Merck Manual

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Vascular Dementia


Juebin Huang

, MD, PhD, Memory Impairment and Neurodegenerative Dementia (MIND) Center, University of Mississippi Medical Center

Last full review/revision Dec 2019| Content last modified Dec 2019
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Vascular dementia is acute or chronic cognitive deterioration due to diffuse or focal cerebral infarction that is most often related to cerebrovascular disease.

Dementia is chronic, global, usually irreversible deterioration of cognition.

Vascular dementia is the 2nd most common cause of dementia among older people. It is more common among men and usually begins after age 70. It occurs more often in people who have vascular risk factors (eg, hypertension, diabetes mellitus, hyperlipidemia, smoking) and in those who have had several strokes. Many people have both vascular dementia and Alzheimer disease.

Dementia should not be confused with delirium, although cognition is disordered in both. The following helps distinguish them:

  • Dementia affects mainly memory, is typically caused by anatomic changes in the brain, has slower onset, and is generally irreversible.

  • Delirium affects mainly attention, is typically caused by acute illness or drug toxicity (sometimes life threatening), and is often reversible.

Other specific characteristics also help distinguish the 2 disorders (see table Differences Between Delirium and Dementia).


Vascular dementia typically occurs when multiple small cerebral infarcts (or sometimes hemorrhages) cause enough neuronal or axonal loss to impair brain function.

Vascular dementias include the following:

  • Multiple lacunar infarction: Small blood vessels are affected. Multiple lacunar infarcts occur deep within hemispheric white and gray matter.

  • Multi-infarct dementia: Medium-sized blood vessels are affected.

  • Strategic single-infarct dementia: A single infarct occurs in a crucial area of the brain (eg, angular gyrus, thalamus).

  • Binswanger dementia (subcortical arteriosclerotic encephalopathy): This uncommon variant of small-vessel dementia is associated with severe, poorly controlled hypertension and systemic vascular disease. It causes diffuse and irregular loss of axons and myelin with widespread gliosis, tissue death due to an infarction, or loss of blood supply to the white matter of the brain.

Symptoms and Signs

Symptoms and signs of vascular dementia are similar to those of other dementias (eg, memory loss, impaired executive function, difficulty initiating actions or tasks, slowed thinking, personality and mood changes, language deficits). However, compared with Alzheimer disease, vascular dementia tends to cause memory loss later and to affect executive function earlier. Also, symptoms can vary depending on where the infarcts occur.

Unlike other dementias, multiple-infarct dementia tends to progress in discrete steps; each episode is accompanied by intellectual decline, sometimes followed by modest recovery. Subcortical vascular dementia caused by small-vessel ischemic damage (which includes multiple lacunar infarction and Binswanger dementia) tends to cause small, incremental deficits; thus, the decline appears to be gradual.

As the disease progresses, focal neurologic deficits often develop:

  • Exaggeration of deep tendon reflexes

  • Extensor plantar response

  • Gait abnormalities

  • Weakness of an extremity

  • Hemiplegias

  • Pseudobulbar palsy with pathologic laughing and crying

  • Other signs of extrapyramidal dysfunction

  • Aphasias

Cognitive loss may be focal. For example, short-term memory may be less affected than in other dementias. Because loss may be focal, patients may retain more aspects of mental function. Thus, they may be more aware of their deficits, and depression may be more common than in other dementias.


  • Generally similar to diagnosis of other dementias

  • Neuroimaging

Diagnosis of vascular dementia is similar to the diagnosis of other dementias. A general diagnosis of dementia requires all of the following:

  • Cognitive or behavioral (neuropsychiatric) symptoms interfere with the ability to function at work or do usual daily activities.

  • These symptoms represent a decline from previous levels of functioning.

  • These symptoms are not explained by delirium or a major psychiatric disorder.

Evaluation of cognitive function involves taking a history from the patient and from someone who knows the patient plus doing a bedside mental status examination or, if bedside testing is inconclusive, formal neuropsychologic testing.

Differentiation of vascular dementia from other dementias is based on clinical judgment. Factors that suggest vascular dementia (or Alzheimer disease with cerebrovascular disease) include the following:

  • Evidence of brain infarcts

  • High Hachinski Ischemic Score

  • Clinical features characteristic of vascular dementia (eg, prominent executive dysfunction, mild or absent memory loss)

Confirmation of vascular dementia requires a history of stroke or evidence of a vascular cause for dementia detected by neuroimaging. If focal neurologic signs or evidence of cerebrovascular disease is present, a thorough evaluation for stroke should be done.

