Trauma and Dissociation: Implications for Borderline Personality Disorder
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- Vermetten, E. & Spiegel, D. Curr Psychiatry Rep (2014) 16: 434. doi:10.1007/s11920-013-0434-8
Psychological trauma can have devastating consequences on emotion regulatory capacities and lead to dissociative processes that provide subjective detachment from overwhelming emotional experience during and in the aftermath of trauma. Dissociation is a complex phenomenon that comprises a host of symptoms and factors, including depersonalization, derealization, time distortion, dissociative flashbacks, and alterations in the perception of the self. Dissociation occurs in up to two thirds of patients with borderline personality disorder (BPD). The neurobiology of traumatic dissociation has demonstrated a heterogeneity in posttraumatic stress symptoms that, over time, can result in different types of dysregulated emotional states. This review links the concepts of trauma and dissociation to BPD by illustrating different forms of emotional dysregulation and their clinical relevance to patients with BPD.
KeywordsDissociationTraumaBorderline personality disorderBPDPosttraumatic stress disorderPTSDEmotion regulation
A vast but still emerging literature concerns the fact that childhood trauma and disruptions in attachment are not only common in the histories of patients with dissociative [1•] and complex posttraumatic stress disorders (PTSD)  but also among those with borderline personality disorder (BPD) [3•, 4–8, 9•, 10]. There is also growing evidence that a trauma history should be taken into account in planning treatment for BPD, which has not always been standard clinical practice. More specifically, BPD patients with trauma histories often meet criteria for both PTSD as well as dissociative disorders, which puts an emphasis on careful assessment , treatment planning  as well as detailed assessment of responses to treatment [13•]. Some authors have expressed an interest in including BPD in the list of ‘trauma spectrum disorders’ [14, 15].
Driven by new developments in biological research and the current diagnostic criteria of trauma-related disorders and in particular BPD, new opportunities for a reappraisal of the contribution of early life trauma have arisen. Critical has been a lack of acknowledgement of psychological trauma as an important factor in the psychopathology of BPD. Also, the DSM-IV-TR criteria for BPD do not adequately describe trauma-related dissociative symptomatology in the disorder. Transient, stress-related paranoid ideation or severe dissociative symptoms were listed in DSM IV as only one of nine criteria, which include a pervasive pattern of instability of interpersonal relationships, self-image, and affects and marked impulsivity characterize BPD . This is quite disproportional to the prevalence of trauma and dissociation in the disorder. A further description of dissociative symptoms or discussion of psychological trauma exposure in the diagnostic criteria for BPD is missing. In DSM5 this situation is not much different for BPD, even though quite a few changes have been made to the diagnosis of BPD as well as to Dissociative Disorders [17, 18•, 19••, 20]. In the latest revision, BPD is described as involving impairment in personality functioning, as part of identity disturbance, and (only) one reference to dissociation is made to ‘dissociative states under stress’. The concept of ‘trauma spectrum disorders’ in which BPD would be given a place next to PTSD, and dissociative disorders was proposed by some, but not adopted in the DSM-5. The initial DSM-5 metastructure proposal did include a chapter labeled Posttraumatic and Dissociative Disorders but was not pursued in the final edition. However, the Dissociative Disorders were placed next to the Trauma and Stressor-Related Disorders to indicate relationships between the two.
Impact of Childhood Trauma on Mental Health and BPD
In general, systematic reviews of the impact of childhood sexual trauma on physical and mental health have shown varied results but all point in the same direction, namely that early life trauma has a profound and long-lasting impact on a wide variety of general and mental health. This can be seen in the impressive series of adverse childhood experiences (ACE) studies started in 1998 by Felitti et al.,  as well as in a series of other systematic reviews [22, 23]. Some explanation of variance in the effect sizes of the various studies can be partially accounted for by sample source and size: smaller studies with positive findings are more likely to be published than smaller studies with null or negative findings . In terms of risk factors for anxiety disorders the evidence is particularly strong; a systematic review of 171 studies showed a significant although general and nonspecific, risk factor for anxiety disorders, especially posttraumatic stress disorder, regardless of gender of the victim and severity of abuse among those with a childhood trauma history .
