Subcortical Sleep Theory and Clinical Evidence
The subcortical theory is based on extensive clinical observations of patients with central nervous system lesions. It has been noted that various pathological processes—such as vascular accidents, tumors, or severe infections affecting the brainstem—lead to marked disturbances in the wake-sleep cycle. Patients suffered either from debilitating insomnia or deep lethargic sleep. A striking historical example was the epidemic of lethargic encephalitis in the late 1920s, which presented with the specific clinical picture of "sleeping sickness."
A critical practical observation was made by Soviet neurologist N.I. Grashchenkov during the Great Patriotic War. During local anesthesia in a wounded soldier with a shrapnel fragment in the diencephalic region (the interbrain), a surprising phenomenon was discovered. The slightest mechanical touch to the tissues of this area provoked the immediate induction of sleep: the patient instantly stopped talking and fell asleep, which directly pointed to the localization of sleep centers in the subcortical structures.
Experimental Evidence (W.R. Hess's Experiments)
Clinical data required rigorous experimental verification. Swiss physiologist W.R. Hess developed a unique technique for implanting chronic electrodes into the deep brain structures of animals (cats). The scientist selectively targeted the posterior structures of the subthalamus and hypothalamus.
During the experiments, it was found that low-frequency electrical stimulation of these zones provoked immediate sleep in the animal. As soon as the electrical stimulation ceased, the cat woke up immediately. These experiments served as undeniable proof that the crucial centers regulating sleep are localized precisely within the subthalamus and hypothalamus.
I.P. Pavlov's Cortical Theory
Despite the persuasiveness of the subcortical concept, it had a significant flaw: its inability to explain the phenomenon of hypnotic sleep (falling asleep on command). A hypnotist's verbal command is perceived by the higher divisions of the CNS—namely, the cerebral cortex—and cannot directly affect the brainstem or hypothalamus. To resolve this contradiction, I.P. Pavlov substantiated the involvement of the cerebral hemispheres in the mechanisms of falling asleep.
In experiments involving conditioned reflexes, it was established that animals consistently fall asleep during prolonged and persistent presentation of an unreinforced conditioned stimulus, as well as when forced to perform overly fine signal differentiation. In both cases, sleep developed against the background of pronounced inhibition of conditioned reflex activity.
Mechanisms of "Sleep" Inhibition
According to Pavlov's teaching, sleep is a direct consequence of internal inhibition processes. This is a profound, generalized inhibition that irradiates (spreads) across both hemispheres and engulfs nearby subcortical formations. To describe this state, the term "sleep" inhibition was introduced.
Three main pathways for the emergence of such inhibition are distinguished:
- Conditioned reflex pathway: based on processes of internal inhibition (reflex extinction, complex differentiation).
- Action of monotonous, weak stimuli: uniform sounds or rocking gradually depress cortical activity.
- Action of supramaximal stimuli: triggers protective inhibition, which acts as a biological defense for nerve cells against critical exhaustion.
Despite its logic, the cortical theory encountered contradictions that were irresolvable at the time. It could not explain why organisms lacking cortical function sleep fully. These included decorticated (hemisphereless) animals in experiments, as well as newborn infants whose cerebral cortex is in a state of marked morphological immaturity.