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Multi-infarct Dementia

Multi-infarct dementia


Multi-infarct dementia is one form of dementia that occurs when small blood vessels in the brain are blocked by blood clots or fatty deposits. The blockage interrupts the flow of blood to regions of the brain (a stroke ), which, if sustained, causes the death of cells in numerous areas of the brain. Another form of multi-infarct dementia is inherited.


Blockage or narrowing of small blood vessels by blood clots or by deposits of fat can impede the flow of blood through the vessel. Deprivation of the essential blood is catastrophic for the regions that are supplied by the vessels. In the brain, such vessel blockage can cause the death of brain cells. This event is also called a stroke. The stroke-related cell death affects the functioning of the brain.

Multi-infarct dementia is the most common form of dementia (the loss of cognitive brain due to disease or injury) due to changes in blood vessels. Alzheimer's disease is the most common of these so-called vascular dementias. The term multi-infarct is used because there are many areas in the brain where cell damage or death occurs. Besides dementia, multi-infarct dementia can cause stroke, headaches of migraine-like intensity, and behavioral disturbances.

An inherited form of multi-infarct dementia is designated as CADASIL, which is an acronym for cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.


Multi-infarct dementia usually begins between the ages of 6075 years. For as-yet-undetermined reasons, it affects men more than women. Multi-infarct dementia is the second most common cause of dementia in older people after Alzheimer's disease, accounting for up to 20% of all progressively worsening dementias.

CADASIL occurs in young male and female adults. It has been diagnosed in Americans, Africans, and Asians, and may occur in other racial groups.

Causes and symptoms

The root cause of multi-infarct dementia is usually small blood clots that lodge in blood vessels in the brain, which results in the death of brain cells. Over time, the series of small strokes (also known as mini-strokes, transient ischemic attacks, or TIAs) magnifies the brain cell damage. Blood clots can result from an elevated blood pressure. Indeed, it is uncommon for someone affected with multi-infarct dementia not to have a history of high blood pressure.

There are a variety of symptoms caused by the brain cell loss. These include mental confusion, problems retaining information even for a short time, loss of recognition of surroundings that are familiar (which can lead to getting lost in previously familiar territory), loss of control of urination and defecation, moving with a rapid shuffling motion, difficulty in following instructions, rapid swings in emotion, and difficulty performing tasks that were previously routine. These symptoms appear in a stepwise manner, from less to more severe. As well, the initial symptoms can be so slight as to be unrecognized, disregarded, or rationalized as being due to other causes such as a temporarily stressful period. These early problems include a mild weakness in an arm or a leg, slurred speech, or dizziness that only lasts for a few days. As more blood vessels become blocked with the occurrence of more strokes, the more severe symptoms associated with mental decline become apparent.

CADASIL is characterized by a series of strokes, which is thought to be triggered by genetically determined deficiencies of small cerebral arteries. The defects affect blood flow to the brain in a similar fashion as occurs in multi-infarct dementia. The symptoms associated with CADASIL range from migraines to a slowly progressing series of symptoms that is similar to the symptoms that develop in multi-infarct dementia.


Multi-infarct dementia is diagnosed based on the history of symptoms, especially of high blood pressure and strokes. A physician will look for several features during the examination, which include arm or leg weakness, speech difficulties, or dizziness. Tests that can be performed in the doctor's office include taking a blood pressure reading, recording the heartbeat (an electroencephalogram, or EEG), and obtaining blood for laboratory analysis. Ultrasound studies of the carotid artery may also be performed.

Diagnosis most often involves the non-destructive imaging of the brain by means of computed tomography (CT ) or magnetic resonance imaging (MRI) to reveal blood clots or the characteristic damaged regions of the brain.

Diagnosis can also be aided by an examination by a psychologist or a psychiatrist to test a person's degree of mental reasoning, ability to learn and retain new information, and attention span. Symptoms can be similar to those of Alzheimer's disease, which can complicate and delay the diagnosis of both disorders. Indeed, a person can have both disorders at the same time, as their causes are different.

Treatment team

A person with multi-infarct dementia can benefit from a support network that includes a family physician, neurologist , pharmacist, nurses, and supportive family members and other care givers. Community resources are also important, such as assisted living facilities, adult day or respite care centers, and local agencies on aging.


There is no specific treatment for multi-infarct dementia, as the damage to the brain cells cannot be reversed. Treatment typically involves trying to limit further deterioration. This focuses on establishing and/or maintaining a lower blood pressure, which lessens the tendency of blood clot formation. Those people who are diabetic will be treated for this condition, as diabetes can contribute to stroke. Other factors that can be involved in lessening blood pressure include maintaining a target cholesterol level, exercise , avoiding smoking, and moderation in alcohol consumption.

Aspirin is known to reduce the tendency of the blood to clot. Some physicians will prescribe aspirin or similarly acting drugs for this purpose. As well, those with high cholesterol may benefit from a diet change and/or the use of cholesterol-lowering drugs such as statins. In some people, surgery that removes blockages in the main blood vessel to the brain (the carotid artery) can be done. Other surgical treatments that increase blood flow through vessels include angioplasty and stenting to increase arterial flow to the brain.

Recovery and rehabilitation

As damage to the brain cannot be reversed, the focus for a person with multi-infarct dementia is placed upon prevention of further brain tissue injury, and maintaining optimum independent functioning.

Clinical trials

As of May 2004, there were no clinical trials underway or in the process of recruiting patients for either multi-infarct dementia or CADASIL. However, research is being funded by agencies such as the National Institute of Neurological Disorders and Stroke and is aimed at under-standing the development of dementia. The hope is that the diagnosis of dementias will be improved. Ultimately, the goal is to reverse or prevent the disorder.


The outlook for people with multi-infarct dementia is poor. While some improvement in mental faculty may occur, this is typically of short-term duration. Over longer time, mental decline is inevitable and marked.

Special concerns

A person with multi-infarct dementia is often reliant on family and friends for daily care and support. Family and caregivers can help by stimulating a person's mental activity and prompting the individual to recall past experiences. Eventually, around-the-clock care may become necessary to provide a safe and stimulating environment.



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National Institute for Neurological Diseases and Stroke (NINDS). P.O. Box 5801, Bethesda, MD 20824. (301) 496-5751. (800) 352-9424. <http://www.ninds/>.

National Institute on Aging (NIA). 31 Center Drive, Rm. 5C27 MSC 2292, Bethesda, MD 20892-2292. (301) 496-1752 or (800) 222-2225. [email protected] <>.

National Institute of Mental Health (NIMH). 6001 Executive Blvd. Rm. 8184, MSC 9663, Bethesda, MD 20892-9663. (301) 443-4513 or (866) 615-6464; Fax: (301) 443-4279. [email protected] <>.

Brian Douglas Hoyle, PhD

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