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KEY FACTS

Terminology
- Vascular dementia (VaD), multiinfarct dementia (MID), vascular cognitive impairment (VCI)
- Stepwise progressive ↓ in cognitive function
- Heterogeneous group of disorders with varying etiologies, pathologic subtypes - VaD often mixed etiology - Can occur alone or in association with Alzheimer disease - MID secondary to repeated cerebral infarctions
- VaD: Dementia caused by cerebrovascular disease or ↓ cerebral blood flow
- VCI: Cognitive impairment caused by or associated with vascular factors
- Can occur alone or in association with Alzheimer disease (AD)
Imaging
- General features - Multifocal infarcts [cortical gray matter (GM), subcortical white matter (WM)] - Basal ganglia (BG), pons - Territorial as well as lacunar lesions - Coexisting microvascular WM disease common - Multiple remote microhemorrhages
- CT - Multifocal infarcts - Single or multiple, lacunar to territorial - WM hypointensities (discrete to confluent)
- FDG PET - Multifocal regions ↓ metabolism in cortex, WM
Top Differential Diagnoses
- AD
- Frontotemporal lobar degeneration
- CADASIL
- Dementia with Lewy bodies
Clinical Issues
- 2nd most common dementia (after AD)
- Mood & behavioral changes more typical than memory loss
Diagnostic Checklist
- Report strategically placed infarcts
- Look for hemorrhage, DWI abnormalities

TERMINOLOGY

Abbreviations
- Vascular dementia (VaD)
Synonyms
- Multiinfarct dementia (MID)
- Vascular cognitive disorder (VCD)
- Vascular cognitive impairment (VCI)
- Subcortical ischemic VaD
- Poststroke dementia
Definitions
- Dementia caused by cerebrovascular disease or ↓ cerebral blood flow (CBF)
- VCI: Cognitive impairment caused by or associated with vascular factors
- Secondary to repeated cerebral infarctions
- Can occur alone or in association with Alzheimer disease (AD)
- 2nd most common cause of dementia next to AD

IMAGING

General Features

Best diagnostic clue

- Multifocal infarcts
        - Cortical gray matter (GM), subcortical white matter (WM)
        - Basal ganglia (BG), pons
        - Territorial as well as lacunar infarcts
        - Changes of microvascular WM ischemia common

Location

- Typically involves cerebral hemispheres & BG
- Usually bilateral but may be unilateral

Size

- Vary from single to multiple, punctate to large/confluent

Morphology

- Small infarcts are rounded or oval; large confluent abnormalities are ill defined

CT Findings

NECT

- Hypodensity in periventricular WM
- Cortical, subcortical, BG infarcts
- Generalized atrophy with focal cortical infarcts typical

MR Findings

T1WI

- Generally have hypointense BG lacunar infarcts
- Atrophy with enlargement of ventricles & sulci

T2WI

- Punctate or confluent regions of hyperintense WM
- Central pontine infarcts
- Large areas of volume loss with widened sulci

FLAIR

- Hyperintense foci within BG
- Multifocal diffuse & confluent WM hyperintensities

T2* GRE

- Multiple blooming hypointensities in cortex & along pial surface

DWI

- ↓ fractional anisotropy & ↑ ADC within lesions, normal-appearing WM (NAWM)
- ↑ in mean diffusivity of NAWM correlates with disability found on tests of executive function

MRA

- Most abnormalities in small arteries, generally not well seen on MRA

MRS

- ↓ NAA in both cortical & WM regions
- Frontal cortex NAA negatively correlated with volume of WM signal hyperintensity

Ultrasonographic Findings
- Transcranial Doppler sonography: Pulsatility indices in large arteries ↑ compared to AD
Nuclear Medicine Findings
- FDG PET - Multiple areas of hypometabolism without specific lobar predominance - Severity of MID neuropsychiatric symptoms correlates with extent of ↓ metabolism in cortex & WM
- SPECT - Iodine-123-iodoamphetamine: ↓ frontal & BG CBF, which correlates with low cognitive scores - Tc-99m hexamethyl propyleneamine oxime: CBF heterogeneity more prominent in anterior portion of brain - Unlike pattern in AD, in which posterior abnormalities predominate

