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CODES

ICD10

F03 Unspecified dementia

G30.9 Alzheimer’s disease, unspecified

F01.50 Vascular dementia without behavioral disturbance

CLINICALPEARLS

Medications for AD show a small, statistically significant improvement in some cognitive measures, but it remains unclear if the improvement is clinically significant.

Do not forget the role of adult protective services in case of elderly abuse. Aparticular concern in nursing homes relates to the use of physical restraints

and antipsychotic medication, which are regulated by Omnibus Reconciliation Act of 1987.

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DEMENTIA, VASCULAR

Birju B. Patel, MD, FACP, AGSF N. Wilson Holland, MD, FACP, AGSF

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.

DESCRIPTION

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.

EPIDEMIOLOGY

Second most common cause of dementia after Alzheimer dementia in the elderly

Incidence

About 6 to 12 cases/1,000/person age >70 years

Incidence of vascular dementia is declining in high-income countries in the past several decades likely due to better management of vascular risks.

Prevalence

~1.2–4.2% in those age >65 years

14–32% prevalence of dementia after a stroke

ETIOLOGYAND PATHOPHYSIOLOGY

On autopsy of those with dementia, many have significant vascular pathology

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that is 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)

Genetics

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, migraine with aura, and vascular dementia.

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

RISK FACTORS

Age

Previous stroke

Smoking

Diabetes (especially with frequent hypoglycemia)

HTN

Atrial fibrillation

PVD

Hyperlipidemia

Metabolic syndrome

Coronary atherosclerotic heart disease (1)

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GENERALPREVENTION

Optimization and aggressive treatment of vascular risk factors, such as HTN, diabetes, and hyperlipidemia (2)[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 (3) [B].

Lifestyle modification: weight loss, physical activity, smoking cessation

Medication management for vascular risk reduction: aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy (4)[B]

COMMONLYASSOCIATED CONDITIONS

CADASIL

Cerebral amyloid angiopathy (CAA) causes ischemic white matter damage due to amyloid deposition in penetrating cortical vessels.

DIAGNOSIS

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.

HISTORY

Gradual, stepwise progression is typical.

Ask about onset and progression of cognitive impairment and the specific cognitive domains involved.

Ask about vascular risk factors and previous attempts to control these risk factors.

Ask about medication compliance.

Ask about urinary incontinence and gait disturbances. Abnormal gait and falls are strong predictors of development of vascular dementia, particularly unsteady, frontal, and hemiparetic types of gait.

Look for early symptoms, including difficulty performing cognitive tasks, memory, mood, and assessment of instrumental activities of daily living (IADLs).

Past history may include TIAs, cerebrovascular accidents (CVAs), coronary

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atherosclerotic heart disease, atrial fibrillation, hyperlipidemia, and/or PVD.

PHYSICALEXAM

Screen for HTN. Average daily BPand not office BPis 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 (5)[C],(6)[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).

DIFFERENTIALDIAGNOSIS

Alzheimer dementia

Depression

Drug intoxication

CNS tumors

Hypothyroidism

Vitamin B12 deficiency

DIAGNOSTIC TESTS & INTERPRETATION

Cognitive testing, such as 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. The Mini-Mental Status Examination is not sensitive in distinguishing Alzheimer dementia from vascular dementia because it does not have good measures of executive function.

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.

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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.

TREATMENT

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

MEDICATION

Acetylcholinesterase inhibitors may be used but are of limited benefit in vascular dementia.

Clinical evidence for use of memantine is limited with the clinical benefit likely modest.

Controlling BPwith any antihypertensive medications, treatment of dyslipidemia (e.g., statins), and treatment of diabetes are very important.

Selective serotonin reuptake inhibitors (SSRIs) may be of benefit for agitation and psychosis in vascular dementia.

ADDITIONALTHERAPIES

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.

SURGERY/OTHER PROCEDURES

Carotid endarterectomy/stenting should be considered if evidence of significant internal carotid artery stenosis (i.e., >70–80%).

COMPLEMENTARY& ALTERNATIVE MEDICINE

Ginkgo biloba should be avoided due to increased risk of bleeding, especially in CAA.

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ADMISSION, INPATIENT, AND NURSING

CONSIDERATIONS

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.

ONGOING CARE

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.

FOLLOW-UPRECOMMENDATIONS

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,

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optimizing vascular risk factors, lifestyle modification counseling, therapeutic interventions

DIET

The American Heart Association diet and Dietary Approaches to Stop Hypertension (DASH) diet is recommended for optimal BPand cardiovascular risk factor control.

Low-fat, decreased concentrated sweets and carbohydrates, especially in those with metabolic syndrome

PATIENT EDUCATION

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 BPmonitoring and glucometer testing of blood sugars if HTN, impaired glucose tolerance, and/or diabetes is present

PROGNOSIS

Lost cognitive abilities that persist after initial recovery of deficits from stroke do not usually return. Some individuals can have intermittent periods of selfreported 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.

COMPLICATIONS

Physical disability from stroke

Severe cognitive impairment

Death

REFERENCES

1.Gorelick PB, Scuteri A, Black SE, et al; for American Heart Association/American Stroke Association. 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.

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2.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.

3.Power MC, Deal JA, Sharrett AR, et al. Smoking and white matter hyperintensity progression: the ARIC-MRI Study. Neurology. 2015;84(8):841–848.

4.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.

5.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.

6.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.

ADDITIONALREADING

Eizaguirre NO, Rementeria GP, González-Torres M, et al. Updates in vascular dementia. Heart Mind. 2017;1(1):22–35.

SEE ALSO

Alzheimer Disease; Depression; Mild Cognitive Impairment

CODES

ICD10

F01.50 Vascular dementia without behavioral disturbance

F01.51 Vascular dementia with behavioral disturbance

CLINICALPEARLS

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

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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. Patients can have mixed etiologies as well.

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