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Cerebral Circulation And Metabolism in a Comatose PatientStudied With a New Method
D. H. INGVAR, MD;
E. HAGGENDAL, MD;
N. J. NILSSON, MD;
P. SOURANDER, MD;
I. WICKBOM, MD;
N. A. LASSEN, MD
Arch Neurol. 1964;11(1):13-21.
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Introduction
Investigations in the last decade have amply demonstrated the vital importance of medially situated brain stem structures for consciousness (Lindsley et al, 1949; Jefferson, 1952; Cairns, 1952; and others). Comatose states following brain stem lesions may, in general, be accompanied by only slight or no EEG disturbances in pontine lesions or severe general abnormalities in lesions of the upper brain stem (Roger, Roger, and Gastaut, 1953; Fishgold, and Mathis, 1959; Kaada, Harkmark, and Stokke, 1961; Chatrian, White, Jr., and Daly, 1963; Marquardsen, and Harvald, 1964).
Comatose states are, in general, accompanied by a reduction of both the cerebral circulation and metabolism (Kety, 1948). However, among such cases so far investigated none due to circumscribed brain stem lesion have been included (Lassen, 1959); and the cerebral circulatory and metabolic consequences of such lesions are, therefore, at present unknown.
In this report we describe a case of permanent coma following a
. . . [Full Text PDF of this Article]
Author Affiliations
GOTHENBURG, SWEDEN
From the departments of Neurology, Clinical Physiology, Radiology II, and Pathology I, Sahlgrenska Sjukhuset, University of Gothenburg.
Footnotes
Submitted for publication Jan 14, 1964; accepted April 4.
On leave of absence from the Department of Neurology, University of Lund (Dr. Ingvar).
Chief, Department of Clinical Physiology, Bispebjerg Hospital, Copenhagen, Denmark (Dr. (Lassen).
D. H. Ingvar was supported by the Swedish Medical Research Council.
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