CARL JUNG, PSYCHOLOGY AND RELIGION : WEST, ANSWER TO JOB
SIGMUND FREUD, THE PSYCHOPATHOLOGY OF EVERYDAY LIFE
Adachi, N., T. Adachi, et al. (2007). "Deja vu experiences in schizophrenia: relations with psychopathology and antipsychotic medication." Compr Psychiatry 48(6): 592-596.
To clarify why patients with schizophrenia show deja vu experiences less frequently, we studied deja vu experiences in 113 schizophrenic patients in relation to psychopathologies and antipsychotic medication. Deja vu experiences were observed in 53.1% of the schizophrenic patients. Patients with increased negative symptoms (blunted affect, motor retardation, emotional withdrawal, conceptual disorganization, and mannerisms) had deja vu experiences less frequently. The other psychopathologies were not significantly associated with presence of deja vu experiences. The dosage of antipsychotic drugs was significantly correlated with the frequency of deja vu experiences. This correlation was not affected by their psychopathologies at the time of examination. The decreased frequency of deja vu experiences in patients with schizophrenia may be mainly due to the negative symptoms. The positive relation between frequency of deja vu experiences and the dosage of neuroleptics remains uncertain.
Adachi, N., N. Akanuma, et al. (2008). "Deja vu experiences are rarely associated with pathological dissociation." J Nerv Ment Dis 196(5): 417-419.
We investigated the relation between deja vu and dissociative experiences in nonclinical subjects. In 227 adult volunteers, deja vu and dissociative experiences were evaluated by means of the inventory of deja vu experiences assessment and dissociative experiences scale (DES). Deja vu experiences occurred in 162 (71.4%) individuals. In univariate correlation analysis, the frequency of deja vu experiences, as well as 5 other inventory of deja vu experiences assessment symptoms and age at the time of evaluation, correlated significantly with the DES score. After exclusion of intercorrelative effects using multiple regression analysis, deja vu experiences did not remain in the model. The DES score was best correlated with a model that included age, jamais vu, depersonalization, and precognitive dreams. Two indices for pathological dissociation (DES-taxon and DES > or = 30) were not associated with deja vu experiences. Our findings suggest that deja vu experiences are unlikely to be core pathological dissociative experiences.
Adachi, N., N. Akanuma, et al. (2010). "Two forms of deja vu experiences in patients with epilepsy." Epilepsy Behav 18(3): 218-222.
Persons with epilepsy experience deja vu phenomena with or without seizure recognition. Deja vu experiences are also common mental phenomena in nonclinical individuals. The purpose of this study was to clarify two forms of deja vu experiences in persons with epilepsy. Deja vu experiences of 312 patients with epilepsy and 402 nonclinical individuals were evaluated using the Inventory of Deja vu Experiences Assessment. In the patients with epilepsy, characteristics of deja vu experiences with seizure recognition (SR form) were compared with those experiences with no seizure recognition (NSR form). The incidence (63.1%) of deja vu experiences in patients with epilepsy was significantly lower than that (76.1%) of nonclinical individuals (chi(2)=14.2, P=0.000). Among the patients with epilepsy, 55.6% had the NSR form and 24.0% had the SR form. Those with the NSR form manifested fewer psychopathological characteristics than did those with the SR form. Patients tended to view the SR form more negatively (i.e., frightened, uncomfortable, or disturbed) than the NSR form. The NSR form was significantly associated with idiopathic generalized epilepsies, less frequent antiepileptic drug administration, and no mesial temporal sclerosis. Although there was a significant association between the frequency of the SR form and patients' habitual seizures, the frequency of the NSR form was not associated with the frequency of the patients' habitual seizures. Persons with epilepsy experience two forms of deja vu which are differently associated with their seizure recognition.
Adachi, T., N. Adachi, et al. (2006). "Deja vu experiences in patients with schizophrenia." Compr Psychiatry 47(5): 389-393.