The relationship between BPD and childhood trauma is documented in numerous studies. More than 25 years ago Judith Herman reported in a landmark study on high rates of trauma exposure for BPD patients: 71 % had been physically abused, 67 % sexually abused, and 62 % had witnessed domestic violence. Histories of early childhood trauma (under age six) were only present in BPD patients versus other personality disorder patients . Other estimates of the incidence of trauma in BPD typically are reported to exceed 70 % and are significantly greater than the incidence of trauma in comparison groups with other mental disorders (e.g., . In the 1990s studies emerged demonstrating that childhood histories of emotional, physical, and sexual abuse were commonly reported by patients with BPD. A general conclusion from these studies was that a relationship between childhood trauma and BPD was quite convincing [27–32], particularly if the relationship was considered as part of a multifactorial etiologic model . It must be noted however, that nearly all these studies relied on self-report.
A decade later, studies emerged in the domain of so-called complex PTSD (labeled Disorders of Extreme Stress Not Otherwise Specified, DESNOS) that described a similar clinical phenotype to BPD suggesting that exposure to multiple traumas, especially in childhood, might be related to a type of PTSD that is associated with a wide range of non-typical PTSD difficulties (e.g., impulsivity, rage, depression, self-harm, somatization, and interpersonal problems) that included dissociation as well as pathological changes in personal identity [2, 34].
Yet, while most existing research lead to a conclusion that a relationship existed between BPD and childhood sexual abuse (CSA), it was also clear that not everyone who had been sexually abused as a child would develop BPD [35, 36]. Some believed that the relationship had been overrepresented in literature and that other moderating variables were more significant in the development of the disorder . A meta-analysis of 21 studies performed between 1980 and 1995 to examine the effect size between BPD and childhood sexual abuse resulted only a moderate effect size (r = .279) between CSA and BPD. Yet, it should be noted that many sexually abused girls appear to be able to maintain adequate social competence while still suffering from high levels of internalizing and clinical symptomatology .
Traumatic Stress and Dissociative Symptomatology
During or in the immediate aftermath of acute trauma, such as a violent physical or sexual abuse, victims can report feeling dazed, unaware of physical injury, or can experience the trauma as if they were in a dream. Many rape victims report floating above their body, feeling sorry for the person being assaulted below them. One rape victim reported: ‘I heard someone screaming and discovered it was me.’ Sexually or physically abused children often report seeking comfort from imaginary playmates or imagined protectors, or by imagining themselves absorbed in the pattern of the wallpaper [38, 39]. Some continue to feel detached and disintegrated for weeks, months or years after trauma. This could lead to a kind of ‘somatic estrangement’ with changes in bodily perceptions: feeling as if one’s entire body or a part of one’s body does not belong to oneself. This typical dissociative symptomatology can include affect compartmentalization, disrupted memory encoding, and time distortion and fugue [40–42]. The disruption of a consistent stream of memory and associated personal identity has been thought of as serving a protective function, at least in response to acute stress. However, over time, these defences may start to interfere with necessary cognitive and affective processing of traumatic experiences, and as a result, lead to failure of integration of episodic and autobiographical memory [42, 43•]. The dissociative spectrum is complex: depersonalization and derealization can be seen as belonging to self-monitoring and identity. Other domains and symptoms that coincide are: (a) emotion (withdrawal/detachment), (b) memory (amnesia, shifts in memory encoding), (c) sensory perception (altered time, visual or contextual perception, proprioception, analgesia, changes in olfaction, taste) and (d) cognition (constricted attention, neglect, confusion, altered associated capacities). Dissociative symptoms are further characterized by: (a) unbidden and unpleasant intrusions into awareness and behavior, with an accompanying loss of continuity in subjective experience: i.e., ‘positive’ dissociative symptoms; and/or (b) an inability to access information or control mental functions that are normally amenable to such access or control: i.e., ‘negative’ dissociative symptoms . The more severe forms of dissociation include stupor, derealization, or depersonalization. Dissociative responses can accompany a multitude of psychiatric disorders, including PTSD, acute stress disorder (ASD), dissociative disorders, panic disorder, mood disorders, and psychoses. Based recent research [45••, 46••, 47••, 48••, 49••] a dissociative subtype has been included in the DSM-5 definition of PTSD . It involves all the intrusion, avoidance, dysphoria, and hyperarousal symptoms plus depersonalization and/or derealization. Moreover, dissociative responses have been reported to occur in several neurological conditions such as epilepsy, migraine headaches, cerebral vascular disease, cerebral neoplasms, and posttraumatic brain damage [51–54].
