Vascular Dementia

Vascular dementia is the second most common form of dementia after Alzheimer Disease (AD). The condition is not a single disease; it is a group of syndromes relating to different vascular mechanisms. As early as 1899, arteriosclerosis and senile dementia were described as different syndromes. In 1969, Mayer-Gross et al described this syndrome and reported that hypertension is the cause in approximately 50% of patients. Patients who have had a stroke are at increased risk for vascular dementia. In 1974, Hachinski et al coined the term multi-infarct dementia. In 1985, Loeb used the broader term vascular dementia. Recently, Bowler and Hachinski introduced a new term, vascular cognitive impairment. Vascular dementia is preventable; therefore, early detection and an accurate diagnosis are important.

Case study

A 70-year-old woman came to the clinic with her son for assessment of her cognitive decline. The son is concerned about her short-term memory problems for the past 10 months. She had a fall 10 months ago; after that fall, she started to ask the same questions over and over. There was another fall 4 months ago and also an episode of dizziness 2 months ago. With these incidents, her son noticed further decline in cognition. Recently, her son noticed that she has become a bit more suspicious of her daughter-in-law and has been hoarding things. She has lost interest in her day-to-day activities and forgets to include the right ingredients when cooking. Family has to remind her to take her medications, and her son is helping with the management of her finances.

The patient has hypertension, diabetes, coronary artery disease, osteoarthritis, and osteoporosis. On the Mini-Mental Status Examination (MMSE), the patient scored 21/30 with abnormal clock drawing. On the Geriatric Depression Scale (GDS), the patient scored 2/15. CT scan of the head showed multiple lacunar infarcts in the right basal ganglia and left cerebellar region.

The DSM-5 divides Neurocognitive Disorders including Vascular Neurocognitive Disorder into Major or Mild based on whether they interfere with independence in everyday activities or not.[1]

Many subtypes of vascular dementia have been described.  The spectrum includes (1) mild vascular cognitive impairment, (2) multi-infarct dementia, (3) vascular dementia due to a strategic single infarct, (4) vascular dementia due to lacunar lesions, (5) vascular dementia due to hemorrhagic lesions, (6) Binswanger disease, (7) subcortical vascular dementia, and (8) mixed dementia (combination of AD and vascular dementia).

Vascular dementia is sometimes further classified as cortical or subcortical dementia.  

Vascular disease produces either focal or diffuse effects on the brain and causes cognitive decline. Focal cerebrovascular disease occurs secondary to thrombotic or embolic vascular occlusions. Common areas of the brain associated with cognitive decline are the white matter of the cerebral hemispheres and the deep gray nuclei, especially the striatum and the thalamus. Hypertension is the major cause of diffuse disease, and in many patients, both focal and diffuse disease are observed together. The 3 most common mechanisms of vascular dementia are multiple cortical infarcts, a strategic single infarct, and small vessel disease.

Mild vascular cognitive impairment can occur in elderly persons. It is associated with cognitive decline that is worse than expected for age and educational level, but the effects do not meet the criteria for dementia. These people have subjective and objective evidence of memory problems, but their daily functional living skills are within normal limits. This would be categorized as Mild Vascular Neurocognitive Disorder in the DSM-5.  

In multi-infarct dementia, the combined effects of different infarcts produce cognitive decline by affecting the neural nets.

In single-infarct dementia, different areas in the brain can be affected, which may result in significant impairment in cognition. This may be observed in cases of anterior cerebral artery infarct, parietal lobe infarcts, thalamic infarction, and singular gyrus infarction.

Small vessel disease affects all the small vessels of the brain and produces 2 major syndromes, Binswanger disease and lacunar state. Small vessel disease results in arterial wall changes, expansion of the Virchow-Robin spaces, and perivascular parenchymal rarefaction and gliosis.

Lacunar disease is due to small vessel occlusions and produces small cavitary lesions within the brain parenchyma secondary to occlusion of small penetrating arterial branches. These lacunae are found more typically in the internal capsule, deep gray nuclei, and white matter. Lacunar state is a condition in which numerous lacunae, which indicate widespread severe small vessel disease, are present.

Binswanger disease (also known as subcortical leukoencephalopathy) is due to diffuse white matter disease. In Binswanger disease, vascular changes observed are fibrohyalinosis of the small arteries and fibrinoid necrosis of the larger vessels inside the brain.

