Hallucinations occur in a great variety of neurological conditions and are facilitated by sensory loss. The common end pathway of their pathophysiology involves the activation of cortical sensory areas implicated in normal sensory processing. Based on the presumed pathophysiology, we here classify the hallucinations in four main groups. In migraine aura and epilepsy, hallucinations result from spontaneous intrinsic overactivity in hyperexcitable sensory cortical areas. Deafferentation, i.e. the loss or impairment of sensory input, facilitates hallucinations in the corresponding sensory modality, probably by leading to chronic hyperexcitability of the corresponding cortical areas. The archetypal example of this mechanism is the Charles Bonnet syndrome, where hallucinations are associated with visual impairment. A third mechanism relies on the dissociation of dream and sleep mechanism, as illustrated by hypnagogic and hypnopompic hallucinations. Finally, in the course of neurodegenerative diseases such as Parkinson's disease and dementia with Lewy bodies, hallucinations are frequent and probably result from a combination of factors, including dysfunction of both bottomup sensory processing and top-down modulatory mechanisms, as well as dream intrusion phenomena and facilitating pharmacological factors.