To investigate whether deja vu experiences are psychopathologic phenomena, we studied the frequency and characteristics of deja vu experiences in patients with schizophrenia. One hundred thirteen patients with schizophrenia and 386 nonclinical control subjects were evaluated with the Inventory of Deja vu Experiences Assessment. The frequency and features of deja vu experiences were compared between the 2 groups. The patients with schizophrenia had deja vu experiences less frequently (53.1%) than did the nonclinical subjects (76.2%). The frequency of deja vu experiences did not correlate significantly with age at evaluation or education level among the patients with schizophrenia. Most characteristics of deja vu experiences of the patients were comparable with those of the control subjects. However, the experiences of the patients tended to be longer and more monotonous. The patients often felt alert, oppressed, and disturbed by the experiences. They appeared to have the experiences under unpleasant mental or physical states. Their deja vu experiences are not primarily different in nature from those of the nonclinical subjects. The decreased frequency of the experiences in the patients may suggest deja vu experiences as nonpathologic phenomena.
Brown, A. S. (2003). "A review of the deja vu experience." Psychol Bull 129(3): 394-413.
For more than a century, the deja vu experience has been examined through retrospective surveys, prospective surveys, and case studies. About 60% of the population has experienced deja vu, and its frequency decreases with age. Deja vu appears to be associated with stress and fatigue, and it shows a positive relationship with socioeconomic level and education. Scientific explanations of deja vu fall into 4 categories: dual processing (2 cognitive processes momentarily out of synchrony), neurological (seizure, disruption in neuronal transmission), memory (implicit familiarity of unrecognized stimuli),and attentional (unattended perception followed by attended perception). Systematic research is needed on the prevalence and etiology of this culturally familiar cognitive experience, and several laboratory models may help clarify this illusion of recognition.
Cleary, A. M., A. J. Ryals, et al. (2009). "Can deja vu result from similarity to a prior experience? Support for the similarity hypothesis of deja vu." Psychon Bull Rev 16(6): 1082-1088.
The strange feeling of having been somewhere or done something before--even though there is evidence to the contrary--is called deja vu. Although deja vu is beginning to receive attention among scientists (Brown, 2003, 2004), few studies have empirically investigated the phenomenon. We investigated the hypothesis that deja vu is related to feelings of familiarity and that it can result from similarity between a novel scene and that of a scene experienced in one's past. We used a variation of the recognition-without-recall method of studying familiarity (Cleary, 2004) to examine instances in which participants failed to recall a studied scene in response to a configurally similar novel test scene. In such instances, resemblance to a previously viewed scene increased both feelings of familiarity and of deja vu. Furthermore, in the absence of recall, resemblance of a novel scene to a previously viewed scene increased the probability of a reported deja vu state for the novel scene, and feelings of familiarity with a novel scene were directly related to feelings of being in a deja vu state.
Guedj, E., S. Aubert, et al. (2010). "Deja-vu in temporal lobe epilepsy: metabolic pattern of cortical involvement in patients with normal brain MRI." Neuropsychologia 48(7): 2174-2181.
To contribute to the identification of brain regions involved in deja-vu, we studied the metabolic pattern of cortical involvement in patients with seizures of temporal lobe origin presenting with or without deja-vu. Using voxel-based analysis of 18FDG-PET brain scans, we compared glucose metabolic rate of 8 patients with deja-vu, 8 patients without deja-vu, and 20 age-matched healthy subjects. Patients were selected after comprehensive non-invasive presurgical evaluation, including normal brain MRI and surface electroclinical features compatible with unilateral temporal lobe epilepsy (TLE). Patients with and without deja-vu did not differ in terms of age, gender, epilepsy lateralization, epilepsy onset, epilepsy duration, and other subjective ictal manifestations. TLE patients with deja-vu exhibited ipsilateral hypometabolism of superior temporal gyrus and of parahippocampal region, in the vicinity of perirhinal/entorhinal cortex, in comparison either to healthy subjects or to TLE patients without deja-vu (p<0.05 FDR-corrected). By contrast, no difference was found between patient subgroups for hypometabolism of hippocampus and amygdala. At an individual-level, in comparison to healthy subjects, hypometabolism of both parahippocampal region and superior temporal gyrus was present in 7/8 patients with deja-vu. Hippocampal metabolism was spared in 3 of these 7 patients. These findings argue for metabolic dysfunction of a medial-lateral temporal network in patients with deja-vu and normal brain MRI. Within the medial temporal lobe, specific involvement of the parahippocampal region, often in the absence of hippocampal impairment, suggests that the feeling of familiarity during seizures greatly depends on alteration of the recognition memory system.
