DALLAS, May 7 -- Researchers have used biochemical markers for the first time to locate the brain injury that is associated with loss of movement in individuals who have had a stroke. The study is reported in this month's Stroke: Journal of the American Heart Association.
The findings are considered significant because scientists are now able to pinpoint an area of the brain associated with loss of movement resulting from a stroke. Identifying the location of brain cell damage provides scientists with a target site for designing treatments that could halt or slow the progression of such cell damage in stroke patients.
To locate this brain region, the scientists measured levels of a biochemical substance found almost exclusively in adult brain cells. They used magnetic resonance spectroscopy (MRS), a technique for quantitative measurements of the concentrations of biochemical substances, to measure levels of N-acetylaspartate (NAA) in various areas of the brain.
The role of NAA in the brain is unclear, but studies suggest it may be associated with protein building and the transmission of signals between nerve cells. The researchers found reduced concentrations of NAA in a particular brain region were linked with weakness in patients with stroke. This region, known as the internal capsule, has nerve pathways that transmit signals to and from the brain.
"When combined with magnetic resonance imaging (MRI), a visualization method for detecting clots or blockages in the brain that trigger most strokes, MRS provides scientists with a panoramic, interactive view of both site and function within the nervous system," says lead researcher Sarah T. Pendlebury, MRCP, at the Centre for Functional Magnetic Resonance of the Brain, John Radcliffe Hospital, Oxford, United Kingdom.
George Hademenos, Ph.D., staff scientist with the American Heart Association,
notes that these findings suggest that the injured brain cells within the
internal capsule could be
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Contact: Florence Antoine
florencea@heart.org
214-706-1135
American Heart Association
6-May-1999