In cerebral amyloid angiopathy–associated vasculopathy, aneurysm formation and stenosis in the leptomeningeal and cortical vessels cause damage to the subcortical white matter. In hereditary cystatin-C amyloid angiopathy, patients have recurrent cerebral hemorrhages before age 40 years that can lead to dementia. Prevalence of cerebral amyloid angiopathy is consistently higher in patients with dementia than in patients without dementia, which indicates its significant role in the pathogenesis of dementia.[2]

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is a rare autosomal dominant condition localized to chromosome arm 19q12 that affects small vessels supplying the deep white matter. Pathologically, multiple small infarcts are observed in the white matter, thalamus, basal ganglia, and pons.

Other less common syndromes may lead to vascular dementia. Rare arteriopathies such as inflammatory arteriopathy (e.g., polyarteritis nodosa, temporal arteritis) and noninflammatory arteriopathy (e.g., moyamoya disease, fibromuscular dysplasia) can cause multiple infarcts and can lead to vascular dementia. Hypoperfusion due to large vessel or cardiac disease can affect the watershed areas of the brain and lead to vascular dementia.

Leukoaraiosis (or white matter hyperintensities) greater than 25% is considered to be pathological. Subcortical vascular dementia is a diffuse small vessel disease with minimal or absent infarction with homogenous pathological and clinical features.[3, 4] White matter ischemic changes affect executive dysfunction and cause slower processing speed, rather than memory and language impairment.[5]

Arterial stiffness, which reflects an alteration in arterial mechanics, can be a risk factor for vascular dementia.[6]

Mixed dementia is diagnosed when patients have evidence of Alzheimer dementia and cerebrovascular disease, either clinically or based on neuroimaging evidence of ischemic lesions. Growing evidence indicates that vascular dementia and Alzheimer dementia often coexist, especially in older patients with dementia. Autopsy studies have shown an association between Alzheimer disease and vascular lesions.[7]

Several recent studies also suggest that the risk of developing Alzheimer disease is increased when a patient is exposed to vascular risk factors such as hypertension, diabetes mellitus, peripheral arterial disease, and smoking, which usually are associated with cerebrovascular disease and vascular dementia. Recent evidence suggests that the vascular processes in both disorders may mutually induce each other. Apolipoprotein E may play a role in Alzheimer disease and vascular dementia. Apolipoprotein E4 also increases the risk of dementia in stroke survivors and is a strong risk factor for the development of cerebral amyloid angiopathy in patients with Alzheimer disease. In elderly individuals, many cases of dementia may be caused by the cumulative effect of cerebrovascular and Alzheimer pathology.

One-third of patients with vascular dementia are found to have significant Alzheimer disease pathology with cholinergic deficits in the nucleus basalis of Meynert.[8]

Vascular cognitive disorder (VCD) is a new term used to describe a particular constellation of cognitive and functional impairment spectrum that ranges from vascular cognitive impairment (VCI) to subcortical vascular dementia, poststroke dementia, and mixed dementia.[4]

Frequency

Vascular dementia is the second most common cause of dementia in the United States and Europe, but it is the most common form in some parts of Asia.

The prevalence rate of vascular dementia is 1.5% in Western countries and approximately 2.2% in Japan. In Japan, vascular dementia accounts for 50% of all dementias that occur in individuals older than 65 years.

In Europe, vascular dementia and mixed dementia account for approximately 20% and 40% of cases, respectively.

In Latin America, 15% of all dementias are vascular.

In community-based studies in Australia, the prevalence rate for vascular and mixed dementia is 13% and 28%, respectively.

The prevalence rate of dementia is 9 times higher in patients who have had a stroke than in controls. One year after a stroke, 25% of patients develop new-onset dementia. Within 4 years following a stroke, the relative risk of incident dementia is 5.5%.

The prevalence of vascular dementia is higher in men than in women.

Mortality/Morbidity

In patients with dementia who have had a stroke, the increase in mortality is significant. The 5-year survival rate is 39% for patients with vascular dementia compared with 75% for age-matched controls.[9]

Vascular dementia is associated with a higher mortality rate than AD, presumably because of the coexistence of other atherosclerotic diseases.

