Personality disorders, attachment and psychodynamic psychotherapy.

Personality Disorders Received: May 27, 2014 Accepted after revision: July 24, 2014 Published online: November 1, 2014

Psychopathology 2014;47:425–436 DOI: 10.1159/000366135

Personality Disorders, Attachment and Psychodynamic Psychotherapy Lissa Weinstein a M. Mercedes Perez-Rodriguez b–d Larry Siever b, c

a

Doctoral Program in Clinical Psychology, City College of New York and Graduate Center, and b Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, N.Y., and c Mental Health Patient Care Center and Mental Illness Research Education and Clinical Center, James J. Peters Veterans Affairs Medical Center, Bronx, N.Y. USA; d CIBERSAM, Autonomous University of Madrid, Fundacion Jimenez Diaz Hospital, Madrid, Spain

Abstract While attachment has been a fruitful and critical concept in understanding enduring individual templates for interpersonal relationships, it does not have a well-understood relationship to personality disorders, where impairment of interpersonal functioning is paramount. Despite the recognition that attachment disturbances do not simply reflect nonoptimal caretaking environments, the relationship of underlying temperamental factors to these environmental insults has not been fully explored. In this paper we provide an alternate model for the role of neurobiological temperamental factors, including brain circuitry and neuropeptide modulation, in mediating social cognition and the internalization and maintenance of attachment patterns. The implications of these altered attachment patterns on personality disorders and their neurobiological and environmental roots for psychoanalytically based treatment models designed to ameliorate difficulties in interpersonal functioning through the medium of increased access to mature forms of mentalization is discussed. © 2014 S. Karger AG, Basel

© 2014 S. Karger AG, Basel 0254–4962/14/0476–0425$39.50/0 E-Mail [email protected] www.karger.com/psp

Introduction

A considerable body of research has shown that attachment patterns evolving early in development can coalesce as maladaptive templates that will influence later adult relationships and contribute to the pathology manifest in the personality disorders [1]. Attachment classifications were derived from the infant’s behavior in the Strange Situation [2], a structured series of separations and reunions between the infant and his caregiver that measured the infant’s capacity to use the caregiver as a ‘safe haven’ in times of distress. While a secure infant would typically seek comforting contact with his caregiver upon her return and successfully reestablish equilibrium, an avoidant/dismissive infant would turn away or ignore the caretaker upon her return, while an anxious/ambivalent infant will seek contact, but be unable to be soothed, and continue to express discomfort and distress. A fourth category – disorganized – was typified by odd, contradictory or bizarre behaviors and, unlike the other three classifications, by the absence of a coherent coping strategy [3]. The development of maladaptive attachment patterns stems from innate temperamental factors including faulty affective regulation, poor impulse/action controls and cognitive distortions interacting with suboptimal environments, with insults ranging from overt abuse and neglect to more subLissa Weinstein, PhD City College of New York and Graduate Center 160 Convent Avenue New York, NY 10031 (USA) E-Mail lissa_weinstein @ hotmail.com

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Key Words Personality disorders · Attachment patterns · Psychodynamic psychotherapy · Interpersonal functioning

Attachment and Personality Disorders

That a relationship exists between personality disorders and attachment seems intuitively obvious given that personality refers to relatively persistent ways of structur426


