Early Shame Experiences and Infant Brain Development · 2016. 2. 8. · 3 Early Shame Experiences...

3Early Shame Experiences

and Infant Brain Development

Allan N. Schore

TheI he scientific study of emotion, begun by Charles Darwin, Sigmund Freud, andWilliam James in the last century, has been neglected for much of this one. Over-shadowed by behavior and cognition, the formal study of internal emotional states,events that are central to the understanding of the human condition, is only re-cently receiving the attention of a growing number of experimental researchersand clinical authors. Within the entire spectrum of emotional states, perhaps thelast to become a focus of observation of scientific scrutiny has been the "hidden"emotion of shame. A rapid expansion of knowledge about this emotion has oc-curred only within the last ten years, as contributions from a variety of disciplinesare now actively attempting to understand more deeply the unique psychologicaland biological properties of shame.

A primary purpose of this chapter is to place shame within the context of veryrecent developmental psychological studies that describe the emergence of emo-tional states over the course of infancy, as well as of developmental neurobiologicalresearch which suggests that these early emotional experiences are required formaturation of the brain in the first two years of life. In pioneering work, H. B. Lewis(1980) referred to shame as "attachment emotion," a theme I will elaborate on byoffering a developmental model of shame that integrates current attachment re-search. In light of the long-established principle that attachment is more than overtbehavior and is "built into the nervous system, in the course and as a result of theinfant's experience of his transactions with the mother" (Ainsworth, 1967, p. 429)and the recently demonstrated finding that parenting directly influences the de-veloping patterns of neuronal connectivity in the infant's brain (Dawson, 1994), Ishall present multidisciplinary evidence which suggests that primordial shameexperiences play a central role in not only psychological but in neurobiologicalhuman development.

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58 INTERPERSONAL BEHAVIOR

To this end I will focus on emotional development in early and then late infancyto demonstrate the tight coupling between the psychobiological processes that un-derlie attachment and shame dynamics. Attachment transactions in the first yearoccur within attuned face-to-face interactions that generate increasingly higher lev-els of positive affects, whereas socialization transactions in the second year involvemisattuned face-to-face interactions that generate shame and inhibit these samepositive states. I will also outline how, at the end of the first year, dyadic nonverbalcommunications of internal, positive affective states directly influence the expe-rience-dependent development of a corticolimbic structure involved in attachmentfunctions that begins a critical period of growth at this time. Socialization expe-riences in the second year that generate stressful levels of shame allow for thefurther maturation of this frontal system, which is expanded in the early maturingright brain. The right hemisphere plays a dominant role in the processing of so-cioemotional information, autonomic activities, and the expression and regulationof primitive emotions, including shame. In the final section, I will discuss theadaptive psychobiological role of cortically regulated shame states.

The developmental models presented are not fixed statements or establishedprinciples but heuristic proposals that can be evaluated by experimental and clin-ical research. A more complete referencing of the interdisciplinary studies pre-sented here can be found in Schore (1991, 1994,1997a,b,c). For conveniences, theterms primary caregiver and mother are used interchangeably throughout thischapter.

Emotional Development in Early Infancy

The last decade has seen a rapid, indeed an explosive, expansion of knowledgeabout emotional development in the first year of human life. Over the course ofthis year, the primary caregiver-infant relationship co-constructs an increasinglycomplex dynamic system of mutual reciprocal influences that mediates the for-mation of an attachment bond within the dyad. This interactive mechanism reg-ulates the infant's psychobiological states, thereby allowing the child to toleratemore intense and longer lasting levels of heightened, yet modulated, arousal. Thisontogenetic achievement, central to human development, enables the infant toexperience very high levels of the positive affects of interest-excitement and en-joyment-joy by the end of the first year.

Dyadic Visuoaffective Transactions and the Development ofAttachment Dynamics

Early socioemotional development is closely tied into the maturation of sensorysystems, and it now appears that, in particular, visual experiences play a para-mount role in social and emotional development (Hobson 1993; Preisler, 1995;Wright, 1991). In fact, the mother's emotionally expressive face is, by far, the mostpotent visual stimulus in the infant's environment, and the child's intense interestin her face, especially in her eyes, leads him or her to track it in space, and toengage in periods of intense mutual gaze. The infant's gaze, in turn, reliably evokes





EARLY SHAME EXPERIENCES AND INFANT BRAIN DEVELOPMENT 59

Figure 3.1. A typical sequence observed during "attuned" interactions of normalinfants and their mothers, here shown split-screen but seated face to face and look-ing at each other: (a) the infant looks at the mother and the mother shows anexaggerated facial expression (mock surprise); (b) the infant and mother smile; (c)the infant laughs, the mother "relaxes" her smile; and (d) the infant looks away,the mother ceases smiling and watches her infant. From Field, 1982. Copyright1982 by Lawrence Erlbaum Associates. Reprinted by permission.

the mother's gaze, thereby acting as a potent interpersonal channel for the trans-mission of reciprocal mutual influences. These face-to-face transactions are quitecommon and can be of very long duration, and they mediate the dialogue betweenmother and child.

