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

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.

[1]  H. Jasper Charting the Sea of Brain Waves. , 1948, Science.

[2]  Françoise Bremer,et al.  Considérations sur l'origine et la nature des ⪡ ondes ⪢ cérébrales , 1949 .

[3]  R. Morison,et al.  SPONTANEOUS ELECTRICAL ACTIVITY OF THE THALAMUS AND OTHER FOREBRAIN STRUCTURES , 1943 .

[4]  H. Jasper,et al.  Diffuse projection systems: the integrative action of the thalamic reticular system. , 1949, Electroencephalography and clinical neurophysiology.

[5]  P. Bailey,et al.  Effects of Lesions of the Periaqueductal Gray Matter in the Cat∗ , 1942 .

[6]  H. Josephy CONGENITAL AGYRIA AND DEFECT OF THE CORPUS CALLOSUM , 1944 .

[7]  Juan Jimenez Castellanos Thalamus of the cat in Horsley‐Clarke coordinates , 1949 .

[8]  Ralph W. Gerard,et al.  Factors influencing brain potentials during sleep. , 1939 .

[9]  G. Moruzzi,et al.  Brain stem reticular formation and activation of the EEG. , 1949, Electroencephalography and clinical neurophysiology.

[10]  S. W. Ranson SOMNOLENCE CAUSED BY HYPOTHALAMIC LESIONS IN THE MONKEY , 1939 .

[11]  P. Bailey,et al.  EFFECTS OF LESIONS OF THE PERIAQUEDUCTAL GRAY MATTER ON THE MACACA MULATTA , 1944 .

[12]  A. J. Derbyshire,et al.  THE EFFECTS OF ANESTHETICS ON ACTION POTENTIALS IN THE CEREBRAL CORTEX OF THE CAT , 1936 .

[13]  P. Davis,et al.  HUMAN BRAIN POTENTIALS DURING THE ONSET OF SLEEP , 1938 .

[14]  N. Kleitman,et al.  SLEEP AND WAKEFULNESS , 1940 .

[15]  R. Morison,et al.  ELECTRICAL ACTIVITY OF THE THALAMUS AND BASAL GANGLIA IN DECORTICATE CATS , 1945 .

[16]  Robert S. Morison,et al.  THE PRODUCTION OF RHYTHMICALLY RECURRENT CORTICAL POTENTIALS AFTER LOCALIZED THALAMIC STIMULATION , 1941 .

[17]  R. Morison,et al.  THE INTERACTION OF CERTAIN SPONTANEOUS AND INDUCED CORTICAL POTENTIALS , 1941 .

[18]  C. W. Watson,et al.  Effects of barbiturates and ether on spontaneous electrical activity of dog brain. , 1949, Journal of neurophysiology.