats of FDG PET in a patient with VaD show hypometabolic areas due to remote territorial infarcts <img src='img/arrows/CS.png'/> and chronic WM ischemic changes <img src='img/arrows/CC.png'/>. (Courtesy J. Singh, MD.)*
|
||||
|
||||
|
||||
*Sagittal (top row), axial (bottom left) and coronal (bottom right) reformats of FDG PET in a patient with VaD show hypometabolic areas due to remote territorial infarcts <img src='img/arrows/CS.png'/> and chronic WM ischemic changes <img src='img/arrows/CC.png'/>. (Courtesy J. Singh, MD.)*
|
||||
|
||||
|
||||
*Axial T2 MR through the pons in a patient with VaD demonstrates remote lacunar infarct <img src='img/arrows/CS.png'/> in pons and also associated chronic WM ischemic changes <img src='img/arrows/CC.png'/>. Note focal gliosis in the left anterior temporal lobe <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial T2 MR through the pons in a patient with VaD demonstrates remote lacunar infarct <img src='img/arrows/CS.png'/> in pons and also associated chronic WM ischemic changes <img src='img/arrows/CC.png'/>. Note focal gliosis in the left anterior temporal lobe <img src='img/arrows/CO.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with VaD shows large remote infarction in the left middle cerebral artery distribution <img src='img/arrows/CS.png'/>. Note associated prominent cortical sulci <img src='img/arrows/CC.png'/> and ex vacuo dilation of left lateral ventricle <img src='img/arrows/CO.png'/> due to parenchymal atrophy.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with VaD shows large remote infarction in the left middle cerebral artery distribution <img src='img/arrows/CS.png'/>. Note associated prominent cortical sulci <img src='img/arrows/CC.png'/> and ex vacuo dilation of left lateral ventricle <img src='img/arrows/CO.png'/> due to parenchymal atrophy.*
|
||||
|
||||
|
||||
*Axial SWI MR in a 73-year-old woman with VaD demonstrates multiple scattered remote microhemorrhagic foci <img src='img/arrows/CS.png'/> predominantly in peripheral distribution.*
|
||||
|
||||
|
||||
*Axial SWI MR in a 73-year-old woman with VaD demonstrates multiple scattered remote microhemorrhagic foci <img src='img/arrows/CS.png'/> predominantly in peripheral distribution.*
|
||||
|
||||
|
||||
*Axial NECT shows WM hypodensity as well as bilateral frontal and parietal evolving cortical remote infarctions <img src='img/arrows/CS.png'/>. Note the associated focal biparietal cortical atrophy <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
*Axial NECT shows WM hypodensity as well as bilateral frontal and parietal evolving cortical remote infarctions <img src='img/arrows/CS.png'/>. Note the associated focal biparietal cortical atrophy <img src='img/arrows/CC.png'/>.*
|
||||
|
||||
|
||||
*Axial FDG PET in a patient with multiinfarct dementia demonstrates multiple wedge-shaped areas of hypometabolism <img src='img/arrows/CC.png'/> due to chronic infarcts. (Courtesy A. Ali, MD.)*
|
||||
|
||||
|
||||
*Axial FDG PET in a patient with multiinfarct dementia demonstrates multiple wedge-shaped areas of hypometabolism <img src='img/arrows/CC.png'/> due to chronic infarcts. (Courtesy A. Ali, MD.)*
|
||||
|
||||
|
||||
### Additional Images
|
||||
|
||||
|
||||
*Sagittal T1WI MR demonstrates frontal cortical thinning with white matter hypointensity <img src='img/arrows/WS.png'/> from infarction. Also note the separate focus of white matter abnormality <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Sagittal T1WI MR demonstrates frontal cortical thinning with white matter hypointensity <img src='img/arrows/WS.png'/> from infarction. Also note the separate focus of white matter abnormality <img src='img/arrows/WO.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows diffuse, confluent white matter hyperintensity in a patient with vascular dementia.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows diffuse, confluent white matter hyperintensity in a patient with vascular dementia.*
|
||||
|
||||
|
||||
*Axial T2WI MR reveals bilateral thalamic lacunar infarctions <img src='img/arrows/BS.png'/>, as well as confluent periventricular white matter hyperintensity. Note the ventricular enlargement from associated atrophy.*
|
||||
|
||||
|
||||
*Axial T2WI MR reveals bilateral thalamic lacunar infarctions <img src='img/arrows/BS.png'/>, as well as confluent periventricular white matter hyperintensity. Note the ventricular enlargement from associated atrophy.*
|
||||
|
||||
|
||||
*Axial FLAIR MR demonstrates only mild white matter hyperintensity, as well as a very small cortical/subcortical infarct <img src='img/arrows/WS.png'/> in a patient with vascular dementia.*
|
||||
|
||||
|
||||
*Axial FLAIR MR demonstrates only mild white matter hyperintensity, as well as a very small cortical/subcortical infarct <img src='img/arrows/WS.png'/> in a patient with vascular dementia.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows changes of late acute/early subacute infarction in the right hemisphere <img src='img/arrows/WS.png'/>, old focal cortical infarcts in the left hemisphere <img src='img/arrows/WC.png'/>, and diffuse confluent white matter disease <img src='img/arrows/WO.png'/> (arteriolosclerosis).*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows changes of late acute/early subacute infarction in the right hemisphere <img src='img/arrows/WS.png'/>, old focal cortical infarcts in the left hemisphere <img src='img/arrows/WC.png'/>, and diffuse confluent white matter disease <img src='img/arrows/WO.png'/> (arteriolosclerosis).*
|
||||
|
||||
|
||||
