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Dementia, Vascular
Birju B. Patel, MD, FACP, AGSF
N. Wilson Holland, MD, FACP, AGSF
image BASICS
Vascular dementia is a heterogeneous disorder caused by the sequel of cerebrovascular disease that manifests in cognitive impairment affecting memory, thinking, language, behavior, and judgment.
  • Vascular dementia (previously known as multi-infarct dementia) was first mentioned by Thomas Willis in 1672. Later, it was further described in the late 19th century by Binswanger and Alzheimer as a separate entity from dementia paralytica caused by neurosyphilis. This concept has evolved tremendously since the advent of neuroimaging modalities.
  • Synonym(s): vascular cognitive impairment (VCI); vascular cognitive disorder (VCD); arteriosclerotic dementia; poststroke dementia; senile dementia due to hardening of the arteries; Binswanger disease. Diagnostic and Statistical Manual of Mental Disorders (DSM-5) categorizes vascular dementia as mild or major VCD.
Second most common cause of dementia after Alzheimer dementia in the elderly
About 6 to 12 cases/1,000/person age >70 years
  • ˜1.2-4.2% in those age >65 years
  • 14-32% prevalence of dementia after a stroke
Upon autopsy of those with dementia, many have significant vascular pathology are present, but this is not necessarily correlated clinically with vascular dementia. No set pathologic criteria exist for the diagnosis of vascular dementia such as those that exist for Alzheimer dementia. Pathology includes the following:
  • Large vessel disease: cognitive impairment that follows a stroke
  • Small vessel disease: includes white matter changes (leukoaraiosis), subcortical infarcts, and incomplete infarction. This is usually the most common cause of multi-infarct dementia.
  • Subcortical ischemic vascular disease: due to small vessel involvement within cerebral white matter, brain stem, and basal ganglia. Lacunar infarcts and deep white matter changes are typically included in this category.
  • Noninfarct ischemic changes and atrophy
  • Transient ischemic attack (TIA)/stroke
  • Vascular, demographic, genetic factors
  • Vascular disease (i.e., hypertension [HTN], peripheral vascular disease [PVD], atrial fibrillation, hyperlipidemia, diabetes)
  • Cerebral autosomal dominant arteriopathy with subcortical infarcts (CADASIL) is caused by a mutation in the NOTCH3 gene on chromosome 19 that results in leukoencephalopathy and subcortical infarcts. This is clinically manifested in recurrent strokes and associated cognitive decline.
  • Apolipoprotein E gene type: Those with ApoE4 subtypes are at higher risk of developing both vascular and Alzheimer dementia.
  • Amyloid precursor protein (APP) gene: leads to a form of vascular dementia called heritable cerebral hemorrhage with amyloidosis (1)
  • Age
  • Previous stroke
  • Smoking
  • Diabetes (especially with frequent hypoglycemia)
  • HTN
  • Atrial fibrillation
  • PVD
  • Hyperlipidemia
  • Metabolic syndrome
  • Coronary atherosclerotic heart disease (2)
  • Optimization and aggressive treatment of vascular risk factors, such as HTN, diabetes, and hyperlipidemia (3)[C]
  • HTN is the single most modifiable risk factor and treatment for it must be optimized.
  • Smoking is associated with white matter changes on imaging which may be associated with small vessel disease and vascular dementia progression (4)[B].
  • Lifestyle modification: weight loss, physical activity, smoking cessation
  • Medication management for vascular risk reduction: aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy (5)[B]
  • Cerebral amyloid angiopathy (CAA): accumulation of amyloid in cerebral vasculature resulting in infarctions and hemorrhages
Differentiation between Alzheimer dementia and vascular dementia can be difficult, and significant overlap is seen in the clinical presentation of these two dementias. The diagnosis of vascular dementia is a clinical diagnosis.
  • Screen for HTN. Average daily BP and not office BP is associated with progression of cerebrovascular disease and cognitive decline in the elderly.