Kovacs, N., T. Auer, et al. (2009). "Neuroimaging and cognitive changes during deja vu." Epilepsy Behav 14(1): 190-196.
OBJECTIVE: The cause or the physiological role of deja vu (DV) in healthy people is unknown. The pathophysiology of DV-type epileptic aura is also unresolved. Here we describe a 22-year-old woman treated with deep brain stimulation (DBS) of the left internal globus pallidus for hemidystonia. At certain stimulation settings, DBS elicited reproducible episodes of DV. METHODS: Neuropsychological tests and single-photon-emission computed tomography (SPECT) were performed during DBS-evoked DV and during normal DBS stimulation without DV. RESULTS: SPECT during DBS-evoked DV revealed hyperperfusion of the right (contralateral to the electrode) hippocampus and other limbic structures. Neuropsychological examinations performed during several evoked DV episodes revealed disturbances in nonverbal memory. CONCLUSION: Our results confirm the role of mesiotemporal structures in the pathogenesis of DV. We hypothesize that individual neuroanatomy and disturbances in gamma oscillations or in the dopaminergic system played a role in DBS-elicited DV in our patient.
Lee, D. J., C. M. Owen, et al. (2009). "Isolated amygdala neurocysticercosis in a patient presenting with deja vu and olfactory auras. Case report." J Neurosurg Pediatr 3(6): 538-541.
Neurocysticercosis is the most common parasitic infection in the CNS and a leading cause of epilepsy. Since it is a circumscribed lesional cause of epilepsy, specific locations of neurocysticercal lesions may lead to specific clinical presentations. The authors describe a 17-year-old Hispanic boy who had a single enhancing bilobar mass in the right amygdala. Initially, the patient presented with secondarily generalized tonic-clonic seizures, which resolved with antiepilepsy drug therapy. On further investigation, he was found to have persistent olfactory and deja vu auras. A right amygdalectomy without hippocampectomy was performed, and both the seizures and auras immediately resolved. Pathological analysis revealed neurocysticercosis. To the authors' knowledge, this case is the first reported instance of 2 distinct mesial temporal aura semiologies associated with localized neurocysticercosis in the amygdala and successfully treated with resection. Uniquely, the case demonstrates that both olfactory and deja vu auras can emanate from the amygdala.
O'Connor, A. R., A. J. Barnier, et al. (2008). "Deja vu in the laboratory: a behavioral and experiential comparison of posthypnotic amnesia and posthypnotic familiarity." Int J Clin Exp Hypn 56(4): 425-450.
This experiment aimed to create a laboratory analogue of deja vu. During hypnosis, 1 group of high hypnotizables completed a puzzle game and then received a posthypnotic amnesia suggestion to forget the game (PHA condition). Another group of highs were not given the game but received a posthypnotic familiarity suggestion that it would feel familiar (PHF condition). After hypnosis, all participants were given the game and described their reactions to it. Whereas 83% of participants in both conditions passed their respective suggestions, more in the PHF condition felt a sense of deja vu. An EAT inquiry revealed that they experienced sensory fascination and confusion about the source of familiarity, akin to everyday deja vu. These findings highlight the value of using hypnosis as a laboratory analogue of deja vu and provide a framework for investigating clinical manifestations of this phenomenon.
