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Treatment of vascular cognitive impairment and dementia

Treatment of vascular cognitive impairment and dementia
Authors:
Eric E Smith, MD
Clinton B Wright, MD, MS
Section Editors:
Steven T DeKosky, MD, FAAN, FACP, FANA
Scott E Kasner, MD
Deputy Editor:
Janet L Wilterdink, MD
Literature review current through: Jan 2024.
This topic last updated: May 24, 2022.

INTRODUCTION — Vascular dementia (VaD) refers to any dementia that is primarily caused by cerebrovascular disease or impaired cerebral blood flow and falls within the spectrum of vascular cognitive impairment, a syndrome that includes all cognitive disorders in which cerebrovascular disease or impaired cerebral blood flow is a contributing causative factor. It is best understood as a heterogeneous syndrome rather than a distinct disease, in which the underlying cause is cerebrovascular dysfunction or disease in some form, and its ultimate manifestation is dementia.

There is considerable overlap between Alzheimer disease (AD) and VaD with regard to comorbidity as well as shared risk factors and even pathogenesis. The combination of pathologies may be more common than either in isolation, and it is often not easy to identify the primary etiologic entity.

This topic will review the treatment and prognosis of VaD. The epidemiology, clinical features, evaluation, and diagnosis of VaD are discussed separately. (See "Etiology, clinical manifestations, and diagnosis of vascular dementia".)

VASCULAR RISK MODIFICATION

Risk factor management — Patients with cognitive impairment and clinical or radiologic evidence of cerebrovascular pathology should be screened and treated for vascular risk factors, especially hypertension. Although these measures may be more helpful in preventing rather than ameliorating dementia, there is a strong rationale for aggressive secondary stroke prevention measures in these patients [1,2]. Recurrent stroke is associated with greater risk of cognitive decline, and poststroke dementia is associated with higher mortality [3,4]. In general, for patients with VaD, we follow the recommendations for secondary stroke prevention, which are described in detail separately. (See "Overview of secondary prevention of ischemic stroke".)

The role of vascular risk factor management in the prevention of dementia is discussed separately. (See "Prevention of dementia", section on 'Vascular risk factor modification'.)

●Antihypertensive therapy – Pending further studies in patients with VaD, we follow standard guidelines for treatment of blood pressure in older adults. (See "Goal blood pressure in adults with hypertension", section on 'Older adults'.)

Although it is clear that hypertension is a risk factor for the condition, blood pressure lowering strategies have not been specifically tested for treatment of VaD. One substudy of a randomized trial in patients without established cerebrovascular disease found that more aggressive blood pressure treatment (target blood pressure 120 versus 140 mmHg) was associated with a smaller mean increase in white matter lesion volume (0.92 versus 1.45 cm3) but a greater decrease in total brain volume (-30.6 versus -26.9 cm3) after four years [5]. In addition, there is some concern that aggressive lowering of blood pressure could potentially compromise cerebral perfusion and actually may be deleterious in patients with established cerebrovascular disease. Pending data from further trials, we do not suggest intensively lowering systolic blood pressure to less than 120 mmHg in patients with symptomatic VaD.

The relationship between blood pressure and incident dementia and the role of antihypertensive therapy in the prevention of dementia are discussed separately. (See "Risk factors for cognitive decline and dementia", section on 'Hypertension' and "Prevention of dementia", section on 'Antihypertensive therapy'.)

●Diabetes management – While unstudied in the treatment of VaD, glucose control is generally recommended for the prevention of complications associated with diabetes [6]. (See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Glycemic management'.)

●Statins – For patients with VaD and a history of ischemic stroke or transient ischemic attack (TIA), we follow guidelines for secondary prevention. (See "Overview of secondary prevention of ischemic stroke", section on 'LDL-C lowering therapy'.)

For patients with VaD who have not had a clinical ischemic stroke or TIA, statin therapy should be administered based on the patient's assessed cardiovascular risk, as discussed separately. (See "Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease", section on 'Indications for statin therapy'.)

