The Origins of Emotion Regulation: Clinical Presentation and Neurobiology
Ruth A. Lanius
Robyn L. Bluhm
Clare Pain
Post-traumatic stress disorder (PTSD), chronic complex PTSD, and borderline personality disorder (BPD) are disorders that show significant clinical overlap; the terminology used to describe their most prominent features is also similar. Asmundson et al. (1) note that PTSD involves four identifiable symptom factors—intrusions, avoidance, dissociation or numbing, and hyperarousal—precipitated by terrifying experiences that threaten death, serious injury, or loss of physical integrity. The three major symptom factors consistently identified in BPD are impaired relatedness (unstable relationships, identity disturbance, and emptiness), behavioral dysregulation (impulsiveness and deliberate self-harm), and affect dysregulation (labile mood and excessive anger, associated with threatened abandonment) (2,3). However, in contrast to PTSD, a history of trauma is not required for a diagnosis of BPD and trauma is not inevitably present (4,5). Several symptoms of BPD and PTSD have similar features, for example, excessive irritability and anger, estrangement and chronic emptiness, emotional reactivity to specific trauma cues and in general, and dissociative symptoms. The BPD criteria generally require more marked persistence, pervasiveness, or relational instability than occur in PTSD, but current symptom levels can be similar (4). In addition, recurrent suicidal threats or behavior, recurrent self-injury, severe impulsivity, markedly unstable relationships, interpersonal manipulation, and avoidance of abandonment are features of complex PTSD and BPD rather than of PTSD alone (4).
The extent to which PTSD and BPD are related to each other and etiologically to trauma is a source of controversy, and we suggest that a better understanding of the
genesis, psychology, and neurobiology of the effects of exposure to trauma, especially during early development, will help to elucidate the relationship between them. Deficits in regulation of emotion observed in each of these disorders are central to their clinical presentation. Explication of the mechanisms of emotion regulation and dysregulation will provide new research directions and, ultimately, a better understanding of the relationship between PTSD and BPD. We note that the diagnostic criteria of both PTSD and BPD fail to capture the full clinical picture of most chronically traumatized individuals, and that the attempt to include such a disorder (disorder of extreme stress not otherwise specified, or DESNOS) in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) failed. This too contributes to the difficulty in clarifying the important clinical similarities and differences between PTSD and BPD.
genesis, psychology, and neurobiology of the effects of exposure to trauma, especially during early development, will help to elucidate the relationship between them. Deficits in regulation of emotion observed in each of these disorders are central to their clinical presentation. Explication of the mechanisms of emotion regulation and dysregulation will provide new research directions and, ultimately, a better understanding of the relationship between PTSD and BPD. We note that the diagnostic criteria of both PTSD and BPD fail to capture the full clinical picture of most chronically traumatized individuals, and that the attempt to include such a disorder (disorder of extreme stress not otherwise specified, or DESNOS) in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) failed. This too contributes to the difficulty in clarifying the important clinical similarities and differences between PTSD and BPD.
The chapter provides an overview of the epidemiology of trauma, PTSD, and BPD and then discusses the proposed role of early life experience in the development of trauma-related psychopathology. Following a brief review of the literature on attachment in infancy and its effects on adult attachment style, we review the work of Allan Schore on the neurobiology of attachment (6). Whereas Schore concentrates on the importance of stressful experiences during infancy on the development of the ability to regulate one’s emotions, we suggest that the potential for traumatic experiences to affect the developing brain may extend into adolescence and adulthood. In discussing the clinical and biologic aspects of trauma in adults, we draw on the neuroimaging literature and suggest that pathologic neural functioning in PTSD and BPD occurs in relation to pathologic emotional experiences and the subject’s response to them over time.
WHAT IS TRAUMATIC STRESS?
POST-TRAUMATIC STRESS DISORDER
The quintessential trauma-related disorder is post-traumatic stress disorder (PTSD). PTSD cannot be diagnosed in the absence of exposure to an event (or events) that cause the individual to fear for his or her life or safety, or that of another person, and to respond with feelings of intense fear, helplessness, or horror. However, differences in clinical presentation are common in PTSD patients, and comorbidity is common. Substance use disorders (7,8,9), persistent anxiety and affective disorders (10,11), eating disorders (12), borderline personality disorder (13,14), physical health impairments (15), and a significantly increased use of medical and mental health services (16) have all been associated with a diagnosis of PTSD.
The National Comorbidity Survey showed that as many as one in two individuals in the general population experiences trauma at some point in life (17). Between 10% and 25% of people exposed to psychological trauma subsequently develop PTSD, a disorder that can have debilitating effects on every facet of daily living, including sleep, work or school, and interpersonal relationships (see Chapter 16 by Kaminer and Seedat in this book) (17,18). Yet these statistics mask important gender differences in the epidemiology of PTSD. Gavranidou and Rosner (19) reviewed the literature on the epidemiology of PTSD and found that three themes were consistently reported: men are more likely than women to experience a traumatic event; the types of traumatic events experienced tend to be different for women than for men; and women are more likely than men to develop PTSD subsequent to exposure to trauma (see Chapter 16). In fact, the national comorbidity survey suggests that the lifetime prevalence of PTSD is 10.4% for women and 5% for men.