O'Connor, A. R. and C. J. Moulin (2008). "The persistence of erroneous familiarity in an epileptic male: challenging perceptual theories of deja vu activation." Brain Cogn 68(2): 144-147.
We report the case of a 39-year-old, temporal lobe epileptic male, MH. Prior to complex partial seizure, experienced up to three times a day, MH often experiences an aura experienced as a persistent sensation of deja vu. Data-driven theories of deja vu formation suggest that partial familiarity for the perceived stimulus is responsible for the sensation. Consequently, diverting attention away from this stimulus should cause the sensation to dissipate. MH, whose sensations of deja vu persist long enough for him to shift his perceptual focus a number of times during the experience, spontaneously reports that these shifts make no difference to the sensation experienced. This novel observation challenges data-driven theories of deja vu formation which have been used to explain the occurrence of deja vu in those with temporal lobe epilepsy and the general population. Clearly, in epilepsy, erratic neuronal firing is the likely contributor, and in this paper we postulate that such brain firing causes higher-order erroneous 'cognitive feelings'. We tentatively extend this account to the general population. Rather than being a reaction to familiar elements in perceptual stimuli, deja vu is likely to be the result of a cognitive feeling borne of the erroneous activation of neural familiarity circuits such as the parahippocampal gyrus, persisting as long as this activation persists.
O'Connor, A. R. and C. J. Moulin (2010). "Recognition without identification, erroneous familiarity, and deja vu." Curr Psychiatry Rep 12(3): 165-173.
Deja vu is characterized by the recognition of a situation concurrent with the awareness that this recognition is inappropriate. Although forms of deja vu resolve in favor of the inappropriate recognition and therefore have behavioral consequences, typical deja vu experiences resolve in favor of the awareness that the sensation of recognition is inappropriate. The resultant lack of behavioral modification associated with typical deja vu means that clinicians and experimenters rely heavily on self-report when observing the experience. In this review, we focus on recent deja vu research. We consider issues facing neuropsychological, neuroscientific, and cognitive experimental frameworks attempting to explore and experimentally generate the experience. In doing this, we suggest the need for more experimentation and a more cautious interpretation of research findings, particularly as many techniques being used to explore deja vu are in the early stages of development.
Pressman, M. R. (2009). "Sleepwalking deja vu." Sleep 32(12): 1542-1543.
Taiminen, T. and S. K. Jaaskelainen (2001). "Intense and recurrent deja vu experiences related to amantadine and phenylpropanolamine in a healthy male." J Clin Neurosci 8(5): 460-462.
We report a case of a 39-year-old caucasian healthy male physician who developed intense and recurrent deja vu experiences within 24h of initiating concomitant amantadine-phenylpropanolamine treatment against influenza. Deja vu experiences terminated on discontinuation of medication. Findings in temporal epilepsy suggest that mesial temporal structures, including hippocampus, are related to paramnesic symptoms. On the other hand, previous case reports have confirmed that both amantadine and phenylpropanolamine alone, and particularly in combination, can induce psychotic symptoms due to their dopaminergic activity. The authors suggest that deja vu experiences may be provoked by increased dopamine activity in mesial temporal structures of the brain.
Thompson, R. G., C. J. Moulin, et al. (2004). "Persistent Deja vu: a disorder of memory." Int J Geriatr Psychiatry 19(9): 906-907.
Tritschler, F., E. Huntzinger, et al. (2010). "Role of GW182 proteins and PABPC1 in the miRNA pathway: a sense of deja vu." Nat Rev Mol Cell Biol 11(5): 379-384.
GW182 proteins have emerged as key components of microRNA (miRNA) silencing complexes in animals. Although the precise molecular function of GW182 proteins is not fully understood, new findings indicate that they act as poly(A)-binding protein (PABP)-interacting proteins (PAIPs) that promote gene silencing, at least in part, by interfering with cytoplasmic PABP1 (PABPC1) function during translation and mRNA stabilization. This recent discovery paves the way for future studies of miRNA silencing mechanisms.
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