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Neurology 2000;55:1883-1894
© 2000 American Academy of Neurology


Articles

Neural correlates of recovery from aphasia after damage to left inferior frontal cortex

H. J. Rosen, MD;, S. E. Petersen, PhD;, M.R. Linenweber, BS;, A. Z. Snyder, MD, PhD;, D.A. White, PhD;, L. Chapman, MA;, A.W. Dromerick, MD;, J. A. Fiez, PhD; and and M. Corbetta, MD

From the Departments of Neurology and Neurological Surgery (Drs. Rosen, Petersen, Snyder, Corbetta, and M. Linenweber), Anatomy and Neurobiology (Drs. Petersen and Corbetta), and Psychology (Dr. Petersen and L. Chapman), and the NeuroImaging Laboratory (Drs. Rosen, Petersen, Snyder, and Corbetta), Mallinkrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO; Department of Psychology (Dr. Fiez), University of Pittsburgh and Center for the Neural Basis of Cognition, University of Pittsburgh/Carnegie Mellon University, PA.

Address correspondence and reprint requests to Dr. Maurizio Corbetta, Department of Neurology and Neurological Surgery, Box 8111, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110; e-mail: mau{at}npg.wustl.edu

OBJECTIVE: To determine neural correlates of recovery from aphasia after left frontal injury.

METHODS: The authors studied the verbal performance of patients with infarcts centered in the left inferior frontal gyrus (IFG), using a battery of attention-demanding lexical tasks that normally activate the left IFG and a simpler reading task that does not normally recruit the left IFG. The authors used positron emission tomography (PET) and functional MRI (fMRI) to record neural activity in the same group of patients during word-stem completion, one of the attention-demanding lexical tasks. To identify potential neural correlates of compensation/recovery, they analyzed the resulting data for the group as a whole (PET, fMRI) and also for each participant (fMRI).

RESULTS: Patients with damage to the left IFG were impaired on all attention-demanding lexical tasks, but they completed the word-reading tasks normally. The imaging studies demonstrated a stronger-than-normal response in the right IFG, a region homologous to the damaged left IFG. The level of activation in the right IFG did not correlate with verbal performance, however. In addition, a perilesional response within the damaged left IFG was localized in the two patients who gave the best performance in the word-stem completion task and showed the most complete recovery from aphasia.

CONCLUSIONS: Right-IFG activity may represent either the recruitment of a preexisting neural pathway through alternative behavioral strategies or an anomalous response caused by removal of the left IFG. Perilesional activity in the left IFG may represent sparing or restoration of normal function in peri-infarctual tissue that was inactive early on after injury. This activity may be of greater functional significance than right IFG activity because it was associated with more normal verbal performance.




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