Vascular Dementia¶

Chapter 444 | Part 13: Neurologic Disorders · Part 13 – Neurologic Disorders

Detailed clinical reference synthesised from Harrison's Principles of Internal Medicine, 22nd Edition

🔑 Key Clinical Points¶

Vascular dementia is traditionally defined by symptomatic strokes but broadly encompasses vascular contributions to cognitive impairment and dementia (VCID).
Mixed dementias (vascular + neurodegenerative) are more prevalent than single-etiology dementias.
Approximately 50% of stroke survivors demonstrate cognitive impairment, with risk increasing over longer periods of follow-up.
SPRINT-MIND trial showed SBP <120 mmHg reduced mild cognitive impairment (HR 0.81) and combined MCI/dementia (HR 0.85).
MRI markers: Lacunar infarcts (3-15mm), Microinfarcts (<3mm), Microbleeds (T2*), White Matter Hyperintensities (FLAIR).
Arteriolosclerosis affects deep penetrating vessels; Cerebral Amyloid Angiopathy affects superficial lobar regions.
Strategic infarcts (thalamus, medial temporal cortex, angular gyrus) can cause specific cognitive deficits.
Poststroke cognitive decline occurs even in patients with good recovery.
Framingham Study showed declining dementia hazard rates correlating with improved BP control.
Diffusion Tensor MRI (DTI) measures white matter disconnection associated with cognitive performance.

📑 Table of Contents¶

1. DEFINITION & OVERVIEW
1.1 Subtypes of Cerebrovascular Disease Associated with VCID
2. EPIDEMIOLOGY
2.1 Epidemiologic Trends and Risk Factors
3. ETIOLOGY & PATHOPHYSIOLOGY
3.1 MRI Markers and Imaging Findings
4. CLINICAL FEATURES
4.1 Cognitive Domains Affected
4.2 Poststroke Cognitive Decline
5. DIFFERENTIAL DIAGNOSIS
5.1 Mixed Dementia Considerations
6. INVESTIGATIONS & DIAGNOSIS
6.1 Diagnostic Imaging Criteria
7. MANAGEMENT & TREATMENT
7.1 Prevention and Risk Factor Management
8. PROGNOSIS & COMPLICATIONS
8.1 Cognitive Decline Trajectories
9. SPECIAL CONSIDERATIONS
9.1 Global Variability
10. KEY PEARLS & CLINICAL TRAPS
10.1 Clinical Pearls
Figures & Illustrations

📋 Figures in This Chapter¶

#	Type	Description
1	🖼 Figure	Magnetic resonance imaging (MRI) markers of cerebral small vessel showing hyperintense rim...
2	🖼 Figure	Magnetic resonance imaging (MRI) markers of cerebral small vessel showing hyperintense rim...
3	🖼 Figure	Magnetic resonance imaging (MRI) markers of cerebral small vessel showing hyperintense rim...
4	🖼 Figure	Magnetic resonance imaging (MRI) markers of cerebral small vessel showing hyperintense rim...
5	🖼 Figure	Magnetic resonance imaging (MRI) markers of cerebral small vessel showing hyperintense rim...

1. DEFINITION & OVERVIEW¶

The term vascular dementia has traditionally been used to describe a subset of dementia cases due primarily to one or more symptomatic strokes.
Considered as such, vascular dementia is usually ranked the second most frequent cause of dementia, exceeded only by Alzheimer's disease.
More recently, this relatively narrow definition of vascular dementia has been substantially broadened to encompass the full impact of cerebrovascular disease on age-related cognitive decline.
The term vascular contributions to cognitive impairment and dementia (VCID) reflects the observation that pathologic changes involving the cerebral vasculature are highly prevalent in the elderly and contribute to cognitive impairment, whether occurring in isolation or—in conjunction with other neurodegenerative processes.
The concept of VCID is one facet of the contemporary understanding of age-related cognitive decline as due to cumulative effects of distinct and overlapping neuropathologic changes.
Multifactorial or 'mixed' dementias appear to be more prevalent than single-etiology dementias and thus represent the rule rather than the exception.
Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
Community-based individuals in the longitudinal Reasons for Geographic and Racial Differences in Stroke study, for example, changed trajectory from an average prestroke cognitive gain of 0.021 points/year to poststroke cognitive loss of –0.035 points/year on the six-item screener global cognitive function scale.
Mechanisms for poststroke cognitive decline likely include ongoing effects of the cerebrovascular disease that gave rise to the index stroke as well as loss of cognitive reserve that makes the brain less resilient to any additional age-related disorders.
Population-based studies also demonstrate substantially increased risk of cognitive impairment among individuals without symptomatic stroke but with MRI evidence of cerebrovascular disease.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.

