This review considers a number of recent theories on the neural basis of consciousness, with particular attention to the theories of Bogen, Crick, Llina Β΄s, Newman, and Changeux. These theories allot different roles to various key brain areas, in particular the reticular and intralaminar nuclei of the thalamus and the cortex. Crick's hypothesis is that awareness is a function of reverberating corticothalamic loops and that the spotlight of intramodal attention is controlled by the reticular nucleus of the thalamus. He also proposed different mechanisms for attention and intention (''will''). The current review presents a new hypothesis, based on elements from these hypotheses, including intermodal attention and olfaction and pain, which may pose problems for Crick's original theory. This work reviews the possible role in awareness and intermodal attention and intention of the cholinergic system in the basal forebrain and the tegmentum; the reticular, the intralaminar, and the dorsomedial thalamic nuclei; the raphe and locus coeruleus; the reticular formation; the ventral striatum and extended amygdala; insula cortex, and other selected cortical areas. Both clinical and basic research data are covered. The conclusion is reached that the brain may work by largely nonlinear parallel processing and much intramodal shifts of attention may be effected by intracortical, or multiple corticothalamic mechanisms (small local ''flashlights'' rather than one major ''searchlight''). But this is constrained by the functional anatomy of the circuits concerned and waking ''awareness'' is modulated by the many ''nonspecific'' systems (cholinergic from the basal forebrain, noradrenergic from the locus coeruleus, dopaminergic from the substantia nigra and ventral tegmentum, and serotoninergic from the raphe). But the principal agents for intermodal attention shifts, the ''searchlight,'' may be two key nuclei of the cholinergic system in the mesencephalon. Clinical loss of consciousness results from damage to these nuclei but not from damage to the cholinergic nucleus basalis of the basal forebrain.