15 Aug Healing of Affect Dysregulation & Dissociation with the therapeutic relationship
The concept of dissociation has a long history of bridging psychiatry, psychology, and neurology. Because dissociation is inextricably linked to trauma, theoretical and clinical models of dissociation have spanned the psycho- logical and biological realms. Although the relationship between childhood trauma and dissociation was noted at the end of the 19th century, only recently has a developmental perspective been used to understand dissocia- tion’s etiological mechanisms. Dissociative phenomena are now being viewed through an interdisciplinary lens.
There is a growing appreciation of the unique contributions that developmental models can make to psychopathogenesis. As Putnam (1995) noted, a developmental view of dissociation offers “potentially very rich models for understanding the ontogeny of environmentally produced psychiatric conditions” (p. 582). In particular, I will suggest that regulation theory (Schore, 1994, 2003a, 2003b) can provide such models. Towards that end I will draw upon (1) recent ndings about infant behavior from developmental psychology, (2) current data on brain development from neuroscience, (3) updated basic research in biological psychiatry on stress mechanisms, and (4) new information from developmental psychobiology on the essential functions of the autonomic nervous system in order to construct a model of the etiology and underly- ing psychoneurobiological mechanisms of pathological dissociation. I will use posttraumatic stress disorder as a paradigm for dissociative disorder. I will discuss the earliest expression of dissociation in human infancy— pediatric posttraumatic stress disorder—and its enduring impact on the experience-dependent maturation of the right brain, including the characterological use of disso- ciation at later points of interpersonal stress.
There is a growing appreciation of the unique contributions that developmental models can make to psychopathogenesis. As Putnam (1995) noted, a developmental view of dissociation offers “potentially very rich models for understanding the ontogeny of environmentally produced psychiatric conditions” (p. 582). In particular, I will suggest that regulation theory (Schore, 1994, 2003a, 2003b) can provide such models. Towards that end I will draw upon (1) recent ndings about infant behavior from developmental psychology, (2) current data on brain development from neuroscience, (3) updated basic research in biological psychiatry on stress mechanisms, and (4) new information from developmental psychobiology on the essential functions of the autonomic nervous system in order to construct a model of the etiology and underly- ing psychoneurobiological mechanisms of pathological dissociation. I will use posttraumatic stress disorder as a paradigm for dissociative disorder. I will discuss the earliest expression of dissociation in human infancy— pediatric posttraumatic stress disorder—and its enduring impact on the experience-dependent maturation of the right brain, including the characterological use of disso- ciation at later points of interpersonal stress.
Dissociation and the Dissociative Disorders
is defined by DSM-IV as “a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment” (American Psychiatric Association, 1994) and by the 10th edition of the International Classification of Diseases (ICD-10) as “a partial or complete loss of the normal integration between memories of the past, awareness of identity and immediate sensations, and control of body movements” (World Health Organization, 1992). Although both stress a deficit in integration, only ICD-10 includes an alteration of bodily processes. Finally, Spiegel and Cardeña (1991) characterized dissociation as “a structured separation of mental processes (e.g., thoughts, emotions, conation, memory, and identity) that are ordinarily integrated” (p. 367). Note that Spiegel and Cardeña include emotion in their definition of dissociation, whereas DSM-IV and ICD-10 did not.
The concept of dissociation can be directly traced to the work of Pierre Janet. Janet (1887, 1889) considered (pathological) dissociation to be a phobia of memories that was expressed as excessive or inappropriate physical responses to thought or memories of old traumas (see Van der Hart & Dorahy, this volume). This dissociation of cognitive, sensory, and motor processes is adaptive in the context of overwhelming traumatic experience, and yet such unbearable emotional reactions result in an altered state of consciousness. Janet described an abaissement du niveau mental, a lowering of the mental level, a regression to a state that is constricted and disunified. Furthermore, Janet speculated that dissociation was the result of a deficiency of psychological energy. Due to early developmental factors, the quantity of psychological energy is lowered below a critical point, and thus individuals with pathological dissociation are deficient in binding together all their mental functions into an organized unity under the control of the self.
Following Charcot (1887), Janet also posited that early trauma is a fundamental psychopathogenic factor in the etiology of hysteria. Freud (1893/1955), who cited Janet in his early pre-psychoanalytic work, defined dissociation as a splitting of consciousness, frequently associated with bizarre physical symptoms. Although Freud initially considered developmental trauma to be essential to hysteria, he soon rejected this idea and posited that repression— not dissociation—was the primary psychopathogenic mechanism.
Summarizing the essentials of Janet’s model, Van der Kolk, Weisaeth, and Van der Hart stated:
Janet proposed that when people experience “vehment emotions,” their minds may become incapable ofmatching their frightening experiences with existing cognitive schemes. As a result the memories of the experience cannot be integrated into personal awareness; instead, they are split off [fusion_builder_container hundred_percent=”yes” overflow=”visible”][fusion_builder_row][fusion_builder_column type=”1_1″ background_position=”left top” background_color=”” border_size=”” border_color=”” border_style=”solid” spacing=”yes” background_image=”” background_repeat=”no-repeat” padding=”” margin_top=”0px” margin_bottom=”0px” class=”” id=”” animation_type=”” animation_speed=”0.3″ animation_direction=”left” hide_on_mobile=”no” center_content=”no” min_height=”none”][dissociated] from consciousness and voluntary control … extreme emotional arousal results in failure to integrate traumatic memories. … The memory traces of the trauma linger as unconscious “ fixed ideas” that cannot be “liquidated” … they continue to intrude as terrifying perceptions, obsessional preoccupations, and somatic reexperiences.
The concept of dissociation can be directly traced to the work of Pierre Janet. Janet (1887, 1889) considered (pathological) dissociation to be a phobia of memories that was expressed as excessive or inappropriate physical responses to thought or memories of old traumas (see Van der Hart & Dorahy, this volume). This dissociation of cognitive, sensory, and motor processes is adaptive in the context of overwhelming traumatic experience, and yet such unbearable emotional reactions result in an altered state of consciousness. Janet described an abaissement du niveau mental, a lowering of the mental level, a regression to a state that is constricted and disunified. Furthermore, Janet speculated that dissociation was the result of a deficiency of psychological energy. Due to early developmental factors, the quantity of psychological energy is lowered below a critical point, and thus individuals with pathological dissociation are deficient in binding together all their mental functions into an organized unity under the control of the self.
Following Charcot (1887), Janet also posited that early trauma is a fundamental psychopathogenic factor in the etiology of hysteria. Freud (1893/1955), who cited Janet in his early pre-psychoanalytic work, defined dissociation as a splitting of consciousness, frequently associated with bizarre physical symptoms. Although Freud initially considered developmental trauma to be essential to hysteria, he soon rejected this idea and posited that repression— not dissociation—was the primary psychopathogenic mechanism.
Summarizing the essentials of Janet’s model, Van der Kolk, Weisaeth, and Van der Hart stated:
Janet proposed that when people experience “vehment emotions,” their minds may become incapable ofmatching their frightening experiences with existing cognitive schemes. As a result the memories of the experience cannot be integrated into personal awareness; instead, they are split off [fusion_builder_container hundred_percent=”yes” overflow=”visible”][fusion_builder_row][fusion_builder_column type=”1_1″ background_position=”left top” background_color=”” border_size=”” border_color=”” border_style=”solid” spacing=”yes” background_image=”” background_repeat=”no-repeat” padding=”” margin_top=”0px” margin_bottom=”0px” class=”” id=”” animation_type=”” animation_speed=”0.3″ animation_direction=”left” hide_on_mobile=”no” center_content=”no” min_height=”none”][dissociated] from consciousness and voluntary control … extreme emotional arousal results in failure to integrate traumatic memories. … The memory traces of the trauma linger as unconscious “ fixed ideas” that cannot be “liquidated” … they continue to intrude as terrifying perceptions, obsessional preoccupations, and somatic reexperiences.
In Janet’s view, traumatized individuals seem to have lost their capacity to assimilate new experiences as well. It is … as if their personality development has stopped at a certain point, and cannot enlarge any more by the addition of new elements. (1911, p. 532) Translating Janet’s concept of personality into contemporary terms, Van der Kolk, Van der Hart, and Marmar concluded that “Dissociation refers to a compartmentalization of experience: Elements of a trauma are not integrated into a unitary whole or an integrated sense of self ”.
At the dawn of modern psychiatry, many major pioneers (e.g., Charcot, Janet, Freud, Hughlings Jackson) were interested in the neurology of dissociation (i.e., its structure-function relationships). Devinsky (2000) has noted that late 19th-century clinicians linked the right hemisphere with emotion (Luys, 1881) and dissociative phenomena (Myers, 1885; Richer, 1881); he cited Jackson’s (1876) work on the duality of the brain, and the role of the right hemisphere in “emotional” speech, as opposed to the left hemisphere’s “voluntary expression and conscious awareness of propositional speech.” Dissociative psychopathology continues to be a focus of the epilepsy literature. Patients with intractable epilepsy show high rates of “dissociative convulsions” (De Wet et al., 2003), and “dissociative pseudoseizures” are common sequelae of traumatic experiences (Harden, 1997), especially in patients with histories of sexual and physical abuse (Alper et al., 1993) and diagnoses of personality disorders and depression (Bowman & Markand, 1996).
Recently, Brown and Trimble (2000) have argued that we must move beyond a purely descriptive approach: “The rst goal must be to provide a precise de nition of dissociation based on a conceptually coherent and empirically justified account of the processes underlying these phenomena” (p. 288). Other investigators have made similar assertions:
At the dawn of modern psychiatry, many major pioneers (e.g., Charcot, Janet, Freud, Hughlings Jackson) were interested in the neurology of dissociation (i.e., its structure-function relationships). Devinsky (2000) has noted that late 19th-century clinicians linked the right hemisphere with emotion (Luys, 1881) and dissociative phenomena (Myers, 1885; Richer, 1881); he cited Jackson’s (1876) work on the duality of the brain, and the role of the right hemisphere in “emotional” speech, as opposed to the left hemisphere’s “voluntary expression and conscious awareness of propositional speech.” Dissociative psychopathology continues to be a focus of the epilepsy literature. Patients with intractable epilepsy show high rates of “dissociative convulsions” (De Wet et al., 2003), and “dissociative pseudoseizures” are common sequelae of traumatic experiences (Harden, 1997), especially in patients with histories of sexual and physical abuse (Alper et al., 1993) and diagnoses of personality disorders and depression (Bowman & Markand, 1996).
Recently, Brown and Trimble (2000) have argued that we must move beyond a purely descriptive approach: “The rst goal must be to provide a precise de nition of dissociation based on a conceptually coherent and empirically justified account of the processes underlying these phenomena” (p. 288). Other investigators have made similar assertions:
Attachment Trauma and the Developing Right Brain
A precise definition of the term “dissociation” must be established, based on a coherent and empirically checkable concept. Furthermore, it is important to discover the primary pathophysiologic mechanism that leads to the dissociative symptoms, using neurobiological research mechanisms. (Prueter, Schultz-Venrath, & Rimpau, 2002, p. 191)
Over the last few decades a few authors have pro- posed neurobiological models of dissociation in adults. Whitlock (1967) and Ludwig (1972) suggested that the primary pathophysiological mechanism of dissocia- tive symptoms is an attentional dysfunction that results from an increase in the corticofugal inhibition of afferent stimulation. This inhibition impairs the processing of essential information, which subsequently fails to be inte- grated into awareness, and thereby generates dissociative symptoms. More recently J. Krystal et al. (1998), Scaer (2001), and Nijenhuis, Van der Hart, and Steele (2002) have made contributions to the psychobiology of dissoci- ation (see also Nijenhuis & Den Boer, 2008, this volume). Current neuroimaging research is also contributing new information about the structure-function relationships of dissociation in mature brain systems.
Several important observations about dissociation have been advanced. In psychological studies of adults, Loewenstein noted that “Dissociation is conceptualized as a basic part of the psychobiology of the human trauma response: a protective activation of altered states of con- sciousness in reaction to overwhelming psychological trauma” (1996, p. 312). In neuropsychiatric studies of adult trauma patients, Bremner and colleagues demon- strated that (1) there are two subtypes of acute trauma response, hyperarousal and dissociation (1999), (2) disso- ciation represents an effective short-term strategy that is detrimental to long-term functioning (Bremner & Brett, 1997), and (3) extreme stress invokes neural mechanisms that produce long-term alterations of brain functioning (Krystal et al., 1998). Finally, Meares concluded that “dissociation, at its rst occurrence, is a consequence of a ‘psychological shock’ or high arousal” (1999, p. 1853).
I will offer evidence that each of the above observa- tions about dissociation in adults applies to infants as well. I will argue that developmental studies offer (1) specific models of the process whereby early trauma alters the human ontogenetic trajectory and creates a predispo- sition for later pathological dissociation. These models, in turn, afford a deeper understanding of the neurobio- logical mechanisms of dissociation. I believe that attach- ment theory, “the dominant approach to understanding early socioemotional and personality development during the past quarter-century of research” (Thompson, 1990,p. 145), best describes the interactions among develop- ment, trauma, and dissociation. Disorganized-disoriented insecure attachment, a primary risk factor for the devel- opment of psychiatric disorders (Main, 1996), has been speci cally implicated in the etiology of the dissociative disorders (Chefetz, 2004; Liotti, 2004; Schore, 1997). Longitudinal attachment studies have demonstrated an association between traumatic childhood events and proneness to dissociation (Ogawa et al., 1997).
Over the last few decades a few authors have pro- posed neurobiological models of dissociation in adults. Whitlock (1967) and Ludwig (1972) suggested that the primary pathophysiological mechanism of dissocia- tive symptoms is an attentional dysfunction that results from an increase in the corticofugal inhibition of afferent stimulation. This inhibition impairs the processing of essential information, which subsequently fails to be inte- grated into awareness, and thereby generates dissociative symptoms. More recently J. Krystal et al. (1998), Scaer (2001), and Nijenhuis, Van der Hart, and Steele (2002) have made contributions to the psychobiology of dissoci- ation (see also Nijenhuis & Den Boer, 2008, this volume). Current neuroimaging research is also contributing new information about the structure-function relationships of dissociation in mature brain systems.
Several important observations about dissociation have been advanced. In psychological studies of adults, Loewenstein noted that “Dissociation is conceptualized as a basic part of the psychobiology of the human trauma response: a protective activation of altered states of con- sciousness in reaction to overwhelming psychological trauma” (1996, p. 312). In neuropsychiatric studies of adult trauma patients, Bremner and colleagues demon- strated that (1) there are two subtypes of acute trauma response, hyperarousal and dissociation (1999), (2) disso- ciation represents an effective short-term strategy that is detrimental to long-term functioning (Bremner & Brett, 1997), and (3) extreme stress invokes neural mechanisms that produce long-term alterations of brain functioning (Krystal et al., 1998). Finally, Meares concluded that “dissociation, at its rst occurrence, is a consequence of a ‘psychological shock’ or high arousal” (1999, p. 1853).
I will offer evidence that each of the above observa- tions about dissociation in adults applies to infants as well. I will argue that developmental studies offer (1) specific models of the process whereby early trauma alters the human ontogenetic trajectory and creates a predispo- sition for later pathological dissociation. These models, in turn, afford a deeper understanding of the neurobio- logical mechanisms of dissociation. I believe that attach- ment theory, “the dominant approach to understanding early socioemotional and personality development during the past quarter-century of research” (Thompson, 1990,p. 145), best describes the interactions among develop- ment, trauma, and dissociation. Disorganized-disoriented insecure attachment, a primary risk factor for the devel- opment of psychiatric disorders (Main, 1996), has been speci cally implicated in the etiology of the dissociative disorders (Chefetz, 2004; Liotti, 2004; Schore, 1997). Longitudinal attachment studies have demonstrated an association between traumatic childhood events and proneness to dissociation (Ogawa et al., 1997).
Current neurobiological models of attachment focus on the formation of the implicit self system, located in the early maturing right brain (Schore, 1994, 2001a). Researchers now assert that fearful arousal and the rela- tional modulation of that arousal lie at the heart of attach- ment theory, and that relational trauma triggers states of hyperarousal and dissociation in the developing brain. I will show that abuse and neglect elicit dissociative defenses in the developing infant. As such, they represent a deleterious in uence during the critical growth period of cortical, limbic, brainstem, and autonomic centers in the early maturing right brain.
Janet’s ideas about early trauma and dissociation are strongly supported by recent developmental studies. A traumatizing caregiver negatively impacts the child’s attachment security, strategies for coping with stress, and sense of self (Crittenden & Ainsworth, 1989; Erickson, Egeland, & Pianta, 1989). There is substantial and con- vincing evidence that childhood trauma arrests affective development; conversely, trauma in adulthood produces a regression in affective development (H. Krystal, 1988). The most signi cant consequence of early relational trauma is the child’s failure to develop the capacity for emotional self-regulation (Toth & Cicchetti, 1998); the child (and subsequent adult) cannot adequately regulate affective intensity and duration (Van der Kolk & Fisler, 1994). This chapter contends that these established prin- ciples of early emotional development must be incorpo- rated into an overarching model of dissociation.
THE NEUROBIOLOGY OF SECURE ATTACHMENT
The essential task of the first year of human life is the creation of a secure attachment bond between the infant and his/her primary caregiver. Secure attachment depends upon the mother’s psychobiological attunement with the infant’s internal states of arousal. Through visual-facial, gestural, and auditory-prosodic communication, caregiver and infant learn the rhythmic structure of the other and modify their behavior to fit that structure, thereby cocreating a specifically fitted interaction. During the bodily based affective communications of mutual gaze, the attuned mother synchronizes the spatiotemporal patterning of her exogenous sensory stimulation with the infant’s spontaneous expressions of endogenous organismic rhythms. Via this contingent responsivity, the mother appraises the nonverbal expressions of her infant’s internal arousal and affective states, regulates them, and communicates them to the infant. To accomplish this, the mother must successfully modulate nonoptimal high or nonoptimal low levels of stimulation which would induce superheightened or extremely low levels of arousal in the infant.
Janet’s ideas about early trauma and dissociation are strongly supported by recent developmental studies. A traumatizing caregiver negatively impacts the child’s attachment security, strategies for coping with stress, and sense of self (Crittenden & Ainsworth, 1989; Erickson, Egeland, & Pianta, 1989). There is substantial and con- vincing evidence that childhood trauma arrests affective development; conversely, trauma in adulthood produces a regression in affective development (H. Krystal, 1988). The most signi cant consequence of early relational trauma is the child’s failure to develop the capacity for emotional self-regulation (Toth & Cicchetti, 1998); the child (and subsequent adult) cannot adequately regulate affective intensity and duration (Van der Kolk & Fisler, 1994). This chapter contends that these established prin- ciples of early emotional development must be incorpo- rated into an overarching model of dissociation.
THE NEUROBIOLOGY OF SECURE ATTACHMENT
The essential task of the first year of human life is the creation of a secure attachment bond between the infant and his/her primary caregiver. Secure attachment depends upon the mother’s psychobiological attunement with the infant’s internal states of arousal. Through visual-facial, gestural, and auditory-prosodic communication, caregiver and infant learn the rhythmic structure of the other and modify their behavior to fit that structure, thereby cocreating a specifically fitted interaction. During the bodily based affective communications of mutual gaze, the attuned mother synchronizes the spatiotemporal patterning of her exogenous sensory stimulation with the infant’s spontaneous expressions of endogenous organismic rhythms. Via this contingent responsivity, the mother appraises the nonverbal expressions of her infant’s internal arousal and affective states, regulates them, and communicates them to the infant. To accomplish this, the mother must successfully modulate nonoptimal high or nonoptimal low levels of stimulation which would induce superheightened or extremely low levels of arousal in the infant.
If attachment is the regulation of interactive synchrony, then attachment stress is an asynchrony in that interac- tional synchrony. In optimal interpersonal contexts, fol- lowing such stress, a period of reestablished synchrony allows the child to recover his/her regulatory equilib- rium. Resilience in the face of stress is an ultimate indi- cator of attachment security. The regulatory processes of affect synchrony in a secure attachment relationship (1) cocreate positive arousal and (2) repair states of negative arousal. Thus, attachment represents biological regula- tion between and within organisms.