With the onset of increasing myelination of the visual areas of the infant's oc-cipital cortex over the second and third quarter of the first year, mutual gaze in-teractions increase significantly. These interactions occur within the context ofsocial play between mother and infant, and they are expressed in synchronousrapid movements and fast changes in affective expressions within the dyad. Anorganized dialogue occurs within milliseconds, and it acts as an interactive matrixin which both partners match states and then simultaneously adjust their socialattention, stimulation, and accelerating arousal in response to the partner's signals.This microregulation continues, as soon after the "heightened affective moment"of an intensely joyful full-gape smile the baby will gaze avert in order to regulatethe potentially disorganizing effect of this intensifying emotion (see figure 3.1].

In order to maintain the infant's positive emotion, the psychobiologically at-tuned mother takes her cue, backs off to reduce her stimulation, and waits for the






baby's signals for reengagement. In this way, not only the tempo of their engage-ment but also of their disengagement and reengagement is coordinated. In thisprocess of contingent responsivity, the more the mother tunes her activity level tothe infant during periods of social engagement, the more she allows him or her torecover quietly in periods of disengagement; and the more she attends to his or herreinitiating cues for reengagement, the more synchronized their interaction. In thismanner, the caregiver facilitates the infant's information processing by adjustingthe mode, amount, variability, and timing of stimulation to the infant's actual in-tegrative capacities. These early experiences of "interaffectivity" (Stern, 1985) arethus organized by ongoing regulations, and the development of such mutuallyattuned synchronized interactions is fundamental to the ongoing affective devel-opment of the infant (Feldman & Greenbaum, 1997; Schore, 1994).

But facia] mirroring exchanges generate much more than overt facial changesin the dyad; they represent a transformation of inner events. To enter into thiscommunication, the mother must be psychobiologically attuned not so much tothe child's overt behavior as to the reflections of his or her internal state. Thehuman face is a unique stimulus whose features display biologically significantinformation, and as the mother and infant synchronize with each other's temporaland affective patterns, each recreates an inner psychophysiological state similar tothe partner's. In this dynamic system, the crescendos and decrescendos of theinfant's psychobiological state are in resonance with similar states of crescendosand decrescendos, cross-modally, of the mother. In physics, a property of reso-nance is sympathetic vibration, the tendency of one resonance system to enlargeand augment through matching the resonance frequency pattern of another reso-nance system. Stern (1985) refers to the delight the infant displays in reacting tothe augmenting effects of his or her mother's playful, empathically attuned behav-ior. The caregiver's attuned resonance with the child's affect thereby allows for amultimodal sensory amplification of the child's state. Consequently, both experi-ence a state transition as they move together from a state of neural affect and arousalto one of heightened positive emotion and high arousal (see figure 3.1). It is nowthought that the attachment relationship is essentially a regulator of arousal (vander Kolk & Fisler, 1994), that regulatory processes are the precursors of psycho-logical attachment and its associated emotions (Hofer, 1994), and that psychobio-logical attunement is the mechanism that mediates attachment bond formation(Field, 1985).

According to Bowlby (1969), vision is central to the establishment of a primaryattachment to the mother, and imprinting is the learning mechanism that underliesattachment bond formation. Imprinting involves a state of mutually entrained cen-tra] nervous system (CNS) propensities and a synchrony between sequential infant-maternal stimuli and behavior (Petrovich & Gewirtz, 1985). Emde (1988) suggeststhat the infant is biologically prepared to engage in visual stimulation to stimulateits brain. This brings us to another level of analysis—the neurobiological level. Inthis "transfer of affect between mother and infant," how are developing systemsof the organizing brain influenced by these interactions with the social environ-ment?

This question is directly addressed by Trevarthen's (1993) studies of maternal-infant "protoconversations," which he describes as an interactive mechanism bywhich older brains engage with mental states of awareness, emotion, and interest






Figure 3.2. Channels of face-to-face communication in protoconversation. Proto-conversation is mediated by eye-to-eye orientations, vocalizations, hand gestures,and movements of the arms and head, all acting in coordination to express inter-personal awareness and emotions. From Trevarthen (1993). Copyright 1993 byCambridge University Press. Reprinted by permission.

in younger brains (figure 3.2). Coordinated with eye-to-eye messages as channelsof communication are auditory vocalizations and tactile and body gestures. A traf-fic of visual and prosodic (variations in pitch, rhythm, and auditory stress thatconvey affect) signals induce instant emotional effects; excitement and pleasureare amplified within the dyad. Indeed, the resonance of the dyad ultimately per-mits the intercoordination of positive affective brain states. Trevarthen's studiesunderscore the fundamental principle that the baby's brain is not only affected bythese transactions, but also that its growth literally requires brain-brain interactionand occurs in the context of a positive affective relationship between mother andinfant. Trevarthen concludes that "the affective regulations of brain growth" areembedded in the context of an intimate relationship and that they promote thedevelopment of cerebral circuits.