ing thought, motivations, emotions, action/impulse and interpersonal relations, all domains related to attachment [10]. While research provides evidence for a link between insecure attachment and psychopathology, and a negative correlation between secure attachment and virtually all personality disorders [11–13], the linking of a precise attachment classification with a specific personality disorder has been harder to demonstrate, leading some to question further whether attachment classifications can truly capture the diverse and idiosyncratic varieties of attachment patterns seen in clinical work [14]. The most consistent findings of a relationship between personality disorder and attachment have been, not surprisingly, found with borderline personality disorder (BPD) as its defining traits of difficulty with affective regulation, episodic aggression, self-harm behaviors and instability in relationships are manifest most prominently in an interpersonal context. Preoccupied and disorganized attachment patterns were found in BPD using the Adult Attachment Interview (AAI) [15], as well as a dimensional scaling of clinician ratings of personality which partialed out the effects of other personality disorder dimensional scales and gender [10]. In a review of 13 empirical studies on attachment and BPD, Agrawal et al. [16] concluded that despite the wide variety of measures used to assess attachment, the numerous targeted assessment relationships, and the variety of insecure attachment types, all of which makes comparisons among the different studies difficult, all of the studies revealed an association between BPD and insecure forms of attachment (e.g. preoccupied, ambivalent, fearful, dismissing, avoidant, unresolved), even if, as several studies note, BPD cannot be tied to a specific form [15, 17]. Additional studies have borne out these general conclusions. Gunderson and Lyons-Ruth [18] noted disorganizedambivalent attachment (a combination of genetic predisposition for high reactivity in interpersonal situations within the context of a maladaptive environment). A meta-analysis of attachment studies using the AAI found insecure-preoccupied and unresolved attachment states of mind to be typical of BPD [19]. In a study evaluating preoccupied attachment and difficulties with emotion regulation in a mixed inpatient sample of BPD, antisocial and avoidant personality disorders, preoccupied attachment was seen to be strongly positively associated with each of the personality disorders, albeit more strongly related to BPD than to the other personality disorder populations [20]. Yet despite any overarching regularities, even with the BPD group, a fraction of patients were classified as secure, Weinstein /Perez-Rodriguez /Siever


tle failures to validate or empathize with the developing child’s particular temperamental vulnerabilities and strengths. These insecure/disorganized attachment patterns rely primarily on immature, emotion contagion systems involving visceral and sensory resonance with other’s emotions rather than more mature reflective systems based on explicit mental state attributions more conducive to appropriate empathic responses that maintain the boundaries between self and other [4, 5]. Psychoanalytically based manualized treatments aim to allow the patient a more flexible access to different empathic networks that are both better attuned to the interpersonal context and also allow continued reflection even in stressful situations. The reworking of these more insecure/disorganized patterns allows for increased mentalization (the ability to understand and represent others’ mental states) about attachment, accounting for the seeming switch in attachment templates following psychodynamic treatment [6]. The current paper presents a model of the complex multidimensional relationship between the neuropeptide oxytocin, the development and maintenance of attachment, social cognition and affective regulation in the personality disorders. A final section will discuss the implications of this research for models of psychodynamic psychotherapy. Initially, personality was seen as organized around 4 psychological dimensions – affective dysregulation or instability, impulsivity, cognitive disorganization, anxiety – that were grounded in underlying biological function [7, 8]; as evidence mounted for direct biological mediation of the interpersonal sphere, a fifth dimension of interpersonal dysfunction was added [9]. These dimensions exist on a continuum, and vulnerabilities in one or several areas will not necessarily eventuate in a personality disorder diagnosis. Susceptibility to the development of a personality disorder will be patterned by genes expressing themselves in these dimensions of temperament, which are further shaped by the environment. In our view, the development of social cognition is central to affect regulation, the ability to delay impulsive action, the smooth deployment of one’s cognitive resources and the experience of anxiety and further that social cognition is determined both by the functioning of neuropeptide systems which are further patterned in the context of the attachment relationship.

