In normal subjects, dream imagery (with sensory hallucinations) is more salient during N1 and rapid eye movement (REM) sleep than during N2–N3 sleep. The occasional leak of dream imagery into wake at sleep onset or offset is viewed as the mechanism of physiological sleep-related hallucinations. Physiological hallucinations are reported before entry into stage N1, and at sleep offset. Visual hallucinations (VHs) are reported in numerous neurological diseases.1 A non-exhaustive list includes neurodegenerative diseases (Parkinson's disease, Lewy body dementia), probably auto-immune diseases (narcolepsy, Guillain-Barré, Morvan's chorea), prion disease (fatal familial insomnia), diencephalic lesion (peduncular hallucinosis), toxic disease (delirium tremens), migraine (hallucinations are more geometrical than complex however), seizures (micropsia), and Charles Bonnet syndrome (complex hallucinations in subjects with major visual disturbances). They share common features, including the frequent vision of human figures or faces (sometimes torsos without heads or the opposite), animals (real or bizarre), sometimes in miniature, or scenery of outstanding beauty. The images are static or moving, vivid, and often silent, projected over the normal background of the room. The observer is usually immobile, and placed in darkness or poorly lighted environment. A common model of these hallucinations includes three main mechanisms: (i) direct irritation of the sensorial or integrative cortex, via epilepsy; (ii) lesions of peripheral and central visual pathway, causing defective visual input and hallucinations as a cortex release phenomenon, as in Charles Bonnet phenomenon; and (iii) brainstem lesions/dysfunctions of ascending serotonergic and cholinergic pathways, that modify the thalamocortical connections, as in peduncular hallucinosis and narcolepsy.1 The hallucinations would be, in all these cases, released or produced by the visual association cortex, hence their strikingly similar phenomenology. In addition, mental confusion, dementia or altered consciousness (that are frequent in neurological diseases) may promote the hallucinations, decrease the insight into their unreality, and favor their transformations into hallucinations-based delusions and psychoses. The consciousness is transiently altered at sleep onset. Indeed, the thalamic deactivation occurring at sleep onset most often precedes that of the cortex by several minutes in normal subjects, possibly promoting the hypnagogic hallucinations.2 In this direction, hallucinations and REM sleep behavior disorder (RBD) may represent manifestations of sleep–wake state dissociation (specifically admixtures of wakefulness and REM sleep), of close but different origins. We will review here the evidences supporting that hallucinations in several of these diseases are hypnagogic and are associated to RBD and to other REM sleep phenomena (especially status dissociatus).