![]() In a series of 32 cases, 11 manifested depersonalization, four with a left-sided focus, three with a right-sided focus, and four with general dysrhythmia (5). ![]() The epilepsy literature describes depersonalization with seizures. Some lines of evidence are consistent with this temporal lobe hypothesis of depersonalization. It is of interest that Penfield and Rasmussen postulated that depersonalization states involve an “alteration in the usual mechanism of comparison of immediate sensory perception with memory records.” “D.A.” experienced illusions of being “far off and out of this world,” produced by stimulation of the middle temporal gyrus. ![]() In “G.A.,” “queer sensations of not being present and floating away” were produced by stimulation of the superior temporal gyrus. They claimed that these perceptual illusions could be produced by stimulation of the cortex only in the temporal region, perhaps extending somewhat into the occipital cortex (p. Half a century ago, Penfield and Rasmussen (13) noted “illusions of unfamiliarity, strangeness and remoteness,” the descriptions of which reflect typical depersonalization experiences. Attempts at localizing depersonalization, although not in depersonalization disorder per se (5– 12), have yielded contradictory results regarding activation, laterality, and regional involvement. Depersonalization can be induced in subjects not suffering from the disorder by means of a pharmacological challenge with tetrahydrocannabinol (THC) (3) or the partial serotonin agonist m-CPP (4). The neurochemistry of depersonalization is poorly understood and does not provide clear indication of a neuroanatomical center. Neuropsychological testing has revealed selective deficits in attention, short-term memory, and spatial reasoning (2). Thirty subjects with DSM-III-R depersonalization disorder have been described (1), showing a mean age of onset in adolescence, an often chronic unremitting course associated with significant morbidity, frequent comorbidity with mood and anxiety disorders but no consistent association with any such disorder, and poor response to pharmacotherapy with the possible exception of benzodiazepines and selective serotonin reuptake inhibitors (SSRIs). ![]() The hallmark of depersonalization is an altered subjective experience regarding the familiarity of self and surroundings, a dissociation of perceptions with intact reality testing. These findings are in good agreement with the phenomenological conceptualization of depersonalization as a dissociation of perceptions as well as with the subjective symptoms of depersonalization disorder.Īlthough depersonalization disorder is one of the four major dissociative disorders, it is a poorly researched condition, and very little is known about its biological underpinnings. CONCLUSIONS: Depersonalization appears to be associated with functional abnormalities along sequential hierarchical areas, secondary and cross-modal, of the sensory cortex (visual, auditory, and somatosensory), as well as areas responsible for an integrated body schema. Dissociation and depersonalization scores among the subjects with depersonalization disorder were significantly positively correlated with metabolic activity in area 7B. RESULTS: Compared to the healthy subjects, subjects with depersonalization disorder showed significantly lower metabolic activity in right Brodmann’s areas 22 and 21 of the superior and middle temporal gyri and had significantly higher metabolism in parietal Brodmann’s areas 7B and 39 and left occipital Brodmann’s area 19. A cortical analysis by individual Brodmann’s areas was performed. The two groups did not differ in age, sex, education, performance on a baseline neuropsychological battery, or performance on a verbal learning task administered during fluorodeoxyglucose uptake. METHOD: Positron emission tomography scans coregistered with magnetic resonance images of eight subjects with depersonalization disorder were compared to those of 24 healthy comparison subjects. OBJECTIVE: The goal of this study was to assess brain glucose metabolism and its relationship to dissociation measures and clinical symptoms in DSM-IV depersonalization disorder.
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