1.1 Subtypes of Cerebrovascular Disease Associated with VCID¶

Large Cerebral Strokes: Symptomatic strokes, whether ischemic or hemorrhagic, reflect irreversible injury to discrete areas of cerebral cortex, subcortical white matter, or other subcortical and infratentorial structures and produce cognitive impairment as a function of their size and location.
Rare individual infarcts in specific strategic locations such as thalamus, medial temporal cortex, anterior corpus callosum, or dominant-side angular gyrus can sufficiently impair episodic memory and functional skills to meet memory-based criteria for dementia.
Cerebral Small-Vessel Disease: Diseases of the brain's small vessels can also cause symptomatic ischemic or hemorrhagic stroke but are more often clinically asymptomatic and recognized only during evaluation for cognitive decline or other symptoms.
The two common age-related cerebral small-vessel pathologies are arteriolosclerosis and cerebral amyloid angiopathy.
Arteriolosclerosis represents thickening of arterioles due to infiltration of plasma proteins into the vessel wall.
Cerebrovascular arteriolosclerosis can present as a cause of ischemic or hemorrhagic symptomatic stroke, both most commonly centered in territories supplied by deep penetrating vessels such as thalamus, basal ganglia, or brainstem.
Cerebral amyloid angiopathy is defined by deposition of the β-amyloid peptide in the walls of small cerebral arteries, arterioles, and capillaries, with consequent loss of normal wall structure.
Cerebral amyloid angiopathy is most often recognized symptomatically as a cause of intracerebral hemorrhage, commonly located in cerebral cortex, subcortical white matter (collectively known as lobar hemorrhages), or the cerebral convexity subarachnoid space.
Despite differences in their underlying pathogenic mechanisms, the two cerebral small-vessel diseases produce a similar range of ischemic and hemorrhagic brain lesions detectable by histopathology at autopsy or MRI scan during life.

Table 1 — MRI Markers of Cerebral Small Vessel Disease¶

Marker	MRI Sequence	Appearance	Location	Pathology
Lacunar Infarct	FLAIR	Hyperintense rim surrounding a hypointense cavitated core	Left thalamus (deep penetrating)	Arteriolosclerosis
Acute Microinfarct	Diffusion-weighted	Small hyperintense lesion	Left centrum semiovale	Small-vessel disease
Cerebral Microbleeds (Deep)	T2*-weighted	Multiple small hypointense lesions	Pons (deep penetrating)	Arteriolosclerosis
Cerebral Microbleeds (Lobar)	T2*-weighted	Multiple small hypointense lesions	Lobar brain regions	Cerebral amyloid angiopathy
White Matter Hyperintensities	FLAIR / T2-weighted	Confluent diffuse hyperintensities	White matter	Gliosis, demyelination, increased water content

2. EPIDEMIOLOGY¶

A review of data from across the globe indicates good evidence for variability in vascular dementia.
Intracranial atherosclerosis is higher in Asians, Hispanics, and American blacks than it is in European and American whites.
Whites may have more extracranial disease.
The causes of these disparities remain under investigation but likely include access to health care, lifestyle factors such as diet, and possible genetic influences.
The population-based Framingham Study reported 5-year age- and sex-adjusted cumulative hazard rates for dementia of 3.6 per 100 persons during the late 1970s to early 1980s, 2.8 in the late 1980s to early 1990s, 2.2 in the late 1990s to early 2000s, and 2.0 in the late 2000s to early 2010s.
These time intervals coincide with parallel trends in hypertension control and stroke prevention, though the associations do not prove causation.
Evidence supporting a potential causative effect of blood pressure control came from the SPRINT-MIND trial targeting systolic blood pressure (SBP) of 30% of postmortem brains and, when present, to each account for ~20% of an individual's premortem cognitive decline.