  • Focal neurologic deficits may be present.
  • Gait assessment is important, especially looking at gait initiation, gait speed, and balance (6)[C],(7)[B].
  • Check for carotid bruits as well as abdominal bruits and assess for presence of PVD.
  • Check body mass index and waist circumference.
  • Do a thorough cardiac evaluation that includes looking for arrhythmias (i.e., atrial fibrillation).
  • Alzheimer dementia
  • Depression
  • Drug intoxication
  • CNS tumors
  • Hypothyroidism
  • Vitamin B12 deficiency
  • Cognitive testing, such as Mini-Mental Status Exam (MMSE), Saint Louis University Mental Status (SLUMS), and Montreal Cognitive Assessment (MOCA), provides more definitive information in terms of cognitive deficits, especially executive function, which may be lost earlier in vascular dementia.
  • Neuropsychological testing may also be beneficial, especially in evaluating multiple cognitive domains and their specific involvements and deficits.
Initial Tests (lab, imaging)
As appropriate, consider CBC, comprehensive metabolic profile, lipid panel, thyroid function, hemoglobin A1C, and vitamin B12.
  • Imaging is used in conjunction with history and physical examination to support a clinical diagnosis of vascular dementia.
  • Cognitive deficits observed clinically do not always have to correlate with findings found on neuroimaging studies.
  • MRI is best in terms of evaluation of subtle subcortical deficits.
  • White matter changes and specific location of these changes can be associated with executive dysfunction and episodic memory impairment (8)[C].
Prevention is the real key to treatment:
  • Control of risk factors, including HTN, hyperlipidemia, and diabetes
  • Avoidance of tobacco and smoking cessation
  • Healthy, low-cholesterol diet

  • Acetylcholinesterase inhibitors may be used but are of limited benefit in vascular dementia (9)[A].
  • Clinical evidence for use of memantine is limited with the clinical benefit likely modest.
  • Controlling BP with any antihypertensive medications, treatment of dyslipidemia (e.g., statins), and treatment of diabetes are very important.
  • Nicardipine has been studied and has been found to have some neuroprotective effects for vascular dementia (10)[B].
  • Selective serotonin receptor inhibitors (SSRIs) may be of benefit for agitation and psychosis in vascular dementia (11)[A].
  • Limit alcohol drink intake to ≤1/day in women and 2/day in men.
  • Heavy sustained alcohol use contributes to HTN.
  • Aspirin and/or clopidogrel may be useful in some cases.
Carotid endarterectomy/stenting should be considered if evidence of significant internal carotid artery stenosis (i.e., >70-80%).
Ginkgo biloba should be avoided due to increased risk of bleeding, especially in CAA.
  • Remain sensitive to functional assessment and avoidance of pressure ulcers after CVAs.
  • Avoid Foley catheter usage unless absolutely necessary due to increased risk of infection.
  • Nonpharmacologic approaches to behavior management should be attempted prior to medication usage.
  • Providing optimal sensory input to patients with cognitive impairment is important during hospitalizations to avoid delirium and confusion. Patients should be given frequent cues to keep them oriented to place and time. They should be informed of any changes in the daily schedule of activities and evaluations. Family and caregivers should be encouraged to be with patients with dementia as much as possible to further help them from becoming confused during hospitalization. Recreational, physical, occupational, and music therapy can be beneficial during hospitalization in avoiding delirium and preventing functional decline.
  • Particular emphasis has to be placed on screening for, and optimizing, the mood of the patient. Depression is very common in older patients, especially those who have had strokes and have become hospitalized. Depression in itself can present as “pseudodementia” with worsening confusion during hospitalization and is a treatable condition.
Vascular dementia is a condition that should be followed with multiple visits in the office setting with goals of optimizing cardiovascular risk profiles for patients. Future planning and advanced directives should be addressed early. Family and caregiver evaluation and burden should also be evaluated.
