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Historically, the relationship between dissociation and trauma dates back to the 19th century (Briquet, 1859; Janet, 1889). Until now, the link between dissociation and posttrau-matic stress disorder (PTSD) remains a source of conceptual controversy (van der Hart, Ni-jenhuis, Steele & Brown, 2004). Dissociation refers to an alternation of the usually inte-grated functions of consciousness, memory, sense of time, body awareness, and perceptions of the environment and the self (Diagnostic and Statistical Manual of Mental Disorder-IV (DSM-IV), American Psychiatric Association, 1994). An evolutionary based model could further the understanding of trauma and dissociation (Schauer & Elbert, 2010). Being con-fronted by life threatening situations, cognitive and motivational adaption play an important role in ensuring the survival. The defense cascade model “freeze-flight-fight-fright-flag-faint” consists of adaptive processes to enhance survival (Lang, Bradley & Cuthbert, 1998).

In life threatening situations, initially, the ongoing perceptual and behavioral processes would be interrupted followed by an enhanced sensory perception towards the threatening stimulus (Graham, 1966; Sokolov, 1963). Porges (2006) suggests that the unmyelinated vagal system is responsible for the reduced cardiac output, which is associated with immobile behavior.

This defense stage presents a transient mechanism and may serve as a preparation of active defense responses such as flight or fight (Bracha, 2004). If the stimulus is threatening then the sympathetic branch of the autonomous nervous system becomes dominant and the release of sympathetic mediated adrenalin is initiated. This bodily adaption supplies the heart and muscles with the required energy for flight or fight. At the same time, the peripheral vessels constrict in order to reduce the potential blood loss in the case of injury. Further the breath-ing changes in order to supply the body optimally with oxygen. In life-threat with extreme fear and physical restraint “fright” or tonic immobility is common (Bracha, 2004). Research with laboratory animals has shown that the termination of tonic immobility is typically abrupt (Gallup, 1977). Reports about tonic immobility from rape survivors describe similar states in humans (Bovin, Jager-Hyman, Gold, Marx & Sloan, 2008; Galliano, Noble, Travis & Puechl, 1993; Fusé, Forsyth, Marx, Gallup & Weaver, 2007). The defense responses escalate as a function of proximity to danger (Bracha, 2004; Marx, Forsyth & Lexington, 2008) and of individual defense possibilities. Maximal proximity such as penile penetration during rape is associated with more dissociative responding (Johnson, Pike & Chard, 2001). Whereas an adult more likely possesses the strength or the power for flight or fight, a child is more likely to show dissociative responding (Heidt, Marx, Forsyth, 2005; Romans, Martin, Morris &

Herbison, 1999). The stages “fright-flag-faint” present further progression on the defense cascade. Dissociative responding consists of functional sensory deafferentation, motor pa-ralysis, alternations of the consciousness and loss of speech perception and production. Ap-parently, traumatic events that involve intense fear, in the presence of fluids with risk of con-tamination (e.g. blood or sperm), perceived ongoing inescability, or a high proximity to dan-ger during life-threat may provoke shutdown dissociation (Marx et al., 2008; Heidt et al., 2005; Schauer & Elbert, 2010). To shutdown the bodily system, the parasympathetic system takes over the dominance resulting in bradycardia, decrease in blood pressure and vasodilata-tion (Scaer, 2001; Schauer & Elbert, 2010). The dorsal vagal complex in the medulla may increase its activity during dissociative responding (Porges, 1995). “Fright-flag-faint” be-comes adaptive when there is no perceived possibility to “flight or fight”. It enhances the survival, because the predator may loose the interest under the assumption that the prey is dead. In contrast to the tonic immobility, the onset of shutdown dissociation is usually slow with a long recovery time. An abrupt onset can only be observed when dissociative respond-ing is conditioned (Bolles and Fanselow, 1980; Schauer & Elbert, 2010).

Figure 1.1: Schematic illustration of the defense cascade model as it progresses along the different defense stages. The active defense stages are presented on the ascent of the curve and the set of dissociative defense stages on the descent.

