Asymmetric sleep in apneic human patients.

Unilateral sleep in marine mammals has been considered to be a defense against airway obstruction, as a sentinel for pod maintenance, and as a thermoregulatory mechanism. Birds also show asymmetric sleep, probably to avoid predation. The variable function of asymmetric sleep suggests a general capability for independence between brain hemispheres. Patients with obstructive sleep apnea share similar problems with diving mammals, but their eventual sleep asymmetry has received little attention. The present report shows that human sleep apnea patients also present temporary interhemispheric variations in dominance during sleep, with significant differences when comparing periods of open and closed airways. The magnitude of squared coherence, an index of interhemispheric EEG interdependence in phase and amplitude, rises in the delta EEG range during apneic episodes, while the phase lag index, a measure of linear and nonlinear interhemispheric phase synchrony, drops to zero. The L index, which measures generalized nonlinear EEG interhemispheric synchronization, increases during apneic events. Thus, the three indexes show significant and congruent changes in interhemispheric symmetry depending on the state of the airways. In conclusion, when confronted with a respiratory challenge, sleeping humans undergo small, but significant, breathing-related oscillations in interhemispheric dominance, similar to those observed in marine mammals. The evidence points to a relationship between cetacean unihemispheric sleep and their respiratory challenges.

Asymmetric sleep in rats.

Five Wistar rats were surgically implanted with cortical and parietal electrodes for conventional polysomnography to test for sleep-related EEG asymmetries during 48 hours of continuous recording. When the animals were grouped not according to right-left dominance (which would represent a population bias) but instead according to preferred vs non-preferred hemisphere, significant light/dark circadian changes in side dominance were found in delta power during NREM; in theta and beta power during REM; and in alpha 1, alpha 2, and theta power during wakefulness. The changes have been interpreted as a response to temporal variations in the capability to respond to environmental challenges.

Evolution of wakefulness, sleep and hibernation: from reptiles to mammals.

Thus far, most hypotheses on the evolutionary origin of sleep only addressed the probable origin of its main states, REM and NREM. Our article presents the origin of the whole continuum of mammalian vigilance states including waking, sleep and hibernation and the causes of the alternation NREM-REM in a sleeping episode. We propose: (1) the active state of reptiles is a form of subcortical waking, without homology with the cortical waking of mammals; (2) reptilian waking gave origin to mammalian sleep; (3) reptilian basking behaviour evolved into NREM; (4) post-basking risk assessment behaviour, with motor suspension, head dipping movements, eye scanning and stretch attending postures, evolved into phasic REM; (5) post-basking, goal directed behaviour evolved into tonic REM and (6) nocturnal rest evolved to shallow torpor. A small number of changes from previous reptilian stages explain these transformations.

The trivial function of sleep.

Rest in poikilothermic animals is an adaptation of the organism to adjust to the geophysical cycles, a doubtless valuable function for all animals. In this review, we argue that the function of sleep could be trivial for mammals and birds because sleep does not provide additional advantages over simple rest. This conclusion can be reached by using the null hypothesis and parsimony arguments. First, we develop some theoretical and empirical considerations supporting the absence of specific effects after sleep deprivation. Then, we question the adaptive value of sleep traits by using non-coding DNA as a metaphor that shows that the complexity in the design is not a definitive proof of adaptation. We then propose that few, if any, phenotypic selectable traits do exist in sleep. Instead, the selection of efficient waking has been the major determinant of the most significant aspects in sleep structure. In addition, we suggest that the regulation of sleep is only a mechanism to enforce rest, a state that was challenged after the development of homeothermy. As a general conclusion, there is no direct answer to the problem of why we sleep; only an explanation of why such a complex set of mechanisms is used to perform what seems to be a simple function. This explanation should be reached by following the evolution of wakefulness rather than that of sleep. Sleep could have additional functions secondarily added to the trivial one, although, in this case, the necessity and sufficiency of these sleep functions should be demonstrated.