The psychoneurobiological mechanism underlying these events is revealed inHofer's (1990) research, which demonstrates that the mother influences the neuralsubstrates for emotion by directly regulating the levels of the catecholamines do-pamine and noradrenaline in the infant's brain. Dopamine is centrally involved inarousal, elation (joy), and the anticipation of reward. Amplified levels of interest-excitement in the mother's face are also accompanied by elevated levels of corti-






cotropin-releasing factor, a neuropeptide produced in paraventricular hypotha-lamic centers that activates the energy-mobilizing sympathetic division of theautonomic nervous system (ANS) and increases in plasma concentrations of no-radrenaline (Brown et al., 1982), thereby intensifying levels of ergotropic (sym-pathetic-dominant) arousal (Gellhorn, 1970) associated with heightened infant ac-tivity levels. The mother's face also triggers high levels of endogenous opiates(endorphins) in the child's growing brain (Hoffman, 1987; Kalin, Shelton, Lynn,1997) that biochemically mediate the pleasurable qualities of social interaction,social affect, and attachment via activation of the ventral tegmental dopamine sys-tem (Bozarth, 1986). Both catecholamines and opioids act as trophic regulators ofneural development.

Infant studies thus reveal that the primary function of early synchronized gazeinteractions is the generation of pleasurable states and that the baby becomes at-tached to the modulating caregiver, who expands opportunities for positive affectand minimizes negative affect. In other words, the affective state underlies andmotivates attachment, and the central adaptive function of dyadic attachment dy-namics is to interactively amplify and maintain optimal levels of the pleasurablestates of what Tomkins (1962) referred to as enjoyment-joy and interest-excitement.

The Onset of a Critical Period for the Maturation of theOrbitofrontal Cortex at the End of the First Year

Attachment functions involve highly visual mechanisms and generate positive af-fect, and they mature near the end of the first year of life. Mary Main, perhaps themost influential attachment researcher, now concludes that "The formation of anattachment to a specified individual signals a quantitative change in infant behav-ioral (and no doubt also brain) organization" (1995, p. 214; italics added). Gilbert(1989) proposes that the mother-child relationship has important and very specificeffects on the maturation of the infant's limbic system. So the question is: Whatspecific limbic areas of the brain are beginning a critical period of growth at 10 to12 months and are involved in attachment functions?

In earlier work (see Schore, 1994,1996), I proposed that dyadic communicationswhich generate intense positive affective states and high levels of dopamine andendogenous opiates represent a growth-promoting environment for the prefrontalcortex, an area that undergoes a major maturational change at 10 to 12 months (Dia-mond & Doar, 1989). The maturation of the prefrontal areas, which represent 30%of the total surface of the human cortex, is completely postnatal, and the limbicorbital prefrontal areas are known to mature before the nonlimbic dorsolateral pre-frontal areas (figure 3.3). Attachment experiences, face-to-face transactions be-tween caregiver and infant, directly influence imprinting, the final circuit wiringof this system. Indeed, there is now evidence to show that activity of the orbitof-rontal cortex, an area which contains neurons that specifically respond to the emo-tional expressions effaces (Scalaidhe, Wilson & Goldmari-Rakic, 1997), is directlyassociated with attachment functions (Steklis & Kling, 1985). This cortical regionplays an essential role in the processing of social signals necessary for the initiationof affiliative behaviors and in the pleasurable qualities of social interaction.






Figure 3.3. Boundaries of functional zones of the human cerebral cortex, showingthe dorsolateral and orbital prefrontal areas. From Kolb & Whishaw (1990). Copy-right 1990 by W. H. Freeman. Reprinted by permission.

The orbital area of the prefrontal cortex (so called because of its relation to theorbit of the eye) is "hidden" in the ventral and medial surfaces of the prefrontallobe. This unique cerebral region is so intimately interconnected limbic areas thatit has been conceived of as an "association cortex" for the limbic forebrain. Inaddition to receiving multimodal input from all sensory association areas of theposterior cortex, it uniquely projects extensive pathways to limbic areas inthe temporal pole and the amygdala, to dopamine neurons in reward centers ofthe ventral tegmental areas of the anterior reticular formation, and to drive centersin the paraventricular hypothalamus that are associated with the sympatheticbranch of the autonomic nervous system. This excitatory limbic circuit, the ventraltegmental limbic forebrain-midbrain circuit (Nauta & Domesick, 1982), is involved






with the generation of positively valenced states associated with motivational re-ward, approach behavior, and active coping strategies.

