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fMRI study of episodic memory in relapsing-remitting MS

Correlation with T2 lesion volume

From the Department of Neurology (J.A.B., S.M.R., L.L., C.E., A.G., J.K., S.D.), Medical College of Wisconsin, Neurognostics, Inc. (S.M.R., C.E.), and Advanced Healthcare SC (L.L., E.M.), Milwaukee, WI.

Address correspondence and reprint requests to Dr Rao, Division of Neuropsychology, Medical College of Wisconsin, 9200 W. Wisconsin Ave., Milwaukee, WI 53226; e-mail: srao{at}mcw.edu

Objective: To determine whether memory loss in patients with multiple sclerosis (MS) results from faulty encoding or retrieval, we correlated extent of T2-weighted lesion involvement with brain activation patterns on fMRI scans obtained while patients performed a verbal episodic memory task.

Methods: We performed a neurologic examination, neuropsychological testing, and an event-related fMRI scan on 36 patients with relapsing-remitting MS. In addition, we obtained T2-weighted structural MRI scans to measure lesion volume. We performed a regression analysis to examine the association between lesion volume and regional brain activation.

Results: Increasing lesion volume correlated with increasing magnitude of brain activation, primarily in the left frontal and parietal association cortices. Significant correlations of function with lesion volume were primarily observed during the memory retrieval phase of the task.

Conclusions: These results extend previous fMRI studies in multiple sclerosis (MS) by demonstrating an association between greater disease burden and increased neural recruitment during episodic memory. In addition, the stronger correlations observed between lesion volume and brain activation during retrieval than encoding would suggest that retrieval processes are more affected by MS-related cerebral pathology.

Supported in part by a Biogen Idec, Inc., Independent Medical Grant (L.L.) and the Medical College of Wisconsin General Clinical Research Center (NIH: M01 RR00058).

Disclosure: The authors report no conflicts of interest.

Received February 1, 2006. Accepted in final form July 6, 2006.

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