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The agraphia of Alzheimer's disease

Department of Neurology, Divisions of Cognitive Neuroscience & Aging, University of Southern California, Los Angeles, CA (Drs. Henderson, Sobel, and Freed)
Department ofNeuroepidemiology, University of Southern California, Los Angeles, CA (Dr. Sobel),
Department of Psychology, University of Southern California, Los Angeles, CA (Drs. Henderson and Freed)
Department of Preventive Medicine, University of Southern California, Los Angeles, CA (Dr. Sobel)
Ethel Percy Andrus Gerontology Center, University of Southern California, Los Angeles, CA (Drs. Henderson, Buckwalter, and Freed, and M.M. Diz)
Program in Neural, Informational, and Behavioral Sciences, University of Southern California, Los Angeles, CA (Dr. Henderson).

Hypothesizing that agraphia in Alzheimer's disease (AD) reflects disturbances in multiple cognitive domains, we evaluated writing samples from 33 patients meeting strict criteria for probable AD. We found agraphia to be common on a standard narrative writing task. When compared with 41 education- and age-matched normal control subjects, AD patients had significantly lower writing scores, wrote significantly fewer words, mentioned significantly fewer categories of information, and were significantly more likely to make writing errors. On stepwise regression procedures, neuropsychological measures of visuoperceptual impairment and disease severity were the strongest predictors of agraphia, but other analyses indicated that measures of language, praxis, and attention could also contribute significantly to agraphia. On two writing tasks, we failed to confirm the previous contention that agraphia is a marker for familial AD. However, there was a highly significant interaction between family history, oral naming, and writing: patients with non familial AD, but not those with a family history of dementia, showed a strong correlation between naming and writing performance. We conclude that agraphia in AD can be variously determined and that agraphia is not a reliable marker for familial disease.

Address correspondence and reprint requests to Dr. Victor W. Henderson, Department of Neurology (MCH-142), University of Southern California School of Medicine, 2025 Zonal Avenue, Los Angeles, CA 90033.

Research was supported in part by NIA grants P50-AG05142 and 1U01-AG06790, and by the Thomas J. and Mary C. Bowles Fund for Alzheimer's and Related Diseases.

Presented in part at the 42nd annual meeting of the American Academy of Neurology, Miami Beach, FL, May 1990.

Received July 25, 1991. Accepted for publication in final form September 19, 1991.

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