Multi-infarct dementia is a heterogeneous disorder caused by the sequel of cerebrovascular disease that manifests in cognitive impairment affecting memory, thinking, language, behavior, and judgment.
Multi-infarct dementia was first mentioned by Thomas Willis in 1672. It was later further described in the late 19th century by Binswanger and Alzheimer as a separate entity from dementia paralytica caused by neurospyhillus (1). This concept has evolved tremendously since the advent of neuroimaging modalities.
Synonym(s): Vascular dementia (VaD); Vascular cognitive impairment (VCI); Vascular cognitive disorder (VCD); Arteriosclerotic dementia; Post-stroke dementia; Senile dementia due to hardening of the arteries; Binswanger’s disease; mixed dementia (2).
- It is the 2nd most common cause of dementia after Alzheimer’s dementia in the elderly.
- After careful consideration of the difficulties in diagnosing multi-infarct dementia and the many geographical and methodological differences, there is a lack of agreement in terms of its prevalence and epidemiology.
About 6–12 cases per 1000 person years >70 (3)
- About 1.2–4.2% in those >65 (3)
- 14–32% prevalence of dementia after a stroke
- Previous stroke
- Atrial fibrillation
- Peripheral vascular disease (PVD)
- Metabolic syndrome
- Coronary atherosclerotic heart disease
- Cerebral autosomal dominant arteriopathy (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 (4).
- Apolipoprotein E gene type: Those with ApoE4 subtypes are at higher risk of developing both multi-infarct and Alzheimer’s dementia.
- Amyloid precursor protein (APP) gene: Leads to a form of vascular dementia called heritable cerebral hemorrhage with amyloidosis (5).
- Optimization and aggressive treatment of vascular risk factors such as hypertension, diabetes, and hyperlipidemia
- Hypertension is the single most modifiable risk factor and must be optimized.
- Lifestyle modification: Weight loss, physical activity, smoking cessation
- Medication management for vascular risk reduction: Aspirin usage, statin therapy for hyperlipidemia, antihypertensive therapy
Upon autopsy of those with dementia, 1/3 have significant vascular pathology present but this is not necessarily correlated clinically with multi-infarct dementia (6). There are no set pathological criteria for the diagnosis of multi-infarct dementia such as those that exist for Alzheimer’s dementia.
- Large vessel disease: Cognitive impairment that follows a stroke
- Small vessel disease: Includes white matter changes (leukoaraisosis), 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, brainstem, and basal ganglia. Lacunar infarcts and deep white matter changes are typically included in this category (7).
- Non-infarct ischemic changes and atrophy (8)
- Transient ischemic attack (TIA)/stroke
- Vascular, demographic, genetic factors
- Vascular disease (i.e., hypertension, PVD, atrial fibrillation, hyperlipidemia, diabetes, etc.)
Commonly Associated Conditions
- Cerebral amyloid angiopathy (CAA): Accumulation of amyloid in cerebral vasculature resulting in infarctions and hemorrhages (9).
Differentiation between Alzheimer’s dementia and multi-infarct dementia can be difficult and there can be significant overlap in the clinical presentation of these two dementias. The diagnosis of multi-infarct dementia is a clinical diagnosis.
- 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.
- Look for early symptoms including difficulty performing cognitive tasks, memory, mood, and assessment of instrumental activities of daily living (IADLs) (8).
- Past history may include TIAs, cerebrovascular accidents, coronary atherosclerotic heart disease, atrial fibrillation, hyperlipidemia, and/or peripheral vascular disease.
- Screen for hypertension
- Focal neurological deficits may be present
- Gait assessment is important especially looking at gait initiation, gait speed, and balance.
- Check for carotid bruits as well as abdominal bruits and assess for presence of peripheral vascular disease.
- Check body mass index and waist circumference.
- Do a thorough cardiac evaluation that includes looking for arrhythmias (i.e., atrial fibrillation).
Diagnostic Tests & Interpretation
- Cognitive screening, such as Mini-Cog, 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 multi-infarct dementia (8).
- Neuropsychological testing may also be beneficial especially in evaluating multiple cognitive domains and their specific involvements and deficits.
As appropriate, consider: Complete blood count, comprehensive metabolic Profile, lipid panel, thyroid function, hemoglobin A1C, vitamin B12.
- Imaging is used in conjunction with history and physical examination to support a clinical diagnosis of multi-infarct dementia.
- Cognitive deficits observed clinically do not always have to correlate with findings found on neuroimaging studies.
- There are no pathognomonic neuroimaging features for multi-infarct dementia (6).