Research supports the proposal (Schore, 1994) that the long-enduring regulatory effects of attachment are due to their impact on brain development. According to Ziabreva et al. (2003): [T]he mother functions as a regulator of the socio- emotional environment during early stages of postnatal development … subtle emotional regulatory interac- tions, which obviously can transiently or permanently alter brain activity levels … may play a critical role dur- ing the establishment and maintenance of limbic system circuits. (p. 5334)
I have suggested that the attachment mechanism is embedded in infant-caregiver right-hemisphere-to-right- hemisphere affective transactions (Schore, 1994, 2000, 2003a, 2003b). Because (1) the human limbic system myelinates in the rst year and a half (Kinney et al., 1988) and (2) the early-maturing right hemisphere (Allman et al., 2005; Bogolepova & Malofeeva, 2001; Chiron et al., 1997; Geschwind & Galaburda, 1987)—which is deeply connected into the limbic system (Tucker, 1992)—is undergoing a growth spurt at this time, attachment expe- riences speci cally impact limbic and cortical areas of the developing right cerebral hemisphere (Henry, 1993; Schore, 1994, 2005b; Siegel, 1999; Wang, 1997).
This model accounts for a body of recent develop- mental neurobiological research. At two months of age, the onset of a critical period during which synaptic connections in the developing occipital cortex are modi- ed by visual experience (Yamada et al., 1997, 2000), infants show right hemispheric activation when exposed to a woman’s face (Tzourio-Mazoyer, 2002). The devel- opment of the capacity to ef ciently process informa- tion from faces requires visual input to the right (and not left) hemisphere during infancy (Le Grand et al., 2003), and mutual gaze activates face-processing areas of the right hemisphere (Pelphrey, Viola, & McCarthy, 2004; Watanabe, Miki, & Kakigi, 2002). Spontaneous gestures that express feeling states communicated within a dyad also activate right hemispheric structures (Gallagher & Frith, 2004). With respect to prosody, the tendency of mothers to cradle infants on their left side “facilitates the ow of affective information from the infant via the left ear and eye to the center for emotional decoding, that is, the right hemisphere of the mother” (Manning et al., 1997, p. 327). Finally, the human maternal response to an infant’s cry is accompanied by activation of the mother’s right brain (Lorberbaum et al., 2002).
Research supports the proposal (Schore, 1994) that the long-enduring regulatory effects of attachment are due to their impact on brain development. According to Ziabreva et al. (2003): [T]he mother functions as a regulator of the socio- emotional environment during early stages of postnatal development … subtle emotional regulatory interac- tions, which obviously can transiently or permanently alter brain activity levels … may play a critical role dur- ing the establishment and maintenance of limbic system circuits. (p. 5334)
I have suggested that the attachment mechanism is embedded in infant-caregiver right-hemisphere-to-right- hemisphere affective transactions (Schore, 1994, 2000, 2003a, 2003b). Because (1) the human limbic system myelinates in the rst year and a half (Kinney et al., 1988) and (2) the early-maturing right hemisphere (Allman et al., 2005; Bogolepova & Malofeeva, 2001; Chiron et al., 1997; Geschwind & Galaburda, 1987)—which is deeply connected into the limbic system (Tucker, 1992)—is undergoing a growth spurt at this time, attachment expe- riences speci cally impact limbic and cortical areas of the developing right cerebral hemisphere (Henry, 1993; Schore, 1994, 2005b; Siegel, 1999; Wang, 1997).
This model accounts for a body of recent develop- mental neurobiological research. At two months of age, the onset of a critical period during which synaptic connections in the developing occipital cortex are modi- ed by visual experience (Yamada et al., 1997, 2000), infants show right hemispheric activation when exposed to a woman’s face (Tzourio-Mazoyer, 2002). The devel- opment of the capacity to ef ciently process informa- tion from faces requires visual input to the right (and not left) hemisphere during infancy (Le Grand et al., 2003), and mutual gaze activates face-processing areas of the right hemisphere (Pelphrey, Viola, & McCarthy, 2004; Watanabe, Miki, & Kakigi, 2002). Spontaneous gestures that express feeling states communicated within a dyad also activate right hemispheric structures (Gallagher & Frith, 2004). With respect to prosody, the tendency of mothers to cradle infants on their left side “facilitates the ow of affective information from the infant via the left ear and eye to the center for emotional decoding, that is, the right hemisphere of the mother” (Manning et al., 1997, p. 327). Finally, the human maternal response to an infant’s cry is accompanied by activation of the mother’s right brain (Lorberbaum et al., 2002).
THE NEUROBIOLOGY OF RELATIONAL TRAUMA
Optimal attachment communications directly affect the maturation of (1) the central nervous system (CNS) lim- bic system that processes and regulates social-emotional stimuli and (2) the autonomic nervous system (ANS) that generates the somatic aspects of emotion. It is important to stress that a growth-facilitating emotional environment is required for a child to develop an internal system that can adaptively regulate arousal and other psychobiologi- cal states (and thereby affect, cognition, and behavior), The good-enough mother offers her securely attached infant access to her after a separation; she tends to respond appropriately and promptly to his/her emotional expressions. She also allows high levels of positive affect to be generated during co-shared play states. Such events as these support an expansion of the child’s coping capacities and illustrate why secure attachment is the primary defense against trauma-induced psychopathology.
In contrast to caregivers who foster secure attachment, abusive caregivers not only play less, but also induce enduring negative affect in the child. Such caregivers provide little protection against other environmental impingements, including that of an abusive father. This caregiver is emotionally inaccessible, given to inappropriate and/or rejecting responses to her infant’s expressions of emotions and stress, and provides minimal or unpredictable regulation of the infant’s states of overarousal. Instead, she induces extreme levels of stimulation and arousal (i.e., the very high stimulation of abuse and/or the very low stimulation of neglect). And finally, because she provides no interactive repair, she leaves the infant to endure intense negative states for long periods of time.
Optimal attachment communications directly affect the maturation of (1) the central nervous system (CNS) lim- bic system that processes and regulates social-emotional stimuli and (2) the autonomic nervous system (ANS) that generates the somatic aspects of emotion. It is important to stress that a growth-facilitating emotional environment is required for a child to develop an internal system that can adaptively regulate arousal and other psychobiologi- cal states (and thereby affect, cognition, and behavior), The good-enough mother offers her securely attached infant access to her after a separation; she tends to respond appropriately and promptly to his/her emotional expressions. She also allows high levels of positive affect to be generated during co-shared play states. Such events as these support an expansion of the child’s coping capacities and illustrate why secure attachment is the primary defense against trauma-induced psychopathology.
In contrast to caregivers who foster secure attachment, abusive caregivers not only play less, but also induce enduring negative affect in the child. Such caregivers provide little protection against other environmental impingements, including that of an abusive father. This caregiver is emotionally inaccessible, given to inappropriate and/or rejecting responses to her infant’s expressions of emotions and stress, and provides minimal or unpredictable regulation of the infant’s states of overarousal. Instead, she induces extreme levels of stimulation and arousal (i.e., the very high stimulation of abuse and/or the very low stimulation of neglect). And finally, because she provides no interactive repair, she leaves the infant to endure intense negative states for long periods of time.
The infant has two psychobiological response patterns to trauma: hyperarousal and dissociation (Perry et al., 1995; Schore, 1997). Beebe describes the “mutually escalating overarousal” of a disorganized attachment pair: Each one escalates the ante, as the infant builds to a frantic distress, may scream, and, in this example, finally throws up. In an escalating overarousal pattern, even after extreme distress signals from the infant, such as ninety-degree head aversion, arching away … or screaming, the mother keeps going. (2000, p. 436)
In this initial stage of threat, the child’s alarm or startle reaction indicates activation of the infant’s right hemisphere (Bradley, Cuthbert, & Lang, 1996). This, in turn, evokes a sudden increase of ANS sympathetic activity, resulting in significantly elevated heart rate, blood pressure, and respiration. Distress is expressed in crying and then screaming. Crying represents an autonomic response to stress, whereby the nucleus ambiguus of the right vagus excites both the right side of the larynx and the sinoatrial node of the heart (Porges et al., 1994).
The infant’s state of frantic distress, or what Perry terms fear-terror, is mediated by sympathetic hyperarousal that is expressed in increased secretion of corticotropin releasing factor (CRF)—the brain’s major stress hormone. CRF regulates sympathetic catecholamine activity (Brown et al., 1982). Thus, brain adrenaline, noradrenaline, and dopamine levels are signicantly elevated, creating a hypermetabolic state within the developing brain. In addition, there is increased secretion of vasopressin, a hypotha- lamic neuropeptide that is released when the environment is perceived to be unsafe and challenging (Kvetnansky et al., 1989, 1990).
Hyperarousal is the infant’s first reaction to stress. Dissociation is a later reaction to trauma, wherein the child disengages from the stimuli of the external world. Traumatized infants are observed to be “staring off into space with a glazed look”: [W]hen infants’ attempts fail to repair the interaction infants often lose postural control, withdraw, and self- comfort. The disengagement is profound even with this short disruption of the mutual regulatory process and break in intersubjectivity. The infant’s reaction is reminiscent of the withdrawal of Harlow’s isolated monkey or of the infants in institutions observed by Bowlby and Spitz. (Tronick & Weinberg, 1997, p. 66)
In this initial stage of threat, the child’s alarm or startle reaction indicates activation of the infant’s right hemisphere (Bradley, Cuthbert, & Lang, 1996). This, in turn, evokes a sudden increase of ANS sympathetic activity, resulting in significantly elevated heart rate, blood pressure, and respiration. Distress is expressed in crying and then screaming. Crying represents an autonomic response to stress, whereby the nucleus ambiguus of the right vagus excites both the right side of the larynx and the sinoatrial node of the heart (Porges et al., 1994).
The infant’s state of frantic distress, or what Perry terms fear-terror, is mediated by sympathetic hyperarousal that is expressed in increased secretion of corticotropin releasing factor (CRF)—the brain’s major stress hormone. CRF regulates sympathetic catecholamine activity (Brown et al., 1982). Thus, brain adrenaline, noradrenaline, and dopamine levels are signicantly elevated, creating a hypermetabolic state within the developing brain. In addition, there is increased secretion of vasopressin, a hypotha- lamic neuropeptide that is released when the environment is perceived to be unsafe and challenging (Kvetnansky et al., 1989, 1990).
Hyperarousal is the infant’s first reaction to stress. Dissociation is a later reaction to trauma, wherein the child disengages from the stimuli of the external world. Traumatized infants are observed to be “staring off into space with a glazed look”: [W]hen infants’ attempts fail to repair the interaction infants often lose postural control, withdraw, and self- comfort. The disengagement is profound even with this short disruption of the mutual regulatory process and break in intersubjectivity. The infant’s reaction is reminiscent of the withdrawal of Harlow’s isolated monkey or of the infants in institutions observed by Bowlby and Spitz. (Tronick & Weinberg, 1997, p. 66)
Winnicott (1958) holds that a particular failure of the maternal holding environment causes a discontinuity in the baby’s need for “going-on-being.” Kestenberg (1985) refers to dead spots in the infant’s subjective experience, an operational de nition of dissociation’s restriction of consciousness.
The child’s dissociation in the midst of terror involves numbing, avoidance, compliance, and restricted affect (the same pattern as adult PTSD). This parasympathet- ic-dominant state of conservation-withdrawal occurs in helpless and hopeless stressful situations in which the individual becomes inhibited and strives to avoid attention in order to become “unseen” (Schore, 1994, 2001b). This state of metabolic shutdown is a primary regulatory process that is used throughout the life span. In conservation-withdrawal, the stressed individual passively disengages in order “to conserve energies … to foster survival by the risky posture of feigning death, to allow healing of wounds and restitution of depleted resources by immobility” (Powles, 1992, p. 213). This parasympathetic mecha- nism mediates the “profound detachment” (Barach, 1991) of dissociation. If early trauma is experienced as “psychic catastrophe” (Bion, 1962), then dissociation is a “detachment from an unbearable situation” (Mollon, 1996), “the escape when there is no escape” (Putnam, 1997), “a last resort defensive strategy” (Dixon, 1998).
The neurobiology of dissociative hypoarousal is different from than of hyperarousal. In this passive state of pain-numbing and pain-blunting, endogenous opiates (Fanselow, 1986) are elevated. The dorsal vagal complex in the brainstem medulla is activated, which decreases blood pressure, metabolic activity, and heart rate— despite increases in circulating adrenaline. This elevated parasympathetic arousal is a survival strategy (Porges, 1997) that allows the infant to maintain homeostasis in the face of the internal state of sympathetic hyperarousal. It is seldom acknowledged that (1) parasympathetic energy-conserving hypoarousal and (2) sympathetic energy-expending hyperarousal are both Janetian states of “extreme emotional arousal.”
Although vagal tone is defined as “the amount of inhibitory influence on the heart by the parasympathetic nervous system” (Field et al., 1995), it is now known that there are two parasympathetic vagal systems. The late- developing “mammalian” or “smart” ventral vagal system in the nucleus ambiguus enables contingent social interactions via the ability to communicate with facial expressions, vocalizations, and gestures. The early developing “reptilian” or “vegetative” system in the dorsal motor nucleus of the vagus shuts down metabolic activity during immobilization, death feigning, and hiding behaviors (Porges, 1997). As opposed to the mammalian ventral vagal complex that can rapidly regulate cardiac output to foster engagement and disengagement with the social environment, the reptilian dorsal vagal complex “contributes to severe emotional states and may be related to emotional states of ‘immobilization’ such as extreme terror” (Porges, 1997, p. 75).
The child’s dissociation in the midst of terror involves numbing, avoidance, compliance, and restricted affect (the same pattern as adult PTSD). This parasympathet- ic-dominant state of conservation-withdrawal occurs in helpless and hopeless stressful situations in which the individual becomes inhibited and strives to avoid attention in order to become “unseen” (Schore, 1994, 2001b). This state of metabolic shutdown is a primary regulatory process that is used throughout the life span. In conservation-withdrawal, the stressed individual passively disengages in order “to conserve energies … to foster survival by the risky posture of feigning death, to allow healing of wounds and restitution of depleted resources by immobility” (Powles, 1992, p. 213). This parasympathetic mecha- nism mediates the “profound detachment” (Barach, 1991) of dissociation. If early trauma is experienced as “psychic catastrophe” (Bion, 1962), then dissociation is a “detachment from an unbearable situation” (Mollon, 1996), “the escape when there is no escape” (Putnam, 1997), “a last resort defensive strategy” (Dixon, 1998).
The neurobiology of dissociative hypoarousal is different from than of hyperarousal. In this passive state of pain-numbing and pain-blunting, endogenous opiates (Fanselow, 1986) are elevated. The dorsal vagal complex in the brainstem medulla is activated, which decreases blood pressure, metabolic activity, and heart rate— despite increases in circulating adrenaline. This elevated parasympathetic arousal is a survival strategy (Porges, 1997) that allows the infant to maintain homeostasis in the face of the internal state of sympathetic hyperarousal. It is seldom acknowledged that (1) parasympathetic energy-conserving hypoarousal and (2) sympathetic energy-expending hyperarousal are both Janetian states of “extreme emotional arousal.”
Although vagal tone is defined as “the amount of inhibitory influence on the heart by the parasympathetic nervous system” (Field et al., 1995), it is now known that there are two parasympathetic vagal systems. The late- developing “mammalian” or “smart” ventral vagal system in the nucleus ambiguus enables contingent social interactions via the ability to communicate with facial expressions, vocalizations, and gestures. The early developing “reptilian” or “vegetative” system in the dorsal motor nucleus of the vagus shuts down metabolic activity during immobilization, death feigning, and hiding behaviors (Porges, 1997). As opposed to the mammalian ventral vagal complex that can rapidly regulate cardiac output to foster engagement and disengagement with the social environment, the reptilian dorsal vagal complex “contributes to severe emotional states and may be related to emotional states of ‘immobilization’ such as extreme terror” (Porges, 1997, p. 75).
There is now agreement that sympathetic nervous system activity manifests in tight engagement with the external environment and high level of energy mobilization and utilization, while the parasympathetic component drives disengagement from the external environment and utilizes low levels of internal energy (Recordati, 2003). Perry’s description of the traumatized infant’s sudden switch from high-energy sympathetic hyperarousal to low-energy parasympathetic dissociation is re ected in Porges’s characterization of the sudden and rapid transition from an unsuccessful strategy of struggling requiring massive sympathetic activation to the metabolically conservative immobilized state mimicking death associated with the dorsal vagal complex. (1997, p. 75)
Similarly, H. Krystal has described the switch from sympathetic hyperaroused terror to parasympathetic hypoaroused hopelessness and helplessness: The switch from anxiety to the catatonoid response is the subjective evaluation of the impending danger as one that cannot be avoided or modi ed. With the perception of fatal helplessness in the face of destructive danger, one surrenders to it. (1988, p. 114–115) Whereas the nucleus ambiguus exhibits rapid and transitory patterns (associated with perceptive pain and unpleasantness), the dorsal vagal nucleus exhibits an involuntary and prolonged pattern of vagal out flow. This prolonged dorsal vagal parasympathetic activation explains the lengthy “void” states that are associated with pathological dissociative detachment (Allen, Console, & Lewis, 1998).
DEVELOPMENTAL NEUROPSYCHOLOGY OF DISSOCIATION
How are the trauma-induced alterations of the developing right brain expressed in the socioemotional behavior of a traumatized toddler? Main and Solomon’s (1986) classic study of attachment in traumatized infants revealed a new attachment category, Type D, an insecure-disorganized/ disoriented pattern that occurs in 80% of maltreated
Similarly, H. Krystal has described the switch from sympathetic hyperaroused terror to parasympathetic hypoaroused hopelessness and helplessness: The switch from anxiety to the catatonoid response is the subjective evaluation of the impending danger as one that cannot be avoided or modi ed. With the perception of fatal helplessness in the face of destructive danger, one surrenders to it. (1988, p. 114–115) Whereas the nucleus ambiguus exhibits rapid and transitory patterns (associated with perceptive pain and unpleasantness), the dorsal vagal nucleus exhibits an involuntary and prolonged pattern of vagal out flow. This prolonged dorsal vagal parasympathetic activation explains the lengthy “void” states that are associated with pathological dissociative detachment (Allen, Console, & Lewis, 1998).
DEVELOPMENTAL NEUROPSYCHOLOGY OF DISSOCIATION
How are the trauma-induced alterations of the developing right brain expressed in the socioemotional behavior of a traumatized toddler? Main and Solomon’s (1986) classic study of attachment in traumatized infants revealed a new attachment category, Type D, an insecure-disorganized/ disoriented pattern that occurs in 80% of maltreated
infants (Carlson et al., 1989). Type D attachment is also associated with pre- and/or postnatal maternal alcohol or cocaine use (Espinosa et al., 2001; O’Connor, Sigman, & Brill, 1987). Hesse and Main (1999) noted that Type D disorganization and disorientation is phenotypically sim- ilar to dissociative states. Main and Solomon (1986) con- cluded that Type D infants have low stress tolerance and that their disorganization and disorientation indicate that the infant is alarmed by the parent. Because infants inevi- tably seek the parent when alarmed, Main and Solomon concluded that frightening parents placed infants in an irresolvable bind wherein they could neither approach their parents, shift their attention, nor ee. These infants are utterly unable to generate a coherent way to cope with their frightening parents.
Main and Solomon detailed the uniquely bizarre behaviors of 12-month-old Type D infants in the Strange Situation procedure. These infants displayed brief (fre- quently only 10 to 30 seconds) but signi cant inter- ruptions of organized behavior. At such times, Type D infants may exhibit a contradictory behavior pattern such as “backing” toward the parent rather than approaching face-to-face.
The impression in each case was that approach move- ments were continually being inhibited and held back through simultaneous activation of avoidant tendencies. In most cases, however, proximity-seeking suf ciently over- rode avoidance to permit the increase in physical proxim- ity. Thus, contradictory patterns were activated but were not mutually inhibited (Main & Solomon, 1986, p. 117).
