A University of Texas at Dallas scientist has received a three-year, $1.7 million grant from the National Institutes of Health (NIH) to support his work on how stroke patients with aphasia may lose the ability to produce or understand speech.
Dr. Roozbeh Behroozmand, associate professor of speech, language, and hearing in the School of Behavioral and Brain Sciences, is the director of the Speech Neuroscience Lab at UT Dallas, where he and his team study the brain mechanisms of speech production and their related disorders in patients with neurological conditions such as post-stroke aphasia.
According to the NIH, about 1 million people in the United States have aphasia, which is caused by damage — most often from a stroke — to one or more of the language areas of the brain.
“The more we learn about the underlying factors that affect brain function, the more we are able to build computational models that yield novel insights into the relationship between the brain and behavior.”
Dr. Roozbeh Behroozmand, associate professor of speech, language, and hearing in the School of Behavioral and Brain Sciences
“Speech production is one of the most complex tasks humans do, involving highly coordinated communications between multiple sensory-motor networks in the brain,” Behroozmand said. “It’s a goal-oriented task, just like reaching for a cup of coffee. When you reach out to produce the right word, your ears help you listen, and other parts of the brain produce the movements in your speech-related muscles.
“Depending on where a stroke happens and what part of the brain has been damaged by a stroke, the ability to produce speech sounds, the perception of one’s own speech or understanding sounds by other people can be lost.”
Behroozmand’s lab uses neuroimaging techniques including MRI at the Sammons BrainHealth Imaging Center to learn what happens when the perception-production loop of speech in the brain breaks down.
“In our experiments, individuals produce different words and sounds that constitute units of speech, and we externally change the auditory feedback of their voice so that they hear something slightly different, like ‘bet’ or ‘bad’ instead of ‘bed,’” he said. “Normal speakers would be able to detect these feedback errors and correct their speech accordingly. Individuals with speech impairment due to stroke often fail to either recognize errors in their production or make the proper adjustment. This can significantly deteriorate their verbal fluency for communication.
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“When we see a behavioral deficit, we can try to identify the neurobiological origin — a brain region that shows an abnormal pattern of neural activity that correlates with the behavioral impairment,” Behroozmand said. “This can be caused by injuries to gray matter brain tissues or white matter tracts that connect different regions together. Depending on how those are damaged, the overall state of the brain network can change in a unique way and affect the person’s ability to produce and perceive speech.”
His research also incorporates computational models to link brain activity patterns to speech outcomes.
“These models help us predict the nature of the impairment,” Behroozmand said. “The more we learn about the underlying factors that affect brain function, the more we are able to build computational models that yield novel insights into the relationship between the brain and behavior.”
Behroozmand said studying the neural causes of speech impairment in stroke patients with aphasia can lead to new insights into the fundamental science of speech production and ultimately benefit future clinical care.
“Studying the post-stroke population can advance our understanding about the neurological mechanisms behind these complex communication tasks,” he said. “Moreover, a better understanding of the neurobiological origins of stroke patients’ impairments can have many clinical implications for developing targeted interventions to improve patients’ communication skills.”