Introduction 15

Numerous retrospective studies show that peritraumatic dissociation plays a key role in the development of PTSD (see Ozer, Best, Lipsey, Weiss, 2003 for review; Ehlers, Mayou &

Bryant, 1998; Shalev, Peri, Canetti & Schreiber, 1996; Weiss, Marmar, Metzler, Ronfeldt, 1995). It is assumed that the peritraumatic responding is linked to a more disturbed immedi-ate memory encoding and processing of the traumatic experiences (van der Kolk & Fisler, 2007). Despite this convincing data, some studies failed to find a significant relationship between peritraumatic dissociation and subsequent PTSD (Harvey & Bryant, 2002).

Whereas a large amount of studies have focused on peritraumatic dissociation, the persistence of these symptoms was long time overlooked. The results of those studies argue for a more central role of ongoing dissociative responding (Briere, Scott & Weathers, 2005; Murray, Ehlers & Mayou, 2002; Panasetis & Bryant, 2003; Werner & Griffin, 2012). Briere, and col-leagues (2005) suggest that it is possible that peritraumatic and persistent dissociation reflect the same phenomenon, but the time course plays a critical role. Their results show, that the association of peritraumatic dissociation and PTSD vanish when the relationship was con-trolled for persistent dissociation. Ongoing dissociation pertains perceptual, somatosensoric and sensual functions (Nijenhuis, Spinhoven, van Dyck, van der Hart & Vanderlinden, 1996) and interferes with an integrative representation of the environment and the self (Schauer &

Elbert, 2010). It is likely that the ongoing disruption of integrative processes would play a key role in the development and maintenance of PTSD. Dissociative responding could then be understood on one hand as an adaption in order to survive during life-threat and on the other hand as a problem resulting in more fragmentation of the past and future memories.

The autobiographical representation of the traumatic memory is disturbed in PTSD (e.g. McNally, Lasko, Macklin, Roger & Pitman, 1995). Traumatic memories consist of sen-sory-perceptual representations as well as cognitive and physiological elements. Repeated exposure to different traumatic event types forms a fear-network that is pathologically de-tached from the context representations (information of where and when), leading to frag-mented memories in patients with PTSD (Elbert, Rockstroh, Kolassa, Schauer & Neuner, 2006). Intrusive memories as well as flashbacks can re-occur at any time when the fear-network is triggered. The intrusion can be understood as displays of elements of the trau-matic event, which can also be accompanied by the dominating physiological response during the traumatic event e.g. sympathetic arousal or dissociative symptoms (Lang, Bradley &

Cuthbert, 1998; Rockstroh & Elbert, 2010). In figure 1.2 the fear-network of one survivor of a sexual assault and vehicle accident is illustrated with both sympathetic and parasympathetic

physiological elements. With repeated exposure to different traumatic event types, the fear-network increases its interconnection between representations of different events and strengthens the network. The parasympathetically dominated shutdown of sensory, func-tional and bodily systems can reoccur whenever the fear-network is triggered e.g. in confron-tation with intrusions, minor stressors or during trauma exposure therapy. Adaptive recovery from traumatic memories requires the reactivation of the elements of the fear-network to be coupled with the contextual features. Accordingly, avoidance and dissociative responding after trauma prevent the recovery, because of suppressed affective involvement (Jaycox, Foa

& Morral, 1998).

 

Figure 1.2: Example of a fear-network memory of two different types of traumatic events (sexual assault and vehicle accident). In the upper part traumatic memory features (sensory contents in the ellipse, emotional con-tents in the pointy cloud, physiological information in the rectangle and cognitions in the think clouds) are shown. The autobiographical content is presented in the lower part. While the elements in the upper part are fairly interconnected, the autobiographical information is weakly associated to the sensory, emotional, cognitive and physiological features. The arrows in the rectangle boxes refer to sympathetic dominance ↑ and parasympa-thetic dominance ↓ of the autonomous nervous system.