Imaging Recommendations

Best imaging tool

- MR
- PET/SPECT may also provide specificity

Protocol advice

- Axial FLAIR to detect WM infarcts
- Axial & coronal T2WI to assess regions of atrophy
- T2* GRE/SWI to identify hemorrhage

DIFFERENTIAL DIAGNOSIS

Alzheimer Disease
- Striking hippocampus & amygdala atrophy
- PET: Bilateral temporoparietal hypoperfusion/hypometabolism (BG spared)
- Often coexists with VaD
Frontotemporal Lobar Degeneration
- Characterized by early onset of behavioral changes with intact visual, spatial skills
- Frontal, temporal lobe atrophy
- Marked atrophy → knife-like gyri
Alcoholic Encephalopathy
- 3rd most common cause of dementia
- Generalized > focal atrophy; superior vermis atrophy
CADASIL
- Most common heritable cause of stroke, VaD in adults
- Earlier age of onset
- Imaging looks like small vessel disease
Dementia With Lewy Bodies
- Hypometabolism of entire brain
- Without infarcts or significant atrophy

PATHOLOGY

General Features

Etiology

- MID is usually due to multiple small infarctions
        - Infarcts involving entire major vessel territories are usually absent
        - Minority may be secondary to single or few large infarctions
- ~ 75% of all MID patients exhibit small vessel disease rather than thromboembolism
- Growing evidence exists for involvement of cholinergic system in VaD
        - Cholinergic deficits well documented in VaD, independent of concomitant AD pathology
        - Cholinergic neuron loss in 70% of AD, 40% of VaD

Genetics

- Apolipoprotein E (*APOE*)
        - Serum protein involved in lipid metabolism
        - Encoded at single gene locus on chromosome 19 by 3 alleles: ε2, ε3, ε4
        - Frequency of ε4 allele significantly higher among patients with AD & VaD compared to controls
        - Odds of developing AD or VaD are 4.4x & 3.7x higher (respectively) in presence of even single ε4 allele
- Paraoxonase (*PON1*)
        - Component of high-density lipoproteins with antioxidative potential
        - 2 *PON1* polymorphisms (Gln192Arg associated with enzyme activity & T-107C associated with enzyme concentration) are independent risk factors for VaD, particularly in *APOE* (ε4)

Staging, Grading, & Classification
- 8 subtypes of VaD - MIDs: Due to large cerebral emboli, usually readily identifiable - Strategically placed infarctions causing dementia - Multiple subcortical lacunar lesions: Develop VaD 5-25x more frequently than age-matched controls - Binswanger disease: Small vessel disease → widespread incomplete infarction of WM - Mixtures of 2 or more VaD subtypes - Hemorrhagic lesions causing dementia - Subcortical dementias due to other causes [e.g., cerebral autosomal dominant arteriopathy with subcortical infarcts & leukoencephalopathy (CADASIL)] - Hybrid forms of AD & VaD
Gross Pathologic & Surgical Features
- Multifocal infarctions with atrophy
Microscopic Features
- Arteriosclerosis & amyloid angiopathy major underlying pathologies in small vessel vascular disease
- Vessels display atheromata, lipohyalinosis, subintimal thickening, fibrinoid necrosis
- Infarcted tissue undergoes necrosis → gliotic wall surrounding CSF cavity
- Myelin & axonal loss with astrocytosis

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- Infarcts with transient focal neurologic deficits
        - Most deficits persist
- Mood & behavioral changes
- Deterioration of executive function & attention, changes in personality (rather than memory loss) predominate
- Severe depression is more common in VaD than AD

Clinical profile

- Main risk factors
        - Advanced age, HTN, diabetes, smoking
        - Hypercholesterolemia, hypercoagulable states

Demographics

Age

- Generally earlier age than AD
- Incidence ↑ with age

Sex
```
- M > F
```

Epidemiology

- 10% of dementias
- 2nd most common dementia (after AD)
- ~ 25% of elderly stroke patients meet VaD criteria
- Cerebral small vessel disease accounted for 33% of dementia risk

Natural History & Prognosis
- Poststroke dementia: Progressive, episodic, stepwise cognitive decline following stroke
- VaD without recent stroke: Progressive or stepwise cognitive decline without concurrent history of symptomatic stroke but with imaging evidence of clinically unrecognized cerebrovascular disease
- Neuropsychiatric & motor signs: VaD accompanied by neuropsychiatric signs, such as depression, abulia, apathy, & psychosis with delusions or hallucinations
- Intervals of clinical stabilization ± limited recovery
- 5-year survival with VaD ~ 50% of age-matched controls
Treatment
- Prevent further vascular insult - Control precipitating factors (e.g., HTN, diabetes)

