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Effect upon the EEG of acute injury to the brain stem activating system

Lindsley, D.B., Bowden, J.W., Magoun, H.W.·1949·Electroencephalography and Clinical Neurophysiology

Abstract

The effect upon the EEG in the unanesthetized "ecéphale isolé" of acute brain stem lesions in a position to involve the ascending reticular activating system has been studied. Elimination of the bulbar segment was without marked effect. Some synchronization followed elimination of the pons, but the most pronounced and prolonged changes occurred as a result of mesencephalic transection, or of discrete injury to the midbrain tegmentum or basal diencephalon, following which the EEG activation pattern of low voltage fast activity was reduced or abolished and the cortical record became dominated by recurring bursts or spindles of high voltage slow waves like those of normal sleep or barbiturate anesthesia. Bursts could be recorded from the intralaminar and other nuclei of the thalamus and these thalamic bursts were abolished by acute decortication. Conversely, cortical bursts were abolished by acute thalamic lesions. Possible interrelations of these regions in this activity is discussed. These results offer an explanation for the clinical observation of somnolence following basal injury to the brain, and suggest that a maintained influence of the ascending brain stem activating system underlies wakefulness, while absence of this influence precipitates sleep.

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Research works printed but not linked: 23

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Metadata

Authors
Lindsley, D. B., Bowden, J. W., & Magoun, H. W.
Venue
Electroencephalography and Clinical Neurophysiology
Publisher
Elsevier BV
Published
1949-01
Volume
1
Issue
1-4
Pages
475-486
ISSN
0013-4694
Cited by
335
References
0
Language
en

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CoChat. (2026). Citation check: Effect upon the EEG of acute injury to the brain stem activating system. https://app.cochat.ai/papers/10.1016/0013-4694(49)90221-7
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Lindsley, D. B., Bowden, J. W., & Magoun, H. W. (1949). Effect upon the EEG of acute injury to the brain stem activating system. Electroencephalography and Clinical Neurophysiology. https://doi.org/10.1016/0013-4694(49)90221-7