While initially attachment was conceived of as relatively stable across the life course, a trait-like variable, numerous studies [28–32] demonstrate discontinuities in attachment status so that assessments in infancy are not perfectly predictive of one’s adult attachment classification; some who start out initially secure become insecure, particularly if adverse life circumstances are encountered. Several developmental periods, for example middle and late adolescence, where the increased separation from parental figures necessitates a redefining of self/other boundaries, leave one vulnerable to shifts in attachment status [33]. Thus, mother-infant attachment alone does not constitute an unyielding prototype for later relationships, nor does secure attachment relate consistently to any one specific personality variable, even if intervening variables are controlled [34]. When found, consistency from infancy to adulthood may be a function of a stable social context, as much as internalized working models [35]. One possibility is that temperament and its underlying neurobiology, new cognitive structures and symbolic capacities continue to factor into the negotiation of all subsequent developmental phases and novel contexts, potentially contributing to the mutability of attachment status across the life span and partly determining how the child will engage and interact with significant others. The difficulty demonstrating a clear relationship between attachment and a specific personality disorder, the lack of a clear predictive line between early attachment and later pathology, and the significant number of individuals from nonclinical and normal samples who can also be classified as insecure all suggest that attachment insecurity should be considered a nonspecific risk factor best measured as a dimensional variable, taking both adaptive and maladaptive forms, that exists along a continuum of severity in all personality disorders. If impairments in relational and emotional functioning are conceptualized as underlying all personality pathology [20, 36], it becomes more efficacious to examine aspects of attachment that more directly reflect emotional and relational functioning, particularly those factors which impact interpersonal assessment and determine approach or avoidance and which can be more specifically linked to neurobiological function, rather than attachment classification itself. Our particular focus is on social cognition and the related development of the capacity for mentalization; the functioning of specific neuropeptides and circuits is central to the formation of the social bonds that support the development of mentalization. Neuropeptides enter into the initial formation of the attachment relationship with-

Personality Disorders, Attachment and Psychodynamic Psychotherapy


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usually between 6 and 8% in studies using interview measures [15]. Nor was insecure attachment limited to a BPD population. In addition to the relationship between several personality disorders and preoccupied attachment [20], research using self-report measures linked avoidant and dependent personality disorders with preoccupied attachment, while schizoid, narcissistic, antisocial and paranoid personality disorders have been linked to dismissing attachment [21, 22]; insecure attachment patterns have also been been linked with cluster B ‘dramatic’ personality disorders [23]. Insecure/dismissing AAI classifications have been linked to adults with conduct or externalizing disorders [19]; Meyer and Pilkonis [24] implicated dismissing attachment, characterized by an inflated internal working model of the self as superior but insufficiently acknowledged and a negative evaluation of the other, in the development of narcissistic personality disorder. Schizoid personality disorder was associated with dismissing attachment in both adults and adolescent samples when clinician ratings of attachment and personality were used [10]. Findings on the relationship between attachment and personality disorder are difficult to interpret for several reasons. First, the high rates of co-occurrence of the axis II disorders were not controlled for in many of the early studies. Further, both attachment disorders and personality disorders are often assessed categorically, while a dimensional approach has proved to be more productive. There are minimal correlations between two of the commonly used measures of attachment in adulthood as they measure different aspects of attachment [25]. The Experiences in Close Relationships and the Experiences in Close Relationships-Revised, using self-report, measure the extent to which respondents are insecure about the availability of current romantic partners and their propensity to either avoid close relations or conversely, feel comfortable depending on others. The AAI measures memories of early significant attachments; classification is made through narrative analysis, not necessarily under the conscious control of the respondent [6]. Depending on which of these two modes of assessment are used, one might be tapping more into generalized trait-like characteristics more likely to be manifest in AAIs, while more situational/relational factors are more apparent on the Experiences in Close Relationships. Self-report inventories, organized around dimensions of avoidance or anxiety, tap into factors that map onto personality traits that are, in part, heritable [26], while studies using the AAI have tended to highlight the effects of the early caretaking environment [for reviews, see 6, 27].