Traumatic dissociation has a longstanding history in both fields of psychiatry and neurology [55–57]. Not unlike what has been the situation for BPD, the psychiatric approach to the dissociative disorders for long time failed to acknowledge any relationship to psychological trauma [58••]. Before DSM III, dissociation was grouped with the old remnant of hysteria, conversion disorder, and was called ‘dissociative hysteria’. Due to this the Dissociative Disorders had difficulty shaking the suspicion that they were not true disorders, or that they were a disguise for secondary gain, malingering, or criminality. The study of dissociative disorders for long time was distanced from mainstream research. In addition, there were the so called ‘memory wars’ in the 1990s of the last century that complicated the situation as well. It was also proposed that dissociation makes individuals prone to fantasy, thereby engendering confabulated memories of trauma . However, the available research evidence contradicts this theory [58••]. There is ample evidence now of the impact of trauma on dissociative symptoms, and that dissociation remains related to trauma history, even when fantasy proneness is controlled. Little support was found for the hypothesis that the dissociation–trauma relationship is due to fantasy proneness or confabulated memories of trauma.
Co-occurrence or Trauma Subtypes?
Given the fact that early trauma is not always associated with the etiology of BPD and is also associated with many other mental disorders, it may not seem justified to categorize BPD as a trauma spectrum disorder. At the same time it is important to emphasize recognition of the role of early trauma in the assessment of mental health problems, and therefore also for BPD, even if it probably is neither a necessary nor a sufficient condition [36, 60]. Some authors proposed to extend the diagnosis of BPD to complex PTSD to characterize a subset of BPD patients with trauma-related disorders [2, 3•, 10, 61–63], in which factors such as duration of the trauma exposure, the developmental phase during which it occurred, genetic vulnerabilities, and other biological variables, in addition to specifics of the traumatic antecedent, as taken into account. Complex PTSD is defined by disturbances of affect regulation, dissociative symptoms and somatization, disturbed self-perception, disturbance of sexuality and relationship formation, and changes in personal beliefs and values. The need for and benefits of the introduction of an additional complex PTSD diagnosis is controversial, in particular because of insufficient construct validity, and potentially high overlap with other psychiatric diagnoses . Its usefulness as a clinical entity is fiercely debated in literature, and it must be clear that not all authors believe BPD is the same as complex PTSD [62, 63, 65].
Relatively few studies have rigorously assessed for both BPD and the Dissociative Disorders. A high endorsement of dissociative symptoms in BPD patients was reported by Korzekwa et al. , calling this a zone of symptomatic overlap. With regard to the dissociative experiences endorsed, most patients reported identity confusion, unexplained mood changes, and depersonalization. BPD patients with mild dissociative disorders reported derealization, depersonalization, and dissociative amnesia. BPD patients with DSM-IV Dissociative Disorder Not Otherwise Specified (DDNOS) reported frequent depersonalization, frequent amnesia, and notable experiences of identity alteration. BPD patients with comorbid Dissociative Identity Disorder (DID) endorsed severe dissociative symptoms in all categories. The authors postulate that three dissociative subgroups can be identified among persons diagnosed with BPD. The first subgroup, about one quarter to one third of BPD patients, have minimal dissociative symptoms, and if symptoms do occur, they are brief and mild. These patients have ‘minimal’ abuse histories compared to the others. The second subgroup, comprising about one third to one half of BPD patients, probably has a disorganized attachment status and a more significant abuse history [67, 68]. The third subgroup appears as the most severe. This group includes DDNOS and DID cases, comprising about 30 % to 40 % of clinical samples of BPD; they also have the most disturbed attachment and serious abuse histories. Recognizing subgroups, or subtypes to BPD are increasingly represented in other recent studies [69–72].
Emotional Modulation as Key Concept in PTSD
If dissociation is viewed as a conditioned form of emotional regulation, if follows that that this can become automatized in situations of chronicity. Moreover, it can also become habitual in response even to minor stressors that require some form of regulating of emotional information. This response process can be well described as ‘modulatory response process’ [48••, 73]. Traumatic reminders are the good examples in that these can evoke strong emotional responses. The typical response to traumatic reminders is the flashback response, in which the person becomes hyperaroused with a concomitant increase in heart rate and an intense feeling of reliving the experience as though it were occurring in the present. This calls for a regulatory system that is capable of managing (read: containing) these typically unregulated and involuntary emotional responses. Recently it has become better understood that there are different response types in individuals with chronic PTSD. These are associated with distinct neural correlates in response to recalling traumatic memories [44, 71, 74–77].