Statins are of interest in the secondary prevention of cerebrovascular disease because of both their lipid-lowering effect and also their pleiotropic effects on vascular function, combining to inhibit atherosclerosis. Their effect on slowing the progression of VaD is uncertain [7]. The role of statins in the prevention of dementia is discussed separately. (See "Prevention of dementia", section on 'Statins'.)

Antithrombotic therapy

●Patients with a history of ischemic stroke or TIA – Patients with VaD and a history of ischemic stroke or TIA should be treated with antithrombotic therapy. Antiplatelet therapy has established efficacy for secondary prevention of ischemic stroke in patients with a history of noncardioembolic stroke or TIA. The choice of antiplatelet agent depends on comorbidities and other factors, as discussed separately. (See "Long-term antithrombotic therapy for the secondary prevention of ischemic stroke".)

For some patients with cardioembolic stroke, anticoagulant therapy may be preferred over antiplatelet therapy for secondary stroke prevention. The observation that oral anticoagulation therapy was associated with a lower incidence of dementia in patients with atrial fibrillation in one registry study provides indirect evidence that stroke prevention strategies may improve cognitive outcomes [8]. The selection of an antithrombotic agent for patients with cardiogenic embolism is discussed separately. (See "Overview of secondary prevention for specific causes of ischemic stroke and transient ischemic attack", section on 'Cardiogenic embolism'.)

●No clinical history or imaging evidence of stroke or TIA – If brain imaging shows white matter lesions only, without history of symptomatic ischemic stroke or imaging evidence of brain infarction, we do not use antithrombotics. This accords with guidelines from the Canadian Conference on Diagnosis and Treatment of Dementia [9] and the European Stroke Organization [10], which recommend against using antiplatelet drugs for stroke or dementia prevention for patients with white matter lesions.

●Imaging evidence of stroke but no clinical history of stroke – For patients that have imaging evidence of brain infarction without history of symptomatic stroke, we often treat with aspirin 50 to 100 mg daily despite the limited evidence. However, we would, in most cases, forego antiplatelet therapy in patients with prior intracranial hemorrhage, evidence of cortical superficial siderosis or multiple microhemorrhages on magnetic resonance imaging, major systemic bleeding, and other potential contraindications to aspirin therapy [11]. For such patients, the Canadian Conference on Diagnosis and Treatment of Dementia gives a weak recommendation that an antiplatelet drug can be considered, based on low-quality evidence, while the European Stroke Organization recommends against their use.

While there is a strong rationale for this treatment approach, there is only limited and indirect evidence to support it. The benefit of aspirin for preventing progression of silent cerebrovascular disease has not been defined [10,12]. A limited number of trials have examined the effect of antiplatelet therapy on cognitive outcomes in patients with a history of stroke [13,14] and in older patients with or without vascular risk factors but no stroke history [15,16]. These studies have not found improved cognitive outcomes, possibly because they were not of sufficient size or duration to detect a benefit. In addition, pooled analysis of two randomized trials of aspirin therapy in patients with Alzheimer disease (AD) suggests the possibility that aspirin is associated with an increased risk of intracerebral hemorrhage: 3.2 versus 0 percent (hazard ratio [HR] 7.6, 95% CI 0.72-81) [17]. While this difference was not statistically significant, it is of potential concern in this population, in whom VaD cannot be reliably distinguished from mixed dementia with AD pathology.

PHARMACOLOGIC THERAPY

Cholinesterase inhibitors — We suggest initiation of cholinesterase inhibitor therapy in patients with VaD who have progressive cognitive decline that cannot be directly attributed to a clinical stroke. This treatment approach is based in part on the knowledge that many such patients will have concomitant Alzheimer disease (AD), and it is difficult to confirm or exclude AD pathology in patients with VaD [7,18,19]. However, the benefit in patients with VaD is likely small, and it is a reasonable choice for some patients to forego this treatment. We do not initiate cholinesterase inhibitor therapy in patients with dementia diagnosed after a stroke if there is not progressive cognitive decline.

