'Silent' Strokes Linked to Dementia

Danish study finds symptomless attacks double risk

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By
HealthDay Reporter

WEDNESDAY, March 26, 2003 (HealthDayNews) -- Older people who have "silent" brain infarcts -- burst blood vessels that produce few or no symptoms -- can suffer dementia similar to Alzheimer's disease, a Dutch study finds.

In a report that stops just short of stating a cause-and-effect relationship, epidemiologists at Erasmus Medical Center in Rotterdam write in the March 27 issue of The New England Journal of Medicine that "elderly people with silent brain infarcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions."

It is the latest chapter in an evolution of medical thought about dementia that has gone on for more than a century, says Dr. John P. Blass, a professor of neurology, medicine and neuroscience at Weill Cornell College and author of an accompanying editorial.

"At the beginning of the last century, senior dementia was attributed entirely to problems with blood vessels in the brain," Blass says. "About 35 years ago, the consensus changed, and a sharp distinction developed between problems caused by vascular [blood vessel] disease and degenerative disease. In the last 10 or 15 years, the pendulum is swinging back toward a midpoint, with vascular disease being recognized as an individual risk factor for development of dementia."

The Danish results come from the Rotterdam Scan Study, which includes 1,015 men and women 60 to 90 years of age who were free of dementia when the study began. Each had neuropsychological testing and magnetic resonance imaging (MRI), which can detect the damage done by brain infarcts, at the start and were monitored for symptoms of dementia an average of 3.6 years.

Dementia developed in 30 of the participants during that time, and "the presence of silent brain infarcts more than doubled the risk of dementia," the researchers report. The increased risk was seen only in people who were found to have suffered infarcts at the beginning of the study and had more infarcts over the following years.

There are several possible explanations for that finding, the researchers say. Perhaps a burst brain vessel speeds the progress of dementia in someone with Alzheimer's disease. Or perhaps infarcts trigger the development of the plaques and nerve tangles seen in Alzheimer's disease.

The study leaves several questions unanswered, Blass says. "This has been a controversial issue, and one epidemiological [study] doesn't settle it," he says. "That is an answer that would have to be provided by an adequately large multi-center trial."

Such a study would indicate what to do about clinically normal people who are found to have experienced a silent infarct by an MRI examination, Blass says. "The possible clinical implication is that these people should be given baby aspirin or other medications to prevent further strokes," he says.

A high incidence of silent infarcts was found in older Americans given MRIs in the Cardiovascular Health Study, funded by the National Heart, Lung, and Blood Institute, says Annette Fitzpatrick, an assistant professor of epidemiology at the University of Washington. "We followed more than 3,600 individuals for five and a half years," she says.

The study found that 28 percent of the participants, all elderly, had experienced silent brain infarcts.

These infarcts sometimes do cause detectable symptoms, Blass says. "If you have had transient neurological symptoms, such as weakness of an arm or leg or tingling of an arm or leg, something may be happening in the brain," he says. "You should see a doctor to learn if you have had a silent infarct."

More information

To learn more about dementia, consult the National Library of Medicine. Read about strokes of all types at the National Stroke Association.

SOURCES: John P. Blass, M.D., Ph.D., professor, neurology, medicine and neuroscience, Weill Cornell Medical College, White Plains, N.Y.; Annette Fitzpatrick, Ph.D., assistant professor, epidemiology, University of Washington Medical School, Seattle; March 27, 2003, The New England Journal of Medicine

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