2.1 Epidemiologic Trends and Risk Factors¶

Vascular dementia is especially common in populations with limited access to medical care, where vascular risk factors are undertreated.
Recent epidemiologic evidence of a decline in age-adjusted dementia incidence hints at the potential public impact of improving vascular health.
Risk factors for arteriolosclerosis include age, hypertension, and diabetes mellitus.
Risk factors for cerebral amyloid angiopathy include advancing age.

Table 2 — Framingham Study Dementia Hazard Rates¶

Time Period	Cumulative Hazard Rate (per 100 persons)	Context
Late 1970s to early 1980s	3.6	Baseline
Late 1980s to early 1990s	2.8	Parallel trends in hypertension control
Late 1990s to early 2000s	2.2	Parallel trends in hypertension control
Late 2000s to early 2010s	2.0	Parallel trends in hypertension control

3. ETIOLOGY & PATHOPHYSIOLOGY¶

Large Cerebral Strokes: Symptomatic strokes, whether ischemic or hemorrhagic, reflect irreversible injury to discrete areas of cerebral cortex, subcortical white matter, or other subcortical and infratentorial structures and produce cognitive impairment as a function of their size and location.
Rare individual infarcts in specific strategic locations such as thalamus, medial temporal cortex, anterior corpus callosum, or dominant-side angular gyrus can sufficiently impair episodic memory and functional skills to meet memory-based criteria for dementia.
Cerebral Small-Vessel Disease: Diseases of the brain's small vessels can also cause symptomatic ischemic or hemorrhagic stroke but are more often clinically asymptomatic and recognized only during evaluation for cognitive decline or other symptoms.
The two common age-related cerebral small-vessel pathologies are arteriolosclerosis and cerebral amyloid angiopathy.
Arteriolosclerosis represents thickening of arterioles due to infiltration of plasma proteins into the vessel wall.
Cerebrovascular arteriolosclerosis can present as a cause of ischemic or hemorrhagic symptomatic stroke, both most commonly centered in territories supplied by deep penetrating vessels such as thalamus, basal ganglia, or brainstem.
Cerebral amyloid angiopathy is defined by deposition of the β-amyloid peptide in the walls of small cerebral arteries, arterioles, and capillaries, with consequent loss of normal wall structure.
Cerebral amyloid angiopathy is most often recognized symptomatically as a cause of intracerebral hemorrhage, commonly located in cerebral cortex, subcortical white matter (collectively known as lobar hemorrhages), or the cerebral convexity subarachnoid space.
Despite differences in their underlying pathogenic mechanisms, the two cerebral small-vessel diseases produce a similar range of ischemic and hemorrhagic brain lesions detectable by histopathology at autopsy or MRI scan during life.
Small (lacunar) infarcts are a common feature of arteriolosclerosis and less commonly of cerebral amyloid angiopathy.
Chronic lacunar infarcts can appear on MRI fluid-attenuated inversion recovery (FLAIR) sequences as a hyperintense rim surrounding a hypointense cavitated core with diameters typically 3–15 mm.
This characteristic appearance evolves in only a subset of small infarctions, and many cannot be readily identified in the chronic stage.
Microinfarcts <3 mm are characteristic of both small-vessel diseases.
They are substantially more numerous than lacunar infarcts but less easily visualized.
Acute microinfarcts may be visible as punctate hyperintensities on diffusion-weighted MRI images, whereas a small subset of chronic microinfarcts is detectable on high-resolution T2-weighted MRI sequences as hyperintense lesions in the cerebral cortex.
Cerebral microbleeds are less numerous than lacunes or microinfarcts but readily detected in their chronic stage because of the paramagnetic effects of iron products.
These appear as round hypointense lesions on T2*-weighted MRI, primarily in deep penetrating brain regions if caused by arteriolosclerosis or lobar regions if caused by cerebral amyloid angiopathy.
Other MRI markers of small-vessel disease identify diffuse injury of the white matter.
White matter hyperintensities on T2-weighted or FLAIR MRI sequences are an almost ubiquitous feature of aging.
Although these lesions are readily visible on clinical MRI, they represent a nonspecific marker of white matter gliosis, demyelination, or increased water content.
Extremely severe diffuse white matter vascular injury is commonly referred to as Binswanger's disease or subcortical arteriosclerotic encephalopathy, recognized as a clinical syndrome with gradual cognitive deterioration and notable white matter changes of small-vessel ischemic disease.
On neuroimaging, a progressive confluent subcortical and periventricular white matter disease is seen.
Diffusion tensor MRI measures of white matter structural integrity show a consistent association with cognitive performance and gait speed, reflecting the central role of disconnection of key brain networks in mediating the effects of cerebral small-vessel disease.
These diffusion tensor–based methods often require complex processing and are typically used in research rather than clinical settings.
A relatively simple diffusion tensor–based metric defined by the peak width of the skeletonized mean diffusivity (PSMD) histogram has emerged as a candidate method for quantifying white matter disconnection.
Functional MRI measurement of cerebrovascular reactivity to physiologic stimuli is generally not performed in clinical practice, but it may become abnormal decades before appearance of structural brain injury and therefore represents a promising outcome marker for identifying disease-modifying interventions aimed to slow or prevent vascular brain injury.
The concept of VCID posits that large strokes and small-vessel disease often occur in combination with neurodegenerative brain diseases, most commonly Alzheimer's disease.
Many clinicopathologic correlation studies have established that the co-occurrence of cerebrovascular and neurodegenerative lesions produces more cognitive and functional impairment than expected from the effects of each disease mechanism.

