Revisiting the etiological aspects of dissociative identity disorder: a biopsychosocial perspective

Abstract

Dissociative identity disorder (DID) is a chronic post-traumatic disorder where developmentally stressful events in childhood, including abuse, emotional neglect, disturbed attachment, and boundary violations are central and typical etiological factors. Familial, societala and cultural factors may give rise to the trauma and/or they may influence the expression of DID. Memory and the construction of self-identity are cognitive processes that appear markedly and centrally disrupted in DID and are related to its etiology. Enduring decoupling of psychological modes may create separate senses of self, and metamemory processes may be involved in interidentity amnesia. Neurobiological differences have been demonstrated between dissociative identities within patients with DID and between patients with DID and controls. Given the current evidence, DID as a diagnostic entity cannot be explained as a phenomenon created by iatrogenic influences, suggestibility, malingering, or social role-taking. On the contrary, DID is an empirically robust chronic psychiatric disorder based on neurobiological, cognitive, and interpersonal non-integration as a response to unbearable stress. While current evidence is sufficient to firmly establish this etiological stance, given the wide opportunities for innovative research, the disorder is still understudied. Comparison of well-selected samples of DID patients with non-dissociative subjects who have other psychiatric disorders would further delineate the neurobiological and cognitive features of the disorder, whereas genetic research on DID would further illuminate the interaction of the individual with environmental stress. As such, DID may be seen as an exemplary disease model of the biopsychosocial paradigm in psychiatry.