Page 15 - PIECES OF THE PUZZLE Eline Vissia

Reinders et al. (2014) proposed an extended PTSD-based neurobiological model for emotion modulation in DID. It was found that hypo-aroused personality states activated the PFC, cingulate, posterior association areas and parahippocampal gyri, thereby overmodulating emotion regulation; hyper-aroused personality states activated the amygdala and insula as well as the dorsal striatum, thereby undermodulating emotion regulation. By including a PTSD group in studies of this thesis, and compare PTSD with DID, we are able to directly test the trauma model on both neuronal and psychological measures.
Etiology debate
Dissociative identity disorder is controversial (Gillig 2009) and probably the most disputed psychiatric diagnosis (Reinders 2008). For decades the disorder has been officially recognized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III (American Psychiatric Association 1980) (defined as Multiple Personality Disorder), DSM-IV (American Psychiatric Association 1994), DSM-5 (American Psychiatric Association 2013)), but many patients with DID share a history of years of misdiagnosis and various hospitalizations similar to Esther’s experience. Genuine DID patients present their dissociative symptoms with great reluctance. Because of the often mild phenomenology and the usually high shame threshold, symptoms have to be actively enquired after, as most patients do not report them spontaneously (Steinberg 1994). Only gradually, in a stable therapeutic environment, dissociative symptoms can be debriefed and explored, which has led skeptics to assume that DID has an iatrogenic origin. According to a survey among practitioners of patients with DID (Putnam et al. 1986), it took an average of seven years from the first contact with social workers to the time of adequate diagnosis, with nearly four prior other diagnoses. Under -and misdiagnosis may be related to unfamiliarity with the spectrum of dissociative disorders, disbelief that they exist, or lack of knowledge and appreciation of their epidemiology (Coons 1998, Brand et al. 2012). High comorbidity rates (Ellason, Ross 1997, Sar et al. 2004, Sar et al. 2006, Rodewald et al. 2011, Ross, Ferrell & Schroeder 2014, Bozkurt et al. 2014) complicate the diagnosis even further. To date, many clinicians and scientists still question the validity and even existence of DID (Merckelbach, Devilly & Rassin 2002, Piper, Merskey 2004a, Sar 2005, Coons 2005, Fraser 2005, Pope et al. 2006, Paris 2012, Lynn et al. 2014).
GENERAL INTRODUCTION
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