3.1 MRI Markers and Imaging Findings¶

Lacunar infarcts: Fluid-attenuated inversion recovery (FLAIR) sequence showing hyperintense rim surrounding a hypointense cavitated core in the left thalamus.
Acute microinfarcts: Diffusion-weighted sequence showing small hyperintense lesion in the left centrum semiovale.
Cerebral microbleeds in deep penetrating brain regions: T2*-weighted sequence showing multiple small hypointense lesions in the pons.
Cerebral microbleeds in lobar brain regions: T2*-weighted sequence showing multiple small hypointense lesions lobar brain regions.
White matter hyperintensities: FLAIR sequence showing confluent diffuse hyperintensities in white matter.
Diffusion tensor MRI: Increased water diffusivity or decreased diffusion directionality associated with cognitive performance and gait speed.

Table 3 — MRI Markers of Cerebral Small Vessel Disease¶

Marker	MRI Sequence	Appearance	Location	Pathology
Lacunar Infarct	FLAIR	Hyperintense rim surrounding a hypointense cavitated core	Left thalamus (deep penetrating)	Arteriolosclerosis
Acute Microinfarct	Diffusion-weighted	Small hyperintense lesion	Left centrum semiovale	Small-vessel disease
Cerebral Microbleeds (Deep)	T2*-weighted	Multiple small hypointense lesions	Pons (deep penetrating)	Arteriolosclerosis
Cerebral Microbleeds (Lobar)	T2*-weighted	Multiple small hypointense lesions	Lobar brain regions	Cerebral amyloid angiopathy
White Matter Hyperintensities	FLAIR / T2-weighted	Confluent diffuse hyperintensities	White matter	Gliosis, demyelination, increased water content