CT and MRI may show

  • Bilateral multiple infarcts in the dominant hemisphere and limbic structures

  • Multiple lacunar strokes

  • Periventricular white-matter lesions extending into the deep white matter

  • In Binswanger dementia, leukoencephalopathy in the cerebrum semiovale adjacent to the cortex, often with multiple lacunae affecting structures deep in the gray matter (eg, basal ganglia, thalamic nuclei)

The Hachinski Ischemic Score is sometimes used to help differentiate vascular dementia from Alzheimer disease (see table Modified Hachinski Ischemic Score).


Modified Hachinski Ischemic Score



Abrupt onset of symptoms


Stepwise deterioration (eg, decline-stability-decline)


Fluctuating course


Nocturnal confusion


Personality relatively preserved




Somatic complaints (eg, body aches, chest pain)


Emotional lability


History or presence of hypertension


History of stroke


Evidence of coexisting atherosclerosis (eg, PAD, MI)


Focal neurologic symptoms (eg, hemiparesis, homonymous hemianopia, aphasia)


Focal neurologic signs (eg, unilateral weakness, sensory loss, asymmetric reflexes, Babinski sign)


* Total score is determined:

  • < 4 suggests primary dementia (eg, Alzheimer disease).

  • 4–7 is indeterminate.

  • > 7 suggests vascular dementia.

MI = myocardial infarction; PAD = peripheral arterial disease.

Adapted from Hachinski VC, Iliff LD, Zilhka E, et al: Cerebral blood flow in dementia. Arch Neurol 32 (9):632-637, 1975.


The 5-year mortality rate for patients with vascular dementia is 61%, which is higher than that for most forms of dementia, presumably because other atherosclerotic disorders coexist.


  • Safety and supportive measures

  • Management of vascular risk factors, including smoking cessation

Safety and supportive measures for vascular dementia are similar to those of other dementias. For example, the environment should be bright, cheerful, and familiar, and it should be designed to reinforce orientation (eg, placement of large clocks and calendars in the room). Measures to ensure patient safety (eg, signal monitoring systems for patients who wander) should be implemented.

Troublesome symptoms can be treated.

Managing vascular risk factors (eg, hypertension, diabetes, hyperlipidemia) may slow the progression of vascular dementia and help prevent future strokes, which could cause more cognitive impairment. Management includes the following:

  • Blood pressure control

  • Cholesterol-lowering therapy

  • Regulation of plasma glucose (90 to 150 mg/dL)

  • Smoking cessation

Drugs, such as cholinesterase inhibitors and memantine, may be helpful if Alzheimer disease could also be present. Cholinesterase inhibitors may improve cognitive function. Memantine, an NMDA (N-methyl-d-aspartate) antagonist, may help slow the loss of cognitive function in patients with moderate to severe dementia and may be synergistic when used with a cholinesterase inhibitor.

However, efficacy of cholinesterase inhibitors and memantine is uncertain in vascular dementia. Nonetheless, a trial of these drugs is reasonable because older patients with vascular dementia may also have Alzheimer disease.

End-of-life issues

Because insight and judgment deteriorate in patients with dementia, appointment of a family member, guardian, or lawyer to oversee finances may be necessary. Early in dementia, before the patient is incapacitated, the patient’s wishes about care should be clarified, and financial and legal arrangements (eg, durable power of attorney, durable power of attorney for health care) should be made. When these documents are signed, the patient’s capacity should be evaluated, and evaluation results recorded. Decisions about artificial feeding and treatment of acute disorders are best made before the need develops.

In advanced dementia, palliative measures may be more appropriate than highly aggressive interventions or hospital care.

Key Points

  • Vascular dementia can occur as a series of discrete episodes (which may seem like a gradual decline) or in a single episode.

  • Focal neurologic signs may help differentiate vascular dementia from other dementias.

  • Confirm that dementia is vascular based on a history of stroke or neuroimaging findings that suggest a vascular cause.

  • Control vascular risk factors, and if Alzheimer disease could also be present, treat with cholinesterase inhibitors and memantine.

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