This area is especially expanded in the right cortex (Falk et al., 1990), whichmatures before the left (Chiron et al., 1997), is known to be specifically affected byearly social experiences, and is centrally involved in attachment experiences(Schore, 1994). Indeed, it is now thought that "The emotional experience of theinfant develops through the sounds, images, and pictures that constitute much ofan infant's early learning experience, and are disproportionately stored or proc-essed in the 'visuospatial' right hemisphere during the formative stages of brainontogeny" (Semrud-Clikeman & Hynd, 1990, p. 198). As the first year draws to aclose, the initial phases of the anatomical maturation of the orbitofrontal cortex, asystem that subserves cognitive-emotional interactions (Barbas, 1995), allows fordevelopmental advances. This system can now generate interactive representa-tions that encode expectations of being matched by, and being able to match, thepartner, as well as "participating in the state of the other" (Beebe & Lachmann,1988). By the end of the first year, a period when the infant begins to toddle andexplore the world, the child can access internal working models of the infant'stransactions with the primary attachment figure in order to appraise self and otherin encounters with the social and physical environments.

Emotional Development in Late Infancy

In optimal growth-promoting environments, the interactive mechanism for gen-erating positive affect becomes so efficient that by the time the infant begins totoddle he or she is experiencing very high levels of elation and excitement. Thesocioemotional environment of the caregiver-infant dyad, however, changes dra-matically from early to late infancy. At 10 months, 90% of maternal behavior con-sists of affection, play, and caregiving. In sharp contrast, the mother of the 13-17-month-old toddler expresses a prohibition on the average of every 9 minutes. Inthe second year, the mother's role now changes from primarily a caregiver to asocializing agent, as she must now persuade the child to inhibit unrestricted ex-ploration, tantrums, bladder and bowel functions; that is, activities that he or sheenjoys.

Socialization Experiences and the Emergence ofthe Attachment Emotion of Shame

In other words, to socialize the child, the mother must now engage in affect reg-ulation to reduce the heightened levels of positive affect associated with the plea-sure of these activities. How does she inhibit and restrict the behaviors that thechild finds pleasurable? In fact, there is one very specific inhibitor of acceleratingpleasurable emotional states. Shame, "the primary social emotion" (Scheff, 1988),acts as a specific inhibitor of the activated ongoing affects of interest-excitementand enjoyment-joy and uniquely reduces self-exposure or exploration powered bythese positive affects (Tomkins, 1963). In earlier work (Schore, 1991, 1994), I pre-sented multidisciplinary developmental data which suggests that shame makes itsinitial appearance at 14 to 16 months.






In the second year, the ambulatory infant, now able to physically separate him-or herself from the mother for longer periods of time, is able to explore realms ofthe physical and social environment that are beyond her watchful eye. Upon returnfrom these forays, the toddler brings the things he or she is exploring and attempt-ing to master to the mother, but now, more than any time previously, these reun-ions can engender interactive stress. Excitedly expecting her "sparkling-eyed plea-sure" (Emde, 1988), the toddler is suddenly and unpreparedly confronted with the"unexpected noncooperation of the mirroring object" (Kohut, 1978). Face-to-faceencounters that at one time elicited only joy become the principal context forstressful shame experiences.

The experience of shame is associated with unfulfilled expectations and is trig-gered by an appraisal of a disturbance in facial recognition, the most salient chan-nel of nonverbal communication. The toddler's attentive focus on the mother'seyes and the frustration of the child's expectation of her participation in eye-to-eye contact and visuoaffective communication may be the key visual cue that trig-gers the visual, nonverbal affect of shame. Reciprocal gaze behavior, the most in-tense form of interpersonal communication, acts as a powerful mediator of affectattunement, but it can also transmit misattunement, because "this visual feedbacksystem carries within it the potential of mutual gratification as well as frustration"(Riess, 1978, p. 382). The impediment to anticipated positive affect is specificallya perception of a facial display which conveys not mirroring but, rather, disgust.M. Lewis (1992) points out that a disgusted face is widely used in the socializationof children, though parents are often unaware that they are producing it.

These developmental data describe the rapid state-transforming events that un-derlie the primordial shame transaction. As a result of earlier dyadic mirroringexperiences, when the senior toddler approaches the caregiver in a state of accel-erating positive affect, he or she expects this state of rising positive arousal to beamplified. Recall that the child now has access to presymbolic representations thatencode the expectation of being matched by, and being able to match, the partner,as well as "participating in the state of the other" (Beebe & Lachmann, 1988).Despite an excited expectation of a psychobiologically attuned shared positiveaffect state with the mother and a dyadic amplification of the positive affects ofexcitement and joy, the infant unexpectedly encounters a facially expressed affec-tive misattunement. The ensuing break in an anticipated visual-affective commu-nication triggers a sudden shock-induced deflation of positive affect, and the infantis thus propelled into a state which he or she cannot yet autoregulate. Shamerepresents this rapid state transition from a preexisting positive state to a negativestate.