4. CLINICAL FEATURES¶

Symptomatic strokes, whether ischemic or hemorrhagic, reflect irreversible injury to discrete areas of cerebral cortex, subcortical white matter, or other subcortical and infratentorial structures and produce cognitive impairment as a function of their size and location.
Rare individual infarcts in specific strategic locations such as thalamus, medial temporal cortex, anterior corpus callosum, or dominant-side angular gyrus can sufficiently impair episodic memory and functional skills to meet memory-based criteria for dementia.
More commonly, strokes occur outside these strategic territories and affect various other aspects of cognition such as executive function, processing speed, and visuospatial performance that fall under the broader VCID concept.
Multiple strokes and larger volumes of infarcted territory are associated with a higher likelihood of poststroke cognitive dysfunction.
Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
Community-based individuals in the longitudinal Reasons for Geographic and Racial Differences in Stroke study, for example, changed trajectory from an average prestroke cognitive gain of 0.021 points/year to poststroke cognitive loss of –0.035 points/year on the six-item screener global cognitive function scale.
Mechanisms for poststroke cognitive decline likely include ongoing effects of the cerebrovascular disease that gave rise to the index stroke as well as loss of cognitive reserve that makes the brain less resilient to any additional age-related disorders.
Population-based studies also demonstrate substantially increased risk of cognitive impairment among individuals without symptomatic stroke but with MRI evidence of cerebrovascular disease.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.
Extremely severe diffuse white matter vascular injury is commonly referred to as Binswanger's disease or subcortical arteriosclerotic encephalopathy, recognized as a clinical syndrome with gradual cognitive deterioration and notable white matter changes of small-vessel ischemic disease.
On neuroimaging, a progressive confluent subcortical and periventricular white matter disease is seen.

4.1 Cognitive Domains Affected¶

Episodic memory (specifically in strategic infarcts like thalamus, medial temporal cortex).
Executive function.
Processing speed.
Visuospatial performance.

4.2 Poststroke Cognitive Decline¶

Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
Trajectory change from average prestroke cognitive gain of 0.021 points/year to poststroke cognitive loss of –0.035 points/year on the six-item screener global cognitive function scale.
Mechanisms include ongoing effects of the cerebrovascular disease that gave rise to the index stroke as well as loss of cognitive reserve that makes the brain less resilient to any additional age-related disorders.

5. DIFFERENTIAL DIAGNOSIS¶

Mixed dementias appear to be more prevalent than single-etiology dementias and thus represent the rule rather than the exception.
The concept of VCID posits that large strokes and small-vessel disease often occur in combination with neurodegenerative brain diseases, most commonly Alzheimer's disease.
Many clinicopathologic correlation studies have established that the co-occurrence of cerebrovascular and neurodegenerative lesions produces more cognitive and functional impairment than expected from the effects of each disease mechanism.

5.1 Mixed Dementia Considerations¶

Co-occurrence of cerebrovascular and neurodegenerative lesions (e.g., Alzheimer's disease).
Produces more cognitive and functional impairment than expected from the effects of each disease mechanism.

6. INVESTIGATIONS & DIAGNOSIS¶

The term vascular dementia has traditionally been used to describe a subset of dementia cases due primarily to one or more symptomatic strokes.
More recently, this relatively narrow definition of vascular dementia has been substantially broadened to encompass the full impact of cerebrovascular disease on age-related cognitive decline.
The term vascular contributions to cognitive impairment and dementia (VCID) reflects the observation that pathologic changes involving the cerebral vasculature are highly prevalent in the elderly and contribute to cognitive impairment, whether occurring in isolation or—in conjunction with other neurodegenerative processes.
Population-based studies also demonstrate substantially increased risk of cognitive impairment among individuals without symptomatic stroke but with MRI evidence of cerebrovascular disease.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.
MRI markers of small-vessel disease identify diffuse injury of the white matter.
White matter hyperintensities on T2-weighted or FLAIR MRI sequences are an almost ubiquitous feature of aging.
Although these lesions are readily visible on clinical MRI, they represent a nonspecific marker of white matter gliosis, demyelination, or increased water content.
Extremely severe diffuse white matter vascular injury is commonly referred to as Binswanger's disease or subcortical arteriosclerotic encephalopathy, recognized as a clinical syndrome with gradual cognitive deterioration and notable white matter changes of small-vessel ischemic disease.
On neuroimaging, a progressive confluent subcortical and periventricular white matter disease is seen.
Diffusion tensor MRI measures of white matter structural integrity show a consistent association with cognitive performance and gait speed, reflecting the central role of disconnection of key brain networks in mediating the effects of cerebral small-vessel disease.
These diffusion tensor–based methods often require complex processing and are typically used in research rather than clinical settings.
A relatively simple diffusion tensor–based metric defined by the peak width of the skeletonized mean diffusivity (PSMD) histogram has emerged as a candidate method for quantifying white matter disconnection.
Functional MRI measurement of cerebrovascular reactivity to physiologic stimuli is generally not performed in clinical practice, but it may become abnormal decades before appearance of structural brain injury and therefore represents a promising outcome marker for identifying disease-modifying interventions aimed to slow or prevent vascular brain injury.