*Axial NECT in a patient with multi-infarct dementia and a history of numerous strokes shows diffuse atrophy with multiple old focal cortical infarcts <img src='img/arrows/WS.png'/> and confluent periventricular white matter hypodensities <img src='img/arrows/WO.png'/>, consistent with arteriolosclerosis and lipohyalinosis.*
|
||||
|
||||
|
||||
*Axial NECT in a patient with multi-infarct dementia and a history of numerous strokes shows diffuse atrophy with multiple old focal cortical infarcts <img src='img/arrows/WS.png'/> and confluent periventricular white matter hypodensities <img src='img/arrows/WO.png'/>, consistent with arteriolosclerosis and lipohyalinosis.*
|
||||
|
||||
|
||||
*Axial T2WI MR in an 82-year-old woman with clinical vascular dementia shows age-appropriate sulcal prominence, enlarged ventricles, and a focal right parietal lacunar infarct <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial T2WI MR in an 82-year-old woman with clinical vascular dementia shows age-appropriate sulcal prominence, enlarged ventricles, and a focal right parietal lacunar infarct <img src='img/arrows/WS.png'/>.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows another lacunar infarct in the right deep hemispheric white matter <img src='img/arrows/BS.png'/>. A few scattered white matter hyperintensities are present <img src='img/arrows/WS.png'/> but within normal limits for the patient's age. MR images do not explain fully the extent of the patient's cognitive impairment.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in the same patient shows another lacunar infarct in the right deep hemispheric white matter <img src='img/arrows/BS.png'/>. A few scattered white matter hyperintensities are present <img src='img/arrows/WS.png'/> but within normal limits for the patient's age. MR images do not explain fully the extent of the patient's cognitive impairment.*
|
||||
|
||||
|
||||
*PET scan in the same patient was performed. Stereotaxic surface projections show normal glucose metabolism in age-matched controls (2nd row). The patient's scan (3rd row) shows multifocal cortical areas of decreased glucose metabolism. Z-scores are shown on the bottom row. (Courtesy N. Foster, MD.)*
|
||||
|
||||
|
||||
*PET scan in the same patient was performed. Stereotaxic surface projections show normal glucose metabolism in age-matched controls (2nd row). The patient's scan (3rd row) shows multifocal cortical areas of decreased glucose metabolism. Z-scores are shown on the bottom row. (Courtesy N. Foster, MD.)*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with vascular dementia shows confluent periventricular white matter hyperintensities <img src='img/arrows/CC.png'/> with volume loss.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a patient with vascular dementia shows confluent periventricular white matter hyperintensities <img src='img/arrows/CC.png'/> with volume loss.*
|
||||
|
||||
|
||||
*Axial SWI in the same patient shows multiple "blooming" hypointense foci due to remote microhemorrhages in the basal ganglia <img src='img/arrows/CS.png'/>, thalami <img src='img/arrows/CO.png'/>, and cerebral cortex <img src='img/arrows/CC.png'/>. This patient had long-standing uncontrolled hypertension and the distribution of the microhemorrhages predominantly in the deep gray nuclei supports that.*
|
||||
|
||||
|
||||
*Axial SWI in the same patient shows multiple "blooming" hypointense foci due to remote microhemorrhages in the basal ganglia <img src='img/arrows/CS.png'/>, thalami <img src='img/arrows/CO.png'/>, and cerebral cortex <img src='img/arrows/CC.png'/>. This patient had long-standing uncontrolled hypertension and the distribution of the microhemorrhages predominantly in the deep gray nuclei supports that.*
|
||||
|
||||
|
||||
*Axial NECT in a 81-year-old woman with multi-infarct dementia shows cystic encephalomalacia in the right parietal lobe <img src='img/arrows/CC.png'/> due to an old infarct. There is marked volume loss with ventricular enlargement. There are confluent white matter hypodensities <img src='img/arrows/CS.png'/> consistent with arteriolosclerosis and lipohyalinosis.*
|
||||
|
||||
|
||||
*Axial NECT in a 81-year-old woman with multi-infarct dementia shows cystic encephalomalacia in the right parietal lobe <img src='img/arrows/CC.png'/> due to an old infarct. There is marked volume loss with ventricular enlargement. There are confluent white matter hypodensities <img src='img/arrows/CS.png'/> consistent with arteriolosclerosis and lipohyalinosis.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 72-year-old man with chronic hypertension and diabetes presenting with mood and behavioral changes shows confluent white matter hyperintensities <img src='img/arrows/CC.png'/> in the periventricular regions. Note the multiple chronic lacunar infarcts in the basal ganglia <img src='img/arrows/CS.png'/> as well as enlargement of the ventricles and cortical sulci.*
|
||||
|
||||
|
||||
*Axial FLAIR MR in a 72-year-old man with chronic hypertension and diabetes presenting with mood and behavioral changes shows confluent white matter hyperintensities <img src='img/arrows/CC.png'/> in the periventricular regions. Note the multiple chronic lacunar infarcts in the basal ganglia <img src='img/arrows/CS.png'/> as well as enlargement of the ventricles and cortical sulci.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows multiple subcortical hyperintensities <img src='img/arrows/CS.png'/> in a 76-year-old normotensive man with clinical diagnosis of vascular dementia. No focal infarcts are seen.*
|
||||
|
||||
|
||||
*Axial FLAIR MR shows multiple subcortical hyperintensities <img src='img/arrows/CS.png'/> in a 76-year-old normotensive man with clinical diagnosis of vascular dementia. No focal infarcts are seen.*
|
||||
|
||||
Reference in New Issue
Block a user