Jul 31, 2008

Neurological Explanations (Part 1)

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A number of researchers have suggested that a deja vu experience results from a neurological dysfunction involving seizure or a change in the speed of normal neural transmission.

Because deja vu is part of the preseizure aura in some TLEs, a logical extension is that deja vu in nonepileptic individuals results from a small temporal lobe seizure (Penfield, 1955; Stevens, 1990). In earlier research, Hughlings-Jackson (1888) attempted to determine whether deja vu was diagnostic of seizure activity, epilepsy, and brain pathology, and Maudsley (1889) suggested that those most susceptible to deja vu have a higher likelihood of developing epilepsy. Such speculation is supported by the fact that stimulation of the amygdala and hippocampus in TLEs can cause a deja vu experience (Bancaud et al., 1994; Gloor et al., 1982; Halgren et al., 1978).

However, the weight of evidence argues against deja vu being more common in people with epilepsy or being diagnostic of seizure pathology (M. A. Harper, 1969; Neppe, 1983e; Richardson & Winokur, 1967). In fact, estimates of the percentage of TLEs with deja vu as part of their aura is generally quite low (< 1% to 6%; Gupta et al., 1983; Lennox & Cobb, 1933; Mullan & Penfield, 1959; Sengoku, Toichi, & Murai, 1997; Weinand et al., 1994), and studies reporting a higher incidence (11% to 86%) usually include TLEs with intractable seizures undergoing medical procedures to correct this problem (Cole & Zangwill, 1963; Gloor et al., 1982; Halgren et al., 1978; M. Harper & Roth, 1962; Neppe,1983c). A variant of this position is that a more general, right hemisphere dysfunction results in deja vu, a conclusion stemming from the consistent observation that TLEs with deja vu have a higher probability of seizure activity originating in the right hemisphere (Cole & Zangwill, 1963; Cutting & Silzer, 1990; Gupta et al., 1983; Jackson, 1880; Mullan & Penfield, 1959; Weinand et al., 1994).

Halgren et al. (1978) used brain stimulation procedures to duplicate a number of components of the preseizure aura in TLEs, among them the deja vu experience. They speculated that during a typical seizure, a similar type of increased electrical “outflow” from the hippocampal gyrus, an area so intimately involved in encoding and retrieval, may be misinterpreted as a sensation of familiarity. Bancaud et al. (1994) supported such speculation and added that because the lateral temporal lobe receives major inputs from the visual and auditory cortices the nonspecific seizure activity in the temporal lobe combined with current sensory input results in an inappropriate feeling of familiarity.