Vein-based treatment could aid stroke recovery
Vein-based treatment could aid stroke recovery
Retrograde transvenous neuroperfusion could help prevent disability in stroke survivors, according to a new study.1Researchers are looking at an emergency treatment that uses veins to send blood back to areas of the brain threatened by stroke. "We’re able to treat patients within the first seven hours after the onset of [stroke] symptoms," writes study author John Frazee, MD, from the University of California at Los Angeles School of Medicine.
His and his colleagues’ technique depends on using the brain’s "other" vascular system — the veins that drain deoxygenated blood back to the lungs and heart. The experimental procedure uses some of those veins to transfer blood to or gans in a retrograde, or opposite-direction, manner.
In experiments with baboons, the team channeled freshly-oxygenated blood from an artery in the animals’ groins into small mechanical pumps, then pumped it into tubes or catheters placed in the back of the head into a major vein. The procedure allows the surgeon to direct the flow of blood backward into the brain or into the tissue that is not getting a blood supply.
All of the baboons used in the study had suffered an artificially-induced stroke one hour prior to the procedure. The researchers report that, by using the venous technique, they effectively reversed stroke-related brain tissue damage in the affected animals. Frazee writes that the success of those studies "has led us to do experimental trials in (human) patients."
The positive results of early human trials suggest that post-stroke neurological damage can be minimized even when venous interventions are initiated as late as seven hours after stroke onset. This is a much wider window of opportunity than that afforded by current emergency stroke treatments, including the use of clot-busting tissue plasminogen activator drugs.
Reference
1. Frazee JG, Luo X, Luan G, et al. Retrograde transvenous neuroperfusion: A back door treatment for stroke. Stroke 1998; 29:1,912-1,916.
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