Updated: Aug 18, 2009
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. Vascular dementia is preventable; therefore, early detection and an accurate diagnosis are important.
Patients who have had a stroke are at increased risk for vascular dementia. Recently, vascular lesions have been thought to play a role in AD.
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. 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.
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. Patient had a fall 10 months ago; after that fall, she started to ask the same questions over and over. Patient had 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.
Many subtypes of vascular dementia have been described to date. 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.
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. 1
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 (eg, polyarteritis nodosa,
temporal arteritis) and noninflammatory arteriopathy (eg, 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 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. 2 3 White matter ischemic changes affect executive dysfunction and cause slower processing speed, rather than memory and language impairment. 4
Arterial stiffness, which reflects an alteration in arterial mechanics, can be a risk factor for vascular dementia. 5
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.6
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. 7
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. 3
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.
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.
Dementia Due to Head Trauma
Dementia Due to HIV Disease
Huntington Disease Dementia
Parkinson Disease Dementia
Other Problems to Be Considered
Normal pressure hydrocephalus
Lewy body dementia
Patients with AD have early language and visuospatial deficits. The deficits in short-term memory are severe, and clues do not help in retrieving information. The onset of the disease is gradual, with a slow progression. Usually, no motor findings are present until the middle or late stages of the disease.
Patients with vascular dementia have patchy cognitive impairment, often with focal neurologic signs and symptoms. Onset may be abrupt, with a stepwise decline.
Patients with Parkinson dementia have cognitive slowing with extrapyramidal signs such as rigidity, bradykinesia, tremor, and gait disturbances. Usually, dementia is seen in later stages of the disease.
Patients with dementia due to head trauma have memory impairment, and other cognitive deficits associated with a history of head trauma occur. The physical findings depend on the location of injury. Usually, it is not progressive unless the person has a history of repeated head trauma (eg, dementia pugilistica).
Patients with HIV dementia have a positive result from an HIV test and cognitive changes with neurological signs.
Frontotemporal dementia is a type of cortical dementia characterized by behavioral and personality disorders more than cognitive issues. Three distinct types are seen: frontotemporal dementia, semantic dementia, and progressive nonfluent aphasia.
Patients with Pick disease have memory problems, personality changes, and deterioration of social skills. Onset is usually between the fifth and sixth decades of life. Upon physical examination, the patient has frontal release signs such as snout and grasp reflex.
Huntington disease is an autosomal dominant disease with an onset of cognitive changes as early as the third decade of life, with physical signs of choreoathetosis.
In Creutzfeldt-Jakob disease, onset is usually seen between the fourth and sixth decades of life, even though it can occur at any, and is associated with signs such as myoclonus, seizures, and ataxia. A rapid progression is typical.
Patients with Lewy body dementia have recurrent visual hallucinations, fluctuating cognitive impairment, and parkinsonism features. Also, the frequency of adverse reactions to antipsychotic medications is high.
In the case of cognitive symptoms secondary to depression, the onset is acute
compared with the insidious onset in most types of dementia. The term pseudodementia
has been used to describe the condition when cognitive symptoms are prominent.
The current and more accurate name for this state is dementia of depression.
Patients with depression usually report their cognitive difficulties, which
is unusual for patients with dementia. Patients with depression tend to state
that they do not know the answers to questions, and they appear to not try
very hard during neuropsychological evaluations. Mood symptoms are prominent
in patients with dementia of depression.
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.
Medical therapy options include antiplatelet and hemorheologic agents.
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.
Prevents platelet-aggregating thromboxane A2 by blocking prostaglandin synthetase action and thereby preventing prostaglandin synthesis.
Aspirin (Anacin, Ascriptin, Bayer aspirin)
Prevents platelet-aggregating thromboxane A2 by blocking prostaglandin synthetase
action and thereby preventing prostaglandin synthesis.