Psychobiological attunement drives the attachment process by acting as a mech-anism that maximizes and expands positive affect and minimizes and diminishesnegative affect. The negative affect of shame is thus the infant's immediate phys-iological-emotional response to a perceived interruption in the flow of an antici-pated maternal regulatory function—psychobiological attunement which gener-ates positive affect—and to the mother's use of misattunement to mediate thesocialization process. In other words, shame, which has been called an "attach-ment emotion" (Lewis, 1980), is the reaction to an important other's unexpectedrefusal to cocreate an attachment bond that allows for the dyadic regulation ofemotion (Sroufe, 1996). Thus, in the prototypical object relation of shame, a sep-






aration response is triggered in the presence of and by the mother, who sponta-neously and unconsciously blockades the child's initial attempt to emotionallyreconnect with her in a positive affective state. It is well established that attach-ment bond disruptions precipitate an imbalance in the regulation of affect. In theshame transaction, instead of encountering the synchronizing function of the sig-nificant other who regulates the child's homeostatic equilibrium, the individualexperiences a traumatic interruption of interpersonal synchronizing processes(Maunder, 1996). The misattunement in shame, as in other negative affects, rep-resents a regulatory failure and is phenomenologically experienced as a disconti-nuity in what Winnicott (1958) calls the child's "going-on-being."

In direct contrast to the psychobiologically energized state, shame, an acutelypainful stress-associated affect, triggers a rapid de-energizing state in the infant inwhich the deflated self, depleted of energy, withdraws, recoils, and attempts todisappear from the view of significant objects. As opposed to processes that pro-mote and prolong contact and facilitate "merging with sources of satisfaction" inorder to generate euphoric emotions and pleasurable activity, shame induces "end-ing contact and halting arousal" {Knapp, 1967). The conscious subjective experi-ence of shame, a sharp gradient of change in emotion, represents a rapid, unex-pected, uncontrollable transition from a "crescendo" to a "decrescendo," an"animate" to an "inanimate" feeling state (Stern, 1985), a switch from an attach-ment-affiliation or exploratory-assertive to an aversive motivational functional sys-tem. Shame stress thus precipitates a rapid and unexpected contraction of the self.

This state is mediated by a different psychobiological pattern than positivestates—corticosteroids are produced in a stress response, and these reduce opioidand corticotropin-releasing factor in the brain. Even short-lived elevations of cor-ticosteroids induce inhibition and withdrawal (Stansbury & Gunnar, 1994). Thepsychobiological components of the shame response involve an influx of auto-nomic proprioceptive and kinesthetic feedback into awareness, reflecting a neu-robiological activation of medullary reticular formation activity in the brain stem.In contrast to the attuned state, shame elicits a painful infant distress state, mani-fested in a sudden decrement in mounting pleasure, a rapid inhibition of excite-ment, and cardiac deceleration by means of vagal impulses in the medulla oblon-gata (Knapp, 1967). This shift reflects the reduced activation of the excitatoryventral tegmerital limbic forebrain-midbrain circuit and increased activation of theinhibitory lateral tegmeiital limbic forebrain-midbrain circuit.

The onset of the interactively triggered shame state thus represents a suddenshift from energy-mobilizing sympathetic to energy-conserving parasympatheticdominant ANS activity, a rapid transition from a hyperaroused to a hypoarousedstate, and a sudden switch from ergotropic (sympathetically driven) to tropho-tropic (parasympathetically driven) arousal. Indeed, Buss (1979) has demonstratedthat shame represents parasympathetic arousal. In such a psychobiological statetransition, sympathetically powered elation, heightened arousal, and elevated ac-tivity level instantly evaporate. This represents a shift into a low-keyed inhibitorystate of parasympathetic conservation-withdrawal that occurs in helpless andhopeless stressful situations (Engel & Schmale, 1972). How long the child remainsin this stress state is an important factor.

In fact, active parental participation in regulating the child's shame state iscritical to enabling the child to shift from the negative affective state of deflation






and distress to a reestablished state of positive affect. In early development, parentsprovide much of the necessary modulation of states, especially after a state dis-ruption and across a transition between states, and this allows for the developmentof self-regulation. This transition involves and highlights the central role of stressrecovery mechanisms in affect regulation. Stress has been defined as the occur-rence of an asynchrony in an interactional sequence; further, "a period of syn-chrony, following the period of stress, provides a 'recovery' period" (Chappie, 1970p. 631). The child's facial display, postural collapse, and gaze aversion act as non-verbal signals of his or her internal distress state. If the caregiver is sensitive, re-sponsive, and emotionally approachable, especially if she reinitiates and reentersinto mutual gaze visual affect regulating transaction, the dyad is psychobiologi-cally reattuned, shame is metabolized and regulated, and the attachment bond isreestablished. The key to this is the caregiver's capacity to monitor and regulateher own affect.