Cholinergic dysfunction has been documented in VaD as well as AD, providing a rationale for investigating these agents in VaD [18,20]. A meta-analysis of six trials of cholinesterase inhibitors in patients with VaD [21-28] (including an unpublished trial of rivastigmine) found an overall statistically significant benefit for each drug, as measured by change in the Alzheimer Disease Assessment Scale-Cognitive Subscale (ADAS-Cog) from baseline [29]. However, the effect was small (approximately two points on the ADAS-Cog scale, which is roughly half the benefit seen in patients with AD), and there was no consistent benefit using measures of global change outcomes or neuropsychiatric symptoms. The investigators concluded that the benefits were small and of uncertain clinical significance.

For clinicians who do choose to administer a trial of cholinesterase inhibitors, there is somewhat better evidence to support the use of donepezil or galantamine than rivastigmine (table 1) [30,31]. The clinical use of these agents including dosing, adverse effects, and monitoring is described separately. (See "Cholinesterase inhibitors in the treatment of dementia".)

Memantine — Memantine, an N-methyl-D-aspartate receptor antagonist, putatively inhibits excitotoxicity and protects against neurologic injury from a variety of mechanisms. We suggest against its use in patients with VaD because the evidence for its benefit is not compelling. Nonetheless, because memantine is approved for treatment of moderate to severe AD, some clinicians may choose to use memantine in patients with VaD because AD cannot be ruled out and is often comorbid with VaD [32].

Two studies have compared memantine 20 mg/day with placebo in patients with mild to moderate VaD [33,34]. These were of short duration, 28 weeks. Benefit was seen on cognitive scales but not on clinical global impression or activities of daily living [29,35]. Memantine was safe and well tolerated.

For clinicians who choose to treat with memantine, it is often used for patients with more severe dementia, typically in combination with a cholinesterase inhibitor. Dosing, administration, and adverse effects are described separately. (See "Treatment of Alzheimer disease", section on 'Memantine'.)

Investigational agents — Many agents, including neuroprotectants and vasodilators, have been studied for VaD, but the trials have mostly been small and without conclusive results [36]. Agents that have inconclusive evidence of benefit in the prevention of cognitive decline in VaD include nimodipine, ergot alkaloids (hydergine, nicergoline) [37-39], cerebrolysin [40], ginkgo biloba [41], xanthine derivatives (propentofylline, pentoxifylline, and denbufylline) [42-44], cytidinediphosphocholine [45], and piracetam [46]. Actovegin is licensed for poststroke cognitive impairment in some countries in Europe and Asia, based on a trial showing more improvement in the ADAS-Cog at six months [47]. None of these therapies are recommended at this time.

NONPHARMACOLOGIC THERAPY — Lifestyle interventions such as exercise and social interactions are suggested for patients with VaD. However, there is not high-quality evidence to support a benefit of exercise, nutrition, and other lifestyle changes in patients with an established diagnosis of VaD. In one small randomized trial in patients with VaD, a six-month, three-days-per-week aerobic exercise training program improved short-term cognitive performance compared with an educational control group, but differences in cognitive outcomes did not persist when participants were retested six months later [48].

Other studies have examined a benefit for these interventions in patients with unspecified forms of dementia as well as in Alzheimer disease (AD). In the aggregate, such studies do not suggest a robust benefit on cognitive outcomes but do suggest a possible benefit for improved functional outcomes. The roles of rehabilitation, nutrition, exercise, and other lifestyle modifications in the management of dementia are discussed separately. (See "Treatment of Alzheimer disease", section on 'Nonpharmacologic therapy and supportive care'.)

Some poststroke rehabilitation programs include cognitive as well as physical rehabilitation. However, the evidence regarding the efficacy of such programs is limited by the inconsistent quality of the studies and the use of nonstandardized interventions [49].

TREATMENT OF BEHAVIORAL SYMPTOMS — Neuropsychiatric symptoms may become troubling in patients with VaD. The evaluation and management of these problems are discussed separately. (See "Management of neuropsychiatric symptoms of dementia".)

