[Characteristics of humoral regulation of functions in dogs following cerebral decortication].
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Detailed observation of a case of laminar necrosis of almost the whole of the cerebral cortex has led to several deductions concerning the physiology of the cortex in man. It suggests that the cortex has a limited influence on sleep, interfering particularly in the electro-encephalographic translation of slow sleep and, curiously, in the organisation of sleep, paradoxical sleep is hardly affected at all. It confirms the importance of the human cortex in the acquisition of elementary skills and describes a new oculomotor pattern in a decorticate man.
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Reduction of cortical inhibition has been suggested as a possible mechanism for the transition from episodic fetal to continuous postnatal breathing. Twelve fetal lambs were chronically decorticated at 112-115 days gestation. Lateral rectus, neck, and diaphragmatic electromyogram (EMG), electrocorticogram (ECoG), and tracheal and arterial blood pressure were monitored after allowing 3 days for recovery. The fetal lambs were studied for 4-28 days in 2- to 4-h sessions/day. There were no episodes of low-voltage high-frequency ECoG activity. The mean duration (+/- SD) of rapid eye movements (REM) measured by lateral rectus EMG [11 +/- 7.9 min and periods of tonic activity or silence [non-REM (NREM)], 14 +/- 7.4 min] in decorticated fetuses were not statistically different from REM (12 +/- 5.1 min) and NREM (15 +/- 6.8 min) sleep periods in intact fetuses. After decortication, the percentage of time (+/- SD) occupied by different states were phasic diaphragmatic EMG activity 36 +/- 7.8%, tonic diaphragmatic EMG 21 +/- 8.6%, and diaphragmatic silence 43 +/- 14.2%. Phasic diaphragmatic EMG activity occurred together with REM, the latter being present 45 +/- 3.7% of the time. Despite decortication, between 115 and 125 days gestation ECoG changed from a trace alternans to a high-voltage low-frequency pattern. We conclude that the cerebral cortex is not responsible for apnea during fetal life. In addition, these data suggest that the cerebral cortex may normally be the source of ECoG synchrony.
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