Yehuda (20) notes that the most salient characteristics of events that lead to PTSD are their severity, duration, type, and predictability. Thus, it seems that the difference in prevalence between genders may be due, in part, to differences in the types of traumatic events experienced by women and men. In particular, women are more likely than men to be abused and to experience sexual abuse as children. Men, by contrast, tend to experience traumatic events such as physical attacks and serious accidents more commonly as adults. Thus, there are differences in the types of “interpersonal” or “social” traumatic events, although there are no gender differences in the reporting of events such as natural disasters or sudden death of a partner or friend (21). Because of this, Gavranidou and Rosner (19) suggest that one explanation for the difference in prevalence of PTSD between men and women is that women are more likely to suffer events that “are subject to heavily negative social sanction.” Interestingly, Brewin, Andrews, and Valentine (22) reported in a meta-analysis of risk factors for PTSD that the gender effect, although substantial among civilians, was not significant in combat settings.
All of this discussion about the nature of trauma and the impact of traumatic events on an individual’s understanding of herself and her place in the world requires a discussion of what counts as a traumatic event. DSM-IV defines a traumatic event in terms of its emotional impact on the individual who experiences it. As described above, a traumatic event is one that causes fear for the life or safety of oneself or another individual and causes a reaction of fear, helplessness, or horror. Two individuals might experience the same event differently. Thus, an event such as a relatively minor accident or a perceived danger of assault might not be traumatic for one individual but might well be experienced as a life-threatening and traumatic event by another individual. In fact, in some cases, individuals with PTSD report precipitating events that seem minor to observers but that clearly are a source of great distress to them (23,24). This has led clinicians to believe that, in many cases, the ability to cope with relatively “minor” traumas depends on the individual’s history. In particular, women with a history of childhood abuse or neglect may lack the ability to cope with sudden stressful experience (23,24).
BORDERLINE PERSONALITY DISORDER
The term “borderline personality” was first used in 1938 by Adolph Stern to describe patients who could be diagnosed neither as neurotic nor as psychotic and who were therefore not appropriate candidates for psychoanalysis. During the 1950s and 1960s, the concept of borderline personality disorder was strongly influenced by object-relations theory. Analysts described the disorder as stemming not from the “classic” Freudian Oedipus complex but from difficulties during an earlier, narcissistic phase. The importance of Winnicott’s “good enough” mothering and later Bowlby and Ainsworth’s “secure” mother-infant attachment is emphasized in Wirth-Cauchon’s (25) recent work: “The fragile process of relating to and differentiating from the mother in the pre-oedipal period is the primary site for the construction of a sense of self or identity. Thus, any aberrations in ‘good enough’ mothering will prove disastrous for the fragile emerging self.” While the current criteria for the diagnosis of BPD concentrate solely on symptomatology and do not discuss this purported etiology, the historical association of the disorder with early difficulties in the relationship with caregiver(s) is influential.
The prevalence of BPD in the general population has been estimated to be 1.3% (26). However, one survey (27) found that in a primary care population, the
lifetime prevalence of BPD was 6.4%. Moreover, prevalence of BPD is dramatically higher in psychiatric populations: estimates for psychiatric inpatients range from 15% to 20% (28) to up to 63% (29). DSM-IV-TR also reports gender differences in the diagnosis of BPD, with approximately 75% of diagnoses occurring in women. Like PTSD, BPD is associated with extensive use of the mental heath system, as compared with other personality disorders and major depressive disorder (30). Individuals with BPD are also at high risk of self-injury or suicide (4,29).
lifetime prevalence of BPD was 6.4%. Moreover, prevalence of BPD is dramatically higher in psychiatric populations: estimates for psychiatric inpatients range from 15% to 20% (28) to up to 63% (29). DSM-IV-TR also reports gender differences in the diagnosis of BPD, with approximately 75% of diagnoses occurring in women. Like PTSD, BPD is associated with extensive use of the mental heath system, as compared with other personality disorders and major depressive disorder (30). Individuals with BPD are also at high risk of self-injury or suicide (4,29).
There is a high degree of comorbidity between BPD and PTSD. In a sample of BPD patients Zanarini, et al. (31), found that 56% had comorbid PTSD. Shea et al. (32) reported that 68% of PTSD patients in their sample also had BPD. Partly because of this comorbidity, it has been hypothesized that both disorders should be considered trauma-spectrum disorders (13,14), although this suggestion is controversial. Other authors, however, deny that BPD and PTSD are variants of the same disorder (5,31), but suggest instead that BPD predisposes individuals to vulnerability to the effects of trauma, thus placing them at risk of developing PTSD as well (33). This separation of the two disorders is congruent with the current diagnostic position of PTSD as an axis I disorder and BPD as an axis II disorder.