325 mg PO qd
Effects may decrease with antacids and urinary alkalinizers; corticosteroids
decrease salicylate serum levels; additive hypoprothrombinemic effects and
increased bleeding time may occur with coadministration of anticoagulants;
may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin
and valproic acid; doses > 2 g/d may potentiate glucose-lowering effect
of sulfonylurea drugs
Documented hypersensitivity; liver damage; hypoprothrombinemia; vitamin K
deficiency; bleeding disorders; asthma; use in children ( <16 y) with flu
(associated with Reye syndrome)
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
May cause transient decrease in renal function and aggravate chronic kidney disease; avoid use in patients with severe anemia, with history of blood coagulation defects, or taking anticoagulants
Used in patients who cannot tolerate aspirin therapy or in whom aspirin therapy
250 mg PO bid
Effects may decrease with coadministration of corticosteroids and antacids;
toxicity increases when taken concurrently with theophylline, cimetidine,
aspirin, and NSAIDs
Documented hypersensitivity; neutropenia or thrombocytopenia; liver damage;
active bleeding disorders
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Discontinue if absolute neutrophil count decreases to <1200/µL or if platelet count falls to <80,000/µL
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
75 mg PO qd
Coadministration with naproxen associated with increased occult GI blood
loss; prolongs bleeding time; safety of coadministration with warfarin not
Documented hypersensitivity; active pathological bleeding (eg, peptic ulcer);
B - Fetal risk not confirmed in studies in humans but has been shown in some
studies in animals
Use caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)
In a multicenter, double-blinded, placebo-controlled trial involving 29 European
centers, improvement in cognitive function at 9 mo was noted.
400 mg PO tid
Coadministration with cimetidine or theophylline increases effects and toxic
potential; increases effect of antihypertensives
Documented hypersensitivity; cerebral or retinal hemorrhage
C - Fetal risk revealed in studies in animals but not established or not
studied in humans; may use if benefits outweigh risk to fetus
Caution in renal impairment
Further Outpatient Care
Patient and family education
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arteriosclerotic dementia, atherosclerotic disease, dementia due
to vascular disease, multiinfarct dementia, multi-infarct dementia, vascular
cognitive impairment, Alzheimer disease, AD, Alzheimer's disease, cognitive
dementia, senility, stroke, old age dementia, senile dementia, Binswanger disease,
Binswanger's disease, mixed dementia, lacunar lesions, cortical dementia, subcortical
dementia, cognitive decline, subcortical leukoencephalopathy, Binswanger dementia,
Alzheimer dementia, cerebrovascular disease, thrombotic vascular occlusions,
embolic vascular occlusions, hypertension
multiple cortical infarct, strategic single infarct, small vessel disease, single-infarct dementia, anterior cerebral artery infarct, parietal lobe infarcts, thalamic infarction, singular gyrus infarction, subcortical leukoencephalopathy, cerebral amyloid angiopathy–associated vasculopathy, hereditary cystatin-C amyloid angiopathy, recurrent cerebral hemorrhages, inflammatory arteriopathy, polyarteritis nodosa, temporal arteritis, noninflammatory arteriopathy, moyamoya disease, fibromuscular dysplasia, apolipoprotein E, apolipoprotein E-IV, cognitive impairment, urinary incontinence, gait disturbances, cerebral autosomal dominant arteriopathy, subcortical infarcts, depression, delusions, Folstein Mini-Mental State Examination, aphasia, apraxia, agnosia, smoking, hypercholesterolemia, diabetes, cardiovascular disease, vascular cognitive disorder
Kannayiram Alagiakrishnan, MD, MBBS, Associate
Professor, Department of Medicine, Division of Geriatric Medicine, University
Kannayiram Alagiakrishnan, MD, MBBS is a member of the following medical societies: American College of Physicians, American Geriatrics Society, and American Medical Association
Disclosure: Nothing to disclose.
Kamal Masaki, MD, Associate Director of
Geriatric Medicine Fellowship, Associate Professor, Department of Internal Medicine,
Division of Geriatric Medicine, University of Hawaii, John Burns School of Medicine
Disclosure: Nothing to disclose.
Mohammed A Memon, MD, Medical Director of
Geriatric Psychiatry, Department of Psychiatry, Spartanburg Regional Hospital
Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior
Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Iqbal Ahmed, MBBS, Professor, Department
of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of
Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department
of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research
Stephen Soreff, MD, President of Education
Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University,
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.