Mentalization

Closely related to the construct ‘theory of mind’, mentalization is ‘a form of social cognition... the imaginative mental activity that enables us to perceive and interpret human behavior in terms of intentional mental states [37, p. 1357]. The capacity for mentalization is conceived of as a developmental achievement, dependent upon how successfully the attachment object was able to mirror the affective states of the child, which in turn would contribute to the child’s recognition of their own mental state, their capacity to regulate their own affect and the development of attentional control. Mentalization, while functioning as a trait-like variable linked to the quality of early attachment, is easily disrupted depending on arousal and stress levels, the degree of intimacy of the relationship between self and other, and the intensity of endogenous and external stimulation [38]. Like the empathic forms to which it is inextricably linked, a distinction is made between more mature forms of mentalization (characterized by being explicit, conscious, less automatic, involving slower processing) which normally cover but do not replace earlier forms of cognition which structure the subjective experience of self in relation to other and to reality. Automatic mentalization, in contrast, is unconscious, nonverbal, sensory as opposed to thought-like and reflexive as opposed to reflective. An interactive model of the relationship between arousal/stress and mentalization [38] posits an inverted U-shaped curve so that the capacity for explicit/controlled mentalization initially increases with increased arousal/stress, but with continually escalating levels there is a switch to automatic mentalizing and ultimately to nonmentalizing more primitive modes of cognition, as cognitive functions initially mediated by the prefrontal cortex are increasingly arbitrated by parietal and subcor428


tical structures. The mobilization or conversely the deactivation of the attachment system is closely related to stress modulation; hence one’s specific attachment history will alter the set point of whether an interaction, such as gazing at one’s infant’s face, is experienced as pleasurable or stressful and at what point controlled mentalization will give way to more automatic processes [39].

Neural Circuitry for Empathic Responsivity

The word empathy was coined by Edward Titchner, a German psychologist interested in introspection and influenced by Fechner’s idea of the ‘just noticeable difference’, the smallest detectable difference between a starting and secondary level of a particular sensory stimulus. A translation of the German ‘Einfühlungsvermögen’, Merriam-Webster’s dictionary defines empathy as ‘the imaginative projection of a subjective state into an object so that the object appears to be infused with it’ and ‘the action of understanding, being aware of, being sensitive to, and vicariously experiencing the feelings, thoughts and experience of another of either the past or present without having the feelings, thoughts and experience fully communicated in an objectively explicit manner’. The definition presages a distinction between different types of empathy, which neurobiologists would later distinguish as reflecting distinct physiological pathways and psychological experiences. Given the scope of the current paper, the reader is referred to Van Overwalle and Baetens [40] and Zaki and Ochsner [41] for reviews of the current research supporting these distinctions. One type of empathy involves shared representations (SRs) of mental states via commonly activated neural networks in observers and targets. Thus, a target’s pain, experience of repulsion, motoric action or sensory experience is felt by the perceiving person as if it is his or her own through a ‘neural resonance’ that engages the same limbic, paralimbic or sensorimotor neural systems (the amygdala, anterior cingulate and anterior insula) [41]. Utilization of SR networks also contains the risk of mirroring the distress of others through a kind of emotional contagion as it involves the immediate, visceral recognition of another’s state without an accompanying conscious awareness or ability to regulate the affective sequelae of that identification. A second type of empathy which supplants, but does not replace, the SR type of empathy more typical of early childhood, is a more reflective and deliberate empathic processing, distinguished by the incorporation of explicWeinstein /Perez-Rodriguez /Siever


in the context of environmental circumstances, but also continue to modulate how interpersonal events are interpreted throughout life. Thus, while the attachment relationship forms an internalized set of representations of expectable human actions, these set expectations can be modified or altered given changes in neuropeptide functioning as well as the intensity or perceived stress of given interactions. It is a hypothesized bidirectional relationship, such that the neuropeptides mediate the experience of trust, but that the attachment relationship provides a set of expectations so that approach may be experienced as pleasurable or distressing.