PROGNOSIS — Because VaD is a heterogenous disorder, it is unsurprising that a consistent clinical progression has not been defined. In the setting of acute stroke, some recovery of cognitive function is expected. After the initial recovery period, further improvement is less likely; some patients will have stable cognitive impairment consistent with their stroke syndrome, while others will experience ongoing cognitive decline. Imaging studies suggest that the severity of white matter changes and the presence of medial temporal lobe atrophy (possibly suggesting comorbid Alzheimer disease [AD]) are risk factors for worsening cognition [50,51]. Other studies suggest that recurrent strokes and baseline impaired cognition prior to the stroke are poor prognostic factors [52]. Less is known about the natural history of VaD in other settings.

Estimates of mortality vary depending on the diagnostic criteria used. Also, many studies are hospital or clinic based, resulting in referral bias [53]. However, evidence from population-based studies suggests an increased mortality for vascular cognitive impairment, VaD, and dementia after stroke [4,54,55].

ADVANCED DEMENTIA — In the late stages of dementia, patients and their caregivers are faced with a range of physical and psychosocial needs. Effective palliative care can improve patients' symptoms, lessen caregiver burden, and help ensure that treatment decisions are well informed and weighed in the context of patient and caregiver goals and needs. Aspects of care that are specific to patients with advanced dementia are discussed separately. (See "Care of patients with advanced dementia".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cognitive impairment and dementia".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Beyond the Basics topic (see "Patient education: Dementia (including Alzheimer disease) (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Vascular risk modification – Patients with cognitive impairment and clinical or radiologic evidence of cerebrovascular pathology should be screened and treated for vascular risk factors, especially hypertension, although this may be more helpful in preventing rather than ameliorating dementia. (See 'Vascular risk modification' above.)

●Antithrombotic therapy – Patients with vascular dementia (VaD) who have had a clinical ischemic stroke or transient ischemic attack (TIA) should be treated with the appropriate antithrombotic therapy according to their stroke subtype in order to prevent recurrent ischemic stroke. (See "Long-term antithrombotic therapy for the secondary prevention of ischemic stroke" and "Overview of secondary prevention for specific causes of ischemic stroke and transient ischemic attack".)

A decision to initiate antiplatelet therapy in patients with VaD who have not had a clinical ischemic stroke or TIA should be individualized. As an example, we often treat patients with aspirin 50 to 100 mg daily when brain imaging demonstrates an infarction but not when there are only white matter lesions. (See 'Antithrombotic therapy' above.)

●Cholinesterase inhibitor therapy – We suggest initiation of cholinesterase inhibitor therapy (donepezil or galantamine) (table 1) in patients with VaD who have progressive cognitive decline that is not directly attributable to a clinical stroke (Grade 2B). The available evidence suggests that this treatment may have a slight benefit on cognitive outcomes that is of uncertain clinical significance. We do not initiate cholinesterase inhibitor therapy in patients with dementia diagnosed after a stroke if there is not progressive cognitive decline. (See 'Cholinesterase inhibitors' above.)

●Other aspects of the treatment

•Many patients with VaD have concomitant Alzheimer disease (AD). (See "Treatment of Alzheimer disease".)

•The management of behavioral and other neuropsychiatric symptoms is discussed separately. (See "Management of neuropsychiatric symptoms of dementia".)

•Supportive and nonpharmacologic management of dementia is discussed separately. (See "Management of the patient with dementia".)

•The care of patients with advanced dementia is discussed separately. (See "Care of patients with advanced dementia".)

●Prognosis – Because VaD is a heterogeneous disorder, the prognosis is not predictable. After acute stroke recovery, some patients have stable cognitive impairment while others decline. Life expectancy appears to be somewhat shortened in patients with VaD. (See 'Prognosis' above.)

ACKNOWLEDGMENT — The views expressed in this topic are those of the author(s) and do not reflect the views of the National Institutes of Health, the Department of Health and Human Services, or the United States government.

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Topic 5086 Version 31.0

References

1 : Prevention of vascular cognitive impairment.

2 : Long-term effects of secondary prevention on cognitive function in stroke patients.

