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Evidence of Post-Stroke Brain Recovery Discovered

Sep. 29, 2010 — The world's largest study using neuroimaging of stroke patients struggling to regain ability to communicate finds that brain cells outside the damaged area can take on new roles.


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Julius Fridriksson, a researcher at the University of South Carolina's Arnold School of Public Health, said the findings offer hope to patients of "chronic stroke," characterized by the death of cells in a specific area of the brain. The damage results in long-term or permanent disability.

"For years, we heard little about stroke recovery because it was believed that very little could be done," Fridriksson said. "But this study shows that the adult brain is quite capable of changing, and we are able to see those images now. This will substantially change the treatment for chronic-stroke patients."

The study, reported in the Sept. 15 issue of the Journal of Neuroscience, involved 26 patients with aphasia, a communication disorder caused by damage to the language regions in the brain's left hemisphere. Aphasia impairs a person's ability to process language and formulate speech.

About 35 percent of stroke patients have speech and/or communication problems. While many patients with aphasia regain some language function in the days and weeks after a stroke, scientists have long believed that recovery is limited after this initial phase. "Stroke is the leading cause of disability among adults, more than accidents or complications from Parkinson's or Alzheimer's diseases," said Fridriksson, director of the university's Aphasia Laboratory and an associate professor in the department of communication sciences and disorders.

"When someone has brain damage as a result of a stroke, the recovery is expected to be limited," he said.

But Fridriksson's study shows that the brain can recover and that a patient's ability to communicate can improve.

Stroke patients underwent a functional magnetic resonance imaging test, also called fMRI, which measures brain activity. Patients received multiple MRI sessions before and after undergoing 30 hours of traditional speech therapy used to improve communication function in patients with aphasia.

By using fMRI -- an imaging technique more improved and widely used in the past decade -- Fridriksson was able to see the healthy areas of the brain that "take over" the functions of the areas damaged as a result of a stroke.

"The areas that are immediately around the section of the brain that was damaged become more 'plastic,' " Fridriksson said. "This 'plasticity,' so to speak, increases around the brain lesions and supports recovery. In patients who responded well with the treatment for anomia [difficulty in recalling words and names], their fMRI showed evidence that areas of the brain took over the function of the damaged cells."

The study found that patients who did not experience these changes did not have as improved a recovery, he said.

This research lays the foundation for future studies of aphasia, including research on the use of low-current, electrical stimulation for the brain.

"Knowing where the brain has been damaged -- and the section that is taking over that function -- will enable us to better use electrical stimulation to promote recovery," said Fridriksson, the lead author of another paper published last month in the Journal of Neuroscience that examined the mapping of brain lesions that cause speech/communication impairment.

"It is believed that electrical currents to the brain will promote secretions of neurotransmitters that support brain plasticity," he said. "This could dramatically improve the quality of life for stroke patients."

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The above story is reprinted from materials provided by University of South Carolina.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. J. Fridriksson. Preservation and Modulation of Specific Left Hemisphere Regions is Vital for Treated Recovery from Anomia in Stroke. Journal of Neuroscience, 2010; 30 (35): 11558 DOI: 10.1523/JNEUROSCI.2227-10.2010
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