it mental state attribution (MSA) and the inclusion of context and perspective. While the utilization of SR networks privileges attention to nonverbal empathic cues, MSA-based empathic responses are related to changes in temporal and parietal regions which can mediate shifts in perspective as well as medial prefrontal regions that integrate semantic, contextual and sensory data. These networks are slower, less immediate, more explicit and available to consciousness [41] and allow the perceiver to represent states that include a wider temporal window as opposed to the immediate present as well as the target’s perspective. This later developing, more cognitive aspect of empathy matures in tandem with cognitive maturation, executive functioning, attentional capacities, inhibitory control and language. Variations in the ability to flexibly access the different empathic networks might then account for the manifest symptom pictures in the personality disorders. For example, the dramatic intractable interpersonal symptoms that epitomize BPD could be, in part, explained by a tendency to rely on excessive SR empathy with a relative inability to access more MSA-based empathic responses, resulting in their difficulty mentalizing about themselves and others [4]. The reliance on SR forms of empathy would explain the demonstrated emotional hyperreactivity to interpersonal events seen in borderline patients [5, 42] and their enhanced sensitivity to facial emotion in laboratory paradigms [43–45]. Despite the theoretical literature on different forms of empathy in psychoanalysis, their impact on the transference/countertransference matrix and their importance as an aspect of the silent/noninterpretive factors which comprise aspects of the analytic cure [46] there is a relative paucity of empirical literature on the functioning of empathy in the personality disorders. New et al. [45] explored group differences in empathy in relation to interpersonal function in patients with BPD, avoidant personality disorder and healthy controls, measuring responses to emotional pictures with a computer task in which subjects focused either on the experience of the individual in the picture or on their own imagined experience. Consistent with a model of higher reliance on SR empathy and lower access to more mature, MSA-based empathic responses, patients with BPD had high levels of alexithymia, more difficulty identifying their own emotions than patients with avoidant personality disorder, and reported higher empathic distress and poorer ability to take the perspective of others. In contrast to the findings in borderline disorders, narcissistic disorders show far less impairment in cognitive empathy, particularly in theory of

mind tasks, but demonstrate more impairment in emotional empathy, bearing some similarity to the pattern noted in psychopathic individuals in whom experimental tasks requiring cognitive empathy are unimpaired, but who show little autonomic response to another’s distress [47]. Thus, the two types of empathy can be dissociated in pathological populations. How reflexive versus how reflective one’s empathic response is depends on the degree to which SR or MSA networks are engaged; to some extent, this determines how potentially adaptive one’s response is. SR networks, as they involve an emotional contagion, make it more difficult to separate one’s own affective response from that of the other, while MSA networks, which are involved in deliberate self-evaluation, allow for self and other to be distinguished, as well as supporting the inhibition of SR responses. While there are individual differences in the utilization of MSA and SR processing, empathic responses are also altered by context such as increasing intimacy or the perception of threat, stimulus complexity or uncertainty, and it is under these conditions (in laboratory studies) that one observes the subtle dysfunction of empathic regulation in BPD patients. However, difficulties in empathic relatedness, rather than being specific to borderline personalities, also characterize histrionic and dependent personalities [48] and are central to schizoptypal [49] and schizoid personality disorders, whose abnormal social cognition acts as a critical obstacle to their functioning, albeit in a different manner than the more dramatic personality disorders.



While researchers have known for some time that neurobiological factors contribute to the initial development of attachment, it has only recently become possible to specify what these neurobiological factors might be. Sexual hormones, neuropeptides such as oxytocin, vasopressin and endogenous opioids, and neurotransmitters including dopamine, among others, play a key role in the development and maintenance of attachment behavior in humans and in other animals [50]. Attachment is a complex behavior, mediated by multiple, interrelated neural systems. For example, primary sensory areas and more specialized structures (e.g. the fusiform face area) are involved in social perceptual processes [51] that are crucial for social recognition, which is 429


The Neuropeptide Oxytocin as a Mediator of Attachment and Social Cognition and the Capacity for Mentalization

