The phenomenon of déjà vu and mesial temporal lobe epilepsy. Clinical lecture

The déjà vu phenomenon, despite its high prevalence in the general population, is a key symptom in patients with mesial temporal lobe epilepsy (MTLE), where it occurs in 50–80 % of cases. This lecture summarizes current concepts of the neurobiological and cognitive mechanisms of déjà vu, examining it through both the model of pathology (MTLE) and its occurrence in healthy individuals. Based on a review of the literature, the article demonstrates that the hippocampal system, particularly the parahippocampal gyrus, is the central neuroanatomical substrate of déjà vu. Direct evidence comes from studies of MTLE patients, where intracranial electroencephalography and electrical stimulation unequivocally link the onset of déjà vu aura to pathological activity in the mesial temporal lobe. Cognitive models (e.g., Dual Processing, Neural Delay/Mismatch, Global Matching hypotheses) interpret déjà vu as a temporary “glitch” in memory systems, involving a dissociation between the feeling of familiarity (mediated by the perirhinal cortex) and the mechanism of detailed contextual recollection (hippocampus). The contribution of specific subregions of the hippocampal formation (dentate gyrus, СА1–СА3 fields, entorhinal cortex) to pattern separation and completion processes, whose impairment underlies false recognition, is examined. Thus, the déjà vu phenomenon serves as a unique “window” into the mechanisms of memory function. The clinical model of MTLE demonstrates its direct link to pathological activity in the mesial temporal lobe, while cognitive models explain its occurrence in healthy people because of transient dysfunction of the same hippocampal mechanisms. Future research should focus on identifying specific electrophysiological patterns and clarifying the role of impaired inhibitory control and pattern separation mechanisms in the genesis of this phenomenon.