6.1 Diagnostic Imaging Criteria¶

Lacunar infarcts: Fluid-attenuated inversion recovery (FLAIR) sequence showing hyperintense rim surrounding a hypointense cavitated core in the left thalamus.
Acute microinfarcts: Diffusion-weighted sequence showing small hyperintense lesion in the left centrum semiovale.
Cerebral microbleeds in deep penetrating brain regions: T2*-weighted sequence showing multiple small hypointense lesions in the pons.
Cerebral microbleeds in lobar brain regions: T2*-weighted sequence showing multiple small hypointense lesions lobar brain regions.
White matter hyperintensities: FLAIR sequence showing confluent diffuse hyperintensities in white matter.
Diffusion tensor MRI: Increased water diffusivity or decreased diffusion directionality associated with cognitive performance and gait speed.

Table 4 — MRI Markers of Cerebral Small Vessel Disease¶

Marker	MRI Sequence	Appearance	Location	Pathology
Lacunar Infarct	FLAIR	Hyperintense rim surrounding a hypointense cavitated core	Left thalamus (deep penetrating)	Arteriolosclerosis
Acute Microinfarct	Diffusion-weighted	Small hyperintense lesion	Left centrum semiovale	Small-vessel disease
Cerebral Microbleeds (Deep)	T2*-weighted	Multiple small hypointense lesions	Pons (deep penetrating)	Arteriolosclerosis
Cerebral Microbleeds (Lobar)	T2*-weighted	Multiple small hypointense lesions	Lobar brain regions	Cerebral amyloid angiopathy
White Matter Hyperintensities	FLAIR / T2-weighted	Confluent diffuse hyperintensities	White matter	Gliosis, demyelination, increased water content

7. MANAGEMENT & TREATMENT¶

Recent epidemiologic evidence of a decline in age-adjusted dementia incidence hints at the potential public impact of improving vascular health.
The population-based Framingham Study reported 5-year age- and sex-adjusted cumulative hazard rates for dementia of 3.6 per 100 persons during the late 1970s to early 1980s, 2.8 in the late 1980s to early 1990s, 2.2 in the late 1990s to early 2000s, and 2.0 in the late 2000s to early 2010s.
These time intervals coincide with parallel trends in hypertension control and stroke prevention, though the associations do not prove causation.
Evidence supporting a potential causative effect of blood pressure control came from the SPRINT-MIND trial targeting systolic blood pressure (SBP) of <120 mmHg versus 140 mmHg in hypertensive individuals aged ≥50 years.
The study ended prematurely because of effective prevention of cardiovascular outcomes in the lower SBP target group but nonetheless demonstrated that SBP reduction reduced rates of mild cognitive impairment (hazard ratio [HR], 0.81; 95% confidence interval [CI], 0.69–0.95) and combined mild cognitive impairment or probable dementia (HR, 0.85; 95% CI, 0.74–0.97), or not dementia alone (HR, 0.83; 95% CI, 0.67–1.04).
It is notable that both these studies measured all-cause cognitive impairment rather than just a vascular dementia subset, underlining the potential importance of VCID as a target for dementia prevention.