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er cortisol response [69]. Effects of oxytocin administration on stress included both decreases in the subjective experience as well as physiological responses such as decreases in salivary cortisol levels, and increases in parasympathetic cardiac control [70]. In terms of affiliative behaviors, oxytocin, as compared to placebo, increased the ability to infer mental states from facial cues and increased gaze duration toward the eyes, slowed reaction times during facial fear recognition, decreased the rate of positive facial expressions miscategorized as negative, and increased memory for faces, but not nonsocial stimuli [cited in 71]. Based on these and similar results, an initial hope was raised that oxytocin administration might serve as a clinically relevant pharmacological treatment for disorders with social deficits – obsessive-compulsive personality disorder, BPD, social anxiety disorder, schizophrenia and autism spectrum disorders. Initial results seemed promising. Systemic infusions of oxytocin reduced repetitive behavior and improved emotion recognition in autism spectrum disorder [72, 73], a single administration of intranasal oxytocin increased the subjective experience of attachment security in a group of male students classified with insecure attachment over placebo [74]; oxytocin administration enhanced the effects of exposure therapy in a group of patients with social anxiety disorder [75] and decreased psychotic symptoms and improved theory of mind and social perception in schizophrenia [76]. No consistent effects were found in obsessive-compulsive patients. The story turned out to be more complex than a direct translation between oxytocin levels and affiliative experience. In both animals and humans, the effects of oxytocin are mediated by experience, and a combination of multiple perceptual, affective sensory and cognitive systems all working synchronously is necessary for the social bond to develop [77], rather than a specific effect of any one neurohormone. For example, in sheep, the effects of oxytocin are more evident in females with a history of parental care. It is not only the receptor sites for oxytocin in the hypothalamus that are increased during pregnancy, there are also changes in brain regions that regulate memory and learning, which are partly, but not solely, mediated by oxytocin. Thus, mother rats are better than virgins at navigating mazes, capturing prey and foraging, while at the same time they suffer less fear and anxiety (as measured by the levels of stress hormones in their blood). In humans, both interindividual differences and context will affect the way an administration of oxytocin is experienced [78, 79]. Higher endogenous oxytocin levels have been associated with increased perception of interpersonWeinstein /Perez-Rodriguez /Siever


a prerequisite for attachment [50]. Emotion processing is regulated in part by regions including the amygdala, in close interaction with the insula, the anterior cingulate cortex and the orbitofrontal cortex [52]. In order for attachment to occur, neural pathways associated with fear and avoidance must be inhibited, while circuits mediating reward and motivation must be activated [50]. In the current paper, we will focus on the role of the neuropeptide oxytocin in social cognition and attachment behavior. Extrapolating from studies of pair bonding in monogamous rodents such as prairie voles, maternal behavior in sheep [53–55] and grooming behavior in maternal rats toward their pups, oxytocin was hypothesized to play a critical role in human bonding as well. In a growing body of literature, the neuropeptides oxytocin and vasopressin have been noted to play a central role in social cognition, stress responses and interaction in human studies [9, 56–59] and are increasingly seen as fundamental to the development of the attachment behaviors which, in turn, are critical in structuring adaptive responses to interpersonal stressors. To summarize briefly, oxytocin, whose receptors are found in brain areas involved in social behaviors, is central to affiliative behaviors in maternal bonding [60] as well as partner bonding, modulating the formation of social and spatial memory as well as responses to stimuli such as facial expressions, making it key to ‘reading’ mental states in others, which is an essential factor in the process of parental marked mirroring through which the child begins to recognize their own mental states as distinct from that of the other [61]. In early infancy, endogenous oxytocin levels prior to birth were correlated with increased mother-infant bonding; higher salivary oxytocin levels in both mothers and fathers were positively associated with affect synchrony, positive communicative sequences between both parents and child and parent-child engagement overall [62]. Later in development, recognition of facial emotions and ingroup trust were both increased when subjects were given intranasal oxytocin [63–65]. Increases in oxytocin were noted in response to stressful sensory experiences such as uncontrollable noise [66] as well as the stress of problematic social relationships [67], leading researchers to hypothesize its role in dampening physiological responses to stress. In lactating women, increases in oxytocin following breastfeeding were linked with lowering levels of stress hormones [68], suggesting a mediating role for oxytocin. When intranasal oxytocin was administered prior to a mildly stressful social stimulus, oxytocin diminished the stress response and in combination with social support resulted in a low-

