Cerebral glucose metabolism as a predictor of recovery from aphasia in ischemic stroke.

OBJECTIVE The recovery of language function seen in poststroke aphasia is significantly related to the severity of the initial neurologic deficit. However, a great deal of variability still remains in the improvement that is actually achieved. To detect predictors that will help in explaining this variability, positron emission tomography (PET) and fluorodeoxyglucose F 18 (18-F-fluorodeoxyglucose) were used and the results were analyzed by stepwise regression. DESIGN Using PET imaging after injection of fluorodeoxyglucose F 18, the regional changes in glucose metabolism in 26 patients at a period of 12 to 18 days following an ischemic stroke involving the left middle cerebral artery were examined. A second PET examination was performed on 17 of our 26 patients who were able to perform speech activation exercises. All patients received an initial and a 4-month follow-up evaluation of language performance. SETTING During the two PET studies and the first language assessment, the patients were hospitalized in a neurologic clinic. The follow-up evaluation of language performance was performed when the patients were ambulatory. PATIENTS Twenty-six patients (10 women, 16 men; aged 38 to 77 years; mean +/- SD, 60 +/- 9.2 years) were selected in the study. Their aphasias were of various types and of varying severity ranging from mild impairment to severe global aphasia. MAIN OUTCOME MEASURES For the stepwise regression analysis of variables, the following variables were analyzed in resting and activation PET to explain residual variance from the first to the second Token Test: regional cerebral metabolic rate for glucose of infarct and mirror region, left and right cerebral and cerebellar hemispheres, left and right Broca's area, left and right Wernicke's area, and left and right temporoparietal cortex. RESULTS As was expected, early and late Token Tests exhibit a high correlation (.85). The stepwise regression analysis shows that only the left cerebral hemisphere glucose value of the resting PET had significant effect on the residual variance of the Token Test regression. Regional metabolic rates during speech activation had the largest contribution to a significant recovery from aphasia. The infarct area and its corresponding mirror region, the left Broca's area, and the entire left cerebral hemisphere accounted for 80% of the residual variance. CONCLUSIONS These results emphasize not only the application of PET activation studies in the prediction of a tissue's potential reserve capacity but also the importance of left hemisphere integrity in the recovery of functional language.

[1]  G. Demeurisse,et al.  Remote cortical dysfunction in aphasic stroke patients. , 1991, Stroke.

[2]  J C Mazziotta,et al.  Temporoparietal cortex in aphasia. Evidence from positron emission tomography. , 1990, Archives of neurology.

[3]  John Hart,et al.  Delineation of single‐word semantic comprehension deficits in aphasia, with anatomical correlation , 1990, Annals of neurology.

[4]  K Wienhard,et al.  Regional metabolic correlates of Token test results in cortical and subcortical left hemispheric infarction , 1989, Neurology.

[5]  J. Greenhouse,et al.  Predictors of language restitution following stroke: a multivariate analysis. , 1989, Journal of Speech and Hearing Research.

[6]  J D Brodie,et al.  Reproducibility of Cerebral Glucose Metabolic Measurements in Resting Human Subjects , 1988, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[7]  R J Zatorre,et al.  Stability of regional cerebral glucose metabolism in the normal brain measured by positron emission tomography. , 1988, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[8]  R L Hewer,et al.  Aphasia after stroke: natural history and associated deficits. , 1986, Journal of neurology, neurosurgery, and psychiatry.

[9]  K Wienhard,et al.  Estimation of Local Cerebral Glucose Utilization by Positron Emission Tomography of [18F]2-Fluoro-2-Deoxy-D-Glucose: A Critical Appraisal of Optimization Procedures , 1985, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[10]  K Wienhard,et al.  Computer Assisted Mapping in Quantitative Analysis of Cerebral Positron Emission Tomograms , 1985, Journal of computer assisted tomography.

[11]  K. Herholz,et al.  Regional Kinetic Constants and Cerebral Metabolic Rate for Glucose in Normal Human Volunteers Determined by Dynamic Positron Emission Tomography of [18F]-2-Fluoro-2-Deoxy-D-Glucose , 1984, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[12]  D. Knopman,et al.  Mechanisms of recovery from aphasia: Evidence from serial xenon 133 cerebral blood flow studies , 1984, Annals of neurology.

[13]  A. Kertesz Neurobiological aspects of recovery from aphasia in stroke. , 1984, International rehabilitation medicine.

[14]  Marshall Rc,et al.  Prognosis for improved verbal communication in aphasic stroke patients. , 1983 .

[15]  S. Wainapel,et al.  Predictors of stroke outcome. , 1983, American family physician.

[16]  L. Sokoloff,et al.  Frequency-dependent activation of glucose utilization in the superior cervical ganglion by electrical stimulation of cervical sympathetic trunk. , 1983, Proceedings of the National Academy of Sciences of the United States of America.

[17]  W. Heiss,et al.  Flow and neuronal density in tissue surrounding chronic infarction. , 1983, Stroke.

[18]  J. Delisa,et al.  Stroke rehabilitation: part I. Cognitive deficits and prediction of outcome. , 1982, American family physician.

[19]  T. Greitz,et al.  A Four Ring Positron Camera System for Emission Tomography of the Brain , 1982, IEEE Transactions on Nuclear Science.

[20]  J. Hartman Measurement of early spontaneous recovery from aphasia with stroke , 1981, Annals of neurology.

[21]  M. Wyke,et al.  Aphasia and Associated Disorders , 1980 .

[22]  G. Demeurisse,et al.  Quantitative Study of the Rate of Recovery From Aphasia Due to Ischemic Stroke , 1980, Stroke.

[23]  Statistical prediction of change in aphasia. , 1980, Journal of speech and hearing research.

[24]  F. Sakai,et al.  Case reports of three dysphasic patients to illustrate rCBF responses during behavioral activation , 1980, Brain and Language.

[25]  A. Alavi,et al.  The [18F]Fluorodeoxyglucose Method for the Measurement of Local Cerebral Glucose Utilization in Mane , 1979, Circulation research.

[26]  A. Kertesz,et al.  Recovery patterns and prognosis in aphasia. , 1977, Brain : a journal of neurology.

[27]  A study of factors related to prognosis for individual aphasic patients. , 1974, The Journal of speech and hearing disorders.

[28]  L. Swisher,et al.  A study of pattern of recovery in aphasia. , 1972, Cortex; a journal devoted to the study of the nervous system and behavior.

[29]  R. C. Oldfield The assessment and analysis of handedness: the Edinburgh inventory. , 1971, Neuropsychologia.

[30]  E. FRANTZEN,et al.  PROTEIN STUDIES ON CEREBROSPINAL FLUID AND NEUROLOGICAL SYMPTOMS IN MYELOMATOSIS , 1969, Acta neurologica Scandinavica.

[31]  J. Marquardsen The natural history of acute cerebrovascular disease: a retrospective study of 769 patients. , 1969, Acta neurologica Scandinavica.

[32]  K. Poeck,et al.  Clinical Validation of a New Test for Aphasia: An Experimental Study on the Token Test , 1966 .

[33]  E. Renzi,et al.  The token test: A sensitive test to detect receptive disturbances in aphasics. , 1962, Brain : a journal of neurology.

[34]  Kurt Goldstein,et al.  Language and Language Disturbances: Aphasic Symptom Complexes and their Significance for Medicine and Theory of Language , 1948 .