This disconnection syndrome implies that functional and reversible disconnection as well as anatomical and irreversible disconnection of two hemispheres can result in similar dissociative conditions, just as neural network model suggests. In this syndrome, the brain is functionally or anatomically split into two hemispheres, each of which as a module harbors an identity and act independently. However, it is to be noted that this is not what typically happens in DID. The number of identities is not limited to only two and the localizations of identities appear to be, unlike two separated hemispheres, highly superimposed or enmeshed to each other.
Another evidence supporting neural network model for dissociation is a recent study reporting that rCBF (regional cerebral blood flow) pattern changes as the switching of identities occur (Reinders, et al. 2007).If these studies suggest the localization of different identities in the brain, what about the neuroscientific substrate for the switching mechanism? Although this issue is largely unclarified yet, at least several locations of the brain are known to be related to it.
It is well known that Penfield (1952) directly stimulated temporo-parietal lobe, hippocampus and amygdala of patients under brain surgery, and some patients reported dreamy state, recollection of the past memories, and other dissociation-like symptoms etc. Since then stimulation of temporal lobe and resultant dissociative state have been reported. Recently Duggal (1999) reported a case with cerebral infarct involving right occipital lobe and right hypothalamus, who reported loss of the sense of reality and depersonalization syndrome. Duggal hypothesized a connection between occipital lobe and dissociation, and decreased function of hypothalamus and depersonalization. Simeon et al. (2000) used PET (positron emission tomography) and examined glucose metabolism and its relationship to depersonalization. They indicated that depersonalization is associated with functional abnormalities along sequential hierarchical areas of the sensory cortex (visual, auditory, and somatosensory). But there are people who suggest that symptoms associated with brain stimulation or decreased brain activities should not be understood as comparable to dissociative symptoms (Schmahl, Bohus, 2007).
Penfield, W. (1952) Memory Mechanisms. AMA Archives of Neurology and Psychiatry 67:178-198.
Duggal HS (1999) A Lesion Approach to Neurobiology of Dissociative Symptoms. Am J Psychiatry, 156;1850-1855.
Simeon D, Guralnik O, Hazlett EA, Spiegel-Cohen JM, Hollander E and Buchsbaum MS (2000) Feeling Unreal: A PET Study of Depersonalization Disorder. Am J Psychiatry, 157;1782-1788.
Schmahl C, Bohus M (2007) Translational Research Issues in Dissociation. In Eric Vermetten E, Dorahy MJ, Spiegel (Ed.) D, M.D. Arlington, Va., American Psychiatric Publishing.
Reinders AA, Nijenhuis ER, Quak J, Korf J, Haaksma J, Paans AM, Willemsen AT, and den Boer JA (2006) Psychobiological Characteristics of Dissociative.
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