In this essential pattern of what Beebe and Lachrnann (1994) call "disruptionand repair," the "good-enough" caregiver who induces a stress response in herinfant through a misattunement reinvokes in a timely fashion her psychobiologi-cally attuned regulation of the infant's negative affect state that she has triggered.This reattunement is mediated by the mother's reengagement in dyadic visuoaf-fective transactions that regenerate positive affect in the child. Her shame-stress-regulating interventions allow for a state transition in the infant—the parasym-pathetic-dominant trophotropic arousal of the shame state is supplanted by thereignition of sympathetic-dominant ergotropic arousal that supports increased ac-tivity and positive affect. Shame transactions are carried out continually through-out the early period of socialization, and a characteristic pattern of regulating andthereby coping (or not coping) with misattuned states and distressing affects de-velops within the dyad. These events are stored within an internal working modelof a secure attachment.

If, on the other hand, an attachment figure frequently humiliates, ridicules, andrejects the child's requests for comfort in stressful situations, the child developsnot only an internal working model of the parent as rejecting but also one of him-orherself as unworthy of help and comfort. I suggest that, as opposed to the elevatedparasympathetic autonomic component which always accompanies shame, hu-miliation, a common accompaniment of early physical trauma, involves an ex-tremely dysregulated state of elevated parasympathetic plus heightened sympa-thetic reactivity. Psychophysiologically this may represent, respectively, a state ofactivated trophotropic arousal versus an intensely stressful state of trophotropiccombined with ergotropic arousal, a state of "shame-rage" (H. B. Lewis, 1987).Clinical observers note that failures of early attachment invariably become sourcesof shame (Kaufman, 1989), that impairments in the parent-child relationship leadto pathology through an enduring disposition to shame (M. Lewis, 1992), and thatearly abuse engenders intense bodily shame (Andrews, 1995). These data implythat it is not shame itself but rather an early developing inefficient capacity toautoregulate or interactively regulate this potent affect that is psychopathogenic.

Specific emotions are now understood to involve a distinctive "core relationaltheme" which describes an essential person-environment relationship (Lazarus,1991) and to be elicited by an appraisal of actual or expected changes that areimportant to the individual (Frijda, 1988). In light of the fact that shame is directly






related to visual phenomena, the core relational shame transaction becomes inter-nalized in implicit, procedural memory as a visual stored image. Nathanson de-scribes shame as "a biological system by which the organism controls its affectiveoutput so that it will not remain interested or content when it may not be safe todo so, or so that it will not remain in affective resonance with an organism thatfails to match its patterns stored in memory" (1992, p. 140). Although the originof shame is dyadic and external, "the experience of being looked at by the Other"(Wright, 1991), it eventually becomes internalized as "the eye of the self gazinginward" (Morrison, 1987). By the end of late infancy, the elicitation of this affectdoes not require the presence of an external person—it can be activated by aninternal image. Morrison (1989) asserts that turning the potential control of shameinward is an important developmental step. Most important, because shame gen-erally inhibits the expression of emotion per se, the capacity to internally regulateshame allows for an ability to experience a broad range of positive and negativeaffects.

The Maturation of the Orbitofrontal Cortex

These advances in emotional functions reflect structural progressions in the limbicsystem, specifically a reorganization and maturation of the orbitofrontal cortex, acorticolirnbic area that is centrally involved in affect regulation (Schore, 1994, in1996; 1997a, b; in press). A period of structural development in this cortex occursin the first year of infancy, and a second period marked by further anatomicalchanges occurs in the second year of human life. This reorganization of the pre-frontal region is "open to interactions with the external world" (Kostovic, 1990).In the second year, such interactions are expressed in dyadic shame and interactiverepair transactions that are part of the socialization process. These experiencestrigger specific psychobiological patterns of hormones and neurotransmitters, andthe resultant biochemical alterations of brain biochemistry influence the experi-ence-dependent maturation of the orbitofrontal cortex.

Specifically, the interactive misattunements generated in socialization trans-actions induce shame, an interruption of interpersonal synchronizing processes.Developmental psychobiological research indicates that interruptions of the at-tachment bond are correlated with increased cortisol and decreased endogenousopioid levels (Trad, 1986). The sudden triggering of shame reflects an alteration ofthe infant's psychobiological state and the onset of a stress reaction, manifested inelevated levels of corticosteroids in the infant's brain. Corticosteroids suppressproduction of corticotropin-releasing factor and thereby reduce endorphin levels.But during critical periods of cortical maturation these neurohormones do morethan just transiently perturb states—in fact, they directly influence brain growth(Meyer, 1985). Developmental shame experiences thus induce a neurobiologicalreorganization of evolving brain circuitries.

