Abstract
A hypothesis is proposed whereby one of the causes of impairments to visual perception in microsleep consists of the spontaneous generation of ponto-geniculo-occipital (PGO) waves. If the eyes are open during microsleep and PGO waves are generated, they can propagate to the thalamic projection nuclei. This degrades the conduction of visual information from the retina to the visual areas of the neocortex and the input structure of the basal ganglia – the striatum. Taking cognizance of our previously proposed mechanism of visual processing, which includes visual attention, the absence of striatal activation by visual stimuli makes it impossible for neurons in the superior colliculi, which conduct visual information to the dopaminergic structures, to be disinhibited via the basal ganglia. As a result, dopamine cannot be released in response to a visual stimulus, so attention to the stimulus is not triggered and its processing in all visual cortical areas is degraded. It should be possible to verify this hypothesis in experiments using an artificially evoked state of microsleep using non-invasive methods seeking correlates of the presence of PGO activity in the brain.
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