A clinical correlation has been found between the experience of déjà vu and disorders such as schizophrenia and anxiety, and the likelihood of the experience increases considerably with subjects having these conditions. However, the strongest pathological association of déjà vu is with temporal lobe epilepsy. This correlation has led some researchers to speculate that the experience of déjà vu is possibly a neurological anomaly related to improper electrical discharge in the brain. As most people suffer a mild (i.e. non-pathological) epileptic episode regularly (e.g. the sudden "jolt", a hypnagogic jerk, that frequently occurs just prior to falling asleep), it is conjectured that a similar (mild) neurological aberration occurs in the experience of déjà vu, resulting in an erroneous sensation of memory.

It has been reported that certain recreational drugs increase the chances of déjà vu occurring in the user. Interestingly, some pharmacological drugs, when taken together, have also been implicated in the cause of déjà vu. Taiminen and Jääskeläinen (2001) reported the case of an otherwise healthy male who started experiencing intense and recurrent sensations of déjà vu on taking the drugs amantadine and phenylpropanolamine together to relieve flu symptoms. He found the experience so interesting that he completed the full course of his treatment and reported it to the psychologists to write-up as a case study. Due to the dopaminergic action of the drugs and previous findings from electrode stimulation of the brain (e.g. Bancaud, Brunet-Bourgin, Chauvel, & Halgren, 1994), Taiminen and Jääskeläinen speculate that déjà vu occurs as a result of hyperdopaminergic action in the mesial temporal areas of the brain.

The similarity between a déjà vu-eliciting stimulus and an existing, but different, memory trace may lead to the sensation. Thus, encountering something which evokes the implicit associations of an experience or sensation that cannot be remembered may lead to déjà vu. In an effort to experimentally reproduce the sensation, Banister and Zangwill (1941) used hypnosis to give participants posthypnotic amnesia suggestions for material they had already seen. When this was later re-encountered, the restricted activation caused by the posthypnotic amnesia resulted in three of the 10 participants reporting what the authors termed paramnesias. Memory-based explanations may lead to the development of a number of non-invasive experimental methods by which a long sought-after analogue of déjà vu can be reliable produced, in order that it can be tested under well-control experimental conditions.

In the late 19th and early 20th Centuries, it was widely believed that déjà vu could be casued by the mis-timing of neuronal firing. This timing error was thought to lead the brain to believe that it was encountering a stimulus for the second time, when in fact, it was simply re-experiencing the same event from a slightly delayed source. A number of variations of these theories exist, with miscommunication of the two cerebral hemispheres and abnormally fast neuronal firing also given as explanations for the sensation. Perhaps the most widely acknowledged neuronal theory is the optical pathway delay theory which explains déjà vu as being the product of a delayed optical input from one eye. Closely following the input from the first eye (when it should be simultaneous), this misleads conscious awareness and suggests a sensation of familiarity when there should not be one. Although intuitively plausible, this theory is untestable due to the minute times involved in neuronal firing, and inconsistent with reports that blind individuals experience déjà vu in the same way as sighted individuals (O'Connor & Moulin, 2006).

Déjà vu is associated with precognition, clairvoyance or extra-sensory perceptions, and it is frequently cited as evidence for "psychic" abilities in the general population. Non-scientific explanations attribute the experience to prophecy, visions (such as received in dreams) or past-life memories.