Multiple Sclerosis May Cause Changes in Thalamus: Study
Small study finds that MS might reduce volume in area of brain affecting thought process
FRIDAY, Dec. 30 (HealthDay News) -- New research suggests that in addition to the disabling lesions it's known to cause, multiple sclerosis also damages the part of the brain that affects thinking skills, motor function and the senses.
"The thalamus is a central area that relates to the rest of the brain and acts as the 'post office,'" study co-author Khader Hasan, an associate professor at University of Texas Health Science Center at Houston, said in a university news release. "It also is an area that has the least amount of damage from lesions in the brain, but we see volume loss, so it appears other brain damage related to the disease is also occurring."
Hasan and colleagues published their observations in a recent issue of the Journal of Neuroscience.
The study authors noted that aging alone can bring about changes in the size of the thalamus region, resulting in some shrinkage after age 70. However, the research team wanted to see if multiple sclerosis (MS) -- which is often associated with the onset of dementia -- accelerates such structural shifts.
The radiology researchers used cutting-edge MRI scanning equipment to analyze brain structure in 109 MS patients, compared to 255 healthy men and women.
The result: MS patients had greater volume loss in the thalamus region than healthy patients, after accounting for age. And the greater the loss in thalamus volume, the more disabled the patient was, the investigators noted.
"This is looking at multiple sclerosis in a different way," Hasan said in the news release. "The thalami are losing cellular content and we can use this as a marker of what's going on. If we can find a way to detect the disease earlier in a more vulnerable population, we could begin treatment sooner."
For more on multiple sclerosis, visit the National Multiple Sclerosis Society.Alan Mozes SOURCE: University of Texas Health Science Center at Houston, news release, Dec. 22, 2011 Related Articles
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