Presents

DAILY DIGEST

REPORTING FROM ACTRIMS

Americas Committee for Treatment and Research in Multiple Sclerosis
West Palm Beach, Florida

FRIDAY, FEBRUARY 28

Fatigue and Cognitive Deficits in Multiple Sclerosis Can Be Quantified Using MRI Measures of Cerebral Metabolism

Kathryn West, PhD, Postdoctoral Research Fellow at the Center for BrainHealth at UT Dallas School of Behavioral and Brain Sciences, reported on research showing that fatigue and cognitive dysfunction can be quantified using an MRI technique that measures energy metabolism in the brain.WEST PALM BEACH, FL — Fatigue and cognitive dysfunction are some of the most common and troubling issues affecting people with multiple sclerosis (MS). They are typically evaluated using patient-reported tools such as the Modified Fatigue Impact Scale (MFIS) and the Single Digit Modalities Test (SDMT), but more objective techniques for monitoring fatigue and cognition in MS are lacking.

At the ACTRIMS Forum on Thursday, February 27, Kathryn West, PhD, from UT Dallas School of Behavioral and Brain Sciences, reported on her research using an MRI measure of baseline cerebral metabolism to predict fatigue and cognition in patients with MS.

"The mechanisms of fatigue and cognitive dysfunction MS remain unknown," Dr. West commented. "The primary hypotheses revolve around inflammation, axonal damage, and immune response." A current hypothesis in MS is that axonal damage is related to energy failure, she said. Demyelination places increased energy demands on axonal cells. While some compensatory mechanisms occur to help conduct impulses across demyelinated axons, this creates a huge demand for energy to maintain cellular function. When compensatory mechanisms fail, this leads to the axon's demise, which then reverses energy demands.

"Imaging has been proposed as a possible way to assess the mechanism of this energy failure in patients with MS," Dr. West noted. Previous studies of oxygen metabolism in the brain were done using PET scans, but these images are highly variable, she said. Her research team used MRI measures of cerebral metabolic rate of oxygen (CMRO2). "Our hypothesis is that demyelination leads to a hypermetabolic state, marked by higher levels of CMRO2. With axonal loss there is much lower use of oxygen, marked by low CMRO2 levels."

The UT Dallas study enrolled 33 patients with relapsing MS and 16 healthy controls matched for age, gender, and education. Most were stable on a disease modifying therapy. Fatigue and cognition scales were performed in both groups and compared with the cerebral metabolism findings. The results showed a significant decline in CMRO2 in patients with MS, indicative of overall hypometabolism. Cerebral metabolism findings correlated with measures of fatigue and cognition, after controlling for factors like patient age, disability, and lesion volume. "The patients with the highest metabolism of CMRO2 had the highest levels of fatigue and the poorest performance on SDMT," Dr. West reported.

"There is potential for this to be a clinically useful tool in MS," she concluded. CMRO2 can be measured with MRI using 90-second resting scans, she said. "In the future, we need to further validate CMRO2 and how it relates to MS symptomology."

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By Katherine Wandersee, for the Consortium of Multiple Sclerosis Centers (CMSC)

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