Introduction 17

1.2 Dissociative Responding and its Interrelations

Current research confirms the link between dissociative responding and trauma, par-ticularly in association with severe/ multiple and/ or sexual abuse in childhood (Ginzburg et al., 2006; Heidt et al., 2005; Romans et al., 1999). Interpersonal trauma (e.g. physical and sexual assault) seem to be more associated with PTSD than other potentially traumatizing event types such as accidents or natural disasters (Kessler, Sonnega, Bromet, Hughes & Nel-son, 1995; Resnick, Kilpatrick, Dansky, Saunders & Best, 1993). Increased levels of disso-ciation were also found in refugees or battered women (Carlson & Rosser-Hogan, 1991;

Weaver & Clum, 1996). A greater exposure to trauma is related to higher levels of dissocia-tion (e.g. Briere, Hodges & Godbout, 2010; Carlson & Rosser-Hogan, 1991). Moreover, dissociative responding is associated with more severe psychopathology such as PTSD, de-pression, self-harming and suicidality (e.g. Brewin, Andrews & Valentine, 2000; Feeny, Zoellner, Fitzgibbons & Foa, 2005; Mollica, McInnes, Poole & Tor, 1998; Weber et al., 2008; Werner & Griffin, 2012). Especially, PTSD diagnosis as well as symptom severity is associated with higher levels of dissociation (e.g. Briere et al., 2010; Halligan, Michael, Clark

& Ehlers, 2003; Murray et al., 2002). The positive associations were found for all the three symptom clusters of PTSD (intrusion, avoidance and hyperarousal) and dissociative respond-ing (e.g. Steuwe, Lanius & Frewen 2012). The inherent relationship can be addressed in terms of symptom overlap of co-morbid entities. For example, emotional numbing is one of the core symptoms of PTSD, but could also be a manifestation of a severe depressive disor-der. Further, emotional numbing describes a type of abnormal affective processing in dis-sociative responding as an emotional overmodulation. Further, dissociation may reflect the severity of PTSD: the upper end of the posttrauma stress symptoms (Hyer, Albrecht, Boudewyns, Woods & Brandsma, 1993; Dalenberg & Carlson, 2012). Taken together, the inherent relationship between psychopathology argues to go beyond categorical consider-ations and to focus on continuous dimensions of the symptoms that arise after traumatic stress.

1.3 The Course of Trauma-related Dissociation

The temporal pattern of trauma-related dissociative responding provides further possibilities regarding the link between trauma and dissociation. Several studies observed the dissociative responding in the aftermath of the trauma (e.g. Cardeña & Spiegel, 1993; Dancu, Riggs, Hearst-Ikeda, Foa & Shoyer, 1996). These studies show a decline in dissociative

re-sponding as a function of the time elapsed since the traumatic event. In contrast, a study of Halligan and colleagues (2003) found that the dissociative responding could increase over the time for those who had developed a PTSD. So far no studies have assessed how cumulative trauma affects the temporal pattern, but it has been shown that dissociative symptoms play a role even after months or years after the traumatic experiences (Carlson, Dalenberg and McDade-Montez, 2012).

Evidence suggests that the exposure-based treatment outcome is lower for patients with dissociative symptoms (Jaycox et al., 1998) and that the current treatment for PTSD may be insufficient. In contrast, another study found that dissociative responding decreases with changes of the PTSD symptom severity (Lynch, Forman, Mendelsohn & Herman, 2008). This link supports the view that both types of symptoms are psychopathologically and phenomenologically related.

1.4 Measures of Dissociative Responding

Beginning in the 1980s, an immense increase of interest of dissociation spurred efforts to develop scales of dissociative responding. The first studies about dissociation in PTSD used the Dissociative Experience Scale (Bernstein & Putnam, 1986). It is a self-rating scale that contains normal and pathological dissociative states. The Dissociative Experience Scale-II represents an update of the original questionnaire with a different response format (Carlson

& Putnam, 1993). Nowadays most of the studies still apply the self-rating scale since it was translated into the most frequent languages. Waller and Ross (1997) developed a subscale of the Dissociative Experience Scale that measures the pathological dissociation. Critic has risen regarding the construct validity and longitudinal stability of the scale (Giesbrecht, Lynn, Lilienfeld & Merckelbach, 2008). There are other types of self-rating questionnaires that measure dissociative responding e.g. the Multiscale Dissociation Inventory (Briere, Weathers

& Runtz, 2005) and the Somatoform Dissociation Questionnaire (Nijenhuis et al., 1996). The Clinician-Administrated Dissociative State Scale consists of a self-rating and ratings scored by a professional observer (Bremner et al., 1998). This questionnaire was applied in several neuroimaging studies (Lanius et al., 2002; 2005). Participants that endorse at least 15 symp-toms on the Clinician-Administrated Dissociative State Scale were included in the dissoci-ative subgroup. The Dissociation Subscale of the Trauma symptom Inventory (Briere, Elliot, Harris & Cotman, 1995) was applied as well in series of studies in PTSD. Further there are structured interviews to assess diagnostic criteria of dissociative symptoms such as Structured