3 : Long-term cognitive transitions, rates of cognitive change, and predictors of incident dementia in a population-based first-ever stroke cohort.

4 : Poststroke dementia predicts poor survival in long-term follow-up: influence of prestroke cognitive decline and previous stroke.

5 : Association of Intensive vs Standard Blood Pressure Control With Cerebral White Matter Lesions.

6 : Cognitive decline and dementia in diabetes mellitus: mechanisms and clinical implications.

7 : Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association.

8 : Less dementia with oral anticoagulation in atrial fibrillation.

9 : Canadian Consensus Conference on Diagnosis and Treatment of Dementia (CCCDTD)5: Guidelines for management of vascular cognitive impairment.

10 : ESO Guideline on covert cerebral small vessel disease.

11 : Antithrombotic therapy in patients with cerebral microbleeds.

12 : Prevention of Stroke in Patients With Silent Cerebrovascular Disease: A Scientific Statement for Healthcare Professionals From the American Heart Association/American Stroke Association.

13 : Effects of aspirin plus extended-release dipyridamole versus clopidogrel and telmisartan on disability and cognitive function after recurrent stroke in patients with ischaemic stroke in the Prevention Regimen for Effectively Avoiding Second Strokes (PRoFESS) trial: a double-blind, active and placebo-controlled study.

14 : Effects of long-term blood pressure lowering and dual antiplatelet treatment on cognitive function in patients with recent lacunar stroke: a secondary analysis from the SPS3 randomised trial.

15 : Low dose aspirin and cognitive function in middle aged to elderly adults: randomised controlled trial.

16 : Effect of Aspirin on Disability-free Survival in the Healthy Elderly.

17 : Aspirin in Alzheimer's disease: increased risk of intracerebral hemorrhage: cause for concern?

18 : Overlap between pathology of Alzheimer disease and vascular dementia.

19 : Editorial comment--How to treat vascular dementia?

20 : Influence of galantamine on vasomotor reactivity in Alzheimer's disease and vascular dementia due to cerebral microangiopathy.

21 : Donepezil for vascular cognitive impairment.

22 : Efficacy of galantamine in probable vascular dementia and Alzheimer's disease combined with cerebrovascular disease: a randomised trial.

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25 : Efficacy, safety and tolerability of rivastigmine capsules in patients with probable vascular dementia: the VantagE study.

26 : Rivastigmine in Chinese patients with subcortical vascular dementia.

27 : A randomized controlled trial of rivastigmine in patients with cognitive impairment no dementia because of cerebrovascular disease.

28 : Efficacy and tolerability of donepezil in vascular dementia: positive results of a 24-week, multicenter, international, randomized, placebo-controlled clinical trial.

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32 : Impact of multiple pathologies on the threshold for clinically overt dementia.

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34 : A double-blind, placebo-controlled multicentre study of memantine in mild to moderate vascular dementia (MMM500).

35 : Memantine for dementia.

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37 : Hydergine for dementia.

38 : A 24-month, double-blind, placebo-controlled multicentre pilot study of the efficacy and safety of nicergoline 60 mg per day in elderly hypertensive patients with leukoaraiosis.

39 : A multicenter randomized double-blind study on the efficacy and safety of nicergoline in patients with multi-infarct dementia.

40 : Cerebrolysin for vascular dementia.

41 : Ginkgo biloba for cognitive impairment and dementia.

42 : Propentofylline for dementia.

43 : European Pentoxifylline Multi-Infarct Dementia Study.

44 : Denbufylline in dementia: a double-blind controlled study.

45 : Cytidinediphosphocholine (CDP-choline) for cognitive and behavioural disturbances associated with chronic cerebral disorders in the elderly.

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52 : Diagnosis and treatment of vascular damage in dementia.

53 : Diagnosis and treatment of vascular damage in dementia.

54 : Prevalence and outcomes of vascular cognitive impairment. Vascular Cognitive Impairment Investigators of the Canadian Study of Health and Aging.

55 : Long-term survival and predictors of mortality in Alzheimer's disease and multi-infarct dementia.

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