Study on causes of death in patients with dementia showed that circulatory system disorders (e.g., ischemic heart disease) is the most common immediate cause of death in vascular dementia, followed by respiratory system diseases (e.g., pneumonia).[10]

A study of hospitalization rates in patients with dementia showed that persons who developed different types of incident dementia, including vascular dementia, were found to have an increased risk of hospitalization, including hospitalization for ambulatory care-sensitive conditions.[11]

Cognitive impairment, acutely or subacutely, after an acute neurologic event with a stepwise progression is a typical history suggestive of vascular dementia. However, this classic history is usually observed with multi-infarct dementia and may not be observed with lacunar state. 

Binswanger disease

The average age of onset is between the fourth and seventh decades of life, and 80% of patients have a history of hypertension. Patients also show progressive motor, cognitive, mood, and behavioral changes over a period of 5-10 years. Mood and behavioral changes are observed early and, in some patients, may be the presenting feature. Patients may be apathetic or abulic.

Intellectual deficits are also observed early in the disease, and patients are frequently described as disoriented, having memory deficits, inattentive, and vague.

Patients with Binswanger dementia often have early-onset urinary incontinence and gait disturbances.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

The onset of the disease occurs between the third and fourth decades of life.

The clinical picture is similar to Binswanger disease but without a history of hypertension and risk factors for cerebrovascular disease.

Vascular dementia in general

Health professionals can perform a Mini-Mental Status Exam (MMSE),[12] depression assessment screen using DSM-5 criteria,[1] the Geriatric Depression Scale (GDS),[13] or the Cornell Scale for depression in dementia,[14]  Health professionals should directly ask patients about suicidal or homicidal ideation (thoughts), intent, and plan.

The mental status is a bedside or interview assessment and includes:

• Appearance
• Interactions with examiner
• Mood
• Affect
• Pattern of speech
• Thought process and associations
• Thought content (common themes, ideas of reference, delusions)
• Perceptual changes (illusions, hallucinations)
• Level of arousal (Alertness)
• Orientation
• Attention/Concentration
• Memory (Immediate/Short-term/Long-term) 
• Suicidal ideation, intent, plan, preparation, and protective factors 
• Homicidal ideation, intent, plan, preparation, and protective factors 
• Judgment and insight

Major depression is widely observed mood disorder in vascular dementia. Severe depression is more common in persons with vascular dementia than in those with AD. Elderly demented patients may not endorse depressed mood and may be socially withdrawn with decreased psychomotor activity. Suicidal thoughts, intent, passive wishes to die and feeling that life is not worthy is seen in these patients and they should be followed closely. Suicide attempts were observed in fewer than 1% of patients with dementia, but those attempts are often associated with depression.[15]

Demented patients may develop psychosis, delusions, hallucinations and paranoia at some point in their disease and sometimes agitation can be dangerous when it manifests into abnormal behavior and in rare circumstances can lead to attempts of homicide.

Patients with vascular dementia commonly have mood and behavioral changes. In some patients with lacunar state and Binswanger disease, such problems may be more prominent than intellectual deficits.

Executive functioning deficits are seen prior to severe memory loss in the early stages of subcortical vascular cognitive impairment.[16]

A commonly used cognitive screening tool is the Folstein Mini-Mental State Examination. Patchy defects are present in persons with vascular dementia. The deficits are global in persons with Alzheimer dementia.

The Folstein Mini-Mental State Examination is as follows:

• Orientation: First, ask the patient the date, day, month, year, and season. The maximum score is 5. Second, ask the patient their current location, i.e., facility, floor, town, state, and country. The maximum score is 5.

• Registration: Name 3 objects (e.g., ball, flag, door), and ask the patient to repeat them. The maximum score is 3.

• Attention: Ask the patient to spell the word "world" backwards or to subtract 7 from 100 serially backwards (stop after 5 answers). The maximum score is 5.

• Recall: Ask the patient to remember the 3 objects from the Registration portion of the test. The maximum score is 3.

• Language

• Ask the patient to identify a pencil and a watch. The maximum score is 2. Ask the patient to repeat the phrase "no ifs, ands, or buts." The maximum score is 1. Ask the patient to follow a 3-step command. The maximum score is 3. Ask the patient to read and obey the phrase "close your eyes." The maximum score is 1. Ask the patient to write a sentence. The maximum score is 1. Ask the patient to copy a set of interlocking pentagons. The maximum score is 1.