Notice the simultaneous activation of the energy- expending sympathetic and energy-conserving para- sympathetic components of the ANS. Maltreated infants exhibit apprehension, confusion, and very rapid shifts of state during the Strange Situation. Main and Solomon describe the child’s entrance into a dissociated state: One infant hunched her upper body and shoulders at hearing her mother’s call, then broke into extravagant laugh-like screeches with an excited forward movement. Her braying laughter became a cry and distress-face without a new intake of breath as the infant hunched forward. Then suddenly she became silent, blank and dazed. (1986, p. 119)
These behaviors are not restricted to the infant’s interactions with the mother; the intensity of the baby’s dysregulated affective state is often heightened when the infant is exposed to the added stress of an unfamiliar person. At a stranger’s entrance, two infants moved away from both mother and stranger to face the wall; another “leaned forehead against the wall for several seconds, looking back in apparent terror.” These infants exhibit “behavioral stilling,” that is, “dazed” behavior and depressed affect. These are behavioral manifestations of dissociation. One infant “became for a moment exces- sively still, staring into space as though completely out of contact with self, environment, and parent.” Another showed “a dazed facial appearance … accompanied by a stilling of all body movement, and sometimes a freez- ing of limbs which had been in motion.” Yet another “fell face-down on the oor in a depressed posture prior to separation, stilling all body movements.” Guedeney and Fermanian (2001) have developed an alarm distress scale that assesses the sustained withdrawal that is asso- ciated with disorganized attachment; it assesses frozen, absent facial expression; total avoidance of eye contact; immobility; absence of vocalization; absence of relating to others; and the impression that the child is beyond reach.
Main and Solomon detailed the uniquely bizarre behaviors of 12-month-old Type D infants in the Strange Situation procedure. These infants displayed brief (fre- quently only 10 to 30 seconds) but signi cant inter- ruptions of organized behavior. At such times, Type D infants may exhibit a contradictory behavior pattern such as “backing” toward the parent rather than approaching face-to-face.
The impression in each case was that approach move- ments were continually being inhibited and held back through simultaneous activation of avoidant tendencies. In most cases, however, proximity-seeking suf ciently over- rode avoidance to permit the increase in physical proxim- ity. Thus, contradictory patterns were activated but were not mutually inhibited (Main & Solomon, 1986, p. 117).
Notice the simultaneous activation of the energy- expending sympathetic and energy-conserving para- sympathetic components of the ANS. Maltreated infants exhibit apprehension, confusion, and very rapid shifts of state during the Strange Situation. Main and Solomon describe the child’s entrance into a dissociated state: One infant hunched her upper body and shoulders at hearing her mother’s call, then broke into extravagant laugh-like screeches with an excited forward movement. Her braying laughter became a cry and distress-face without a new intake of breath as the infant hunched forward. Then suddenly she became silent, blank and dazed. (1986, p. 119)
These behaviors are not restricted to the infant’s interactions with the mother; the intensity of the baby’s dysregulated affective state is often heightened when the infant is exposed to the added stress of an unfamiliar person. At a stranger’s entrance, two infants moved away from both mother and stranger to face the wall; another “leaned forehead against the wall for several seconds, looking back in apparent terror.” These infants exhibit “behavioral stilling,” that is, “dazed” behavior and depressed affect. These are behavioral manifestations of dissociation. One infant “became for a moment exces- sively still, staring into space as though completely out of contact with self, environment, and parent.” Another showed “a dazed facial appearance … accompanied by a stilling of all body movement, and sometimes a freez- ing of limbs which had been in motion.” Yet another “fell face-down on the oor in a depressed posture prior to separation, stilling all body movements.” Guedeney and Fermanian (2001) have developed an alarm distress scale that assesses the sustained withdrawal that is asso- ciated with disorganized attachment; it assesses frozen, absent facial expression; total avoidance of eye contact; immobility; absence of vocalization; absence of relating to others; and the impression that the child is beyond reach.
Dissociation in infants has also been studied with the still-face procedure, an experimental paradigm of trau- AQ1 matic neglect (see Figure 8.1). In the still-face procedure, the infant is exposed to a severe relational stressor; the
mother maintains eye contact with the infant, but she suddenly inhibits all vocalization and suspends all emo- tionally expressive facial expressions and gestures. This triggers an initial increase of interactive behavior and arousal in the infant. According to Tronick (2004), the infant’s confusion and fearfulness at the break in con- nection is accompanied by the idea that “this is threat- ening.” This is rapidly followed by bodily collapse, loss of postural control, withdrawal, gaze aversion, sad facial expression, and self-comforting behavior.
Most interestingly, this behavior is accompanied by a “dissipation of the infant’s state of consciousness” and a diminishment of self-organizing abilities that re ect “disorganization of many of the lower level psychobio- logical states, such as metabolic systems.” Recall that dissociation, a hypometabolic state, has been de ned in the DSM as “a disruption in the usually integrated func- tions of consciousness” and described as “a protective activation of altered states of consciousness in reaction to overwhelming psychological trauma” (Loewenstein, 1996). Tronick (2004) suggests that infants who have a history of chronic breaks of connections exhibit an “extremely pathological state” of emotional apathy; she equates this state with Spitz’s concept of hospitalism and Romanian orphans who fail to grow and develop. Such infants ultimately adopt a communication style of “stay away, don’t connect.” This defensive stance is a very early forming, yet already chronic, pathological dissociation that is associated with loss of ventral vagal activation and dominance of dorsal vagal parasympa- thetic states.
Most interestingly, this behavior is accompanied by a “dissipation of the infant’s state of consciousness” and a diminishment of self-organizing abilities that re ect “disorganization of many of the lower level psychobio- logical states, such as metabolic systems.” Recall that dissociation, a hypometabolic state, has been de ned in the DSM as “a disruption in the usually integrated func- tions of consciousness” and described as “a protective activation of altered states of consciousness in reaction to overwhelming psychological trauma” (Loewenstein, 1996). Tronick (2004) suggests that infants who have a history of chronic breaks of connections exhibit an “extremely pathological state” of emotional apathy; she equates this state with Spitz’s concept of hospitalism and Romanian orphans who fail to grow and develop. Such infants ultimately adopt a communication style of “stay away, don’t connect.” This defensive stance is a very early forming, yet already chronic, pathological dissociation that is associated with loss of ventral vagal activation and dominance of dorsal vagal parasympa- thetic states.
The still-face induction of hyperarousal and dissocia- tion occurs face-to-face with the mother. The mother’s face is the most potent visual stimulus in the child’s world; it is well known that direct gaze can mediate not only loving, but aggressive messages. Hesse and Main (1999, p. 511) described a mother’s frightening behavior: “in non-play contexts, stiff-legged ‘stalking’ of infant on all fours in a hunting posture; exposure of canine tooth accompanied by hissing; deep growls directed at infant.” Thus, during the trauma, the infant is presented with an aggressive expression on the mother’s face. Both the image of this aggressive face and the associated altera- tions in the infant’s bodily state are indelibly imprinted into limbic circuits; they are stored in the imagistic pro- cedural memory of the visuospatial right hemisphere, the locus of implicit (Hugdahl, 1995) and autobiographical (Fink et al., 1996; Greenberg et al., 2005; Markowitsch et al., 2000) memory.
Main and Solomon (1986) noted that Type D infants often encounter a second kind of disturbing maternal behavior: a maternal expression of fear-terror. This occurs when the mother withdraws from the infant as though the infant were frightening; such mothers of Type D infants exhibit dissociated, trancelike, and fearful behavior. Current studies have shown a link between frightening maternal behavior, dissociation, and disorganized infant attachment (Schuengel, Bakersmans-Kranenburg, & Van IJzendoorn, 1999). In recent work, Hesse and Main observe that when the mother enters a dissociative state, a fear alarm state is triggered in the infant. The caregiver’s entrance into the dissociative state is expressed as “par- ent suddenly completely ‘freezes’ with eyes unmoving, half-lidded, despite nearby movement; parent addresses infant in an ‘altered’ tone with simultaneous voicing and devoicing” (2006, p. 320). In describing the mother as she submits to the freeze state, they note:
Here the parent appears to have become completely unresponsive to, or even aware of, the external surround, including the physical and verbal behavior of their infant. … [W]e observed one mother who remained seated in an immobilized and uncomfortable position with her hand in the air, blankly staring into space for 50 sec. (p. 321)
Main and Solomon (1986) noted that Type D infants often encounter a second kind of disturbing maternal behavior: a maternal expression of fear-terror. This occurs when the mother withdraws from the infant as though the infant were frightening; such mothers of Type D infants exhibit dissociated, trancelike, and fearful behavior. Current studies have shown a link between frightening maternal behavior, dissociation, and disorganized infant attachment (Schuengel, Bakersmans-Kranenburg, & Van IJzendoorn, 1999). In recent work, Hesse and Main observe that when the mother enters a dissociative state, a fear alarm state is triggered in the infant. The caregiver’s entrance into the dissociative state is expressed as “par- ent suddenly completely ‘freezes’ with eyes unmoving, half-lidded, despite nearby movement; parent addresses infant in an ‘altered’ tone with simultaneous voicing and devoicing” (2006, p. 320). In describing the mother as she submits to the freeze state, they note:
Here the parent appears to have become completely unresponsive to, or even aware of, the external surround, including the physical and verbal behavior of their infant. … [W]e observed one mother who remained seated in an immobilized and uncomfortable position with her hand in the air, blankly staring into space for 50 sec. (p. 321)
During these episodes, I suggest that the infant is matching the rhythmic structures of the mother’s dysreg- ulated states, and that this synchronization is registered in the ring patterns of the stress-sensitive corticolim- bic regions of the infant’s brain, especially in the right brain, which is in a critical period of growth. It has been established that maternal care in uences both the infant’s reactivity (Menard et al., 2004) and the infant’s defen- sive responses to threat; these “serve as the basis for the transmission of individual differences in stress responses from mother to offspring” (Weaver et al., 2004, p. 847). Because many mothers suffer from unresolved trauma, their chaotic and dysregulated alterations of state become imprinted into the developing brain and self-system of the child. This is the psychopathogenetic mechanism for the intergenerational transmission of (1) trauma and (2) dissociative defenses against overwhelming and dysregu- lating affective states.
RIGHT BRAIN PROCESSES AND DISSOCIATION THROUGHOUT THE LIFE SPAN
Early traumatic attachment takes place when infants and toddlers repeatedly encounter massive misattunement from caregivers who trigger (and do not repair) long- lasting intensely dysregulated states in the child. The growth-inhibiting environment of relational trauma generates dense and prolonged levels of negative affect associated with extremely stressful states of hyper- and hypoarousal. In self-defense the child severely restricts overt expression of attachment need and signi cantly reduces the output of the emotion-processing, limbic- centered, attachment system. When the child is stressed, defensive functions are rapidly initiated that quickly shift the brain from interactive regulatory modes into long- enduring, less complex autoregulatory modes. These patterns are primitive strategies for survival that remain online for long intervals of time, periods in which the developing brain is in a hypometabolic state that is detri- mental to the substantial amounts of energy required for critical period biosynthetic processes. This hypometabolic brain state (Janetian de ciency of psychological energy) causes dissociative “encoding failures” (Allen et al., 1998) in the autobiographical memory of the developing self.
Attachment trauma thus sets the stage for charac- terological use of primitive autoregulation—that is, pathological dissociation during subsequent stages of development. In accord with this model, (1) severe early maternal dysfunction is associated with high dissociation in psychiatric patients (Draijer & Langeland, 1999); (2) physical abuse and parental dysfunction by the mother— not the father—is associated with somatoform dissocia- tive symptoms (Roelofs et al., 2002); and (3) individuals with Type D attachment utilize dissociative behaviors in later stages of life (Van IJzendoorn et al., 1999). Allen and Coyne describe the characterological use of dissociation:
RIGHT BRAIN PROCESSES AND DISSOCIATION THROUGHOUT THE LIFE SPAN
Early traumatic attachment takes place when infants and toddlers repeatedly encounter massive misattunement from caregivers who trigger (and do not repair) long- lasting intensely dysregulated states in the child. The growth-inhibiting environment of relational trauma generates dense and prolonged levels of negative affect associated with extremely stressful states of hyper- and hypoarousal. In self-defense the child severely restricts overt expression of attachment need and signi cantly reduces the output of the emotion-processing, limbic- centered, attachment system. When the child is stressed, defensive functions are rapidly initiated that quickly shift the brain from interactive regulatory modes into long- enduring, less complex autoregulatory modes. These patterns are primitive strategies for survival that remain online for long intervals of time, periods in which the developing brain is in a hypometabolic state that is detri- mental to the substantial amounts of energy required for critical period biosynthetic processes. This hypometabolic brain state (Janetian de ciency of psychological energy) causes dissociative “encoding failures” (Allen et al., 1998) in the autobiographical memory of the developing self.
Attachment trauma thus sets the stage for charac- terological use of primitive autoregulation—that is, pathological dissociation during subsequent stages of development. In accord with this model, (1) severe early maternal dysfunction is associated with high dissociation in psychiatric patients (Draijer & Langeland, 1999); (2) physical abuse and parental dysfunction by the mother— not the father—is associated with somatoform dissocia- tive symptoms (Roelofs et al., 2002); and (3) individuals with Type D attachment utilize dissociative behaviors in later stages of life (Van IJzendoorn et al., 1999). Allen and Coyne describe the characterological use of dissociation:
Although initially they may have used dissociation to cope with traumatic events, they subsequently dissoci- ate to defend against a broad range of daily stressors, including their own posttraumatic symptoms, perva- sively undermining the continuity of their experience. (1995, p. 620)
This psychic-deadening defense is maladaptive not only because the individual resorts to dissociation at low levels of stress, but also nds it dif cult to exit this state of conservation-withdrawal. During these episodes, the person is impermeable to attachment communications and interactive regulation. This deprives the person of input that is vital to emotional development. Dissociative detachment (Allen et al., 1998) thus becomes an attractor state whereby social intimacy is habitually deemed to be dangerous (because such intimacy is always a potential trigger of “vehement emotions”). The avoidance of emo- tional connections, especially those that contain novel and complex affective information, prevents emotional learning; this, in turn, precludes advances in right brain emotional intelligence (Schore, 2001a) or what Janet (1889) called “enlargement” of personality development.
A fundamental question that must be addressed in any developmental model of dissociation is: What is the pre- cise mechanism by which the early psychological events of “maltreatment-related” (Beer & De Bellis, 2002) or “pediatric” (Carrion et al., 2001) posttraumatic stress disorder affect the later behavior of the self system as it develops at further stages of the life cycle? I maintain that a purely psychological conception cannot answer this question; a psychoneurobiological perspective that integrates both biological structure and psychologi- cal function is required. Research clearly indicates that “the overwhelming stress of maltreatment in childhood is associated with adverse in uences on brain develop- ment” (1999, p. 1281).
During the rst years of life when the right brain is growing (Trevarthen, 1996) and dominant (Chiron et al., 1997), adverse in uences on brain development particu- larly impact the right brain (Allman et al., 2005). During this time, states of the infant brain become traits (Perry et al., 1995); thus, early relational trauma and dissociation
This psychic-deadening defense is maladaptive not only because the individual resorts to dissociation at low levels of stress, but also nds it dif cult to exit this state of conservation-withdrawal. During these episodes, the person is impermeable to attachment communications and interactive regulation. This deprives the person of input that is vital to emotional development. Dissociative detachment (Allen et al., 1998) thus becomes an attractor state whereby social intimacy is habitually deemed to be dangerous (because such intimacy is always a potential trigger of “vehement emotions”). The avoidance of emo- tional connections, especially those that contain novel and complex affective information, prevents emotional learning; this, in turn, precludes advances in right brain emotional intelligence (Schore, 2001a) or what Janet (1889) called “enlargement” of personality development.
A fundamental question that must be addressed in any developmental model of dissociation is: What is the pre- cise mechanism by which the early psychological events of “maltreatment-related” (Beer & De Bellis, 2002) or “pediatric” (Carrion et al., 2001) posttraumatic stress disorder affect the later behavior of the self system as it develops at further stages of the life cycle? I maintain that a purely psychological conception cannot answer this question; a psychoneurobiological perspective that integrates both biological structure and psychologi- cal function is required. Research clearly indicates that “the overwhelming stress of maltreatment in childhood is associated with adverse in uences on brain develop- ment” (1999, p. 1281).
During the rst years of life when the right brain is growing (Trevarthen, 1996) and dominant (Chiron et al., 1997), adverse in uences on brain development particu- larly impact the right brain (Allman et al., 2005). During this time, states of the infant brain become traits (Perry et al., 1995); thus, early relational trauma and dissociation
will be imprinted and embedded into the core structure of the developing right brain. Indeed, evidence shows that early relational trauma is particularly expressed in right hemisphere de cits. Recent studies reveal that maltreated children diagnosed with PTSD manifest right-lateralized metabolic limbic abnormalities (De Bellis et al., 2000), and that adults severely abused in childhood (Raine et al., 2001) and diagnosed with PTSD (Galletly et al., 2001) show reduced right hemisphere activation during a working memory task. This research supports earlier assertions that (1) the symptoms of PTSD fundamentally re ect an impairment of the right brain (Schore, 1997; Van de Kolk, 1996) and (2) the right hemisphere is par- amount in the perceptual and cognitive processing and the regulation of biological responses in PTSD patients (Spivak et al., 1998).
Thus, neurobiological research suggests that there is continuity over the life span in the expression of the cop- ing de cits of PTSD and the use of pathological dissocia- tion in persons who have a childhood history of relational trauma. The principle that severe attachment pathology frequently copes with Janetian “vehement emotions” via primitive modes of autoregulation can be translated into the clinical tenet that in PTSD (and other early form- ing severe pathologies of the self), the individual is cut off (disassociated) from experiencing intense affective states: “traumatic stress in childhood could lead to self- modulation of painful affect by directing attention away from internal emotional states” (Lane et al., 1997, p. 840). The right hemisphere is dominant not only for attach- ment regulation of affects, but also for attention (Raz, 2004) and pain processing (Symonds et al., 2006). Thus, the right brain strategy of dissociation represents the ulti- mate defense for blocking emotional pain.
This affective de cit ensues when attachment trauma produces an enduring impairment of the “affective core” (Emde, 1983), the primordial central integrating struc- ture of the nascent self. Joseph (1992) describes this as the “childlike central core” that maintains the self-image and all associated emotions, cognitions, and memories that are formed during childhood. Joseph localizes this core system in the right brain and limbic system. Recall (1) Devinsky’s (2000) assertion that optimal right hemi- spheric functions allow for “a coherent, continuous, and uni ed sense of self,” and (2) Devinsky’s citation of 19th century authors who postulated a connection between right hemispheric dysfunction and dissociation.
Both developmental (Perry et al., 1995; Schore, 1997) and adult (Bremner, 1999) studies support the proposition that there are two subtypes of acute trauma response in PTSD, hyperarousal and dissociative. I suggest that, in all stages of life, dissociation is a consequence of a psy- chological shock or high arousal (Meares, 1999) and that “at extremely high levels of arousal, coherent integration of sensory information breaks down and dissociative symptoms emerge” (J. Krystal et al., 1995). According to Gadea et al. (2005) mild to moderate negative affective experiences activate the right hemisphere, but an intense experience “might interfere with right hemisphere pro- cessing, with eventual damage if some critical point is reached” (p. 136). This damage is speci cally hyper- arousal-induced apoptotic cell death in the hypermeta- bolic right brain. Thus, via a switch into a hypoarousal, a hypometabolic state allows for cell survival at times of intense stress (Schore, 2003a).
Thus, neurobiological research suggests that there is continuity over the life span in the expression of the cop- ing de cits of PTSD and the use of pathological dissocia- tion in persons who have a childhood history of relational trauma. The principle that severe attachment pathology frequently copes with Janetian “vehement emotions” via primitive modes of autoregulation can be translated into the clinical tenet that in PTSD (and other early form- ing severe pathologies of the self), the individual is cut off (disassociated) from experiencing intense affective states: “traumatic stress in childhood could lead to self- modulation of painful affect by directing attention away from internal emotional states” (Lane et al., 1997, p. 840). The right hemisphere is dominant not only for attach- ment regulation of affects, but also for attention (Raz, 2004) and pain processing (Symonds et al., 2006). Thus, the right brain strategy of dissociation represents the ulti- mate defense for blocking emotional pain.