PTSD patients with histories of early, repeated or prolonged trauma, such as occurs in situations of childhood maltreatment or after prolonged combat trauma, these habitual responses can turn to differently regulated processes, and different manifestations of modulation of emotional responses. What is seen here is a predominantly dissociative response [49••] with no concomitant increase in psychophysiology, yet with feelings of depersonalization and derealization, can be labeled as emotional over-modulation. There is accumulating evidence that in chronic early trauma dissociation can be habituated (read overmodulated) to an involuntary emotion modulation strategy that can emerge in response to major and sometimes also even minor stressors.
The concept of emotional under-modulation has been proposed to emphasize the failure of inhibition of conditioned fear circuitry [48••]. While approximately 70 % of patients with PTSD report this experiencing of the traumatic event in response to traumatic script-driven imagery concomitant with psychophysiological hyperarousal [78••, 79•], it has recently been shown that a minority report symptoms of derealization, depersonalization, numbing and a feeling of emotional detachment while evidencing no significant increase in heart rate .
A closer look learns that two pathways to this emotion dysregulation can be identified: 1) the first pathway describes emotion dysregulation as an outcome of fear conditioning through stress sensitization and kindling; 2) the second pathway views emotion dysregulation as a distal vulnerability factor and hypothesizes a further exacerbation of fear and other emotion regulatory problems, including the development of PTSD after exposure to one or several traumatic event(s) later in life [80••]. Investigations of PTSD to date have focused predominantly on cross sectional studies, which are not able to directly address the causal relationships just described. However, the pathways described above pave a road map for subsequent longitudinal studies that examine this crucial causal relationship in order to elucidate the neuronal underpinnings of PTSD in a prospective manner [80••].
The model of emotional modulation has further been validated by modulation of startle reflex and electrodermal responses  as well as converging neuroimaging data from a study that compared brain activation patterns during the processing of consciously and non-consciously perceived fear stimuli . PTSD patients with high state-dissociation scores showed enhanced activation in the ventromedial prefrontal cortex (PFC) during conscious fear processing as compared to those with low state-dissociation scores. Interestingly, during processing of non-conscious fear, high dissociative symptomatology at the time of the scan in PTSD was associated with increased activation in the bilateral amygdala, insula and left thalamus as compared to those with low state-dissociation. This further supported the theory that dissociation can be seen as a regulatory emotional strategy that plays a role in coping with extreme arousal in PTSD, but also illustrated that this strategy appears to function only during conscious processing of threat.
A Dissociative Subtype of PTSD
In 1992, Judith Herman had proposed a construct, Complex PTSD (labeled Disorders of Extreme Stress Not Otherwise Specified, DESNOS) which defined a non-PTSD posttraumatic syndrome in which dissociative symptoms were a prominent feature. Although DESNOS was not included in the DSM-IV, clinicians and investigators continue to observe dissociative symptoms such as depersonalization and derealization among a significant minority of patients. Based on this as well as new research evaluating the relationship between posttraumatic stress disorder (PTSD) and dissociation has accumulated, leading to the implementation of dissociative subtype of PTSD in DSM5. This subtype is defined primarily by symptoms of derealization (i.e., feeling as if the world is not real) and depersonalization (i.e., feeling detached from oneself, or as though one were not real) .
The addition of a dissociative subtype of PTSD in the new DSM-5 was based on three lines of evidence. First, as reviewed in here neurobiological studies suggested that depersonalization and derealization responses in PTSD were distinct from the anxiety based re-experiencing/hyperarousal reactivity. The distinct neurocircuitry pattern that distinguished individuals with PTSD from those with PTSD plus dissociative symptoms also contributed to this subtype [48••]. As discussed, typically individuals who re-experienced their traumatic memory and showed concomitant psychophysiological hyperarousal exhibited reduced activation in the medial prefrontal- and the rostral anterior cingulate cortex and had increased amygdala reactivity to traumatic reminders. Their reliving responses therefore were thought to be mediated by failure of prefrontal inhibition or top-down control of limbic regions (emotional undermodulation); whereas individuals with PTSD plus dissociative symptoms demonstrated a reversal of this pattern with increased prefrontal activity associated with diminished amygdala activity (emotional overmodulation) [49••, 83••]. Second, studies using latent class, taxometric, epidemiological, and confirmatory factor analyses conducted on PTSD symptom endorsements collected from veteran and civilian PTSD samples indicated that a subgroup of individuals (roughly 15-30 %) suffering from PTSD reported symptoms of depersonalization and derealization [45••, 46••, 84••]. Individuals with the dissociative subtype were more likely to be male, have experienced repeated traumatization and early adverse experiences, have comorbid psychiatric disorders, and evidenced greater suicidality and functional impairment [47••]. The subtype was also replicated cross-culturally. The third line of evidence suggested that symptoms of depersonalization and derealization in PTSD are relevant to treatment decisions in PTSD individuals with PTSD who exhibited symptoms of depersonalization and derealization tended to respond better to treatments that included cognitive restructuring and skills training in affective and interpersonal regulation in addition to exposure-based therapies [85••, 86••]. It was felt that recognizing a dissociative subtype of PTSD carries the potential to improve the assessment and treatment outcome of patients with PTSD.
