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From the Departments of Neurology (Drs. Mendez, Clark, Shapira, and Cummings) and Psychiatry and Biobehavioral Sciences (Drs. Mendez and Cummings), David Geffen School of Medicine, University of California at Los Angeles.
Address correspondence and reprint requests to Dr. M.D. Mendez, Neurobehavior Unit (116AF), VA Greater Los Angeles Healthcare System, 11301 Wilshire Blvd., Los Angeles, CA 90073; e-mail: mmendez{at}ucla.edu
Background: Progressive nonfluent aphasia (PA) is a slow deterioration of language that remains relatively isolated from other cognitive or behavioral deficits for at least 2 years. The differentiation of PA from early Alzheimers disease (AD) is important, given the presence of early language changes in AD.
Methods: A language assessment was administered to 15 patients who met established criteria for PA, 15 patients with clinically probable AD and mild dementia, and 15 normal control subjects. The language battery included verbal fluency, the Boston Naming Test with cuing and recognition, and an aphasia test battery with a motor speech exam.
Results: Pronounced literal paraphasic errors distinguished the PA patients from the AD patients. The PA group had anomia, decreased letter fluency, neologisms, difficulty on phrase repetition, decreased phrase length, and a decreased rate of verbal output. Interference from paraphasic anomia accounted for much of their decreased fluency.
Conclusion: Many patients with PA have a primary defect in accessing sound-based representation of speech (phonemes), similar to conduction aphasia, possibly as a consequence of disturbed white matter tracts in the left superior temporal region.
Received March 14, 2003. Accepted in final form June 23, 2003.
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