7.1 Prevention and Risk Factor Management¶

Hypertension control: SPRINT-MIND trial targeting systolic blood pressure (SBP) of <120 mmHg versus 140 mmHg in hypertensive individuals aged ≥50 years.
SBP reduction reduced rates of mild cognitive impairment (hazard ratio [HR], 0.81; 95% confidence interval [CI], 0.69–0.95).
SBP reduction reduced combined mild cognitive impairment or probable dementia (HR, 0.85; 95% CI, 0.74–0.97).
SBP reduction did not reduce dementia alone (HR, 0.83; 95% CI, 0.67–1.04).
Stroke prevention: Parallel trends in hypertension control and stroke prevention coincide with declining dementia hazard rates.
Vascular risk factors: Access to health care, lifestyle factors such as diet, and possible genetic influences contribute to disparities in intracranial atherosclerosis.

Table 5 — SPRINT-MIND Trial Outcomes¶

Outcome	Hazard Ratio (HR)	95% Confidence Interval (CI)	Target SBP
Mild Cognitive Impairment	0.81	0.69–0.95	<120 mmHg vs 140 mmHg
Combined MCI or Probable Dementia	0.85	0.74–0.97	<120 mmHg vs 140 mmHg
Dementia Alone	0.83	0.67–1.04	<120 mmHg vs 140 mmHg

8. PROGNOSIS & COMPLICATIONS¶

Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
Community-based individuals in the longitudinal Reasons for Geographic and Racial Differences in Stroke study, for example, changed trajectory from an average prestroke cognitive gain of 0.021 points/year to poststroke cognitive loss of –0.035 points/year on the six-item screener global cognitive function scale.
Mechanisms for poststroke cognitive decline likely include ongoing effects of the cerebrovascular disease that gave rise to the index stroke as well as loss of cognitive reserve that makes the brain less resilient to any additional age-related disorders.
Population-based studies also demonstrate substantially increased risk of cognitive impairment among individuals without symptomatic stroke but with MRI evidence of cerebrovascular disease.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.
Many clinicopathologic correlation studies have established that the co-occurrence of cerebrovascular and neurodegenerative lesions produces more cognitive and functional impairment than expected from the effects of each disease mechanism.

8.1 Cognitive Decline Trajectories¶

Prestroke cognitive gain: 0.021 points/year.
Poststroke cognitive loss: –0.035 points/year on the six-item screener global cognitive function scale.
Mechanisms: Ongoing effects of the cerebrovascular disease that gave rise to the index stroke as well as loss of cognitive reserve that makes the brain less resilient to any additional age-related disorders.

9. SPECIAL CONSIDERATIONS¶

The causes of these disparities remain under investigation but likely include access to health care, lifestyle factors such as diet, and possible genetic influences.
Vascular dementia is especially common in populations with limited access to medical care, where vascular risk factors are undertreated.

9.1 Global Variability¶

Intracranial atherosclerosis is higher in Asians, Hispanics, and American blacks than it is in European and American whites.
Whites may have more extracranial disease.
The causes of these disparities remain under investigation but likely include access to health care, lifestyle factors such as diet, and possible genetic influences.

10. KEY PEARLS & CLINICAL TRAPS¶

Mixed dementias appear to be more prevalent than single-etiology dementias and thus represent the rule rather than the exception.
Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.
Extremely severe diffuse white matter vascular injury is commonly referred to as Binswanger's disease or subcortical arteriosclerotic encephalopathy, recognized as a clinical syndrome with gradual cognitive deterioration and notable white matter changes of small-vessel ischemic disease.
On neuroimaging, a progressive confluent subcortical and periventricular white matter disease is seen.

10.1 Clinical Pearls¶

Mixed dementias appear to be more prevalent than single-etiology dementias and thus represent the rule rather than the exception.
Stroke patients who make good cognitive recovery nonetheless demonstrate accelerated poststroke cognitive decline.
The high risk for subsequent cognitive impairment or dementia conferred by MRI markers of otherwise silent vascular brain injury highlights the cumulative impact of small distributed brain injuries—often associated with small-vessel brain disease—on compromising brain function.
Extremely severe diffuse white matter vascular injury is commonly referred to as Binswanger's disease or subcortical arteriosclerotic encephalopathy, recognized as a clinical syndrome with gradual cognitive deterioration and notable white matter changes of small-vessel ischemic disease.
On neuroimaging, a progressive confluent subcortical and periventricular white matter disease is seen.