The new criteria for PTSD in DSM-5 have also moved beyond the conceptualization of PTSD as predominantly a fear response and include dysregulation of a variety of emotional states, including fear, anger, guilt, and shame in addition to dissociation and numbing [87–89]. The term ‘emotion dysregulation’ could start to be used to collectively refer to disturbances in a variety of emotional responses. A model that describes the relationship between fear circuitry and emotional modulation in PTSD had thus far been lacking.
Overlapping Emotion Modulation Strategies in PTSD and BPD?
As reviewed in the landmark work of Marsha Linehan on BPD, emotion dysregulation is considered to be a core symptom in patients with BPD [81, 90–92]. Several authors also highlighted affective instability in the disorder [93, 94] that can be seen as a downstream component of the emotional dysregulation. Emotion dysregulation has been characterized by highly sensitized responding to emotional stimuli as well as delayed habituation to such events. Only recently have studies begun to explicitly examine emotion dysregulation in BPD patients. Yet, the empirical psychophysiological and neurobiological evidence for this model in BPD has thus far been scarce. The majority of these studies exclusively focused on the patients' self-report of emotional experience . New studies indicate that, especially in BPD patients, dissociative symptoms are frequently present and may influence psychophysiological reactions to emotional stimuli [72, 81, 96] as well as neural processing of painful stimuli in response to personalized scripts . The novel perspective that recently is being proposed here is to look at emotional dysregulation represented as derealization, depersonalization and dissociative amnesia; all considered dissociative symptoms . Up until recently in many studies dissociative symptoms had not been considered to be part of the emotional spectrum of response types in BPD.
There are recent studies that investigated the moderating impact of dissociation on baseline startle response in BPD [81, 97]. In these habituation studies, the authors found overall increased startle reactivity in BPD patients relative to controls, but these group differences were modulated by participants' dissociative experiences at the beginning of the experiment. Patients experiencing no dissociative symptoms showed larger overall startle response magnitude compared with patients with high dissociative experiences. Furthermore, experimental studies found reduced pain sensitivity in patients with BPD under stress conditions [98, 99] and revealed a significant correlation between self-reported pain insensitivity and dissociative features  found no differences in emotional reactivity during an imagery task in electrodermal activity controlling for dissociation. In this study dissociation was used only as a covariate and no mediation analyses were conducted. These are the first studies to suggest that individual differences in dissociation among BPD individuals may help to explain the apparent discrepancies in the patterns of findings across psychophysiological studies.
A recent meta-analysis of neural correlates subserving negative emotionality in BPD further supported the emotion modulation dichotomy. It showed that compared with healthy control subjects, BPD patients demonstrated greater activation within the insula and posterior cingulate cortex. Conversely, they showed less activation than control subjects in a network of regions that extended from the amygdala to the subgenual anterior cingulated cortex (ACC) and dorsolateral PFC . So, when thinking of negative emotions as carrying elements of dissociation it is important to realize that these are subserved by an abnormal reciprocal relationship between limbic structures (representing the degree of dissociation or subjectively experienced negative emotion) and anterior brain regions that support the modulation or regulation of emotion [48••, 101].
It is clear that for all victims of recent childhood trauma, early intervention as well as careful monitoring over time for potential negative outcomes that may present during adulthood must be a priority to decrease the risk of psychiatric disorders. All children who have been sexually abused recently should be assessed for the presence of psychological problems. With the current state of knowledge, it is highly appropriate to target available treatment resources at symptomatic children, because sexually abused children who have symptoms (e.g., symptoms of PTSD or behavioral problems) are likely to perceive benefit from psychotherapy [102, 103]. Yet, it must be noted that services for abused children must have a long-term orientation, because these children may experience enduring problems, such as attachment problems, or BPD, or the later onset of other forms of mental illness.