Perform regular follow-up with a primary care provider or geriatrician for risk factor modification and education on importance of regular physical and mental exercises as tolerated.
Patient Monitoring
Appropriate evaluation and diagnosis of this condition, need for future planning, optimizing vascular risk factors, lifestyle modification counseling, therapeutic interventions
  • The American Heart Association diet and dietary approaches to stop hypertension (DASH) diet is recommended for optimal BP and cardiovascular risk factor control.
  • Low-fat, decreased concentrated sweets and carbohydrates, especially in those with metabolic syndrome
  • Lifestyle modification is important in vascular risk reduction (smoking cessation, exercise counseling, dietary counseling, weight-loss counseling).
  • Optimizing vascular risk factors via medications (i.e., HTN, diabetes, atrial fibrillation, PVD, heart disease)
  • Avoiding smoking, including secondhand smoke
  • Home BP monitoring and glucometer testing of blood sugars if HTN, impaired glucose tolerance and/or diabetes is present.
  • Lost cognitive abilities that persist after initial recovery of deficits from stroke do not usually return. Some individuals can have intermittent periods of self-reported improvement in cognitive function.
  • Risk factors for progression of cognitive and functional impairment poststroke include age, prestroke cognitive abilities, depression, polypharmacy, and decreased cerebral perfusion during acute stroke.
1. Russell MB. Genetics of dementia. Acta Neurol Scand Suppl. 2010;(190):58-61.
2. Gorelick PB, Scuteri A, Black SE, et al. Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(9):2672-2713.
3. Hasnain M, Vieweg WV. Possible role of vascular risk factors in Alzheimer's disease and vascular dementia. Curr Pharm Des. 2014;20(38): 6007-6013.
4. Power MC, Deal JA, Sharrett AR, et al. Smoking and white matter hyperintensity progression: the ARIC-MRI Study. Neurology. 2015;84(8):841-848.
5. White WB, Wolfson L, Wakefield DB, et al. Average daily blood pressure, not office blood pressure, is associated with progression of cerebrovascular disease and cognitive decline in older people. Circulation. 2011;124(21):2312-2319.
6. Montero-Odasso M, Verghese J, Beauchet O, et al. Gait and cognition: a complementary approach to understanding brain function and the risk of falling. J Am Geriatr Soc. 2012;60(11):2127-2136.
7. Verghese J, Lipton RB, Hall CB, et al. Abnormality of gait as a predictor of non-Alzheimer's dementia. N Engl J Med. 2002;347(22):1761-1768.
8. Smith EE, Salat DH, Jeng J, et al. Correlations between MRI white matter lesion location and executive function and episodic memory. Neurology. 2011;76(17):1492-1499.
9. Kavirajan H, Schneider LS. Efficacy and adverse effects of cholinesterase inhibitors and memantine in vascular dementia: a meta-analysis of randomised controlled trials. Lancet Neurol. 2007;6(9):782-792.
10. Amenta F, Lanari A, Mignini F, et al. Nicardipine use in cerebrovascular disease: a review of controlled clinical studies. J Neurol Sci. 2009;283(1-2):219-223.
11. Seitz DP, Adunuri N, Gill SS, et al. Antidepressants for agitation and psychosis in dementia. Cochrane Database Syst Rev. 2011;(2):CD008191.
See Also
Alzheimer Disease; Depression; Mild Cognitive Impairment
  • F01.50 Vascular dementia without behavioral disturbance
  • F01.51 Vascular dementia with behavioral disturbance
Clinical Pearls
  • Executive dysfunction and gait abnormalities are often seen early and are more pronounced in vascular dementia as opposed to Alzheimer dementia.
  • Memory is relatively preserved in vascular dementia when compared with Alzheimer dementia in the early stages of this disease.
  • Stepwise progression, as opposed to progressive decline in Alzheimer dementia, is typical.
  • Considerable overlap exists between vascular dementia and Alzheimer dementia in clinical practice and classification into one of these categories is often difficult.