We suggest that this controversy can only be resolved by approaching the problem of psychological trauma from a number of different perspectives. Traditionally, the concept of psychological trauma was associated etiologically with hysteria by Freud but was developed quite differently by Janet, whose work has been “rediscovered” by van der Hart and van der Kolk (34,35,36) in the last few years, proffering possible theoretical underpinnings to dissociative phenomena. The development of attachment theory through the midtwentieth and twenty-first centuries continues to refine our understanding. However, more recently, clinicians who work from a more biologic perspective have begun to develop techniques for elucidating biologic markers associated with PTSD and BPD. These biologic approaches, which include neuroimaging and endocrinology, promise to give a new insight into the etiology of trauma-related disorders. One of the central themes of this chapter is that in order to develop an understanding of trauma and of trauma-related psychiatric disorders, it will be necessary to integrate the insights of those disciplines that have investigated trauma; no one approach on its own can be sufficient to allow us to understand or to treat the effects of trauma. In the following sections, we will discuss trauma-related disorders in terms of a deficiency in emotion regulation, from both a clinical and a neurobiologic perspective. We will describe work that links early life experiences to the process of brain maturation after birth and then turn to a consideration of neuroimaging studies that elucidate brain function associated with emotional experience in both PTSD and BPD.
ATTACHMENT AND EARLY DEVELOPMENT
Psychodynamic approaches to trauma have emphasized the importance of early experiences and their permanent effects on the developing infant. The role of mother-infant attachment has been accentuated, with deviations from “good enough” mothering etiologically linked to a number of later diagnoses, most notably borderline personality disorder.
Traditionally, developmental theorists have focused on the importance of early relationships, primarily with the mother, in helping an infant to learn how to
moderate her own affective states. Taylor, Bagby, and Parker (37) noted, “studies on attachment styles in infancy and childhood have confirmed that the sensitivity and responsiveness of the primary caregiver to the child’s emotional states is a major determinant of the way the child learns to regulate distressing affects and to relate to other people.” Securely attached children are better able than their insecurely attached counterparts to respond both behaviorally and emotionally to changing conditions in their environment (38). Such psychological theories of attachment have recently begun to be integrated with research in developmental neurobiology, primarily by Schore (6), who has offered an account of infant development that considers the effects of an infant’s environment, particularly her social environment, on brain development. Schore emphasizes that the genetically encoded developmental sequence, which provides the basis for our biologic and psychological characteristics, is not completed at the time of our birth. Rather, the most advantageous unfolding of this sequence is dependent upon the infant’s interaction with the environment. In the case of biologic development, this point seems obvious; without proper nutrition and the opportunity to move about and explore the environment, the infant’s growth and development will be suboptimal. However, the same is true for the infant’s psychological development, in particular for the emergence of a sense of self. In Schore’s view, “The relationship between the dynamics of early interactional development and the ontogeny of the emergent function for self-regulation is perhaps the most fundamental problem of development.”
moderate her own affective states. Taylor, Bagby, and Parker (37) noted, “studies on attachment styles in infancy and childhood have confirmed that the sensitivity and responsiveness of the primary caregiver to the child’s emotional states is a major determinant of the way the child learns to regulate distressing affects and to relate to other people.” Securely attached children are better able than their insecurely attached counterparts to respond both behaviorally and emotionally to changing conditions in their environment (38). Such psychological theories of attachment have recently begun to be integrated with research in developmental neurobiology, primarily by Schore (6), who has offered an account of infant development that considers the effects of an infant’s environment, particularly her social environment, on brain development. Schore emphasizes that the genetically encoded developmental sequence, which provides the basis for our biologic and psychological characteristics, is not completed at the time of our birth. Rather, the most advantageous unfolding of this sequence is dependent upon the infant’s interaction with the environment. In the case of biologic development, this point seems obvious; without proper nutrition and the opportunity to move about and explore the environment, the infant’s growth and development will be suboptimal. However, the same is true for the infant’s psychological development, in particular for the emergence of a sense of self. In Schore’s view, “The relationship between the dynamics of early interactional development and the ontogeny of the emergent function for self-regulation is perhaps the most fundamental problem of development.”
This interaction begins as early as 2 months of age. By this time, and peaking at 9 or 10 months, the infant and her mother respond to each other’s facial expressions. On the basis of the mother’s ability to modulate the infant’s response to her facial expression, the infant learns to tolerate increasingly intense positive emotions. By the age of about 10 months, when the infant is beginning to interact more with the environment, the mother’s responses to her child’s emotional state teach the infant to modulate her own emotions. Schore draws on the work of developmental psychologists who observe these mother-child interactions to argue that “the mother induces a mood modification in the infant (39) and is directly influencing the infant’s learning of ‘how to feel,’ ‘how much to feel,’ and ‘whether to feel’ about particular objects in the environment.” Schore further cites studies that indicate that this relationship promotes the maturation of specific neural circuits in the brain that are necessary for appropriate emotion regulation in the adult. The infant brain, particularly the prefrontal cortex, is a locus of great change. The development and maturation of neural circuits occur throughout infancy and are dependent upon environmental conditions; Schore believes that if these environmental conditions are outside of a certain normal range, the effects on the infant’s development are permanent.
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