• Scoring: The maximum score possible is 30. Generally, any score less than 24 is considered abnormal, but the cutoff varies with the patient's level of education. Because the results for this test can vary over time, and for some people results can vary during the day, record when (i.e., the time and date) this test was performed.[17]

Diagnostic criteria

DSM-5

Several specific diagnostic criteria can be used to diagnose vascular dementia, including the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria, the International Classification of Diseases, Tenth Edition criteria, the National Institute of Neurological Disorders and Stroke-Association International pour la Recherché at L'Enseignement en Neurosciences (NINDS-AIREN) criteria, the Alzheimer's Disease Diagnostic and Treatment Center criteria, and the Hachinski ischemic score.

DSM-5 categorizes vascular dementia as an etiological subtype of either major or mild neurocognitive disorder. A summary of the DSM-5 diagnostic criteria is as follows:[1]

• Evidence of modest (mild) or significant (major) cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor or social cognition based on: 1) Concern of the individual, a knowledgeable informant, or the clinician that there has been a decline in cognitive function and 2) An impairment in cognitive performance (modest or significant) documented by standardized testing or another qualified assessment.

• The clinical features are consistent with a vascular etiology as suggested by either of the following: 1) Onset of the cognitive deficits is temporally related to one or more cerebrovascular events; or 2) Evidence for decline is prominent in complex attention (including processing speed) and frontal executive functions.

• There is evidence of the presence of cerebrovascular disease from history, physical examination, and/or neuroimaging considered sufficient to account for the neurocognitive deficits.

• The symptoms are not better explained by another brain disease or systemic disorder.

• Probable vascular neurocognitive disorder is diagnosed if one of the following is present:1) Clinical criteria are supported by neuroimaging evidence of significant parenchymal injury attributed to cerebrovascular disease;2) The neurocognitive syndrome is temporarily related to one or more documented cerebrovascular events; 3)Both clinical and genetic evidence of cerebrovascular disease is present

• Possible vascular neurocognitive disorder is diagnosed if the clinical criteria are met but neuroimaging is not available and the temporal relationship of the neurocognitive syndrome with one or more cerebrovascular events is not established.

NINDS-AIREN

The NINDS-AIREN criteria are the most specific of all available criteria and are used most commonly in research. They provide 3 levels of certainty: definite, probable, and possible.

Lateralizing signs such as hemiparesis, bradykinesia, hyperreflexia, extensor plantar reflexes, ataxia, pseudobulbar palsy, and gait and swallowing difficulties may be observed.

Subcortical vascular dementia signs include balance problems, gait disorder, and urinary incontinence; focal lesions may be subtle.

Neuropsychological testing is as follows:

Patients with vascular dementia have patchy neuropsychological deficits. With vascular dementia, patients have better free recall and fewer recall intrusions compared with patients with AD. Apathy early in the disease is more suggestive of vascular dementia because it usually occurs in the later stages of AD.

Patients with vascular dementia have poor verbal fluency and more perseverative behavior compared with patients with AD. They may even have other signs of executive dysfunction such as cognitive slowing, difficulty in shifting sets, and problems with abstraction. Commonly used mental status tests include the Folstein Mini-Mental State Examination and the Cognitive Abilities Screening Instrument.

Some cognitive patterns may help to differentiate vascular dementia clinically from AD. Patients with vascular dementia tend to show greater deficits on measures of frontal executive functioning than patients with AD, whereas patients with AD show greater long-term memory deficits than patients with vascular dementia.

Neuropsychological findings vary with the site and severity of cerebrovascular disease.

For patients with single or multiple large infarcts, deficits correlate with the site and extent of the infarct.

In patients with extensive deep white matter disease, impairments may be observed in tests of psychomotor speed, dexterity, executive function, and motor aspects of speech (e.g., dysarthria, reduced verbal output). Patients with subcortical vascular dementia show reduced ability to set and reach goals with mental slowing and gradual executive dysfunction.

Cerebral amyloid angiopathy may present with progressive cognitive impairment, transient ischemic attacks or amyloid spells and sudden focal neurological deficits related to intracerebral hemorrhage. Amyloid spells could be early clinical indicators of cerebral amyloid angiopathy.[18]

Behavioral problems assessment: Behavioral disturbances are common in dementia and are associated with adverse outcomes, increased disability, caregiver stress, and earlier institutionalization. Patients should be assessed for the following disturbances:

Agitation/aggression: Patient exhibits restlessness, physical agitation, or verbal or sexual aggression. Patient is hard to handle or resistant to care.