This affective de cit ensues when attachment trauma produces an enduring impairment of the “affective core” (Emde, 1983), the primordial central integrating struc- ture of the nascent self. Joseph (1992) describes this as the “childlike central core” that maintains the self-image and all associated emotions, cognitions, and memories that are formed during childhood. Joseph localizes this core system in the right brain and limbic system. Recall (1) Devinsky’s (2000) assertion that optimal right hemi- spheric functions allow for “a coherent, continuous, and uni ed sense of self,” and (2) Devinsky’s citation of 19th century authors who postulated a connection between right hemispheric dysfunction and dissociation.
Both developmental (Perry et al., 1995; Schore, 1997) and adult (Bremner, 1999) studies support the proposition that there are two subtypes of acute trauma response in PTSD, hyperarousal and dissociative. I suggest that, in all stages of life, dissociation is a consequence of a psy- chological shock or high arousal (Meares, 1999) and that “at extremely high levels of arousal, coherent integration of sensory information breaks down and dissociative symptoms emerge” (J. Krystal et al., 1995). According to Gadea et al. (2005) mild to moderate negative affective experiences activate the right hemisphere, but an intense experience “might interfere with right hemisphere pro- cessing, with eventual damage if some critical point is reached” (p. 136). This damage is speci cally hyper- arousal-induced apoptotic cell death in the hypermeta- bolic right brain. Thus, via a switch into a hypoarousal, a hypometabolic state allows for cell survival at times of intense stress (Schore, 2003a).
HYPERAROUSAL
Current research indicates that both hyperarousal and dis- sociative responses are essentially driven by right brain processes. Metzger et al. (2004) report “PTSD arousal symptoms are associated with increased right-sided pari- etal activation” (p. 324). Bonne et al. (2003) note that “regional blood ow in right precentral, superior tempo- ral, and fusiform gyri in posttraumatic stress disorder was higher than in healthy controls” (p. 1077), a nding that “may represent continuous preparatory motor activation, re ecting an increased basal level of anxiety and arousal.” They suggest that “this may re ect a component common to all survivors of trauma” (p. 1081). Similarly, Rabe et al. nd that PTSD patients show a pattern of right hemisphere activation that is associated with anxious arousal during processing of trauma-speci c information. In perhaps the most extensive investigation, Lanius et al. (2004) observe that PTSD patients (as opposed to traumatized patients without PTSD) who experience traumatic memories with heart rate increases (i.e., hyperarousal) show a pattern of right brain connectivity: activation of the right posterior cingulate, right caudate, right occipital, and right parietal lobe. They deduced that this right-lateralized pattern “may account for the nonverbal nature of traumatic memory in PTSD subjects” and cited other studies showing that “sub- jects who had experienced early trauma displayed … right dominance during memory recall.”
HYPOAROUSAL
Dissociation in PTSD is also centered in right brain pro- cesses. fMRI research of PTSD patients while they were in a dissociative state (as re ected in a lack of increase in heart rate when exposed to their traumatic script) revealed:
activation effects in the superior and middle tempo- ral gyrus, anterior cingulate, medial parietal lobe, and medial frontal gyres in the dissociated PTSD subjects were lateralized to the right side. The possibility that childhood trauma sets the stage for lateralized responses is given credence by report from Schiffer et al. (1995) who showed right hemisphere activation … during recall of unpleasant memories in adults with a history of child- hood abuse. (Lanius et al., 2002, p. 309)
These authors concluded that “prefrontal and limbic structures underlie dissociative responses in PTSD” and stated that activation of the right superior and middle temporal gyri in dissociated PTSD patients is consistent with a corticolimbic model of dissociation. In a more recent study, Lanius et al. (2005) reported predomi- nantly right-hemispheric frontal and insula activation in PTSD patients while they are dissociating, and con- cluded that patients dissociate in order to escape from the overwhelming emotions associated with the trau- matic memory, and that dissociation can be interpreted as representing a nonverbal response to the traumatic memory.
Gundel et al. (2004) noted that dissociating (and alexithymic) patients “have dif culties in integrating aspects of certain neuropsychological functions, namely memories and feelings, into current awareness” and pro- posed that the right anterior cingulate “may represent the structural, neuroanatomical correlate of an active inhibitory system causing a down regulation of emo- tional processing during the … expressive aspects of emotion” (p. 138). Very similar ndings were reported by Spitzer et al. (2004) in a transcranial magnetic stimu- lation study; they argue that their data show that disso- ciation may involve a lack of integration in the right hemisphere. This cor- responds with the idea that the right hemisphere has a distinct role in establishing, maintaining, and process- ing personally relevant aspects of an individual’s world. Thus a right hemispheric dysfunction might result in an altered sense of personally relevant familiarity, which resembles phenomenologically the dissociative symptoms of depersonalization and derealization … trauma-related conditions, which themselves are closely- associated with dissociative psychopathology, lack right hemispheric integration. (p. 167)
Citing the DSM-IV, they conclude, “In dissociation- prone individuals, a trauma that is perceived and pro- cessed by the right hemisphere will lead to a ‘disruption in the usually integrated functions of consciousness’” (p. 168).
These authors concluded that “prefrontal and limbic structures underlie dissociative responses in PTSD” and stated that activation of the right superior and middle temporal gyri in dissociated PTSD patients is consistent with a corticolimbic model of dissociation. In a more recent study, Lanius et al. (2005) reported predomi- nantly right-hemispheric frontal and insula activation in PTSD patients while they are dissociating, and con- cluded that patients dissociate in order to escape from the overwhelming emotions associated with the trau- matic memory, and that dissociation can be interpreted as representing a nonverbal response to the traumatic memory.
Gundel et al. (2004) noted that dissociating (and alexithymic) patients “have dif culties in integrating aspects of certain neuropsychological functions, namely memories and feelings, into current awareness” and pro- posed that the right anterior cingulate “may represent the structural, neuroanatomical correlate of an active inhibitory system causing a down regulation of emo- tional processing during the … expressive aspects of emotion” (p. 138). Very similar ndings were reported by Spitzer et al. (2004) in a transcranial magnetic stimu- lation study; they argue that their data show that disso- ciation may involve a lack of integration in the right hemisphere. This cor- responds with the idea that the right hemisphere has a distinct role in establishing, maintaining, and process- ing personally relevant aspects of an individual’s world. Thus a right hemispheric dysfunction might result in an altered sense of personally relevant familiarity, which resembles phenomenologically the dissociative symptoms of depersonalization and derealization … trauma-related conditions, which themselves are closely- associated with dissociative psychopathology, lack right hemispheric integration. (p. 167)
Citing the DSM-IV, they conclude, “In dissociation- prone individuals, a trauma that is perceived and pro- cessed by the right hemisphere will lead to a ‘disruption in the usually integrated functions of consciousness’” (p. 168).
DYSREGULATION OF RIGHT- LATERALIZED LIMBIC-AUTONOMIC CIRCUITS AND DISSOCIATION
These studies re ect the ontogenetic development of an early-dysregulated system, and provide further evi- dence that prefrontal cortical and limbic areas, particu- larly of the right hemisphere, are central to dissociative response. More so than the left, the right hemisphere is densely interconnected with limbic regions and subcorti- cal areas that generate the physiological aspect of emo- tions, including fear-terror (Adamec, 1999; Adolphs, Tranel, & Damasio, 2001; Borod, 2000; Gainotti, 2000; Tucker, 1992). Hecaen and Albert (1978) have described the much overlooked importance of hierarchical vertical corticosubcortical functional systems:
Cortical neural mechanisms of one hemisphere would be responsible for a particular performance, and subcortical structures connected to these cortical zones would par- ticipate in the realization of the performance, creating a complex, corticosubcortical functional system speci c to each hemisphere. (p. 414)
This “vertical” model of cortical-subcortical circuits directly applies to the right hemisphere, “the emotional brain”:
Neural processing of emotions engages diverse structures from the highest to the lowest levels of the neuraxis. On the one hand, high-order association areas are necessary to understand the signi cance of an emotional situa- tion, and on the other hand, low level structures must be activated to express the emotion through changes in the rhythm of peripheral organs. (Barbas et al., 2003)
These vertical circuits also account for the fact that the right hemisphere contains the major circuitry of emo- tion regulation (Brake et al., 2000; Porges, Doussard- Roosevelt, & Maiti, 1994; Schore, 1994; Sullivan & Dufresne, 2006).
I suggest that dissociation, a primitive coping strategy of affect regulation, is best understood as a loss of verti- cal connectivity between cortical and subcortical limbic areas within the right hemisphere. In contrast, J. Krystal et al. (1998) emphasize “shifts in interhemispheric pro- cessing” and “cortical disconnectivity” between higher frontal and limbic structures. Ontogenetically, however, dissociation appears well before the frontal areas of the cerebral cortex are myelinated and before callosal connec- tions are functional (Bergman, Linley, & Fawcus, 2004; Schore, 2001a). Thus, models of early dissociative defense
Cortical neural mechanisms of one hemisphere would be responsible for a particular performance, and subcortical structures connected to these cortical zones would par- ticipate in the realization of the performance, creating a complex, corticosubcortical functional system speci c to each hemisphere. (p. 414)
This “vertical” model of cortical-subcortical circuits directly applies to the right hemisphere, “the emotional brain”:
Neural processing of emotions engages diverse structures from the highest to the lowest levels of the neuraxis. On the one hand, high-order association areas are necessary to understand the signi cance of an emotional situa- tion, and on the other hand, low level structures must be activated to express the emotion through changes in the rhythm of peripheral organs. (Barbas et al., 2003)
These vertical circuits also account for the fact that the right hemisphere contains the major circuitry of emo- tion regulation (Brake et al., 2000; Porges, Doussard- Roosevelt, & Maiti, 1994; Schore, 1994; Sullivan & Dufresne, 2006).
I suggest that dissociation, a primitive coping strategy of affect regulation, is best understood as a loss of verti- cal connectivity between cortical and subcortical limbic areas within the right hemisphere. In contrast, J. Krystal et al. (1998) emphasize “shifts in interhemispheric pro- cessing” and “cortical disconnectivity” between higher frontal and limbic structures. Ontogenetically, however, dissociation appears well before the frontal areas of the cerebral cortex are myelinated and before callosal connec- tions are functional (Bergman, Linley, & Fawcus, 2004; Schore, 2001a). Thus, models of early dissociative defense
against organismic threat must move down the neuraxis into the brain stem that generates states of arousal.
In a congruent model, Scaer postulates that dissociation is elicited by internal and external cue-specific stimuli, but because the threat itself has not been resolved, internal cues persist without inhibition from external messages of safety, and kindling is triggered in the cortical, limbic, and brainstem centers. (2001, p. 84, my italics)
Notice that Scaer’s reference to brain stem centers and external and internal cues clearly implies both top- down and bottom-up processing. Pathological dissociative detachment is a defensive state, driven by fear, in which the stressed individual copes by pervasively and diffusely disengaging attention “from both the outer and inner worlds” (Allen et al., 1998, p. 164, my italics). In a similar conceptualization, Putnam (1997) describes dissociation between “an observing and experiencing ego.” Such terms (i.e., “inner world,” “experiencing ego”), however, have not been clearly de ned by the dissociation literature.
I have suggested that what is “experienced” are bodily states, and that the “inner world,” the source of “internal cues,” is more so than cognitions, the realm of bodily processes, central components of emotional states (Schore, 1994). According to Allen and his col- leagues, “dissociatively-detached individuals are not only detached from the environment, but also from the self—their body, their own actions, and their sense of identity” (p. 165). This is reminiscent of the ICD-10 de – nition of dissociation: “a partial or complete loss of the normal integration between memories of the past, aware- ness of identity and immediate sensations, and control of body movements.”
Speci cally, recent ndings about the autonomic ner- vous system, or what Jackson (1931) called the “physi- ological bottom of the mind,” are vital to understanding the mind-body alterations of trauma and the mechanism of dissociation (Schore, 2001b, 2002). Indeed, the higher regulatory systems of the right hemisphere form exten- sive reciprocal connections with the limbic, sympathetic, and parasympathetic branches of the ANS (Aftanas et al., 2005; Critchley et al., 2000; Erciyas et al., 1999; Spence, Shapiro, & Zaidel, 1996; Tucker, 1992; Yoon et al., 1997). These control the somatic components of many emotional responses, especially autonomic physi- ological responses to social stimuli. Adaptive right- brain emotion processing depends upon an integration of the activities of the CNS and the ANS (Hagemann, Waldstein, & Thayer, 2003).
In a congruent model, Scaer postulates that dissociation is elicited by internal and external cue-specific stimuli, but because the threat itself has not been resolved, internal cues persist without inhibition from external messages of safety, and kindling is triggered in the cortical, limbic, and brainstem centers. (2001, p. 84, my italics)
Notice that Scaer’s reference to brain stem centers and external and internal cues clearly implies both top- down and bottom-up processing. Pathological dissociative detachment is a defensive state, driven by fear, in which the stressed individual copes by pervasively and diffusely disengaging attention “from both the outer and inner worlds” (Allen et al., 1998, p. 164, my italics). In a similar conceptualization, Putnam (1997) describes dissociation between “an observing and experiencing ego.” Such terms (i.e., “inner world,” “experiencing ego”), however, have not been clearly de ned by the dissociation literature.
I have suggested that what is “experienced” are bodily states, and that the “inner world,” the source of “internal cues,” is more so than cognitions, the realm of bodily processes, central components of emotional states (Schore, 1994). According to Allen and his col- leagues, “dissociatively-detached individuals are not only detached from the environment, but also from the self—their body, their own actions, and their sense of identity” (p. 165). This is reminiscent of the ICD-10 de – nition of dissociation: “a partial or complete loss of the normal integration between memories of the past, aware- ness of identity and immediate sensations, and control of body movements.”
Speci cally, recent ndings about the autonomic ner- vous system, or what Jackson (1931) called the “physi- ological bottom of the mind,” are vital to understanding the mind-body alterations of trauma and the mechanism of dissociation (Schore, 2001b, 2002). Indeed, the higher regulatory systems of the right hemisphere form exten- sive reciprocal connections with the limbic, sympathetic, and parasympathetic branches of the ANS (Aftanas et al., 2005; Critchley et al., 2000; Erciyas et al., 1999; Spence, Shapiro, & Zaidel, 1996; Tucker, 1992; Yoon et al., 1997). These control the somatic components of many emotional responses, especially autonomic physi- ological responses to social stimuli. Adaptive right- brain emotion processing depends upon an integration of the activities of the CNS and the ANS (Hagemann, Waldstein, & Thayer, 2003).
According to Porges et al. (1994), the lower right side of the brain stem that controls the ANS is innervated by the amygdala and unnamed higher limbic structures; this “vagal circuit of emotion regulation” provides the primary central regulation of homeostasis and physi- ological reactivity. Porges’s model emphasizes the lower structures of a vertical system. Although he details the brain stem components, he refers to the higher structures as the “cortex” that processes information from the social environment. And yet, his model clearly implies a bidi- rectional system in which both top-down and bottom-up processes are responsible for generating adaptive regula- tory functioning.
Benarroch (1997) describes such CNS-ANS limbic- autonomic circuits in his model of a central autonomic network (CAN)—an internal regulation system through which the brain controls visceromotor, neuroendo- crine, and behavioral responses. Like Porges’s model, Benarroch’s CAN is a bidirectional hierarchical system. Benarroch, however, focuses more on higher limbic structures than lower brain stem structures. The CAN is composed of (1) limbic areas in the ventromedial (orbital) prefrontal cortex, anterior cingulate, insula, and amygdala, (2) diencephalic areas in the hypothalamus, (3) brain stem structures in the periaqueductal grey mat- ter, and (4) the nucleus of the solitary tract and nucleus ambiguus in the medulla. Hagemann, Waldstein, and Thayer (2003) characterize the CAN as
a network of neural structures that generate, receive, and integrate internal and external information in the service of goal-directed behavior and organism adaptability…. These structures are reciprocally interconnected such that information ows in both directions—top-down and bottom-up. The primary output of the CAN is mediated through the preganglionic sympathetic and parasympa- thetic neurons. These neurons innervate the heart via the stellate ganglia and the vagus nerve. (pp. 83–84)
When this network is either completely uncoupled or rigidly coupled, the individual is less able to dynamically and adaptively assemble the components of the network to meet an environmental challenge, thereby displaying de cits in emotional expression and affect regulation (Demaree et al., 2004). This nding leads back to the problem of psychopathogenesis—what events could be responsible for such de cits?
Authors are now describing the developmental pro- cess of “cerebral maturation in the vertical dimension” (Luu & Tucker, 1996). Both the ANS and the CNS con- tinue to develop postnatally; importantly, the assembly of these limbic-autonomic circuits (Rinaman, Levitt, & Card, 2000) is experience dependent (Schore, 1994, 2001a). These experiences are provided by attachment transactions of the rst and second year, during which the primary caregiver provides complex interpersonal stim- uli and interactive regulation of the infant’s core systems of central and autonomic arousal. Optimal environments promote secure attachments that facilitate the organiza- tion of limbic-autonomic circuits and a right hemispheric limbic-modulated ventral vagal parasympathetic circuit of emotion regulation that mediates both emotion and communication processes (Porges et al., 1994).
Benarroch (1997) describes such CNS-ANS limbic- autonomic circuits in his model of a central autonomic network (CAN)—an internal regulation system through which the brain controls visceromotor, neuroendo- crine, and behavioral responses. Like Porges’s model, Benarroch’s CAN is a bidirectional hierarchical system. Benarroch, however, focuses more on higher limbic structures than lower brain stem structures. The CAN is composed of (1) limbic areas in the ventromedial (orbital) prefrontal cortex, anterior cingulate, insula, and amygdala, (2) diencephalic areas in the hypothalamus, (3) brain stem structures in the periaqueductal grey mat- ter, and (4) the nucleus of the solitary tract and nucleus ambiguus in the medulla. Hagemann, Waldstein, and Thayer (2003) characterize the CAN as
a network of neural structures that generate, receive, and integrate internal and external information in the service of goal-directed behavior and organism adaptability…. These structures are reciprocally interconnected such that information ows in both directions—top-down and bottom-up. The primary output of the CAN is mediated through the preganglionic sympathetic and parasympa- thetic neurons. These neurons innervate the heart via the stellate ganglia and the vagus nerve. (pp. 83–84)
When this network is either completely uncoupled or rigidly coupled, the individual is less able to dynamically and adaptively assemble the components of the network to meet an environmental challenge, thereby displaying de cits in emotional expression and affect regulation (Demaree et al., 2004). This nding leads back to the problem of psychopathogenesis—what events could be responsible for such de cits?
Authors are now describing the developmental pro- cess of “cerebral maturation in the vertical dimension” (Luu & Tucker, 1996). Both the ANS and the CNS con- tinue to develop postnatally; importantly, the assembly of these limbic-autonomic circuits (Rinaman, Levitt, & Card, 2000) is experience dependent (Schore, 1994, 2001a). These experiences are provided by attachment transactions of the rst and second year, during which the primary caregiver provides complex interpersonal stim- uli and interactive regulation of the infant’s core systems of central and autonomic arousal. Optimal environments promote secure attachments that facilitate the organiza- tion of limbic-autonomic circuits and a right hemispheric limbic-modulated ventral vagal parasympathetic circuit of emotion regulation that mediates both emotion and communication processes (Porges et al., 1994).
Under stress, this complex system manifests itself as a exible coping pattern in which homeostatic increases in the activity in one ANS division are associated with decreases in the other. An autonomic mode of coupled reciprocal sympathetic-parasympathetic control is evi- dent when an organism responds alertly and adaptively to a personally meaningful (especially social) stressor, yet promptly returns to the relaxed state of autonomic bal- ance as soon as the context is appraised as safe. Thus, the ANS is not only sensitive to environmental demands and perceived stresses and threats, but will also, in a predictable order, rapidly reorganize to different neural- mediated states (Porges, 2001).