In optimal socialization experiences in the second year, the child is exposednot only to interpersonal transactions that induce negatively valenced shame andinhibition and withdrawal behaviors but also to interactive regulations that repairthis state and resume positively valanced excitatory activities and approach be-haviors. These distinct types of socioemotional experiences allow for the critical-period experience-dependent structural maturation of the orbitofrontal cortex. (In






contrast, misattuned relational environments that generate high and long-enduringlevels of negative affect act as growth-inhibiting environments for developing fron-tolimbic systems; Schore, 1996). This organization includes the fine-tuning of de-scending projections from the prefrontal cortex to subcortical structures that areknown to mature during infancy. Of particular importance is the growth of pre-frontal axons back down to subcortical targets on noradrenergic neurons in thenucleus of the solitary tract of the brain stem caudal reticular formation and thevagal complex in the medulla (Yasui, Itoh, Kaneko, Shigemoto, & Mizuno, 1991)and in parasympathetic autonomic areas of the hypothalamus (Kita & Oomura,1981). By this process the organization of the lateral tegmental forebrain-midbrainlimbic circuit that brakes arousal and activates the onset of an inhibitory state iscompleted. Along with the earlier developing ventral tegmental limbic forebrain-midbrain circuit, the orbitofrontal system now connects into both the excitatoryand the inhibitory limbic circuits. Its direct connections with the hypothalamusenable it to act as a major center of central nervous system control over the energy-mobilizing sympathetic and energy-conversing parasympathetic branches of theautonomic nervous system (Neafsey, 1990).

Because of the organization of its dense connections, with sites in both thecortex and subcortex, this corticolimbic system plays an essential adaptive regu-latory role. At the orbitofrontal level cortically processed exteroceptive informa-tion concerning the external environment (such as visual and prosodic informationemanating from an emotional face) is integrated with subcortically processed ex-teroceptive information regarding the internal visceral environment (such as con-current changes in the emotional or bodily state). This adaptive function allowsfor incoming social information to be associated with emotional and motivatedstates. Orbitofrontal areas are involved in the generation of high-level psycholog-ical representations of other individuals (Brothers & Ring, 1992) and in the self-regulation of bodily states (Luria, 1980). According to Hofer (1984), internal rep-resentations of external human relationships serve an important intrapsychic roleas "biological regulators" that control physiological processes. The essential activ-ity of this ventromedial system in emotional behavior (Damasio, 1994; Price, Car-michael, & Drevets, 1996) and in mediating processes relevant to the organism'sparticipation in social groups (Zald & Kim, 1996) is thus the adaptive switching ofinternal bodily states in response to changes in the external social environmentthat are appraised to be personally meaningful (Schore, in press, c). This includesthe onset of a parasympathetically driven inhibitory shame state in response to theappraisal of a facially (visually and prosodically) expressed stressful alteration ofthe interpersonal environment.

Over 60 years ago, MacCurdy (1930) proposed that the immobility seen inshame is due to a shift in balance in the autonomic nervous system, with an offsetof sympathetic activity and an onset of vagal activity, leading to cardiac deceler-ation and a fall in blood pressure. The shame state is manifested in a rapid inhi-bition of excitement, a sudden decrement in mounting pleasure, and cardiac de-celeration by means of vagal impulses (Knapp, 1967). Activation of theorbitofrontal cortex, a cortical area that receives direct vagal inputs (Hardstaff,Jagadeesh, & Newman, 1973) and acts as a "nonspecific system governing internalinhibition" (Velasco & Lindsley, 1965), psychobiologically mediates the onset ofsocially-induced stressful shame states, since direct projections from frontal cor-






ticolimbic areas down to subcortical autonomic sites allows for an orbital role in"vagal restraint" and in the energy-conserving inhibition of autonomic function(Kaada, Pribram, & Epstein, 1949). Stimulation of particular orbitofrontal sites trig-gers an almost instantaneous inhibition of gastrointestinal motility, respiratorymovements of inspiration, and somatic locomotor activity and a dramatic precip-itous fall in blood pressure, thereby accounting for the influx of autonomic feed-back into awareness that accompanies shame. The involvement of orbitofrontal-vagal connections in shame is suggested by the "active restraining quality" of thisaffect, which brakes arousal and triggers a "partial paralysis of outer activity"(Knapp, 1967), since orbital activity inhibits muscle tone and brain-stem-regulatedsomatic reflexes (Sauerland, Knauss, Nakamura, & Clernente, 1967). The centralrole played by frontolimbic areas in shame states is also expressed in its neuro-hormonal regulatory operations—orbitofrontal activation triggers increases of hy-pothalamico-pituitary-adrenocortical corticosteroid levels (Hall & Marr, 1975), afunction mediated by the parasympathetic branch of the ANS (Henry & Stephens,1977).

Indeed, this prefrontolimbic region comes to act in the capacity of an executivecontrol function for the entire right cortex (see figure 3.4). The right hemisphere isparticularly well connected reciprocally with limbic (Tucker, 1992) and autonomic(Spence, Shapiro, & Zaidel, 1996) areas, and is therefore dominant in controllingfundamental physiological and endocrinological functions whose primary controlcenters are located in subcortical regions of the brain (Wittling & Pfluger, 1990).These authors point out that the right cortex is also centrally involved in regulatingcorticosteroid activity. Furthermore, a right hemispheric vagal circuit of emotionregulation, hierarchically dominated by the right orbitofrontal cortex, has beenrecently described by Porges, Doussard-Roosevelt, and Maiti (1994). I suggest thatthe activity of this right brain cortical-subcortical circuit, identical to the arousal-braking, inhibitory lateral tegmental forebrain-midbrain limbic circuit, mediatesall forms of shame-related emotional behaviors. Neurobiological studies show thatthe orbitofrontal system plays a major role in the adjustment or correction of emo-tional responses (Rolls, 1986; Schore, 1994), that is, affect regulation. It acts as arecovery mechanism that efficiently monitors and autoregulates the duration, fre-quency, and intensity of not only positive but also negative affect states, includingstressful shame states.