- Magnetic resonance imaging (MRI) is best in terms of evaluation of subtle subcortical deficits.
- Alzheimer’s dementia
- Drug intoxication
- Central nervous system tumors
- Vitamin B12 deficiency
Prevention is the real key to treatment.
- Control of risk factors including hypertension, hyperlipidemia, and diabetes.
- Avoidance of tobacco and stopping smoking.
- Healthy, low-cholestrol diet
- Acetylcholinesterase inhibitors may be used but are of limited benefit in multi-infarct dementia (6,10).
- The clinical evidence for use of memantine is not as strong as for acetylcholinesterase inhibitors and therefore the clinical benefit is likely modest (6).
- Controlling blood pressure with any antihypertensive medications, treatment of dyslipidemia (e.g., statins), and treatment of diabetes are very important.
- Limit alcohol intake to ≤1 drink per day in women and 2 per day in men.
- Heavy sustained alcohol use contributes to hypertension.
- Aspirin and/or clopidogrel may be useful in some cases.
Complementary and Alternative Medicine
Ginkgo biloba should be avoided due to increased risk of bleeding especially in cerebral amyloid angiopathy.
Carotid endarterectomy or stenting if evidence of significant internal carotid artery stenosis (i.e., >70-80%).
- Remain sensative to functional assessment and avoidance of pressure ulcers after cerebrovascular accients.
- Urinary incontinence treatment may be needed after CVA.
- Avoid Foley catheter usage unless absolutely necessary due to increased risk of infection.
- Nonpharmacological 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 that have had strokes and have become hospitalized. Depression in itself can present as “pseudodementia” with worsening confusion during hospitalization and is a treatable condition.
Multi-infarct 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.
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.
Appropriate evaluation and diagnosis of this condition, need for future planning, optimizing vascular risk factors, lifestyle modification counseling, therapeutic interventions
- American Heart Association diet and DASH diet recommended for optimal blood pressure 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., hypertension, diabetes, atrial fibrillation, PVD, heart disease)
- Avoiding smoking including secondhand smoke.
- Home blood pressure monitoring and glucometer testing of blood sugars if hypertension, impaired glucose tolerance and/or diabetes is present.
- Instruct patients to call 911 for any TIA type symptoms.
- 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 (6).
- Physical disability from stroke
- Severe cognitive impairment
1. Román G et al. Vascular dementia: a historical background. Int Psychogeriatr. 2003;15 Suppl 1:11–3.
2. Jellinger KA et al. The pathology of “vascular dementia”: a critical update. J. Alzheimers Dis. 2008;14:107–23.
3. Hébert R, Brayne C et al. Epidemiology of vascular dementia. Neuroepidemiology. 1995;14:240–57.
4. Pinkston JB, Alekseeva N, González Toledo E et al. Stroke and dementia. Neurol. Res. 2009;31:824–31.
5. Russell MB et al. Genetics of dementia. Acta Neurol. Scand., Suppl. 2010;:58–61.
6. Rojas-Fernandez CH, Moorhouse P et al. Current concepts in vascular cognitive impairment and pharmacotherapeutic implications. Ann Pharmacother. 2009;43:1310–23.
7. Chui HC et al. Subcortical ischemic vascular dementia. Neurol Clin. 2007;25:717–40, vi
8. Moorhouse P, Rockwood K et al. Vascular cognitive impairment: current concepts and clinical developments. Lancet Neurol. 2008;7:246–55.
9. Rockwood K, Ebly E, Hachinski V, Hogan D et al. Presence and treatment of vascular risk factors in patients with vascular cognitive impairment. Arch. Neurol. 1997;54:33–9.
10. Kavirajan H, Schneider LS et al. Efficacy and adverse effects of cholinesterase inhibitors and memantine in vascular dementia: a meta-analysis of randomised controlled trials. Lancet Neurol. 2007;6:782–92.
See Also (Topic, Algorithm, Electronic Media Element)
Alzheimer’s Dementia, Depression, and Mild Cognitive Impairment
290.40 Vascular dementia, uncomplicated
- 56267009 multi-infarct dementia (disorder)
- 429998004 vascular dementia (disorder)
- Executive dysfunction and gait abnormalities are often seen early and are more pronounced in multi-infarct dementia as opposed to Alzheimer’s dementia (48).
- Memory is relatively preserved in multi-infarct dementia when compared to Alzheimer’s dementia in the early stages of this disease (4).
- Stepwise progression as opposed to progressive decline in Alzheimer’s dementia is typical.