In contrast to this healthy developmental scenario, traumatizing primary caregivers amplify the infant’s states of hyperarousal and/or dissociative hypoarousal. This relational intersubjective context inhibits the expe- rience-dependent maturation of CNS-ANS links (which are more extensive on the right side of the brain). In this manner, dysregulation of the developing right brain is associated in the short term with traumatic attachment and in the long term with the psychopathogenesis of dis- sociation. An extensive apoptotic parcellation of vertical circuits in the developing right brain would lead to an inef cient regulation of the ANS by higher centers in the CNS, functionally expressed as a dissociation of central regulation of sympathetic and hypothalamic-pituitary- adrenal systems (Young, Ross, & Landsberg, 1984).
This model of dissociation as a stress-induced discon- nect between right brain CNS and ANS systems directly applies to the etiology and psychobiological mechanism of “somatoform dissociation,” which is an outcome of early onset traumatization, often involving physical abuse and threat to life by another person. In somatoform dis- sociation there is a lack of integration of sensorimotor experiences, reactions, and functions of the individual and his/her self-representation (Nijenhuis, 2000). Recall Devinsky’s (2000) assertion: optimal right hemispheric functions allow for the operations of “a coherent, con- tinuous, and uni ed sense of self.”
In contrast to this healthy developmental scenario, traumatizing primary caregivers amplify the infant’s states of hyperarousal and/or dissociative hypoarousal. This relational intersubjective context inhibits the expe- rience-dependent maturation of CNS-ANS links (which are more extensive on the right side of the brain). In this manner, dysregulation of the developing right brain is associated in the short term with traumatic attachment and in the long term with the psychopathogenesis of dis- sociation. An extensive apoptotic parcellation of vertical circuits in the developing right brain would lead to an inef cient regulation of the ANS by higher centers in the CNS, functionally expressed as a dissociation of central regulation of sympathetic and hypothalamic-pituitary- adrenal systems (Young, Ross, & Landsberg, 1984).
This model of dissociation as a stress-induced discon- nect between right brain CNS and ANS systems directly applies to the etiology and psychobiological mechanism of “somatoform dissociation,” which is an outcome of early onset traumatization, often involving physical abuse and threat to life by another person. In somatoform dis- sociation there is a lack of integration of sensorimotor experiences, reactions, and functions of the individual and his/her self-representation (Nijenhuis, 2000). Recall Devinsky’s (2000) assertion: optimal right hemispheric functions allow for the operations of “a coherent, con- tinuous, and uni ed sense of self.”
Psychopathological regulatory systems thus contain poorly evolved CNS-ANS limbic-autonomic switching mechanisms that are inef cient or incapable of uncou- pling and recoupling the sympathetic and parasympa- thetic components of the ANS in response to changing environmental circumstances. This “nonreciprocal mode of autonomic control” (Berntson et al., 1991) is unable to adapt to stress; in fact, the coping limitations of patho- logical dissociation are essentially de ned by these sys- tems’ overly rigid and continuing inhibition of certain internal systems. In other words, dissociation re ects the inability of the right brain cortical-subcortical system to (1) recognize and co-process exteroceptive information from the relational environment and (2) on a moment-to- moment basis integrate this information from moment to moment with interoceptive information from the body. Neuroscience writers now refer to “a dissociation between the emotional evaluation of an event and the physiologi- cal reaction to that event, with the process being depen- dent on intact right hemisphere function” (Crucian et al., 2000, p. 643).
An immature right brain circuit of emotion regulation would show de cits in “intense emotional-homeostatic processes” (Porges et al., 1994), that is, it would too easily default from fast-acting ventral vagal to slow-acting dor- sal vagal systems in moments of “vehement emotions” and, thereby, be unable to exibly shift internal states and overt behavior in response to stressful external demands. Indeed, the ventral vagal complex is known to be defec- tive in PTSD patients (Sahar, Shalev, & Porges, 2001); this may account for the basal hyperarousal and high heart rates of these patients (Sack, Hopper, & Lamprecht, 2004). I suggest that under high stress an unstable ventral vagal system could be rapidly displaced by a dorsal vagal system; this would account for the low heart rate of dis- sociative hypoarousal.
The disassociation of higher corticolimbic areas of the CAN internal regulation system and Porges’s right brain circuit of emotion regulation precludes (1) top-down con- trol of lower brain stem and autonomic functions and (2) adaptive integration of CNS exteroceptive and ANS intero- ceptive information processing. This disinhibition releases lower control structures in the right amygdala via a mecha- nism that Hughlings Jackson (1958) called dissolution:
The higher nervous arrangements inhibit (or control) the lower, and thus, when the higher are suddenly rendered functionless, the lower rise in activity. What do we know about higher control systems? Current neuroimaging research indicates that the highest level of regulatory control structures in the human brain are located in frontolimbic systems of the right hemisphere.
An immature right brain circuit of emotion regulation would show de cits in “intense emotional-homeostatic processes” (Porges et al., 1994), that is, it would too easily default from fast-acting ventral vagal to slow-acting dor- sal vagal systems in moments of “vehement emotions” and, thereby, be unable to exibly shift internal states and overt behavior in response to stressful external demands. Indeed, the ventral vagal complex is known to be defec- tive in PTSD patients (Sahar, Shalev, & Porges, 2001); this may account for the basal hyperarousal and high heart rates of these patients (Sack, Hopper, & Lamprecht, 2004). I suggest that under high stress an unstable ventral vagal system could be rapidly displaced by a dorsal vagal system; this would account for the low heart rate of dis- sociative hypoarousal.
The disassociation of higher corticolimbic areas of the CAN internal regulation system and Porges’s right brain circuit of emotion regulation precludes (1) top-down con- trol of lower brain stem and autonomic functions and (2) adaptive integration of CNS exteroceptive and ANS intero- ceptive information processing. This disinhibition releases lower control structures in the right amygdala via a mecha- nism that Hughlings Jackson (1958) called dissolution:
The higher nervous arrangements inhibit (or control) the lower, and thus, when the higher are suddenly rendered functionless, the lower rise in activity. What do we know about higher control systems? Current neuroimaging research indicates that the highest level of regulatory control structures in the human brain are located in frontolimbic systems of the right hemisphere.
THE ESSENTIAL ROLE OF RIGHT FRONTOLIMBIC STRUCTURES IN THE REGULATION OF DISSOCIATION
Note that the neuroanatomy of the right brain allows for a reciprocal connection between the highest level of the limbic system (the orbitofrontal and medial frontal cor- tices) and the brain stem medullary vagal systems that regulate parasympathetic hypoarousal and dissociation. A similar model is proposed by Phillips et al. (2003), who described a “ventral” regulation system, includ- ing orbitofrontal cortex, insula, anterior cingulate, and amygdala. As opposed to a nonlimbic “dorsal” effortful regulation system in the dorsolateral cortex, hippocam- pus, and other structures involved in explicit processing of the “verbal components of emotional stimuli,” this ventral system is important for the implicit identi ca- tion of the emotional signi cance of environmental stimuli, and is central to the “automatic regulation and mediation of autonomic responses to emotional stimuli and contexts that accompany the production of affective states” (p. 510).
I have described a model of dual limbic-autonomic circuits, a hierarchical sequence of interconnected limbic areas in the orbitofrontal cortex, insular cortex, anterior cingulate, and amygdala (Schore, 1994, 1996). Each component of this “rostral limbic system” inter- connects with the other and with brain stem bioamin- ergic arousal and neuromodulatory systems, including vagal nuclei in the medulla and hypothalamic neuroen- docrine nuclei that regulate the sympathetic and para- sympathetic nervous systems (Schore, 1994, 2003a, 2003b). Of particular importance are the highest levels of this vertical cortical-subcortical system, especially the orbitofrontal cortex, which monitors and con- trols responses initiated by other brain regions and is involved in the selection and active inhibition of neu- ral circuits associated with emotional responses (Rule, Shimamura, & Knight, 2002). This prefrontal sys- tem performs a “hot’” executive function—regulating affect and motivation via control of basic limbic system functions (Zelazo & Muller, 2002).
According to Barbas and her colleagues (2003),
Axons from orbitofrontal and medial prefrontal cortices converge in the hypothalamus with neurons project- ing to brainstem and spinal autonomic centers, linking the highest with the lowest levels of the neuraxis….Descending pathways from orbitofrontal and medial prefrontal cortices [anterior cingulate], which are linked with the amygdala, provide the means for speedy in u- ence of the prefrontal cortex on the autonomic system, in processes underlying appreciation and expression of emotions…. Repetitive activation of the remarkably spe- ci c and bidirectional pathways linking the amygdala with the orbitofrontal cortex may be necessary for con- scious appreciation of the emotional signi cance of events.
This top-down in uence can either be excitatory or inhibitory; the latter expressed in the documented activa- tion of the orbitofrontal cortex during defensive responses (Roberts et al., 2001). Recall Lanius’s et al. (2002) con- clusion that prefrontal and limbic structures underlie dis- sociative responses in PTSD, and Gundel’s et al. (2004) proposal that the right anterior cingulate can act as an inhibitory system that down-regulates emotional process- ing, resulting in dissociation (i.e., an inability to integrate feelings into conscious awareness).
Indeed, this limbic-autonomic circuit is right-lateral- ized. The right orbitofrontal cortex, the hierarchical apex of the limbic system, exercises executive control over the entire right brain. Right orbitofrontal areas are more crit- ical to emotional functions than left orbitofrontal areas (Tranel, Bechara, & Denburg, 2002). Within the orb- itofrontal cortex, the lateral orbital prefrontal areas are specialized for regulating positive emotional states, while medial orbitofrontal areas are specialized for processing negative emotional states (Northoff et al., 2000; Schore, 2001a). The functioning of these two limbic-autonomic circuits, one capped by the lateral orbitofrontal cortex and the other by the medial orbitofrontal cortex (which in earlier writings I termed the excitatory ventral teg- mental limbic forebrain-midbrain circuit and the inhibi- tory lateral tegmental limbic forebrain-midbrain circuits, respectively; Schore, 1994) are organized by the attach- ment experiences of the rst and second year.
Optimal maturation of this prefrontolimbic system allows for the highest level of integration of exteroceptive and interoceptive information. The right orbitofrontal cortex, in conjunction with the right anterior insula, sup- ports a representation of visceral responses accessible to awareness, and provides a substrate for subjective feeling states and emotional depth and awareness (Craig, 2004; Critchley et al., 2004). In contrast, recall that pathological dissociation is de ned in ICD-10 as a loss of “awareness of identity and immediate sensations, and control of body movements.” Just as secure attachment constrains trauma and dissociation, so does optimal functioning of the orb- itofrontal system oppose somatoform dissociation.
Indeed, this limbic-autonomic circuit is right-lateral- ized. The right orbitofrontal cortex, the hierarchical apex of the limbic system, exercises executive control over the entire right brain. Right orbitofrontal areas are more crit- ical to emotional functions than left orbitofrontal areas (Tranel, Bechara, & Denburg, 2002). Within the orb- itofrontal cortex, the lateral orbital prefrontal areas are specialized for regulating positive emotional states, while medial orbitofrontal areas are specialized for processing negative emotional states (Northoff et al., 2000; Schore, 2001a). The functioning of these two limbic-autonomic circuits, one capped by the lateral orbitofrontal cortex and the other by the medial orbitofrontal cortex (which in earlier writings I termed the excitatory ventral teg- mental limbic forebrain-midbrain circuit and the inhibi- tory lateral tegmental limbic forebrain-midbrain circuits, respectively; Schore, 1994) are organized by the attach- ment experiences of the rst and second year.
Optimal maturation of this prefrontolimbic system allows for the highest level of integration of exteroceptive and interoceptive information. The right orbitofrontal cortex, in conjunction with the right anterior insula, sup- ports a representation of visceral responses accessible to awareness, and provides a substrate for subjective feeling states and emotional depth and awareness (Craig, 2004; Critchley et al., 2004). In contrast, recall that pathological dissociation is de ned in ICD-10 as a loss of “awareness of identity and immediate sensations, and control of body movements.” Just as secure attachment constrains trauma and dissociation, so does optimal functioning of the orb- itofrontal system oppose somatoform dissociation.
Furthermore, the right prefrontal cortex, the “senior executive of limbic arousal” (Joseph, 1996), is most directly linked to stress-regulatory systems (Brake et al., 2000) and, therefore, is essential for the regulation of the hyperaroused and hypoaroused states that accompany traumatic stress. During the acquisition of conditioned fear (Fischer et al., 2002), the right prefrontal brain is activated. This cortical-subcortical regulatory mecha- nism allows for orbitofrontal modulation of the right amygdala that is specialized for fear conditioning (Baker & Kim, 2004; Moses et al., 2007) and processing fright- ening faces (Whalen et al., 1998; Adolphs, Tranel, & Damasio, 2001). The right amygdala directly projects to the brain stem startle center (Bradley, Cuthbert, & Lang, 1996; Davis, 1989) and to the dorsal motor vagal nucleus (Schwaber et al., 1982), and the amygdala’s connections with the dorsolateral periaqueductal gray in the brain stem mediate the defensive freeze response (Oliveira et al., 2004; Vianna et al., 2001). In this manner, the right orbitofrontal cortex “organizes the appropriate cortical and autonomic response based on the implications of … sensory information for survival. The orbitofrontal cortex therefore functions as a master regulator for organization of the brain’s response to threat” (Scaer, 2001, p. 78).
These data strongly suggest that an individual with an impaired or developmentally immature orbitofron- tal system resulting from early relational trauma will be vulnerable to pathological dissociation under stress. Without orbital prefrontal feedback regarding the level of threat, the organism remains in an amygdala-driven defensive response state longer than necessary (Morgan & LeDoux, 1995). In humans, conditioned fear acquisi- tion and extinction are associated with right-hemisphere- dominant amygdala function (La Bar et al., 1998). Such amygdala-driven startle and fear-freeze responses are intense because they are totally unregulated by the orbit- ofrontal (and medial frontal) cortex. Indeed, dysfunction of the right frontal lobe is involved in PTSD symptoma- tology (Freeman & Kimbrell, 2001) and dissociative ashbacks (Berthier et al., 2001).
In classic neurological primate research, Ruch and Shenkin (1943) lesioned the orbitofrontal cortex (Brodman area 13) and observed a “de nite reduction in emotional expression” and an elimination of fear and aggressive behaviors (that were replaced by “gazing into the dis- tance with a blank expression”). Neurological patients with orbitofrontal damage show a “dissociation among autonomic measures” and an altered response to a startle. Such patients show a decrease in heart rate in anticipa- tion of, or in response to, an aversive stimulus (Roberts et al., 2004). This is reminiscent of the deceleration of heart rate that has been observed in traumatized dissoci- ating infants and dissociating adult psychiatric patients.
These data strongly suggest that an individual with an impaired or developmentally immature orbitofron- tal system resulting from early relational trauma will be vulnerable to pathological dissociation under stress. Without orbital prefrontal feedback regarding the level of threat, the organism remains in an amygdala-driven defensive response state longer than necessary (Morgan & LeDoux, 1995). In humans, conditioned fear acquisi- tion and extinction are associated with right-hemisphere- dominant amygdala function (La Bar et al., 1998). Such amygdala-driven startle and fear-freeze responses are intense because they are totally unregulated by the orbit- ofrontal (and medial frontal) cortex. Indeed, dysfunction of the right frontal lobe is involved in PTSD symptoma- tology (Freeman & Kimbrell, 2001) and dissociative ashbacks (Berthier et al., 2001).
In classic neurological primate research, Ruch and Shenkin (1943) lesioned the orbitofrontal cortex (Brodman area 13) and observed a “de nite reduction in emotional expression” and an elimination of fear and aggressive behaviors (that were replaced by “gazing into the dis- tance with a blank expression”). Neurological patients with orbitofrontal damage show a “dissociation among autonomic measures” and an altered response to a startle. Such patients show a decrease in heart rate in anticipa- tion of, or in response to, an aversive stimulus (Roberts et al., 2004). This is reminiscent of the deceleration of heart rate that has been observed in traumatized dissoci- ating infants and dissociating adult psychiatric patients.
In support of earlier proposals (Schore, 1994), it is now well established that orbitofrontal maturation is experience dependent (Neddens et al., 2001; Poeggel, Nowicki, & Braun, 2003), that human prefrontal func- tions emerge around the end of the rst year (Happeney, Zelazo, & Stuss, 2004), and that conditions that modify early maternal variability in infancy produce “signi – cant differences in right but not left adult prefrontal vol- umes, with experience-dependent asymmetric variation most clearly expressed in ventral medial cortex” (Lyons et al., 2002, p. 51). During these critical periods extensive hypometabolic states preclude optimal organization and optimal functional capacity of the highest frontolimbic levels of the right brain. Pathological dissociation re ects an impairment of the affect regulatory functions of the higher centers in the orbitofrontal cortex. Through its connections with the ANS the orbitofrontal system is implicated in “the representation of emotional informa- tion and the regulation of emotional processes” (Roberts et al., 2004, p. 307) and “the conscious appreciation of the emotional signi cance of events” (Barbas et al., 2003). In the dorsal vagal parasympathetic-dominant state of dissociation, however, the individual is cut off (dis-associated) from both the external and the internal environment and, therefore, emotions are not consciously experienced.
Although triggered by subcortical mechanisms, dis- sociation is regulated by higher corticolimbic centers. Pathological dissociation is the product of an inef – cient frontolimbic system that cannot regulate the onset and offset of the dissociative response. Instead, for long periods of time, disinhibited lower subcortical centers (especially the right amygdala) drive the dissociative response; this re ects a Janetian regression to a con- stricted and disuni ed state. Adequate orbitofrontal activ- ity is needed to integrate information from the external world and the internal world (especially “messages of safety”); “such integration might provide a way whereby incoming information may be associated with motiva- tional and emotional states to subserve processes such as selective attention and memory formation and retrieval” (Pandya & Yeterian, 1985, p. 51). Loss of orbitofrontal functions that maintain “the integration of past, present, and future experiences, enabling adequate performance in behavioral tasks, social situation, or situations involv- ing survival (Lipton et al., 1999, p. 356) is re ected in pathological dissociation: “a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment” (APA, 1994). Indeed,
Although triggered by subcortical mechanisms, dis- sociation is regulated by higher corticolimbic centers. Pathological dissociation is the product of an inef – cient frontolimbic system that cannot regulate the onset and offset of the dissociative response. Instead, for long periods of time, disinhibited lower subcortical centers (especially the right amygdala) drive the dissociative response; this re ects a Janetian regression to a con- stricted and disuni ed state. Adequate orbitofrontal activ- ity is needed to integrate information from the external world and the internal world (especially “messages of safety”); “such integration might provide a way whereby incoming information may be associated with motiva- tional and emotional states to subserve processes such as selective attention and memory formation and retrieval” (Pandya & Yeterian, 1985, p. 51). Loss of orbitofrontal functions that maintain “the integration of past, present, and future experiences, enabling adequate performance in behavioral tasks, social situation, or situations involv- ing survival (Lipton et al., 1999, p. 356) is re ected in pathological dissociation: “a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment” (APA, 1994). Indeed,
patients using pathological dissociation who experience severe alterations of consciousness and loss of identity— dissociative identity disorder—show signi cant reduc- tion of blood ow and therefore hypoactivation of the orbitofrontal cortices (S ̧ar et al., in press).
FURTHER SPECULATIONS ON THE BIOLOGICAL MECHANISM OF DISSOCIATION
As previously noted, Prueter (2002) has called for an understanding of the “primary pathophysiologic mech- anism that leads to the dissociative symptoms, using neurobiological research mechanisms.” Towards that end, I have used regulation theory to offer a model of the earliest psychobiological expression of dissociation in human infancy. I argued that dissociation is a basic survival mechanism for coping with intense states of energy-expending hyperarousal by shifting into an energy- conserving hypometabolic state. This regulation strategy of hypoarousal, which is re ected in heart rate decelera- tion in response to stress, remains unchanged over the life span. This model is based in part on (1) Main’s observa- tions (Main & Solomon, 1986; Main & Hesse, 1999, 2006; i.e., that the disorganization and disorientation of type D attachment phenotypically resembles dissociative states), and (2) Tronick’s (Tronick & Weinberg, 1997; Tronick, 2004) still-face procedure—a threatening interpersonal context that triggers “massive disengagement.”