Introduction 19

Clinical Interview for DSM-IV (Steinberg, 1994) and Dissociative Disorder Interview Schedule (Ross et al., 1989). The Multidimensional Inventory of Dissociation is a 218-item self-administered instrument, especially for clinical research and diagnostic assessment (Dell, 2006). Further studies have focused on the peritraumatic response using retrospective self-ratings such as the Peritraumatic Dissociation Experience Questionnaire (Marmar et al., 1994; Marmar, Weiss & Metzler, 1997) or the Tonic Immobility Scale (Forsyth, Marx, Fusé, Heidt, & Gallup, 2000; Fusé et al., 2007).

To summarize, numerous measures of peritraumatic responses, persistent dissociative responses as well as diagnostic interviews of dissociative disorder exist and were applied in the context of dissociative responding in PTSD. Most of these instruments consist of self-rating items. In resource-poor settings, self-assessment seems to be unsuitable. Additionally, it is difficult to apply these questionnaires in low educated samples. We designed a struc-tured interview to assess the tendency of shutdown dissociation: the Shutdown Dissociation Scale. Based on the defense cascade model by Schauer and Elbert (2010), the parasympa-thetic dominant responses are characterized by progressive symptoms of functional sensory deafferentation, reduced nociception, numbing, motor paralysis, loss of language functions, pseudoneurological symptoms and signs of pre-syncope (e.g. vomiting). The present thesis used the Shutdown Dissociation Scale as a measurement of the severity of dissociative re-sponding (the Shutdown Dissociation Scale and administration information are attached in the appendix).

1.5 Physiological, Endocrinological and Neurobiological Differences and Correlates Research has begun to investigate the physiological, endocrinological and neurobi-ological differences as well as correlates of dissociative responding in PTSD. Larger startle responses are a robust physiological correlate of PTSD (Pole, 2007). Exaggerated physio-logical responding has also been found in samples of female nurse veterans and survivors of sexual assault (Carson et al., 2007; Metzger et al., 1999; Rothbaum, Kozak, Foa & Whitaker, 2001). Growing literature suggests that high dissociative PTSD patients show different auto-nomic responses. For example, Griffin, Resick and Mechanic (1997) examined a group of female rape survivors and found that those subjects with high peritraumatic dissociation hibit lower heart rate and skin conductance when they were talking about their traumatic ex-periences. Further studies found evidence that ongoing traumatic stressors such as family violence were correlated with reduced startle reactivity in adult women (Medina, Mejia,

Schell, Dawson & Margolin, 2001). Thus, it seems that although there is strong evidence for cardiac hyperreactivity in PTSD, there is also a significant number of studies showing an opposite hyporeactivity. It is clear that we need a different explanatory framework of PTSD and physiological response to reconcile these apparently contradictory findings. Current psy-chophysiological theories about the physiological reactivity in PTSD that could be observed in the laboratory state that it recapitulates the response that occurred during the trauma (e.g.

Lang et al., 1998). Whereas former views primarily focused on the sympathetic branch of the autonomic nervous system (DSM-IV, American Psychiatric Association, 1994; Buckely &

Kaloupek, 2001), the evolutionary based defense cascade model emphasizes that both parts of the autonomous nervous system the sympathetical and parasympathetical branch contrib-ute to the physiological responding. Thus, active defensive behavior, such as flight or fight, as well as passive defense behavior, such as fright-flag-faint, are adaptive to life-threat (Schauer & Elbert, 2010) and can therefore explain the differences in physiological studies.