Hallucinations: Patient sees or hears things that are not there.

Delusions/paranoia: Patient harbors false beliefs, is suspicious of family members regarding stealing money or belongings, or suspects neighbors are planning to harm him.

Sundowning: Abnormal behaviors typically occur in the late afternoon or evening in a circadian rhythm fashion. Patients may exhibit mood swings, become upset or disoriented, or wander.

Risk factors for vascular dementia include hypertension, smoking, hypercholesterolemia, diabetes mellitus, and cardiovascular and cerebrovascular disease.

A large cohort study published in 2010 followed 21,123 heavy midlife smokers (more than 2 packs per day) for a mean of 23 years. These individuals were found more than 2 decades later to have a greater than 100% increased risk of dementia, Alzheimer disease, and vascular dementia in both sexes and across ethnic groups.[19]

Vascular dementia development after stroke can be influenced by many factors. Some of the important factors that can lead to the development of dementia are older age, lower education level, family history of dementia, left-sided lesions, larger lesions, larger periventricular white matter ischemic lesions, and strokes in thalamic artery territory, inferomedian temporal lobes, hippocampus, and watershed infarcts involving superior frontal and parietal regions.[20]

Laboratory tests should be performed to rule out other causes of dementia. These tests should routinely include a CBC count, erythrocyte sedimentation rate, glucose level, renal and liver function tests, serologic tests for syphilis, vitamin B-12 and red blood cell folate levels, and thyroid function tests.

In selected patients, optional tests include HIV serology testing, lupus anticoagulant testing, antiphospholipid antibody testing, antinuclear antibody testing, and antineutrophil cytoplasmic antibody testing.

Neuroimaging studies may include CT brain scanning and MRI of the brain. The absence of cerebrovascular lesions on CT scanning or MRI is evidence against vascular etiology. The features on CT scanning or MRI that are suggestive of vascular dementia are bilateral multiple infarcts located in the dominant hemisphere and limbic structures, multiple lacunar strokes, or periventricular white matter lesions extending into the deep white matter.

Patients with vascular mild cognitive impairment (MCI), which is a prodromal stage for subcortical vascular dementia, have MRI features that differ from patients with amnestic MCI, which is the prodromal stage for AD. Vascular MCI shows more extensive white matter lacunar infarcts and leukoaraiosis and minimal hippocampal and entorhinal cortical atrophies, whereas the opposite is true for amnestic MCI.

Functional imaging may also be used for diagnosis. According to a 2000 study by Nagata et al,[21] positron emission tomography may be useful for differentiating vascular dementia from AD. Hypoperfusion and hypometabolism can be observed in the frontal lobe, including the cingulate and superior frontal gyri, in patients with vascular dementia; a parietotemporal pattern is observed in patients with AD. Starkstein et al in 1996[22] and other authors have demonstrated that single-photon emission CT scanning produce similar findings.

Cerebral angiography is not performed routinely during the evaluation of vascular dementia, but it is performed before carotid artery surgery. It also is useful in cases of possible cerebral vasculitis; cerebral vessels can demonstrate beading.

Tests that may be useful for evaluation of stroke and in certain cases of vascular dementia include the following:

• Echocardiography

• Holter monitoring

• Carotid duplex Doppler scanning

The mainstay of management of vascular dementia is the prevention of new strokes. This includes administering antiplatelet drugs and controlling major vascular risk factors. Aspirin has also been found to slow the progression of vascular dementia.

Recent guidelines from the American Psychiatric Association provide both treatment principles and possible specific therapies.

Drug treatment is primarily used to prevent further worsening of vascular dementia by treating the underlying disease such as hypertension, hyperlipidemia, and diabetes mellitus. Antiplatelet agents are indicated.

Pentoxifylline and, to a more limited extent, ergoloid mesylates (Hydergine), may be useful for increasing cerebral blood flow. In the European Pentoxifylline Multi-Infarct Dementia Study, which is a double-blinded, placebo-controlled, multicenter study, treatment with pentoxifylline was found to be beneficial for patients with multi-infarct dementia. Significant improvement was observed in the scales used for assessing intellectual and cognitive function.