The Adaptive Psychobiological Role ofCortically Regulated Shame States

The emergent capacity of experiencing and autoregulating the intensely negativeaffect of shame thus reflects the experience-dependent maturation of a right front-limbic system that can access cortically processed social information in order tomodulate subcortical autonomic functions that underlie various emotional states.There is now a large body of evidence which indicates that negative emotionsactivate and are modulated by the right (not left) hemisphere (e.g., Davidson, Ek-man, Saron, Senulis, & Friesen, 1990; Heilman & Bowers, 1990; Heller, 1993,Schore, 1997b). This hemisphere, which contains a "primitive affect system" (Gaz-zaniga, 1985) and a "nonverbal affect lexicon" of facial expressions (Bowers,






Figure 3.4. Relationships of brain stem structures to the orbital surface of the righthemisphere. From Smith (1981). Copyright 1981 by Urban & Schwarzenberg. Re-printed by permission.

Bauer, & Heilman, 1993), is dominant for the regulation of the autonomic correlatesof emotional arousal (Heilman, Schwartz, & Watson, 1977). These data stronglysuggest that "primitive, biologically based" shame (Broucek, 1982), perhaps themost painful and least tolerable negative affect, is a right-brain phemonenon. In-deed, a neuropsychological study shows that the words "shame" and "humilia-tion," when presented tachistoscopically, specifically activate and prime the righthemisphere (Van Strien & Morpugo, 1992).

Almost 50 years ago, Erikson (1950) offered the classical conception of shameas a feeling of being visible and exposed to the eyes of an Other, which leads to anurge to hide and cover one's face. The importance of regulating and thereby beingable to tolerate shame from toddlerhood through adulthood lies in the adaptivecapacity of conservation-withdrawal. Powles characterizes this state, in which theinhibited organism passively disengages in order to attempt to become "unseen,"as the organismic strategy "to conserve energies and strive to avoid attention, tofoster survival by the risky posture of feigning death, to allow healing of woundsand restitution of depleted resources by immobility" (1992, p. 213). This primaryregulatory process for organismic homeostasis allows for a passive coping mech-anism that improves survival efficiency through inactive disengagement and un-responsiveness to environmental input in order to conserve resources and to assureorganismic autonomy until environmental conditions are once again more com-






patible (Engel & Schmale, 1972). As opposed to sympathetically driven "fight-flight" active coping strategies, parasympathetically mediated passive copingmechanisms expressed in immobility and withdrawal associated with "giving up"(Benus, Bohus, Koolhaas, & Van Oortmersen, 1991) and submission (Gilbert, 1992)and in seeking a physical environment of "refuge," a place to hide without beingseen (Mealey & Theis, 1995), represent an alternative but equivalent strategy foreffectively regulating social interactional stress. In contrast to "problem focusedcoping," which entails direct action on the self or on the environment to removethe source of stress, this "emotion focused coping" is directed toward the reductionof the emotional impact of stress through psychological processes (Folkman & Laz-arus, 1980).

The physiological expression of emotion is dependent upon the coordinatedresponses of both the sympathetic and parasympathetic components of the ANS,and this allows for parasympathetically dominant shame states to combine withsympathetically driven states of, for example, fear, anger, and joy. It is known thatparasympathetic inhibitory systems, such as in the frontal lobes, develop moreslowly than sympathetic excitatory processes (Thompson, 1990), that emotion ex-pression changes developmentally as a function of the experience-dependent mat-uration of neural inhibitory mechanisms (Izard, Hembree, & Huebner, 1987), andthat the maturation of the frontal region in the second year is responsible for affectregulation and the development of complex emotions such as shame (Fox, 1991).In light of the fact that affects in general serve the critical adaptive function ofinforming the individual who is tracking biologically relevant goals (Gilbert, 1992)and that specific emotions help to prepare for and sustain the person-environmentrelationship (Lazarus, 1991), successful emotional adaptation requires the capacityto tolerate both positive and negative affects of formidable intensity. Internal work-ing models are now thought to essentially encode coping stategies of affect regu-lation which are unconsciously used to regulate distress in situations that normallyelicit attachment behaviors. The attachment dynamic continues in adult life, andthe ability to cope with the stressful ruptures of attachment that elicit shame isessential to ongoing development, because this affect, which is generated by vir-tually constant monitoring of the self in relationship to others, comes to play acentral role in the regulation of all emotional expression and therefore all humaninteraction.

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