Fighting stroke damage Health: Advances in brain imaging and drugs lead to the conclusion that stroke is treatable as an emergency "brain attack."

August 27, 1996|By Marie McCullough | Marie McCullough,KNIGHT-RIDDER NEWS SERVICE

Hope is growing that the damage caused by a stroke may soon be minimized -- or even averted.

Instead of standing by, almost powerless to intervene as stroke injures the brain, physicians will be able to give medications that protect the brain and restore vital blood flow.

The first emergency drug for strokes caused by blood clots was approved in June by the federal Food and Drug Administration. The drug is called tissue plasminogen activator, or TPA. Dozens of other drugs are now in testing.

This revolution has been fueled by advances in brain imaging technology, insights into the biomechanics of the brain and a recognition that stroke must be treated as a medical emergency.

"From today forward, stroke must be viewed as a 'brain attack,' a medically treatable, emergency condition just as critical as a heart attack," the National Institute of Neurological Disorders and Stroke said in trumpeting the approval of TPA for stroke. The drug is widely used for heart attacks.

Hopeful news about stroke began to emerge a decade ago. First, researchers proved that controlling major risk factors -- particularly hypertension, smoking and diabetes -- could prevent strokes.

Then came progress in controlling subtler risks. Doctors now know that atrial fibrillation (a type of irregular heart beat) or a damaged heart valve can cause blood clots in the heart that may break free and go to the brain. Aspirin or other blood-thinning medications can reduce this stroke risk.

Doctors also know that when the lining of the principal arteries of the neck and head are thickened by atherosclerosis, blood thinners or surgical cleaning of the clogged artery can reduce the risk of ischemic strokes -- caused by blood clots that block blood flow in the brain.

But prevention isn't enough. The new research frontier is treatment.

Scientists have discovered that damage results not only from the loss of oxygen-rich blood supply in the brain, but also from secondary changes in brain cells. Small but toxic amounts of calcium, sodium and other particles enter nerve cells, which in turn produce their own destructive molecules. In addition, chemical messengers called neurotransmitters are released in abundance, overstimulating nerve cells until they self-destruct.

Since the worst of this chain reaction occurs within about eight hours of a stroke, the window of opportunity for treatment is narrow, stroke experts say. TPA, for example, must be administered within three hours of the onset of stroke symptoms -- or it can make the brain damage worse.

Research has focused on two types of treatments -- clot-dissolving agents called thrombolytics and cell-preserving agents called neuroprotectives.

Bleeding in the brain is the major risk of thrombolytics, such as TPA.

That's why these agents cannot be used to treat hemorrhagic strokes, which occur when a blood vessel in the brain leaks, either because a weak spot in the vessel ruptures, or because a large clot breaks through the vessel. Brain scan technology is used to exclude unsuitable patients.

The TPA study leading to its approval found that patients who received it within three hours of a stroke were 30 percent more likely to have little or no disability after three months than a control group.

However, another thrombolytic called streptokinase was recently shown to be unsuitable for stroke treatment. It caused a third of patients to die of cerebral hemorrhage.

At least two other thrombolytics -- ancrod and pro-urokinase -- are currently in clinical trials. Even more promising, researchers say, are a host of neuroprotectives now under investigation, among them citicoline, lubeluzole, eliprodil, cervene and cerestat.

Wayne Clark, director of the stroke center at Oregon Health Sciences University, announced in March that, in a small study, citicoline appeared to limit the size of patients' ischemic strokes, speed recovery and improve their mental functioning. What's more, the drug seemed to be effective up to 24 hours after a stroke -- without serious side effects.

Experts speculate that neuroprotectives, unlike thrombolytics, may prove to help hemorrhagic stroke victims, although tests on such patients have not yet been conducted.

Medical science is still far from being able to repair brain damage after it occurs. But someday, experts say, an arsenal of treatments may minimize that damage.

"In the very near future," said Rodney D. Bell, director of the stroke unit at Thomas Jefferson University in Philadelphia, "a large percentage of stroke victims will remain functional -- they'll be able to dress, walk, talk and take care of themselves."

Pub Date: 8/27/96

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