Neuroprotective drugs such as nimodipine, propentofylline, and posatirelin are currently under study and may be useful for vascular dementia. Nicardipine is a dihydropyridine calcium channel blocker that was studied on the treatment of cognitive deterioration of vascular origin. Preliminary studies showed decrease in cognitive deterioration in patients with cerebrovascular disease.[23]

Increasing evidence supports the involvement of the cholinergic system in vascular dementia, similar to that seen in Alzheimer dementia. However, no cholinesterase inhibitors have been approved to date for the treatment of vascular dementia, despite positive results in clinical trials with this medication.

The general management of dementia includes appropriate referral to community services, judgment and decision-making regarding legal and ethical issues (eg, driving, competency, advance directives), and consideration of caregiver stress.

Agitation and psychosis are common in older adults with dementia and are challenging to manage. Relatively few studies have examined the use of antidepressants for the treatment of agitation and psychosis in dementia; however, the selective serotonin reuptake inhibitors (SSRIs) sertraline and citalopram appear to be associated with a reduction in symptoms of agitation when compared with placebo.[24] Both appear to be reasonably well tolerated when compared with placebo, typical antipsychotics, and atypical antipsychotics. However, more studies are needed to determine if SSRIs, trazodone, or other antidepressants are safe and effective treatments for agitation and psychosis in dementia.

In the Rotterdam study, an increased risk of vascular dementia was associated with total fat intake, whereas fish consumption was inversely related to dementia.

Low levels of folate, vitamin B-6, and vitamin B-12 are associated with increased homocysteine levels, a risk factor for stroke.

In a 44-year longitudinal population study of Swedish women, researchers found that a high cardiovascular fitness in midlife was associated with a decreased risk of subsequent dementia. Data show women with high fitness levels had an 88% lower risk of developing dementia compared with women who were moderately fit in midlife. Additionally, when the highly fit women did develop dementia, they developed the disease an average of 11 years later than women who were moderately fit.[25, 26]

Heavy drinking is the strongest potentially modifiable risk factor for dementia, according to a retrospective analysis involving 30 million people in France. Data from the study show that those with a history of alcohol use disorders had a threefold increased risk for dementia and that over half those with early-onset dementia had a history of alcohol problems. Of 57,000 patients who had developed dementia under the age of 65 years, 57% had a history of alcohol use disorders (66% of men and 37% of women).[27]

Medical therapy options include antiplatelet and hemorheologic agents.

Class Summary

Studies have shown antiplatelet agents are useful for preventing recurrent stroke. In vascular dementia, a pilot study showed that aspirin has positive effects on cognitive deficits. Recent studies have shown it may have some neuroprotective effects. Other antiplatelet agents are ticlopidine and clopidogrel.

Aspirin (Anacin, Ascriptin, Bayer aspirin)

Prevents platelet-aggregating thromboxane A2 by blocking prostaglandin synthetase action and thereby preventing prostaglandin synthesis.

Ticlopidine (Ticlid)

Used in patients who cannot tolerate aspirin therapy or in whom aspirin therapy fails.

Clopidogrel bisulfate (Plavix)

Antiplatelet drug that acts by direct inhibition of ADP binding to the platelet receptor and of subsequent ADP-mediated activation of the glycoprotein IIb/IIIa complex.

Class Summary

Improve flow properties of blood by lowering viscosity, improving erythrocyte flexibility, inhibiting platelet aggregation and thrombus formation, and suppressing leukocyte adhesion.

Pentoxifylline (Trental)

In a multicenter, double-blinded, placebo-controlled trial involving 29 European centers, improvement in cognitive function at 9 mo was noted.

Regular follow-up every 4-6 months is recommended to assess the patient's general condition and cognitive and noncognitive symptoms.

Frequent visits may be needed for patients with behavioral problems and patients who are on specific therapies such as neuroprotective agents.

Treatment of risk factors such as hypertension, hypercholesterolemia, and diabetes mellitus require special attention.

In a randomized controlled trial, no significant differences were found in the follow-up coordination of care either in the memory clinics or with general practitioners in patients diagnosed to have mild to moderate dementia with regards to quality of life, mood and behavioral problems[28] .

If depressed patients do not respond to medical management or if the depression is severe (ie, with life-threatening behavior such as suicide attempts), electroconvulsive therapy is indicated and patients should be hospitalized.

