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Neurology 2000;54:2336-2339
© 2000 American Academy of Neurology
Brief Communications

Apraxic agraphia due to thalamic infarction

T. Ohno, MD, M. Bando, MD, H. Nagura, MD, K. Ishii, MD and H. Yamanouchi, MD

From the Department of Neurology, Tokyo Metropolitan Geriatric Hospital (Drs. Ohno, Bando, Nagura, and Yamanouchi); and the Positron Medical center, Tokyo Metropolitan Institute of Gerontology (Dr. Ishii), Tokyo, Japan.

Address correspondence and reprint requests to Dr. T. Ohno, Department of Neurology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan; e-mail: ttakae-tky{at}umin.ac.jp

The authors report a patient of pure apraxic agraphia with normal praxis due to left thalamic infarction. 15O-gas-PET showed reduced oxygen metabolism in the left thalamus and the left dorsolateral premotor area, while MRI and 11C-fulumazenil-PET showed no remarkable lesions in the frontal cortex. The patient’s word imaging remained normal. The authors hypothesize that thalamic destruction causes pure apraxic agraphia by exerting a remote effect on left dorsolateral premotor area and blocking somewhere between graphemic area and motor programming.

Key words: Apraxic agraphia—Left thalamic infarction—Dorsolateral premotor—PET.




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P. Marien, J. Verhoeven, R. Brouns, L. De Witte, A. Dobbeleir, and P. P. De Deyn
APRAXIC AGRAPHIA FOLLOWING A RIGHT CEREBELLAR HEMORRHAGE
Neurology, August 28, 2007; 69(9): 926 - 929.
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