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On Cerebral Metabolism and Aphasia-Reply

On Cerebral Metabolism and Aphasia-Reply Abstract In Reply. —The letter by Dr Mark challenges our work on four grounds: (1) the adequacy of the Western Aphasia Battery, (2) the value of resting glucose metabolism in predicting regional dysfunction, (3) whether our conclusions regarding conduction aphasia are warranted, and (4) the failure to use dynamic subtraction studies. We will address these points individually.The purpose of our two articles1,2 was to relate glucose metabolic patterns to traditional clinical aphasic syndromes, and not to use the Western Aphasia Battery3 as a means of determining underlying neurolinguistic disturbances. The Western Aphasia Battery was developed to provide a standardized procedure to assist in clinical aphasia classification by providing fixed criteria, thus allowing for a consistent and repeatable diagnosis. Dr Mark is correct in pointing out that the test was not designed to probe the underlying "neurolinguistic" basis of aphasia. Neurolinguistic analyses are particularly important in determining the nature of the References 1. Kempler D, Metter EJ, Jackson CA, et al. Disconnection and cerebral metabolism: the case of conduction aphasia . Arch Neurol . 1988;45:275-279.Crossref 2. Metter EJ, Kempler D, Jackson C, et al. Cerebral glucose metabolism in Wernicke's, Broca's, and conduction aphasias . Arch Neurol . 1989;46:27-34.Crossref 3. Kertesz A. Western Aphasia Battery . New York, NY: Grune & Stratton; 1981. 4. Illes J, Metter EJ, Dennings R, Jackson C, Kempler D, Hanson WR. Spontaneous language production in mild aphasia: relationship to left prefrontal glucose hypometabolism. Aphasiology. In press. 5. Metter EJ. Neuroanatomy and physiology of aphasia: evidence from positron emission tomography . Aphasiology . 1987;1:3-33.Crossref 6. Metter EJ, Riege WH, Hanson WR, et al. Subcortical structures in aphasia: an analysis based on (F-18)—fluorodeoxyglucose positron emission tomography and computed tomography . Arch Neurol . 1988;45:1229-1335.Crossref 7. Metter EJ, Hanson WR, Jackson CA, Kempler D, Van Lancker D. Temporoparietal cortex: the common substrate for aphasia. In: Prescott T, ed. Clinical Aphasiology 1988. San Diego, Calif: College-Hill Press. In press. 8. Metter EJ, Riege WH, Hanson W, Camras L, Kuhl DE, Phelps ME. Correlations of cerebral glucose metabolism and structural damage to language function in aphasia . Brain Lang . 1984;21:187-207.Crossref 9. Metter EJ, Mazziotta JC, Itabashi HH, et al. Comparison of x-ray, CT, glucose metabolism, and postmortem data in a patient with multiple in farctions . Neurology . 1985;35:1695-1701.Crossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Neurology American Medical Association

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References (9)

Publisher
American Medical Association
Copyright
Copyright © 1989 American Medical Association. All Rights Reserved.
ISSN
0003-9942
eISSN
1538-3687
DOI
10.1001/archneur.1989.00520480014010
Publisher site
See Article on Publisher Site

Abstract

Abstract In Reply. —The letter by Dr Mark challenges our work on four grounds: (1) the adequacy of the Western Aphasia Battery, (2) the value of resting glucose metabolism in predicting regional dysfunction, (3) whether our conclusions regarding conduction aphasia are warranted, and (4) the failure to use dynamic subtraction studies. We will address these points individually.The purpose of our two articles1,2 was to relate glucose metabolic patterns to traditional clinical aphasic syndromes, and not to use the Western Aphasia Battery3 as a means of determining underlying neurolinguistic disturbances. The Western Aphasia Battery was developed to provide a standardized procedure to assist in clinical aphasia classification by providing fixed criteria, thus allowing for a consistent and repeatable diagnosis. Dr Mark is correct in pointing out that the test was not designed to probe the underlying "neurolinguistic" basis of aphasia. Neurolinguistic analyses are particularly important in determining the nature of the References 1. Kempler D, Metter EJ, Jackson CA, et al. Disconnection and cerebral metabolism: the case of conduction aphasia . Arch Neurol . 1988;45:275-279.Crossref 2. Metter EJ, Kempler D, Jackson C, et al. Cerebral glucose metabolism in Wernicke's, Broca's, and conduction aphasias . Arch Neurol . 1989;46:27-34.Crossref 3. Kertesz A. Western Aphasia Battery . New York, NY: Grune & Stratton; 1981. 4. Illes J, Metter EJ, Dennings R, Jackson C, Kempler D, Hanson WR. Spontaneous language production in mild aphasia: relationship to left prefrontal glucose hypometabolism. Aphasiology. In press. 5. Metter EJ. Neuroanatomy and physiology of aphasia: evidence from positron emission tomography . Aphasiology . 1987;1:3-33.Crossref 6. Metter EJ, Riege WH, Hanson WR, et al. Subcortical structures in aphasia: an analysis based on (F-18)—fluorodeoxyglucose positron emission tomography and computed tomography . Arch Neurol . 1988;45:1229-1335.Crossref 7. Metter EJ, Hanson WR, Jackson CA, Kempler D, Van Lancker D. Temporoparietal cortex: the common substrate for aphasia. In: Prescott T, ed. Clinical Aphasiology 1988. San Diego, Calif: College-Hill Press. In press. 8. Metter EJ, Riege WH, Hanson W, Camras L, Kuhl DE, Phelps ME. Correlations of cerebral glucose metabolism and structural damage to language function in aphasia . Brain Lang . 1984;21:187-207.Crossref 9. Metter EJ, Mazziotta JC, Itabashi HH, et al. Comparison of x-ray, CT, glucose metabolism, and postmortem data in a patient with multiple in farctions . Neurology . 1985;35:1695-1701.Crossref

Journal

Archives of NeurologyAmerican Medical Association

Published: Dec 1, 1989

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