As dementia progresses, more troubling behaviors such as agitation, aggression, wandering, sleep disorders, and inappropriate sexual behavior are observed. The decision for placement in institutions is usually made when problem behaviors become unmanageable, when more assistance is necessary in performing activities of daily living, when caring duties exceed the capacity of the caregiver, or when a breakdown in the family caregiver's health occurs.

Vascular cognitive impairment is modifiable and preventable. Modifying vascular risk factors (eg, hypertension, diabetes mellitus, smoking, hyperhomocystinemia) and dietary factors (eg, hypercholesterolemia) in midlife may help to prevent stroke and vascular dementia. The single most important risk factor is hypertension. Epidemiologic cohort studies and intervention trials with antihypertensive medications demonstrated the usefulness of antihypertensive drugs in the prevention of vascular dementia.

Appropriate treatment for atrial fibrillation, coronary artery disease, congestive heart failure, and stroke is also recommended.

Adequate management of vascular risk factors, stroke, and heart disease in middle age may be the most effective way to prevent vascular dementia later in life. The distinction between vascular dementia and Alzheimer dementia is becoming increasingly blurred because vascular risk factors play a role in both diseases.

In patients with early cognitive impairment or with neuroimaging findings that demonstrate leukoaraiosis or stroke, secondary prevention can be facilitated by applying standard stroke-preventive therapies such as antiplatelet agents, warfarin, or carotid endarterectomy according to accepted guidelines.

A study by Vercambre et al examined data from participants in the Women's Antioxidant Cardiovascular Study; the findings revealed a significant difference in the rate of cognitive decline over 5 years (p< .003) among elderly women who had physical activity equivalent to daily 30 minutes walk at a brisk pace. Exercise may improve brain vascular health and strengthen the mechanisms underlying brain plasticity.[29]

See the list below:

• Behavioral problems, including wandering, delusions, hallucinations, and poor judgment

• Depression

• Falls and gait abnormality

• Aspiration pneumonia

• Decubitus ulcers

• Caregiver burden and stress: This should be considered a complication of any dementia, including vascular dementia. This can lead to increased psychiatric and medical morbidity in the caregiver.

• Syndrome of delayed posthypoxic leukoencephalopathy (DPHL): Patients who had a period of prolonged hypoxia secondary to cardiac arrest can develop neuropsychiatric complications. It is a demyelinating syndrome and a slow gradual recovery can happen over a 3- to 12-month period. Neuroimaging can show diffuse demyelination sparing cerebellum and brain stem. In some patients, cognitive impairment, especially with domains of attention and executive function, can be permanent.[30]

According to some studies, vascular dementia shortens life expectancy by approximately 50% in men, in persons with lower education, and in persons who perform worse on neuropsychological tests.

The causes of death are due to complications of dementia, cardiovascular disease, and miscellaneous factors, including malignancy.

In addition to patient education, caregiver education is important to dementia management.

Structured, respectful, and friendly caregiving is best, and it forms the most important aspect of behavioral care for patients with vascular dementia. Educating the caregiver on how to take care of these patients, how to react to certain behaviors and agitation, and how to reorient the patient improves the quality of care and treatment in these patients. Well-informed caregivers are best equipped to address the problems that vascular dementia presents.

Guidelines for caregiver education are as follows:

• Use short simple sentences when communicating with patients with dementia.

• Simplify and create a routine for all self-care tasks such as bathing and dressing.

• Establish a daily routine for all activities such as meals, medication administration, recreation, exercise, and sleep.

• To reorient the patient, use signs and pictures, clocks and calendars, family photos, and a list of daily activities.

• Use distraction, not confrontation, to control irritable or socially inappropriate behaviors.

Initiate discussion about long-term care planning, including nursing home placement and issues regarding caregiver stress and respite care. Respite care is a community resource that gives the caregiver relief for a short period.

Day programs can also provide relief for families, particularly working families, and can provide structure and activities for patients with dementia.

• Additional patient and family education can be accessed at the following sites:

• Alzheimer's Association: Vascular Dementia

National Institute of Neurological Disorders and Stroke: NINDS Multi-Infarct Dementia Information Page

For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education articles Dementia in Head Injury, Dementia Overview, Possible Early Dementia, Dementia Medication Overview, Stroke, and Stroke-Related Dementia.

See other resources for caregivers at The National Institute on Aging and Family Caregiver Alliance.