For all adults with psychiatric disorders as well as with medical problems which are psychological in origin, a review of child sexual experiences should be a routine part of the clinical history. There is strong evidence, for example, that depressed individuals with trauma histories respond better to psychotherapy, while those with depression but without a trauma history respond better to antidepressant medication . Given that a certain number of individuals who seek psychiatric treatment have a history of child sexual abuse, this places a clear responsibility on mental health services in the first instance to enquire about early abuse within admission procedures.
A few years after Herman’s landmark study in 1993 Gunderson and Chu, in a paper on treatment implications of past trauma in BPD, stated that ‘when early trauma is in the form of childhood abuse, clinicians could be better able to understand the difficulties these patients experience in relational skills, affect tolerance, behavioral control, self-identity, and self-worth’. They stated that ‘clinicians should be able to facilitate a strong therapeutic alliance through acknowledgement of the patient's victimization and empathy with the effects of early trauma on the patient's life‘ . They considered it essential that the therapist reframe the patient's experience as a consequence of childhood trauma, especially when making traditional interventions like interpretation and confrontation. They also emphasized the role of trauma in the development of BPD and suggested the need for modification of models of individual, family, and group psychotherapies to allow more productive and successful treatment. Many other authors have followed since.
As has been reviewed earlier in this paper, dissociation occurs in up to two thirds of people with BPD. It is important to note that while dissociative responses during and immediately after psychological trauma are common and often adaptive, persistent dissociation that is lasting weeks, months or even years may prevent the necessary working through of traumatic memories and emotions. Individuals with dissociative symptoms often feel strangely in control of events at the time of the trauma, in an attempt to regulate their emotions in an ability to cope with the situation, but experience intrusive thoughts, flashbacks, nightmares, numbing, amnesia and hyperarousal as a kind of retraumatization. These symptoms seem to sensitize rather than produce habituation to traumatic experiences, producing and perpetuating acute stress disorder (ASD), PTSD, and dissociative disorders.
The development of dialectical behavior therapy has been based on the biosocial theory that views BPD as a dysfunction of emotion regulation system . As has been reviewed here there is new research that the emotion regulating system can have dissociative qualities, characterized by derealization and depresonalization, and that both are seen in patients with complex manifestations of PTSD. Distinguishing the dimensions of emotional modulation (over-modulation versus under-modulation) may also help to clarify differences in dissociation and affect dysregulation between and within BPD. Specific interventions addressing over-modulation in BPD, or under-modulation in PTSD, should be added to disorder-specific evidence-based treatments. There are several treatments for BPD, yet these may differentially address the under- and over-modulation of affect depending on the response type, e.g., mentalization can be seen as a therapeutic spin off of the acknowledgement of early trauma in the development of BPD [107–109]. Critical in these approaches is that the process that is started needs to be contingent on an optimal level of arousal that sustains prefrontal functioning , warranting development and recruitment of cortical structures needed to regulate emotional involvement and affective states. Successful therapy needs to engage the mental processes that make psychotherapy yield lasting change.
Trauma can trigger dissociative responses, in part because traumatic stress is a sudden discontinuity of experience, substituting threat for safety, fear, pain and uncertainty for constancy of the external and internal environment. Traumatic dissociation can be considered a unique descriptor for a set of categorically related phenomena in patients exposed to extreme traumatizing events. It relates to a breakdown of usually integrative functions. As the studies in this paper indicate, major advances have been made in our understanding of traumatic dissociation. Several lines of evidence have been put forward to understand this as a form of emotional modulation response. This perspective can serve to bridge response types that we formerly reserved for distinct disorders. We also now have more systematic measures of the dissociative phenotype, and a better understanding of the neural subsystems involved in dissociative symptoms and emotion modulation responses. The recognition that trauma is widespread in patients with BPD, the perspective of a co-occurrence with dissociative symptoms and a supportive neurobiology of emotional modulation is a result of cross fertilization of related fields in psychiatry, psychology, neurobiology, and psychophysiology. This has already opened new research for a disorder that had long been considered unsuited for this perspective. Our patients will benefit.
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Conflict of Interest
Eric Vermetten and David Spiegel declare that they have no conflict of interest.
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This article does not contain any studies with human or animal subjects performed by any of the authors.