The purpose of this paper and its pair is to provide a comprehensive review, from the different perspectives of neurology and neuropsychiatry, of the phenomenology and mechanisms of hallucinatory experience in epilepsy. We emphasise the clinical and electrophysiological features, and make comparisons with the primary psychoses. In this paper, we consider definitions and elementary hallucinatory phenomena. Regarding definition, there is a clearly divergent evolution in meaning of the terms delusion, illusion and hallucination in the separate traditions of neurology and psychiatry. Psychiatry makes clear distinctions between the terms and has focussed on the empirical use of descriptive psychopathology in order to delineate the various psychiatric syndromes, including those in epilepsy. These distinctions in psychiatry have stood the test of time and are useful in clinical descriptive terms, but do not help to understand the basic mechanisms. The focus of neurology has been to regard delusions, illusions and hallucinations in epilepsy as a result of localised or network based neuronal epileptic activity that can be investigated especially using intracranial stereoelectroencephalography (SEEG). The neurological approach leads to a more synoptical definition of 'hallucination' than in psychiatry and to the conclusion that there is little point in differentiating hallucination from illusion or delusion in view of the overlap in the physiological bases of the phenomena. The semiologically derived differentiation of these terms in psychiatry is not supported by similarly discrete electrophysiological signatures. However, as discussed in the second paper, some psychotic states are associated with similar electrophysiological changes. The wide range of hallucinatory symptoms occurring during epileptic seizures recorded during intracranial SEEG and brain stimulation are reviewed here, including: experiential and interpretive phenomena, affective symptoms, as well as auditory, olfactory, gustatory, somatic and visual hallucinatory phenomena. Several conclusions can be drawn. First, it is clear that there is only limited anatomical specificity of many hallucinatory states. Repeated seizures or stimulation of a single area, even within the same patient can produce different psychic responses, whilst stimulation of widely distinct areas (especially in the limbic system) within the same individual can produce remarkably similar phenomena. This lack of specificity applies particularly to psychic symptoms, including experiential phenomena, and complex hallucinatory states. The most anatomically specific areas from this point of view are the elementary hallucinations arising from primary visual and auditory cortices. Involvement of the limbic cortex is a pre-requisite for the occurrence of complex hallucinatory states. It is clear that on the basis of these findings, as has been recognised at least since the 1960s, that even apparently focal epileptic seizures, (especially in the mesial temporal lobe, insula and limbic cortices), must involve widely distributed neuronal networks.