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Research Article Free access | 10.1172/JCI105584
Department of Neurology, University of Miami School of Medicine, Miami, Fla.
†Address requests for reprints to Dr. Peritz Scheinberg, Dept. of Neurology, University of Miami, 1601 N. W. 11th Ave., Miami, Fla. 33136.
*Submitted for publication September 1, 1966; accepted February 1, 1967.
Supported by U. S. Public Health Service grant NB 05820-01.
Find articles by Shimojyo, S. in: PubMed | Google Scholar
Department of Neurology, University of Miami School of Medicine, Miami, Fla.
†Address requests for reprints to Dr. Peritz Scheinberg, Dept. of Neurology, University of Miami, 1601 N. W. 11th Ave., Miami, Fla. 33136.
*Submitted for publication September 1, 1966; accepted February 1, 1967.
Supported by U. S. Public Health Service grant NB 05820-01.
Find articles by Scheinberg, P. in: PubMed | Google Scholar
Department of Neurology, University of Miami School of Medicine, Miami, Fla.
†Address requests for reprints to Dr. Peritz Scheinberg, Dept. of Neurology, University of Miami, 1601 N. W. 11th Ave., Miami, Fla. 33136.
*Submitted for publication September 1, 1966; accepted February 1, 1967.
Supported by U. S. Public Health Service grant NB 05820-01.
Find articles by Reinmuth, O. in: PubMed | Google Scholar
Published May 1, 1967 - More info
Cerebral blood flow and metabolism were measured by the iodoantipyrine-4-131I method in nine patients and by the nitrous oxide method in three patients with the Wernicke-Korsakoff syndrome.
Cerebral blood flow and cerebral oxygen and glucose consumption were strikingly reduced from the normal, whereas cerebral vascular resistance was increased.
Total cerebral metabolism and blood flow may be greatly reduced even though the cerebral metabolic defect is confined to circumscribed anatomical areas. Profound reduction in brain metabolism is not necessarily reflected in alterations of consciousness or awareness as has been previously suggested, or in electroencephalographic abnormalities. This appears to provide cogent support for the neurophysiological principle that disturbance of consciousness is a function of the location of the lesion, not the over-all degree of metabolic defect.
The absence of improvement of cerebral metabolic functions in two patients who were restudied after an additional 2 to 3 weeks of treatment confirms the clinical impression of incomplete recovery in many such patients.