Gola and colleagues (2011) investigated plasma and saliva cortisol in raped (high proximity to danger) and non-raped (lower proximity to danger) trauma survivors and found modula-tions of the cortisol response to a structured interview about the traumatic experiences. An-other study, that has focused on salivary cortisol found no evidence of differential responding during a stressful interview, but 24 hours later in high dissociative women (Koopman et al., 2003). Trauma-related symptoms such as anxiety, depression, sleep disturbances and disso-ciation predicted the cortisol responses in women in an interpersonal conflict task (Power et al., 2006). These studies suggest that dissociative responding is related to hypothalamic-pituitary-adrenal axis reactivity. Neuroimaging studies of the neuronal circuitry of traumatic memories suggest that there may be distinctive response patterns to trauma memories that distinguish individuals with dissociative from those with non-dissociative PTSD (Lanius et al., 2002; Lanius, Bluhm, Lanius & Pain, 2006). A subgroup of PTSD patients that showed more hyperarousal symptoms also displayed lower bilateral medial frontal activity and left anterior cingulate activity. Whereas a subgroup of patients with dissociative PTSD had in-creased right medial frontal, right medial prefrontal, right anterior cingulate activity com-pared to controls. The higher prefrontal activity seems to co-occur with reduced amygdala activity in dissociative PTSD. These results were interpreted as a form of emotional over-modulation in dissociative PTSD, whereas an emotional underover-modulation mediated by less intensive prefrontal inhibition of the limbic system was found in non-dissociative PTSD (Lanius et al., 2010). To summarize, the current controversial physiological and

endocri-Introduction 21

nological as well as neurophysiological findings suggest that there may be hints for a disso-ciative subtype in PTSD, but our knowledge of the role of dissodisso-ciative responding is limited.

1.6 Group Comparison or Dimensional Approaches

Methodologically, dissociative responding following posttraumatic stress can be ceptualized in a qualitative approach, comparing subtypes or in a dimensional approach con-sidering symptom severities. Although there are individual differences in dissociative re-sponding within the PTSD, the question arises whether those symptoms might predominate one distinctive subtype with elevated PTSD or whether those symptoms are distributed di-mensionally. Studies using taxometic or latent class analysis have addressed this question.

Waelde, Silvern and Fairbank (2005) examined 316 male trauma-exposed Vietnam veterans with the Dissociative Experiences Scale. They found that not all individuals who meet the criteria of PTSD, show high dissociative responding and there was a subgroup of high dis-sociative people without PTSD. Their results indicate that there is a distinctive subgroup of severe PTSD with higher levels of dissociative responding. Theses results are in line with the findings of Waller and Ross (1997). They identified a dissociative taxon that included 18%

of the PTSD sample, but the severity of PTSD was not considered in this study. In contrast to the findings, Ruscio, Ruscio and Keane (2002) found support for a continuous stress re-sponse with PTSD presenting the upper end of the dimension. Additionally, the results of the taxometric study of combat veterans (Forbes, Haslam, Willimas & Craemer, 2005) favour the uni-dimensional model of PTSD. A recent study of Wolf and colleagues (2012) examined male and female veterans that were exposed to a variety of traumatic experiences (e.g. com-bat experiences and sexual assaults). The latent structure analysis indicated a three group model (moderate, high and high PTSD coupled with dissociation) in male and female veter-ans. Furthermore, to support the subtype hypothesis, it is necessary to describe the symptom profiles and differentiating factors. Using signal detection analysis, Ginzburg and colleagues (2006) examined symptom profiles of low and high dissociative PTSD. A foreshortened fu-ture and two hyperarousal symptoms -hypervigilance and sleep difficulties- were more pro-nounced in high dissociative compared to low dissociative PTSD. A recent study by Steuwe and colleagues (2012) explored the symptom profile with a latent profile analyses and

of the PTSD sample, but the severity of PTSD was not considered in this study. In contrast to the findings, Ruscio, Ruscio and Keane (2002) found support for a continuous stress re-sponse with PTSD presenting the upper end of the dimension. Additionally, the results of the taxometric study of combat veterans (Forbes, Haslam, Willimas & Craemer, 2005) favour the uni-dimensional model of PTSD. A recent study of Wolf and colleagues (2012) examined male and female veterans that were exposed to a variety of traumatic experiences (e.g. com-bat experiences and sexual assaults). The latent structure analysis indicated a three group model (moderate, high and high PTSD coupled with dissociation) in male and female veter-ans. Furthermore, to support the subtype hypothesis, it is necessary to describe the symptom profiles and differentiating factors. Using signal detection analysis, Ginzburg and colleagues (2006) examined symptom profiles of low and high dissociative PTSD. A foreshortened fu-ture and two hyperarousal symptoms -hypervigilance and sleep difficulties- were more pro-nounced in high dissociative compared to low dissociative PTSD. A recent study by Steuwe and colleagues (2012) explored the symptom profile with a latent profile analyses and