I have suggested that these paradigms describe the same state of dissociation that clinicians have described as “profound detachment” (Barach, 1991), “detachment from an unbearable situation” (Mollon, 1996), and “dis- sociative detachment” (Allen et al., 1998). At all points in the life span, the functional aspects of Janetian “extreme emotional arousal” and dissociation re ect a structural alteration in arousal systems in the brain stem associ- ated with a loss of ventral vagal, and dominance of dorsal vagal, parasympathetic states. In this section I will offer further speculations about the basic biological mecha- nisms that underlie dissociation.
Under stress, Type D infants show “a dazed facial appearance … accompanied by a stilling of all body movement, and sometimes a freezing of limbs which had been in motion” (Main & Solomon, 1986). Experiences of traumatic freezing are encoded in enduring implicit- procedural memory, representing what Janet termed unconscious “ xed ideas” that cannot be “liquidated.” Indeed, the relationship between freeze behavior and dissociation has been noted by authors from various disciplines. In psychophysiological research, Porges (1997) described a trauma-induced “immobilized state” associated with the dorsal vagal complex. In one of the most important psychiatric texts on trauma written in the last century, Henry Krystal (1988) described a traumatic “catatonoid” affective reaction to “the perception of fatal helplessness in the face of destructive danger,” and equates this “pattern of surrender” with the “cataleptic immobility” of animals. In the trauma literature, I have described (1) the “frozen watchfulness” of the abused child who waits warily for parental demands, responds quickly and compliantly, and then returns to her previous vigilant state, and (2) the “frozen state” of speechless ter- ror seen in adult PTSD patients (Schore, 2001a).
FURTHER SPECULATIONS ON THE BIOLOGICAL MECHANISM OF DISSOCIATION
As previously noted, Prueter (2002) has called for an understanding of the “primary pathophysiologic mech- anism that leads to the dissociative symptoms, using neurobiological research mechanisms.” Towards that end, I have used regulation theory to offer a model of the earliest psychobiological expression of dissociation in human infancy. I argued that dissociation is a basic survival mechanism for coping with intense states of energy-expending hyperarousal by shifting into an energy- conserving hypometabolic state. This regulation strategy of hypoarousal, which is re ected in heart rate decelera- tion in response to stress, remains unchanged over the life span. This model is based in part on (1) Main’s observa- tions (Main & Solomon, 1986; Main & Hesse, 1999, 2006; i.e., that the disorganization and disorientation of type D attachment phenotypically resembles dissociative states), and (2) Tronick’s (Tronick & Weinberg, 1997; Tronick, 2004) still-face procedure—a threatening interpersonal context that triggers “massive disengagement.”
I have suggested that these paradigms describe the same state of dissociation that clinicians have described as “profound detachment” (Barach, 1991), “detachment from an unbearable situation” (Mollon, 1996), and “dis- sociative detachment” (Allen et al., 1998). At all points in the life span, the functional aspects of Janetian “extreme emotional arousal” and dissociation re ect a structural alteration in arousal systems in the brain stem associ- ated with a loss of ventral vagal, and dominance of dorsal vagal, parasympathetic states. In this section I will offer further speculations about the basic biological mecha- nisms that underlie dissociation.
Under stress, Type D infants show “a dazed facial appearance … accompanied by a stilling of all body movement, and sometimes a freezing of limbs which had been in motion” (Main & Solomon, 1986). Experiences of traumatic freezing are encoded in enduring implicit- procedural memory, representing what Janet termed unconscious “ xed ideas” that cannot be “liquidated.” Indeed, the relationship between freeze behavior and dissociation has been noted by authors from various disciplines. In psychophysiological research, Porges (1997) described a trauma-induced “immobilized state” associated with the dorsal vagal complex. In one of the most important psychiatric texts on trauma written in the last century, Henry Krystal (1988) described a traumatic “catatonoid” affective reaction to “the perception of fatal helplessness in the face of destructive danger,” and equates this “pattern of surrender” with the “cataleptic immobility” of animals. In the trauma literature, I have described (1) the “frozen watchfulness” of the abused child who waits warily for parental demands, responds quickly and compliantly, and then returns to her previous vigilant state, and (2) the “frozen state” of speechless ter- ror seen in adult PTSD patients (Schore, 2001a).
In neurological writings, Scaer (2001) postulates that dissociation “is initiated by a failed attempt at defensive/ escape efforts at the moment of a life threat, and is per- petuated if spontaneous recovery of the resulting freeze response is blocked or truncated” (p. 84, my italics):
If deterrence of the threat through defense or ght fails, the animal enters a state of helplessness, associated by a marked increase in dorsal vagal complex tone, initiat- ing the freeze/immobility response…. The extremes of vagal parasympathetic tone as manifested in the state of dorsal vagal activation, therefore, contribute greatly to the generation of severe emotions, especially those of terror and helplessness. Although freeze/immobility states … may be useful for short-term survival, prolon- gation or repeated activation of that state clearly has serious implications for health and long-term survival. (Scaer, 2001, p. 81)
Several studies indicate that the freeze response is right lateralized. Freezing in primate infants, which is elicited by eye contact, correlates with extreme right frontal EEG activity and high basal cortisol levels (Kalin et al., 1998). Right parietal lesions in rats are associated with a con- ditioned freezing de cit (Hogg, Sanger, & Moser, 1998). In human catatonia, a basic somatic defense mechanism associated with “immobilization of anxieties,” there is a right lower prefronto-parietal cortical dysfunction (Northoff et al., 2000).
But other studies in the developmental literature, those of Tronick, describe not freeze behavior but a collapsed AQ2 state of “profound disengagement” (see Figure 8.2). Tronick (2004) observed both a suspension of spontane- ous emotional expression and gesture, and a “dissipation of the infant’s state of consciousness” that is associated with “the disorganization of many of the lower level psychobiological states, such as metabolic systems.” How does this relate to freezing? Keep in mind that the
If deterrence of the threat through defense or ght fails, the animal enters a state of helplessness, associated by a marked increase in dorsal vagal complex tone, initiat- ing the freeze/immobility response…. The extremes of vagal parasympathetic tone as manifested in the state of dorsal vagal activation, therefore, contribute greatly to the generation of severe emotions, especially those of terror and helplessness. Although freeze/immobility states … may be useful for short-term survival, prolon- gation or repeated activation of that state clearly has serious implications for health and long-term survival. (Scaer, 2001, p. 81)
Several studies indicate that the freeze response is right lateralized. Freezing in primate infants, which is elicited by eye contact, correlates with extreme right frontal EEG activity and high basal cortisol levels (Kalin et al., 1998). Right parietal lesions in rats are associated with a con- ditioned freezing de cit (Hogg, Sanger, & Moser, 1998). In human catatonia, a basic somatic defense mechanism associated with “immobilization of anxieties,” there is a right lower prefronto-parietal cortical dysfunction (Northoff et al., 2000).
But other studies in the developmental literature, those of Tronick, describe not freeze behavior but a collapsed AQ2 state of “profound disengagement” (see Figure 8.2). Tronick (2004) observed both a suspension of spontane- ous emotional expression and gesture, and a “dissipation of the infant’s state of consciousness” that is associated with “the disorganization of many of the lower level psychobiological states, such as metabolic systems.” How does this relate to freezing? Keep in mind that the
full manifestation of the fear-freeze response is a late- occurring behavior; in human infants, it occurs in the second half of the rst year. But dissociation is seen in the hypoxic human fetus (Reed et al., 1999) and soon after birth (Bergman et al., 2004).
Again, clues come from studies in basic biology and neuroscience. Citing this literature, Scaer states that freeze behavior is a state of alert immobility in the pres- ence of a predator. He points out that a freeze may be suc- ceeded by ight or, if attacked and captured by a predator, by a “deeper state of freeze—one associated with appar- ent unresponsiveness and with marked changes in basal autonomic state” (2001, p. 76, my italics). This state of helplessness lasts for up to 30 minutes, and is accompa- nied by marked bradycardia (heart rate deceleration) and a pronounced state of “deep” parasympathetic vagal tone. Recall that Porges (1995) described an “involuntary and often prolonged characteristic pattern of vagal out ow from the dorsal vagal nucleus” (1995, p. 228). I equate this with a deep dissociative state which, if prolonged, is the psychobiological engine of pathological dissociation.
Studies in basic biology offer further information about the psychobiological mechanism of this deeper state of freeze. Gabrielsen and Smith (1985) have explored the physiological responses that underlie basic defenses (i.e., “threat-induced behavior”) in all animals. In reac- tion to an environmental threat (a predator), an organism can respond in various ways: the organism may ght or ee in fear. Both responses are associated with tachy- cardia and increased activity, re ective of sympathetic hyperarousal. Gabrielson and Smith describe two active defenses (i.e., fight or flight) and two passive defenses (i.e., freezing and paralysis). The passive, immobile defenses differ; freezing occurs in response to visual or auditory stimuli of a predator’s approach, whereas paralysis occurs in response to strong tactile stimulation by the predator.
Again, clues come from studies in basic biology and neuroscience. Citing this literature, Scaer states that freeze behavior is a state of alert immobility in the pres- ence of a predator. He points out that a freeze may be suc- ceeded by ight or, if attacked and captured by a predator, by a “deeper state of freeze—one associated with appar- ent unresponsiveness and with marked changes in basal autonomic state” (2001, p. 76, my italics). This state of helplessness lasts for up to 30 minutes, and is accompa- nied by marked bradycardia (heart rate deceleration) and a pronounced state of “deep” parasympathetic vagal tone. Recall that Porges (1995) described an “involuntary and often prolonged characteristic pattern of vagal out ow from the dorsal vagal nucleus” (1995, p. 228). I equate this with a deep dissociative state which, if prolonged, is the psychobiological engine of pathological dissociation.
Studies in basic biology offer further information about the psychobiological mechanism of this deeper state of freeze. Gabrielsen and Smith (1985) have explored the physiological responses that underlie basic defenses (i.e., “threat-induced behavior”) in all animals. In reac- tion to an environmental threat (a predator), an organism can respond in various ways: the organism may ght or ee in fear. Both responses are associated with tachy- cardia and increased activity, re ective of sympathetic hyperarousal. Gabrielson and Smith describe two active defenses (i.e., fight or flight) and two passive defenses (i.e., freezing and paralysis). The passive, immobile defenses differ; freezing occurs in response to visual or auditory stimuli of a predator’s approach, whereas paralysis occurs in response to strong tactile stimulation by the predator.
Intriguingly, the organism is alert during a freeze, but “unconscious” during paralysis; parasympathetic heart- rate deceleration, which they term emotional bradycar- dia, occurs in both. Biologists call this fear bradycardia or alarm bradycardia (Jacobsen, 1979). I suggest that the differentiation of freeze versus paralysis is the same dif- ference as (1) Scaer’s freeze versus deeper state of freeze, and (2) Main’s type D freezing when the infant is “alarmed by the parent” versus Tronick’s still-face collapse, loss of postural control, and “dissipation of consciousness.” Because high levels of dorsal vagal activation are asso- ciated with dangerous bradycardia, these data strongly suggest that the mother’s failure to repair infant dissocia- tive states of deep freeze would be a potent generator of psychopathogenesis. Recall Bremner and Brett’s (1997) caution: “dissociation represents an effective short-term strategy that is detrimental to long-term functioning.”
Gabrielsen and Smith (1985) discussed another term for the deep freeze state—feigned death—a defense mechanism that is utilized by a number of vertebrates, amphibians, reptiles, birds, and mammals (including humans). A mild threat (the face of a human in this study) to the American opossum elicited freezing and a 12% decrease in heart rate. A more severe threat (vigor- ous tactile shaking), however, induced death feigning and a stunning 46% decrease of heart rate deceleration. In a conception that is congruent with the neurobiological model of dissociation outlined in this chapter, Gabrielsen and Smith (1985) have postulated that (1) the sudden depression in heart rate and respiration strongly indicates that higher CNS structures are directly controlling the parasympathetic cardiovascular “centres” in the medulla and (2) this alteration re ects a severe decrease in oxygen consumption and body temperature.
I propose: (1) the freeze response is a dorsal vagal para- sympathetic energy-conserving state that is coupled with, but dominant over, a weaker state of energy-expending sympathetic arousal; and (2) during the collapsed state of death feigning, the two ANS components are uncoupled. Thus, in the deep freeze there is no sympathetic activity (low levels of vasopressin, catecholamines, cortisol) and pure dorsal vagal activation that produces massive bra- dycardia (Cheng et al., 1999) and a hypometabolic state. This decrease in oxygen consumption during dissociative death feigning is congruent with the role of the dorsal vagal system in hypoxic responses (Porges, 2001; Potter & McCloskey, 1986) and with the reptilian diving re ex, an energy conservation strategy of heart rate deceleration that acts as a “metabolic defense” (Boutiler, 2001; Guppy & Withers, 1999).
Gabrielsen and Smith (1985) discussed another term for the deep freeze state—feigned death—a defense mechanism that is utilized by a number of vertebrates, amphibians, reptiles, birds, and mammals (including humans). A mild threat (the face of a human in this study) to the American opossum elicited freezing and a 12% decrease in heart rate. A more severe threat (vigor- ous tactile shaking), however, induced death feigning and a stunning 46% decrease of heart rate deceleration. In a conception that is congruent with the neurobiological model of dissociation outlined in this chapter, Gabrielsen and Smith (1985) have postulated that (1) the sudden depression in heart rate and respiration strongly indicates that higher CNS structures are directly controlling the parasympathetic cardiovascular “centres” in the medulla and (2) this alteration re ects a severe decrease in oxygen consumption and body temperature.
I propose: (1) the freeze response is a dorsal vagal para- sympathetic energy-conserving state that is coupled with, but dominant over, a weaker state of energy-expending sympathetic arousal; and (2) during the collapsed state of death feigning, the two ANS components are uncoupled. Thus, in the deep freeze there is no sympathetic activity (low levels of vasopressin, catecholamines, cortisol) and pure dorsal vagal activation that produces massive bra- dycardia (Cheng et al., 1999) and a hypometabolic state. This decrease in oxygen consumption during dissociative death feigning is congruent with the role of the dorsal vagal system in hypoxic responses (Porges, 2001; Potter & McCloskey, 1986) and with the reptilian diving re ex, an energy conservation strategy of heart rate deceleration that acts as a “metabolic defense” (Boutiler, 2001; Guppy & Withers, 1999).
Parasympathetic vagal tone also increases “during entrance in hibernation, a long lasting disengagement from the external environment characterized by decreases in heart rate, breathing frequency, and metabolic rate” (Recordati, 2003, p. 4). The hypometabolic changes in brain plasticity (Von der Ohe et al., 2006) and in mito- chondrial energy generation (Eddy et al., 2006) during the hibernation state of torpor (apathy, low responsive- ness) may thus be directly related to the neurobiological mechanism of dissociation. This shift into hypoxia also mediates “suspended animation” in developing systems (Padilla & Roth, 2001; Teodoro & O’Farrell, 2003). These data support my model of dissociation as a hypo- metabolic state (Schore, 2001b), a Janetian de ciency of psychological energy.
Note the similarity of this “emotional bradycardia” to (1) the earlier psychoneurobiological portraits of the infant’s parasympathetic-driven heart rate deceleration and dis- sociative response to attachment trauma, (2) Kestenberg’s (1985) dead spots in the infant’s subjective experience, and (3) Powles’s (1992) state of conservation-withdrawal in which the stressed individual passively disengages by “the risky posture of feigning death.” The clinical litera- ture refers to dissociation as “a last resort defensive strat- egy” (Dixon, 1998) and “a submission and resignation to the inevitability of overwhelming, even psychically dead- ening danger” (Davies & Frawley, 1994, p. 65).
CONCLUSIONS AND IMPLICATIONS FOR DSM–V
We are currently experiencing a period of rapid change within, and perhaps more importantly between, the theo- retical and applied sciences. The DSM-V conception of dissociation should be substantially impacted by the advances in basic science and clinical knowledge that have occurred during “the decade of the brain.”
With what we now understand about development and brain behavior (structure-function) relationships, can we now more precisely characterize the classic statement of Classen, Koopman, and Spiegel: Trauma victims who lack the cognitive and emotional structures to immediately assimilate the experience use the state of consciousness known as dissociation to escape from the full psychological impact of the event. (1993, p. 29) In other words, how do cognition and emotion relate to dissociation? Can we now locate these cognitive and emotional structures in known brain systems?
Note the similarity of this “emotional bradycardia” to (1) the earlier psychoneurobiological portraits of the infant’s parasympathetic-driven heart rate deceleration and dis- sociative response to attachment trauma, (2) Kestenberg’s (1985) dead spots in the infant’s subjective experience, and (3) Powles’s (1992) state of conservation-withdrawal in which the stressed individual passively disengages by “the risky posture of feigning death.” The clinical litera- ture refers to dissociation as “a last resort defensive strat- egy” (Dixon, 1998) and “a submission and resignation to the inevitability of overwhelming, even psychically dead- ening danger” (Davies & Frawley, 1994, p. 65).
CONCLUSIONS AND IMPLICATIONS FOR DSM–V
We are currently experiencing a period of rapid change within, and perhaps more importantly between, the theo- retical and applied sciences. The DSM-V conception of dissociation should be substantially impacted by the advances in basic science and clinical knowledge that have occurred during “the decade of the brain.”
With what we now understand about development and brain behavior (structure-function) relationships, can we now more precisely characterize the classic statement of Classen, Koopman, and Spiegel: Trauma victims who lack the cognitive and emotional structures to immediately assimilate the experience use the state of consciousness known as dissociation to escape from the full psychological impact of the event. (1993, p. 29) In other words, how do cognition and emotion relate to dissociation? Can we now locate these cognitive and emotional structures in known brain systems?
COGNITIVE STRUCTURES AND DISSOCIATION
DSM-IV de nes dissociation as a disruption in the usu- ally integrated functions of consciousness, perception, and memory. It is now well established that memory is not a single process; DSM-V’s de nition of dissociation should re ect this fact. In fact studies on trauma and dissociation have made important contributions to the distinction between declarative-explicit-semantic mem- ory (i.e., conscious recall of traumatic experiences) and procedural-implicit-nonverbal memory (i.e., unconscious organization of emotional memories and storage of con- ditioned sensorimotor traumatic responses). According to Scaer, “Although declarative memory may account for much of the arousal-based cognitive symptoms of PTSD, procedural memory provides the seemingly unbreak- able conditioned link that perpetuates the neural cycle of trauma and dissociation” (2001, p. 76).
Recent data from developmental and affective neu- roscience re ect the importance of implicit-procedural memory in dissociation. Kandel (1999) has noted that “the infant relies primarily on its procedural memory sys- tems” during “the rst 2-3 years of life,” a period of right hemispheric dominance (Chiron et al., 1997). Relational trauma can be stored at an early age: “The clinical data, reinforced by research ndings, indicate that preverbal children, even in the rst year of life, can establish and retain some form of internal representation of a traumatic event over signi cant periods of time” (Gaensbauer, 2002, p. 259). This early representation is encoded in nonverbal implicit-procedural memory that matures well before verbal explicit-declarative memory does. Such representations of attachment trauma are encoded as a “frozen whole” (Gendlin, 1970); they include “non- verbal presymbolic forms of relating” that “protect the infant from trauma and continue to be used by patients to avoid retraumatization” (Kiersky & Beebe, 1994, p. 389), that is, the right brain defensive regulatory strategy of dissociation.
A growing body of studies show that “the right hemi- sphere has been linked to implicit information process- ing, as opposed to the more explicit and more conscious processing tied to the left hemisphere” (Happaney et al., 2004, p. 7). Recall, pathological dissociative detachment “escapes conscious control and is often experienced pas- sively, as automatic or re exive” (Allen et al., 1998, p. 163). Although trauma seriously impairs left-lateralized
declarative memory and hippocampal function, dissocia- tive mechanisms are ef ciently encoded in right-lateral- ized amygdala-driven implicit memory that is primarily regulatory, automatized, and unconscious. Research on the memory mechanisms of PTSD has recently focused on de cits in hippocampal function and impairments of con- scious explicit memory. Stress-induced elevations of corti- sol impair declarative memory (Kirschbaum et al., 1996). Hippocampal dysfunction in PTSD is more lateralized to the left hemisphere (Mohanakrishnan Menon et al., 2003).