DIAGNOSTIC CHECKLIST

Image Interpretation Pearls
- Not single entity but large group of conditions with variable clinical & imaging findings
Reporting Tips
- Report strategically placed infarcts, hemorrhagic components, DWI abnormalities, pattern of cortical volume loss if present

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References

Selected References

Images

Selected Images

Axial graphic of vascular dementia (VaD) shows diffuse cerebral atrophy, focal volume loss due to multiple chronic infarcts , an acute left occipital lobe infarct , and small lacunar infarcts in the basal ganglia/thalami .

Axial T2 MR in a 72-year-old man with VaD demonstrates multiple remote lacunar infarcts in bilateral deep gray nuclei and extensive white matter (WM) hyperintensity due to chronic WM ischemic changes. Also note prominent cortical sulci 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 due to chronic ischemic changes and a remote lacunar infarct in right coronal radiata . Note the prominent cortical sulci due to diffuse parenchymal volume loss.

Axial SWI MR in the same patient demonstrates multiple scattered remote microhemorrhagic foci 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 and chronic WM ischemic changes . (Courtesy J. Singh, MD.)

Axial T2 MR through the pons in a patient with VaD demonstrates remote lacunar infarct in pons and also associated chronic WM ischemic changes . Note focal gliosis in the left anterior temporal lobe .

Axial FLAIR MR in a patient with VaD shows large remote infarction in the left middle cerebral artery distribution . Note associated prominent cortical sulci and ex vacuo dilation of left lateral ventricle due to parenchymal atrophy.

Axial SWI MR in a 73-year-old woman with VaD demonstrates multiple scattered remote microhemorrhagic foci predominantly in peripheral distribution.

Axial NECT shows WM hypodensity as well as bilateral frontal and parietal evolving cortical remote infarctions . Note the associated focal biparietal cortical atrophy .

Axial FDG PET in a patient with multiinfarct dementia demonstrates multiple wedge-shaped areas of hypometabolism due to chronic infarcts. (Courtesy A. Ali, MD.)

Additional Images

Sagittal T1WI MR demonstrates frontal cortical thinning with white matter hypointensity from infarction. Also note the separate focus of white matter abnormality .

Axial FLAIR MR shows diffuse, confluent white matter hyperintensity in a patient with vascular dementia.

Axial T2WI MR reveals bilateral thalamic lacunar infarctions , 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 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 , old focal cortical infarcts in the left hemisphere , and diffuse confluent white matter disease (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 and confluent periventricular white matter hypodensities , 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 .

Axial FLAIR MR in the same patient shows another lacunar infarct in the right deep hemispheric white matter . A few scattered white matter hyperintensities are present 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.)

Axial FLAIR MR in a patient with vascular dementia shows confluent periventricular white matter hyperintensities with volume loss.

Axial SWI in the same patient shows multiple "blooming" hypointense foci due to remote microhemorrhages in the basal ganglia , thalami , and cerebral cortex . 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 due to an old infarct. There is marked volume loss with ventricular enlargement. There are confluent white matter hypodensities 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 in the periventricular regions. Note the multiple chronic lacunar infarcts in the basal ganglia as well as enlargement of the ventricles and cortical sulci.

Axial FLAIR MR shows multiple subcortical hyperintensities in a 76-year-old normotensive man with clinical diagnosis of vascular dementia. No focal infarcts are seen.

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KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Clinical Issues

Diagnostic Checklist

TERMINOLOGY

Abbreviations

Synonyms

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Size

Morphology

CT Findings

NECT

MR Findings

T1WI

T2WI

FLAIR

T2* GRE

DWI

MRA

MRS

Ultrasonographic Findings

Nuclear Medicine Findings

Imaging Recommendations

Best imaging tool

Protocol advice

DIFFERENTIAL DIAGNOSIS

PATHOLOGY

General Features

Etiology

Genetics

Staging, Grading, & Classification

Gross Pathologic & Surgical Features

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Clinical profile

Demographics

Age

Sex

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Image Interpretation Pearls

Reporting Tips

References

Selected References

Images

Selected Images

Additional Images

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