ABSTRACT
The recent scientific explosion of interest in dreaming has led to the strong consensus that this unique psychological state is the concomitant of rapid eye movement sleep. Investigations in animals have further provided convincing evidence that the cortical activation of REM is basically modulated by the brain stem. But how the REM-activated cortex actually elaborates the dream is still to be understood. Experimental evidence of cortical influences on some REM sleep-related phenomena (e.g., rapid eye movements; Jeannerod, Mouret, & Jouvet, 1965) have been obtained from animal studies, but it is obviously impossible to gain from such studies any information on the higher cognitive processes leading to the production and the retrieval of a dream. An alternative investigative strategy could be to look at experiments of nature in humans. An analysis of the effects of brain damage on the higher neurocognitive processes and on dreaming, could determine what damaged areas and functions are common to clinical cases of dreaming loss, alteration or maintenance.