PTSD models are now shifting from the hippocam- pus to the amygdala, from explicit memory of places to implicit memory of faces. Chronic stress induces con- trasting patterns of dendritic remodeling in hippocam- pal and amygdaloid neurons, leading to (1) a loss of hippocampal inhibitory control, (2) a gain of excitatory control by the amygdala, and (3) a resulting imbalance in HPA functioning (Vyas, Mitra, Shankaranarayana Rao, & Chattarji, 2002). Recent clinical models of PTSD sug- gest that the amygdala inhibits hippocampal functioning during high levels of arousal, thereby mediating a diminu- tion of explicit memory for peritraumatic events (Layton & Krikorian, 2002). McNally and Amir (1996) argue that the amygdala is centrally involved in the consolidation of the traumatic experience and in the storage of perceptual implicit memory for trauma-related information.
It is important to note that dissociation not only impairs explicit memory, but also impairs higher levels of implicit memory. J. Krystal and his colleagues are describing the disconnection that occurs under extremes of arousal between the explicit dorsal regulation system involved in the “verbal components of emotional stimuli” and the implicit ventral regulation system involved in the automatic regulation of emotional stimuli (Phillips et al., 2003). This disconnection produces cognitive dissocia- tion. On the other hand, somatic dissociation—indeed the fundamental mechanism of pathological dissociation itself—re ects an impairment in the ventral regulation system and, thus, a de cit in the implicit identi cation and regulation of autonomic responses and the produc- tion of affective states.
Two common misunderstandings have confounded the dissociation literature. The rst common misunderstand- ing is to de ne consciousness narrowly as (1) re ective consciousness and (2) correlated with left hemispheric verbal functions. In fact, another form of consciousness exists; primary consciousness relates emotional and vis- ceral information about the biological self to information about outside reality. Edelman (1989) claims that pri- mary consciousness is lateralized to the right brain. Thus, somatic dissociation represents a disruption of primary consciousness. The second common misunderstand- ing is to equate cognition with conscious verbal menta- tion and to view the left hemisphere as the sole domain of cognition. This is untrue. Cognition is the faculty of knowledge, but knowing can be both conscious and nonconscious. Information about external and internal environments is appraised via nonconscious as well as conscious mechanisms.
PTSD models are now shifting from the hippocam- pus to the amygdala, from explicit memory of places to implicit memory of faces. Chronic stress induces con- trasting patterns of dendritic remodeling in hippocam- pal and amygdaloid neurons, leading to (1) a loss of hippocampal inhibitory control, (2) a gain of excitatory control by the amygdala, and (3) a resulting imbalance in HPA functioning (Vyas, Mitra, Shankaranarayana Rao, & Chattarji, 2002). Recent clinical models of PTSD sug- gest that the amygdala inhibits hippocampal functioning during high levels of arousal, thereby mediating a diminu- tion of explicit memory for peritraumatic events (Layton & Krikorian, 2002). McNally and Amir (1996) argue that the amygdala is centrally involved in the consolidation of the traumatic experience and in the storage of perceptual implicit memory for trauma-related information.
It is important to note that dissociation not only impairs explicit memory, but also impairs higher levels of implicit memory. J. Krystal and his colleagues are describing the disconnection that occurs under extremes of arousal between the explicit dorsal regulation system involved in the “verbal components of emotional stimuli” and the implicit ventral regulation system involved in the automatic regulation of emotional stimuli (Phillips et al., 2003). This disconnection produces cognitive dissocia- tion. On the other hand, somatic dissociation—indeed the fundamental mechanism of pathological dissociation itself—re ects an impairment in the ventral regulation system and, thus, a de cit in the implicit identi cation and regulation of autonomic responses and the produc- tion of affective states.
Two common misunderstandings have confounded the dissociation literature. The rst common misunderstand- ing is to de ne consciousness narrowly as (1) re ective consciousness and (2) correlated with left hemispheric verbal functions. In fact, another form of consciousness exists; primary consciousness relates emotional and vis- ceral information about the biological self to information about outside reality. Edelman (1989) claims that pri- mary consciousness is lateralized to the right brain. Thus, somatic dissociation represents a disruption of primary consciousness. The second common misunderstand- ing is to equate cognition with conscious verbal menta- tion and to view the left hemisphere as the sole domain of cognition. This is untrue. Cognition is the faculty of knowledge, but knowing can be both conscious and nonconscious. Information about external and internal environments is appraised via nonconscious as well as conscious mechanisms.
In fact, right brain appraisal of threat in the social environment is performed implicitly and very quickly, below conscious awareness (see Schore, 2003b, 2004, 2005a). Thus, cognition includes right-lateralized social cognition of faces; this allows for the appraisal of extero- ceptive social cues in a relational intersubjective context. Interoceptive sensitivity (Barrett et al., 2004), the track- ing of somatovisceral information coming up from the body, is also a cognitive process. Both exteroceptive pro- cessing of social cues and interoceptive sensitivity to the body are cognitive operations of the right hemisphere, the locus of implicit learning (Hugdahl, 1995).
Pathological dissociation impairs implicit cognitive appraisal of the external world and the internal world. New models of dissociation must re ect these ndings that shift the emphasis from explicit to implicit memory and from left hemisphere to right hemisphere.
RIGHT BRAIN EMOTIONAL STRUCTURES AND DISSOCIATION
In DSM-IV, the clinical manifestations of dissociation include derealization and amnesia for autobiographical information and derealization, phenomena that re ect a heavy emphasis on cognition. However, psychiatry, psy- chology, and neuroscience are now emphasizing the pri- macy of affect and affect regulation. This convergence suggests that DSM-V should (re)incorporate emotion into the de nition of dissociation. The contemporary revital- ization of the work of Janet (Nemiah, 1989; Putnam, 1989; Van der Hart, Nijenhuis, & Steele, 2006) clearly implies a return to a model of dissociation in which “vehement emotions” and “extreme emotional arousal” are central, rather than secondary, to cognition. A large body of con- verging clinical and experimental research suggests that severe affect dysregulation lies at the core of the dis- integration that occurs in the dissociative response to overwhelming traumatic experience.
The original Janetian concept of dissociation implies that the trigger for disintegration is an unbearable emo- tional reaction and an appraisal that the experience is overwhelming. What is disassociated is a structural system that rapidly detects, processes, and copes with unbearable emotional information and overwhelming survival threat. This characterization applies to the right brain, which is dominant for the reception (Adolphs et al., 1996; Anderson & Phelps, 2000; Borod et al., 1998; George et al., 1996; Lucas et al., 2003; Nakamura et al., 1999) and expression (Borod, Haywood, & Koff, 1997; Mandal & Ambady, 2004) of emotion, as well as respond- ing to preattentive negative emotional stimuli (Kimura et al., 2004), coping with negative affects (Davidson et al., 1990; Silberman & Weingartner, 1986), and controlling vital functions that support survival and enable the organ- ism to cope with stressors (Wittling & Schweiger, 1993).
Pathological dissociation impairs implicit cognitive appraisal of the external world and the internal world. New models of dissociation must re ect these ndings that shift the emphasis from explicit to implicit memory and from left hemisphere to right hemisphere.
RIGHT BRAIN EMOTIONAL STRUCTURES AND DISSOCIATION
In DSM-IV, the clinical manifestations of dissociation include derealization and amnesia for autobiographical information and derealization, phenomena that re ect a heavy emphasis on cognition. However, psychiatry, psy- chology, and neuroscience are now emphasizing the pri- macy of affect and affect regulation. This convergence suggests that DSM-V should (re)incorporate emotion into the de nition of dissociation. The contemporary revital- ization of the work of Janet (Nemiah, 1989; Putnam, 1989; Van der Hart, Nijenhuis, & Steele, 2006) clearly implies a return to a model of dissociation in which “vehement emotions” and “extreme emotional arousal” are central, rather than secondary, to cognition. A large body of con- verging clinical and experimental research suggests that severe affect dysregulation lies at the core of the dis- integration that occurs in the dissociative response to overwhelming traumatic experience.
The original Janetian concept of dissociation implies that the trigger for disintegration is an unbearable emo- tional reaction and an appraisal that the experience is overwhelming. What is disassociated is a structural system that rapidly detects, processes, and copes with unbearable emotional information and overwhelming survival threat. This characterization applies to the right brain, which is dominant for the reception (Adolphs et al., 1996; Anderson & Phelps, 2000; Borod et al., 1998; George et al., 1996; Lucas et al., 2003; Nakamura et al., 1999) and expression (Borod, Haywood, & Koff, 1997; Mandal & Ambady, 2004) of emotion, as well as respond- ing to preattentive negative emotional stimuli (Kimura et al., 2004), coping with negative affects (Davidson et al., 1990; Silberman & Weingartner, 1986), and controlling vital functions that support survival and enable the organ- ism to cope with stressors (Wittling & Schweiger, 1993).
The human threat detection system is located in the subcortical areas of the right brain, especially in the right amygdala, which is specialized for detecting “unseen fear” (Morris et al., 1999), for fear conditioning (Fischer et al., 2002), for stress and emotionally related processes (Scicli et al., 2004), and for the expression of memory of aversively motivated experiences (Coleman-Mesches & McGaugh, 1995). In a study of predator-related stress- activation of the right amygdala and periaqueductal gray, Adamaec, Blundell, and Burton (2003) reported ndings that “implicate neuroplasticity in right hemispheric lim- bic circuitry in mediating long-lasting changes in nega- tive affect following brief but severe stress” (p. 1264). The right amygdala is regulated by the right insula, right anterior cingulate, and right orbitofrontal cortex; this pre- frontal hierarchical apex of the limbic system is activated in “situations involving survival” (Lipton et al., 1999) and functions as “a master regulator for organization of the brain’s response to threat” (Scaer, 2001). Indeed, “the right ventral medial prefrontal cortex plays a primary role in optimizing cautious and adaptive behavior in potentially threatening situations” (Sullivan & Gratton, 2002, p. 69).
Earlier in this chapter, I showed that secure attachment experiences allow for optimal maturation of the right orb- itofrontal cortex. Accordingly, the psychological princi- ple that secure attachment is the primary defense against trauma-induced psychopathology is directly related to the developmental neurobiological tenet that healthy attach- ment experiences facilitate the experience-dependent maturation of a right-lateralized affect regulatory sys- tem that can ef ciently modulate the extreme emotional arousal and vehement emotions of trauma. The capacity to consciously experience regulated negative (and posi- tive) emotional states is profoundly adaptive. Affects pro- vide an internal evaluation of our encounters with the environment (Lazarus, 1991); they allow for actual or expected changes in events that are important to the indi- vidual (Frijda, 1988).
Earlier in this chapter, I showed that secure attachment experiences allow for optimal maturation of the right orb- itofrontal cortex. Accordingly, the psychological princi- ple that secure attachment is the primary defense against trauma-induced psychopathology is directly related to the developmental neurobiological tenet that healthy attach- ment experiences facilitate the experience-dependent maturation of a right-lateralized affect regulatory sys- tem that can ef ciently modulate the extreme emotional arousal and vehement emotions of trauma. The capacity to consciously experience regulated negative (and posi- tive) emotional states is profoundly adaptive. Affects pro- vide an internal evaluation of our encounters with the environment (Lazarus, 1991); they allow for actual or expected changes in events that are important to the indi- vidual (Frijda, 1988).
In contrast, the relational context of a disorganized- disoriented insecure attachment acts as a growth-inhibiting environment that generates immature and inef cient orb- itofrontal systems, thereby precluding higher complex forms of affect regulation. Under stress, these immature prefrontal corticolimbic systems rapidly disorganize, dis- inhibiting lower subcortical systems that activate either states of hyperarousal or the primitive defense of dissoci- ation that counterbalances these states. When dissociated from top-down orbitofrontal in uences, an “exaggerated amygdala” response to masked facially expressed fearful reminders of traumatic events occurs in PTSD patients (Rauch et al., 2000). Characterological use of this “last- resort defensive strategy” precludes the capacity to con- sciously experience affective states, thereby forfeiting their adaptive use in interpersonal and intraorganismic functioning and further emotional development.
The symptomatology of dissociation re ects a struc- tural impairment of a right brain regulatory system and its accompanying de ciencies of affect regulation. The clinical principle that dissociation is detrimental to long- term functioning (Bremner & Brett, 1997) is directly related to the developmental observations that early- forming yet enduring disorganized insecure attachment associated with dissociative states is a primary risk factor for the development of mental disorders (Hesse & Main, 1999; Main, 1996), and to the neuropsychiatric observa- tions that affect dysregulation and right hemisphere dys- function play a prominent role in all psychiatric disorders (Cutting, 1992; Taylor et al., 1997).
Returning to Classen’s dictum (i.e., that individuals who lack the cognitive and emotional structures to assimilate trauma are predisposed to dissociation), it is important to note that ef cient orbitofrontal function is essential for “the conscious appreciation of the emotional signi cance of events” (Barbas et al., 2003). In normal subjects, the right orbitofrontal cortex shows “an enhanced response to consciously perceived, as opposed to neglected fearful faces” (Winston, Vuillemer, & Dolan, 2003, p. 1827); in PTSD patients that exhibit dissociative ashbacks, their right frontal lobe is dysfunctional (Berthier et al., 2001).
The orbitofrontal system is also critical for process- ing cognitive-emotional interactions (Barbas, 1995). This “thinking part of the emotional brain” (Goleman, 1995) functions as an “internal re ecting and organizing agency” (Kaplan-Solms & Solms, 1996) that is involved in “emotion-related learning” (Rolls, Hornak, Wade, & McGrath, 1994). It acts to “integrate and assign emotional- motivational signi cance to cognitive impressions; the association of emotion with ideas and thoughts” (Joseph, 1996) and “presents an important site of contact between emotional or affective information and mechanisms of action selection” (Rogers et al., 1999). These data suggest that dissociating trauma victims’ de cient cognitive and emotional structures are located in the right orbitofrontal structure and its cortical and subcortical connections.
The symptomatology of dissociation re ects a struc- tural impairment of a right brain regulatory system and its accompanying de ciencies of affect regulation. The clinical principle that dissociation is detrimental to long- term functioning (Bremner & Brett, 1997) is directly related to the developmental observations that early- forming yet enduring disorganized insecure attachment associated with dissociative states is a primary risk factor for the development of mental disorders (Hesse & Main, 1999; Main, 1996), and to the neuropsychiatric observa- tions that affect dysregulation and right hemisphere dys- function play a prominent role in all psychiatric disorders (Cutting, 1992; Taylor et al., 1997).
Returning to Classen’s dictum (i.e., that individuals who lack the cognitive and emotional structures to assimilate trauma are predisposed to dissociation), it is important to note that ef cient orbitofrontal function is essential for “the conscious appreciation of the emotional signi cance of events” (Barbas et al., 2003). In normal subjects, the right orbitofrontal cortex shows “an enhanced response to consciously perceived, as opposed to neglected fearful faces” (Winston, Vuillemer, & Dolan, 2003, p. 1827); in PTSD patients that exhibit dissociative ashbacks, their right frontal lobe is dysfunctional (Berthier et al., 2001).
The orbitofrontal system is also critical for process- ing cognitive-emotional interactions (Barbas, 1995). This “thinking part of the emotional brain” (Goleman, 1995) functions as an “internal re ecting and organizing agency” (Kaplan-Solms & Solms, 1996) that is involved in “emotion-related learning” (Rolls, Hornak, Wade, & McGrath, 1994). It acts to “integrate and assign emotional- motivational signi cance to cognitive impressions; the association of emotion with ideas and thoughts” (Joseph, 1996) and “presents an important site of contact between emotional or affective information and mechanisms of action selection” (Rogers et al., 1999). These data suggest that dissociating trauma victims’ de cient cognitive and emotional structures are located in the right orbitofrontal structure and its cortical and subcortical connections.
The DSM and ICD de nitions of dissociation both refer to a dis-association of a normally integrated system, but neither the DSM nor the ICD identify this system. In 1994, I described the unique neuroanatomical intercon- nectivity of the right hemisphere: This hemisphere, with dense reciprocal interconnections with limbic and subcortical structures (Tucker, 1981), is specialized to regulate arousal (Levy, Heller, Banich, & Burton, 1983) and to integrate perceptual processes (Semmes, 1968)…. It contains larger cortical areas than the left of intermodal associative zones that integrate pro- cessing of the three main sensory modalities (Goldberg & Costa, 1981)…. This right hemisphere, more so than the left, is structurally specialized for greater cross- modal integration (Chapanis, 1977; Tucker, 1992), per- haps due to the facts that it contains more myelinated bers that optimize transfer across regions than the left (Gur et al., 1980), and that it is specialized to represent multiple information channels in parallel (Bradshaw & Nettleton, 1981).
Recent studies demonstrate that when the intracorti- cal connections within this hemisphere are functioning in an optimal manner, the hemisphere adaptively integrates cross-sensory information and thereby subserves the inte- gration of different representational information systems (Calvert et al., 2001; Raij et al., 2000). However, under the extreme stress of both hyperarousal and hypoarousal, the right cortical hemisphere loses its capacity to inte- grate posterior cortical sensory processing, thus causing the disruption in the integration of perceptual informa- tion depicted in the current DSM-IV. Moreover, under these intensely stressful periods, the right brain also loses its capacity to act as an integrated vertical cortical- subcortical system.
When this happens, limbic-autonomic information is processed only at the lowest right amygdala level and blocked from access to higher right anterior cingulate and orbitofrontal areas. Such “partially processed” informa- tion (Whitlock, 1967; Ludwig, 1972) cannot be integrated into awareness as a conscious, subjectively experienced emotion. Instead, such “partially processed” somatic information is expressed as what Janet termed “excessive or inappropriate physical responses” and Freud described as “bizarre physical symptoms.” In short, dissociation refers to the loss of the integrative capacity of the verti- cally organized emotional right brain.
Recent studies demonstrate that when the intracorti- cal connections within this hemisphere are functioning in an optimal manner, the hemisphere adaptively integrates cross-sensory information and thereby subserves the inte- gration of different representational information systems (Calvert et al., 2001; Raij et al., 2000). However, under the extreme stress of both hyperarousal and hypoarousal, the right cortical hemisphere loses its capacity to inte- grate posterior cortical sensory processing, thus causing the disruption in the integration of perceptual informa- tion depicted in the current DSM-IV. Moreover, under these intensely stressful periods, the right brain also loses its capacity to act as an integrated vertical cortical- subcortical system.
When this happens, limbic-autonomic information is processed only at the lowest right amygdala level and blocked from access to higher right anterior cingulate and orbitofrontal areas. Such “partially processed” informa- tion (Whitlock, 1967; Ludwig, 1972) cannot be integrated into awareness as a conscious, subjectively experienced emotion. Instead, such “partially processed” somatic information is expressed as what Janet termed “excessive or inappropriate physical responses” and Freud described as “bizarre physical symptoms.” In short, dissociation refers to the loss of the integrative capacity of the verti- cally organized emotional right brain.
These neurobiological data mirror the ICD-10 descrip- tion of dissociation—as a partial or complete loss of control of body movements. Recall Crucian’s (2000) description of a right hemisphere-dependent dissocia- tion between the emotional evaluation of an event and the physiological reaction to that event, and Spitzer’s (2004) observation that the dissociative symptoms of deperson- alization re ect a lack of right hemispheric integration. In a study of “out-of-body” experiences (i.e., episodes in which “a person’s consciousness seems to become detached from the body and take up a remote viewing position”), Blanke et al. (2002) report that “the experi- ence of dissociation of self from the body is a result of failure to integrate complex somatosensory and vestibu- lar function” (p. 269). Importantly, right medial temporal lobe activation is seen during the patient’s dissociative AQ3 episode (see Figure 8.3).
Thus, the assertion that “impaired self-awareness seems to be associated predominantly with right hemi- sphere dysfunction” (Andelman et al., 2004, p. 831) refers to a de cit in the right brain corporeal self during dis- sociative disruptions of identity. Scaer (2001) contends that the least appreciated manifestations of traumatic dissociation are perceptual alterations and somatic symptoms. In earlier work, I have offered a model by which attachment trauma alters the development of right-lateralized limbic-autonomic circuits that process visceral-somatic information and set the stage for the characterological predisposition to somatoform dissocia- tion (Schore, 2001b, 2002). This chapter elaborates this model and strongly indicates that somatoform dissocia- tion should be incorporated into DSM-V.
This model also gives important clues for identifying psychobiological markers of somatoform dissociation. I have described the hypoarousal and heart rate decelera- tion of dissociating human infants and adults. In addi- tion I have also presented biological data to show that this passive defense mechanism is common to all vertebrates. In this “last resort defensive strategy,” bradycardia occurs in response to survival threat. This rapid shift from a hypermetabolic state of hyperarousal into a hypometa- bolic state of hypoarousal re ects a signi cant homeo- static alteration of brain-cardiovascular interactions through higher CNS adjustments of the sympathetic and especially the medullary dorsal vagal parasympathetic energy-conserving branches of the ANS. The activation of “the escape when there is no escape” (i.e., somatic dis- sociation) represents a reorganization of vertical circuits in the right hemisphere, which is dominant for cardiovas- cular (Erciyas et al., 1999; Yoon et al., 1997) and survival (Wittling & Schweiger, 1993) functions.
In traumatizing contexts where active coping mech- anisms are blocked or irrelevant, lateralized limbic- autonomic structures of the central autonomic network (ventromedial prefrontal cortex, anterior cingulate, insula, and amygdala) trigger an instantaneous reorga- nization of the vagal circuit of emotion regulation on the right side of the brain (Porges et al., 1994)—speci cally, a shift in dominance from ventral vagal to dorsal vagal parasympathetic systems. Bradycardia is controlled by orbitofrontal, cingulate, and insula cortices (Buchanan, Powell, & Valentine, 1984; Hardy & Holmes, 1988; Kaada, 1960). Tracing down this limbic-autonomic ver- tical circuit, each of these cortical structures, like the central nucleus of the amygdala, regulates the lateral hypothalamus (Loewy,1991); the lateral hypothalamus modulates dorsal vagal complex neurons (Jiang, Fogel, & Zhang, 2003); cardiac vagal motoneurons lateralized on the right side of the medulla, down the right vagus, regulate the heart (Rentero et al., 2002); and ultimately. parasympathetic efferent neurons that are primarily located in the right atrial ganglionated plexus (Stauss, 2003) trigger a hypometabolic response of “emotional bradycardia.”
In traumatizing contexts where active coping mech- anisms are blocked or irrelevant, lateralized limbic- autonomic structures of the central autonomic network (ventromedial prefrontal cortex, anterior cingulate, insula, and amygdala) trigger an instantaneous reorga- nization of the vagal circuit of emotion regulation on the right side of the brain (Porges et al., 1994)—speci cally, a shift in dominance from ventral vagal to dorsal vagal parasympathetic systems. Bradycardia is controlled by orbitofrontal, cingulate, and insula cortices (Buchanan, Powell, & Valentine, 1984; Hardy & Holmes, 1988; Kaada, 1960). Tracing down this limbic-autonomic ver- tical circuit, each of these cortical structures, like the central nucleus of the amygdala, regulates the lateral hypothalamus (Loewy,1991); the lateral hypothalamus modulates dorsal vagal complex neurons (Jiang, Fogel, & Zhang, 2003); cardiac vagal motoneurons lateralized on the right side of the medulla, down the right vagus, regulate the heart (Rentero et al., 2002); and ultimately. parasympathetic efferent neurons that are primarily located in the right atrial ganglionated plexus (Stauss, 2003) trigger a hypometabolic response of “emotional bradycardia.”
Electrodes stimulated at right hemispheric sites trigger depersonalization reactions in a 43-year-old woman with right temporal lobe (starred) epilepsy. Locations are magenta, motor; green, somatosensory cortex; turquoise, audi- tory cortex. Yellow, site at which out-of-body experience, body- part illusions and vestibular responses were induced (arrow). During these dissociative states the patient states “I see myself lying on the bed, from above, but I only see my legs and lower trunk.” From Blanke et al., 2002.
This pattern of dis-organization, which also occurs in “posttraumatic stress disorders and the consequences of child abuse,” is described by Porges (2000):
[W]hen mobilization strategies ( ght- ight behaviors) are ineffective in removing the individual from the stressor and modulating stress, then the nervous sys- tem may degrade to a phylogenetically earlier level of organization … (This) may re ect a neural strategy associated with immobilization (e.g. passive avoidance, death feigning, dissociative states) that would require a reduction of energy resources. (p. 15, my italics)
I have cited several clinical studies that indicate that parasympathetic emotional bradycardia is a psychobio- logical marker of pathological dissociation. Peritraumatic dissociation associated with low heart rate has been reported by Grif n, Resick, and Mechanic (1997), Lanius et al. (2002), Koopman et al. (2004), and Williams, Haines, and Sale (2003). In a clinical study, Schmahl and colleagues (2002) documented a heart rate decline while a PTSD patient with a history of childhood abuse was right insula is activated by perceptual awareness of threat (Critchley, Mathias, & Dolan, 2002), anticipa- tion of emotionally aversive visual stimuli (Simmons et al., 2004) and harm avoidance (Paulus et al., 2003). In normal functioning, the right insula supports a repre- sentation of visceral responses accessible to awareness (Critchley et al., 2004). On the other hand, neurological damage of the right insula in infancy is associated with abnormal bradycardia (Seeck et al., 2003). Increased right insula activity is also found in adult subjects with bradycardia (Volkow et al., 2000). These studies suggest that the right insula may play a key role in somatoform dissociation.
In short, developmental and neurobiological data suggest that DSM-V can specify a neuropsychobiologi- cal marker for somatic dissociation—namely, heart rate deceleration in response to intersubjective contexts that are associated with nonconsciously perceived survival threat.
EARLY ATTACHMENT TRAUMA AND THE PSYCHOPATHOGENESIS OF DISSOCIATION
In the nal part of this work, I would like to return to the problem of psychopathogenesis. Over 15 years ago, Van der Kolk and Van der Hart (1989), and Spiegel and Cardeña (1991) returned to the work of Janet, proposing
[W]hen mobilization strategies ( ght- ight behaviors) are ineffective in removing the individual from the stressor and modulating stress, then the nervous sys- tem may degrade to a phylogenetically earlier level of organization … (This) may re ect a neural strategy associated with immobilization (e.g. passive avoidance, death feigning, dissociative states) that would require a reduction of energy resources. (p. 15, my italics)
I have cited several clinical studies that indicate that parasympathetic emotional bradycardia is a psychobio- logical marker of pathological dissociation. Peritraumatic dissociation associated with low heart rate has been reported by Grif n, Resick, and Mechanic (1997), Lanius et al. (2002), Koopman et al. (2004), and Williams, Haines, and Sale (2003). In a clinical study, Schmahl and colleagues (2002) documented a heart rate decline while a PTSD patient with a history of childhood abuse was right insula is activated by perceptual awareness of threat (Critchley, Mathias, & Dolan, 2002), anticipa- tion of emotionally aversive visual stimuli (Simmons et al., 2004) and harm avoidance (Paulus et al., 2003). In normal functioning, the right insula supports a repre- sentation of visceral responses accessible to awareness (Critchley et al., 2004). On the other hand, neurological damage of the right insula in infancy is associated with abnormal bradycardia (Seeck et al., 2003). Increased right insula activity is also found in adult subjects with bradycardia (Volkow et al., 2000). These studies suggest that the right insula may play a key role in somatoform dissociation.
In short, developmental and neurobiological data suggest that DSM-V can specify a neuropsychobiologi- cal marker for somatic dissociation—namely, heart rate deceleration in response to intersubjective contexts that are associated with nonconsciously perceived survival threat.
EARLY ATTACHMENT TRAUMA AND THE PSYCHOPATHOGENESIS OF DISSOCIATION
In the nal part of this work, I would like to return to the problem of psychopathogenesis. Over 15 years ago, Van der Kolk and Van der Hart (1989), and Spiegel and Cardeña (1991) returned to the work of Janet, proposing
that dissociation is a response to “overwhelming” emo- tional experience, particularly in childhood. At the end of the last decade, several major theoreticians in traumatol- ogy echoed this conclusion. Putnam et al. asserted that “numerous clinical studies have established that elevated levels of dissociation are signi cantly associated with histories of antecedent trauma” (1996, p. 673). Van der Kolk and colleagues stated that “numerous studies have demonstrated a strong relation between trauma and dis- sociative symptoms” (1996, p. 85). Indeed, a large body of research in the psychiatric and psychological (e.g., Bowman & Markand, 1996; Chu & Dill, 1990; Coons et al., 1989; Draijer & Langeland, 1999; Gershuny & Thayer, 1999; Irwin, 1994; Lipschitz et al., 1996; Merckelbach
As this patient diagnosed with PTSD and bor- derline personality disorder heard her trauma script, she dis- played an intense emotional reaction and her heart rate rose by 11 bpm. While listening to an abandonment script she dissoci- ated. She had the impression that things were moving in slow motion, that things seemed unreal, and that she was watching the situtation as an observer. She felt disconnected from her own body and the sense of her body felt changed. Duing this period her heart rate fell by 14 bpm. After the interview the dissociative state lasted for a few more minutes. From Schmahl et al. 2002. & Muris, 2001; Mulder et al., 1998; Nash et al., 1993; Sanders, McRoberts, & Tollefsin, 1989) and neurological (Alper et al., 1993; Kuyk et al., 1999) literatures now sup- ports the link between childhood trauma and pathologi- cal dissociation.
Although these studies are convincing, the precise psychopathogenetic mechanism by which early trauma produces a later predisposition to pathological dissocia- tion has not been identi ed. The more general develop- mental question of how early traumatic psychological experience generates de cits of later adaptive function- ing is, in fact, the central issue of psychopathogenesis. Here, an interdisciplinary perspective can provide more detailed and complex models. Developmental psychopa- thology provides a theoretical perspective for “under- standing the causes, determinants, course, sequelae, and treatment of psychopathological disorders by inte- grating knowledge from multiple disciplines within an ontogenetic framework” (Cicchetti, 1994, p. 286). Developmental psychologists have demonstrated a strong link between early attachment trauma and dis- sociation (Ogawa et al., 1997; Carlson, Yates, & Sroufe, this volume; Dutra, Bianchi, Lyons-Ruth, & Siegel, this volume). Neuropsychiatrists have established that “the overwhelming stress of maltreatment in childhood is associated with adverse in uences on brain develop- ment” (De Bellis, 1999, p. 1281).
My work in developmental psychopathology inte- grates attachment theory, psychiatry, and developmental affective neuroscience in order to explore how attach- ment trauma alters the developmental trajectory of the right brain (Schore, 1994, 2003a, 2003b). From a devel- opmental viewpoint, early abuse and neglect generates disorganized-disoriented attachment which endures into adolescence and adulthood, and acts as a risk fac- tor for later psychiatric disorders (Schore, 2001b). From a psychiatry viewpoint, “maltreatment-related” (Beer & De Bellis, 2002) or “pediatric” (Carrion et al., 2001) PTSD is the short-term negative effect; a predisposition to later psychiatric disorders is the negative long-term effect. From a developmental neuroscience viewpoint, early abuse and neglect have immediate impact on the developing right brain during a critical growth period; this produces an immature right brain that has a limited capacity to regulate intense affective states. These per- spectives converge on a basic developmental principle: early trauma is critical to the genesis of an enduring pre- disposition to pathological dissociation.
I have offered extensive evidence to show that rela- tional traumatic attachment experiences are “affectively burnt in” (Stuss & Alexander, 1999) limbic-autonomic
My work in developmental psychopathology inte- grates attachment theory, psychiatry, and developmental affective neuroscience in order to explore how attach- ment trauma alters the developmental trajectory of the right brain (Schore, 1994, 2003a, 2003b). From a devel- opmental viewpoint, early abuse and neglect generates disorganized-disoriented attachment which endures into adolescence and adulthood, and acts as a risk fac- tor for later psychiatric disorders (Schore, 2001b). From a psychiatry viewpoint, “maltreatment-related” (Beer & De Bellis, 2002) or “pediatric” (Carrion et al., 2001) PTSD is the short-term negative effect; a predisposition to later psychiatric disorders is the negative long-term effect. From a developmental neuroscience viewpoint, early abuse and neglect have immediate impact on the developing right brain during a critical growth period; this produces an immature right brain that has a limited capacity to regulate intense affective states. These per- spectives converge on a basic developmental principle: early trauma is critical to the genesis of an enduring pre- disposition to pathological dissociation.
I have offered extensive evidence to show that rela- tional traumatic attachment experiences are “affectively burnt in” (Stuss & Alexander, 1999) limbic-autonomic
circuits of the cortical and subcortical components of the right brain during its critical period of growth. Basic research in neuroscience and neuropsychiatry rmly supports the following principles: (1) “early adverse developmental experiences may leave behind a per- manent physiological reactivity in limbic areas of the brain” (Post, Weiss, & Leverich, 1994); (2) emotional and social deprivation interfere with the normal devel- opment of the synaptic architecture and lead to “neu- rological scars” which underlie “subsequent behavioral and cognitive de cits” (Poeggel & Braun, 1996; Poeggel et al., 1999); and (3) “early adverse experiences result in an increased sensitivity to the effects of stress later in life and render an individual vulnerable to stress-related psychiatric disorders” (Graham et al., 1999). Although I have focused here on PTSD, in other works I have shown that this same developmental neurobiological descrip- tion applies to the ontogeny of pathological dissocia- tion in borderline personality disorder (Schore, 2003b, 2003c).
In the introduction, I cited Brown and Trimble’s (2000) call for a more “precise definition of dissociation based on a conceptually coherent and empirically justified account of the processes underlying these phenomena.” This chapter suggests that such a definition must include a developmental model of dissociative phenomena. In total, the interdisciplinary data cited here indicate that the developing brain imprints not only the overwhelming affective states that are at the core of attachment trauma, but also the early appearing primitive defense used against these affects—the regulatory strategy of dissociation. The developmental principle, that maltreatment in childhood is associated with adverse influences on brain development, specifically refers to an impairment of higher corticolimbic modulation of the vagal circuit of emotion regulation on the right side of the brain that generates the psychobiological state of dissociation. This model accounts for the findings that somatoform dissociation is specifically associated with maternal dysfunction, and that early onset traumatization via emotional neglect and abuse and interpersonal threat to the body predict somatoform dissociation. The model also strongly supports Putnam’s (1995) assertion that dissociation offers “very rich models for understanding the ontogeny of environmentally produced psychiatric conditions.”
Although dissociation has been quite controversial, there is now solid convergent evidence from different dis- ciplines that there is a direct relationship between early trauma and pathological dissociation. The next DSM should reflect this advance in our knowledge.
In the introduction, I cited Brown and Trimble’s (2000) call for a more “precise definition of dissociation based on a conceptually coherent and empirically justified account of the processes underlying these phenomena.” This chapter suggests that such a definition must include a developmental model of dissociative phenomena. In total, the interdisciplinary data cited here indicate that the developing brain imprints not only the overwhelming affective states that are at the core of attachment trauma, but also the early appearing primitive defense used against these affects—the regulatory strategy of dissociation. The developmental principle, that maltreatment in childhood is associated with adverse influences on brain development, specifically refers to an impairment of higher corticolimbic modulation of the vagal circuit of emotion regulation on the right side of the brain that generates the psychobiological state of dissociation. This model accounts for the findings that somatoform dissociation is specifically associated with maternal dysfunction, and that early onset traumatization via emotional neglect and abuse and interpersonal threat to the body predict somatoform dissociation. The model also strongly supports Putnam’s (1995) assertion that dissociation offers “very rich models for understanding the ontogeny of environmentally produced psychiatric conditions.”
Although dissociation has been quite controversial, there is now solid convergent evidence from different dis- ciplines that there is a direct relationship between early trauma and pathological dissociation. The next DSM should reflect this advance in our knowledge.
Trauma Recovery Institute offers unparalleled services and treatment approach. Trauma Recovery Institute provides unique individual and group psychotherapy specialising in personality disorders, complex trauma & neglect, sexual trauma, chronic illness and relationship difficulties. We also offer specialised group psychotherapy for psychotherapists and psychotherapy students, People struggling with addictions and substance abuse, sexual abuse survivors, people suffering with cancer or recovering from cancer and their family members, Parents exploring the art of conscious parenting and people looking to function in life at a higher level. Trauma recovery Institute offers a very safe supportive space for deep relational work with highly skilled and experienced psychotherapists accredited with Irish Group Psychotherapy Society (IGPS), which holds the highest accreditation standard in Europe. Trauma Recovery Institute uses a highly structured relationship and body focused psychotherapeutic approach called Dynamic Psychosocialsomatic Psychotherapy (DPP). To explore our unique approach come in for an initial consultation by filling out the form below.
Dynamic Psychosocialsomatic Psychotheyapy (DPP)
Dynamic Psychosocialsomatic Psychotherapy (DPP) is a highly structured, once to twice weekly-modified psychodynamic treatment based on the psychoanalytic model of object relations. This approach is also informed by the latest in neuroscience, interpersonal neurobiology and attachment theory. As with traditional psychodynamic psychotherapy relationship takes a central role within the treatment and the exploration of internal relational dyads. Our approach differs in that also central to the treatment is the focus on the transference and countertransference, an awareness of shifting bodily states in the present moment and a focus on the client’s external relationships, emotional life and lifestyle.
Dynamic Psychosocialsomatic Psychotherapy (DPP) is an integrative treatment approach for working with complex trauma, borderline personality organization and dissociation. This treatment approach attempts to address the root causes of trauma-based presentations and fragmentation, seeking to help the client heal early experiences of abandonment, neglect, trauma, and attachment loss, that otherwise tend to play out repetitively and cyclically throughout the lifespan in relationship struggles, illness and addictions. Clients enter a highly structured treatment plan, which is created by client and therapist in the contract setting stage. The Treatment plan is contracted for a fixed period of time and at least one individual or group session weekly.
“Talk therapy alone is not enough to address deep rooted trauma that may be stuck in the body, we need also to engage the body in the therapeutic process and engage ourselves as clients & therapists to a complex interrelational therapeutic dyad, right brain to right brain, limbic system to limbic system in order to address and explore trauma that persists in our bodies as adults and influences our adult relationships, thinking and behaviour.”
At Trauma Recovery Institute we address three of the core Attachment Styles, their origin’s the way they reveal themselves in relationships, and methods for transforming attachment hurt into healing. We use the latest discoveries in Neuroscience which enhances our capacity for deepening intimacy. The foundation for establishing healthy relationships relies on developing secure attachment skills, thus increasing your sensitivity for contingency and relational attunement. According to Allan Schore, the regulatory function of the brain is experience-dependent and he says that, as an infant, our Mother is our whole environment. In our relational trauma recovery approach you will learn to understand how the early patterns of implicit memory – which is pre-verbal, sub-psychological, and non-conceptual – build pathways in our brain that affect our attachment styles. Clinically, we can shift such ingrained associative patterns in our established neural network by bringing in new and different “lived” experiences in the Here and Now.
The Role of the Therapist in transforming attachment trauma: Healing into wholeness takes the active participation of at least one other brain, mind, and body to repair past injuries – and that can be accomplished through a one-to-one therapeutic relationship, a therapeutic group relationship or one that is intimate and loving. In exploring the “age and stage” development of the right hemisphere and prefrontal cortex in childhood, we discover how the presence of a loving caregiver can stimulate certain hormones, which will help support our growing capacity for social engagement and pleasure in all of our relationships. Brain integration leads to connection and love throughout our entire life span. At trauma recovery institute we bring a deep focus to the role of Neuroscience in restoring the brain’s natural attunement to Secure Attachment. Our brain is a social brain – it is primed for connection, not isolation, and its innate quality of plasticity gives it the ability to re-establish, reveal and expand one’s intrinsic healthy attachment system.
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