Proposed Models for the Effects of Exogenous Oxytocin on Mentalization

The specific mechanisms through which exogenous oxytocin exerts its effects on mentalization are mostly unknown, and are the object of much current research. Some data suggest that changes in mentalization and social recognition after oxytocin administration may be mediated by changes in the salience or rewarding properties of social stimuli [84, 85] including modulation of mesocorticolimbic dopaminergic motivational networks [86]. Oxytocin-induced increases in social cognitive ability correlate with increased pupil dilation, which is in turn coupled with increased locus caeruleus firing [87, 88]. Moreover, oxytocin administration increases attention toward the eye region as measured by eye gaze or reaction time [89–92]. There is also evidence that oxytocin affects social cognition through modulation of amygdala activity and subcortical attention/orienting networks [93, 94]. Two alternate models have been hypothesized to explain the effect of oxytocin on mentalization and social cognition more broadly (fig. 1–3). One, an optimizing model, suggests that oxytocin will enhance mentalization and social cognitive functioning in all populations, regardless of baseline social cognitive skills. Thus, oxytocin Personality Disorders, Attachment and Psychodynamic Psychotherapy

administration would aid cognition in populations seen as deficient in social cognition (schizophrenia and schizoid personality disorder patients) as well as populations where social cognition is excessive and/or distorted (e.g. BPD). A second, interactionist model suggests that baseline social cognition skills will modulate oxytocin’s effects. There is a hypothesized optimal point of oxytonergic tone/social cognition with optimal social recognition, salience and attention to emotional stimuli, resulting in optimal mentalization. Below this optimal point, social cognition will be deficient with low activity and altered emotional modulation of social cognitive networks, poor emotion recognition, low mentalizing accuracy with hypomentalizing errors [95], deficient salience/reward processing of social information, and low attention to social cues. In these individuals, the administration of exogenous oxytocin will have a positive effect [76, 88, 96–99]. Beyond the hypothesized optimal point, social cognition becomes distorted through excessive salience/attention towards social stimuli and attentional biases [78, 89] resulting in overactive, poorly controlled and distorted mentalization termed hypermentalizing [100, 101], and hence, oxytocin administration will have a negative effect. This second, interactionist model is similar to the inverted U-shaped model proposed by Fonagy et al. [102] with regard to arousal/stress and mentalization but allows for a more precise delineation and testing of dose response curves after oxytocin administration within the context of different attachment styles. Although these models remain untested, the literature on intranasal oxytocin administration in BPD seems to support an interactionist model, with effects of oxytocin on social cognition ranging from positive to negative across studies [82, 89, 90, 103, 104]. The type of model subscribed to will also have implications for how a psychodynamic-based treatment is organized. Furthermore, the effects of oxytocin appear to be modulated by other factors, including gender, context, attachment style and history of childhood adversity [78, 83, 105].

Implications for Psychodynamic Treatment

Research on oxytocin opened the exciting possibility that endogenous modulators of attachment could be used to enhance the therapeutic relationship [58]. However, there is accumulating evidence that a simple optimizing model is insufficient as internal biology is experienced and cognized in varied and individual ways so that dePsychopathology 2014;47:425–436 DOI: 10.1159/000366135

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al distress [80]; oxytocin administration decreased cooperation when participants had to interact with strangers rather than people they were familiar with [81]. Attachment status affected the results of oxytocin administration so that securely attached males were more likely to remember their mothers positively following oxytocin administration (as compared to placebo), but oxytocin had the opposite effect on anxiously attached individuals, who remembered their mothers as less caring afterward. When oxytocin was given to BPD patients, oxytocin decreased social game cooperation as opposed to placebo [82]. Thus, rather than negate, in some circumstances, oxytocin may magnify the effects of an already existing attachment schema, while in other cases oxytocin administration seems to reduce stress and cortisol responses for those who are deficient in social relating, but not those who are unimpaired [for a detailed account of the extant literature, see 79, and for a meta-analysis 83]. In sum, although administration of oxytocin holds promise as a treatment for social cognitive impairment, the mechanism, dosing and effects across disorders are unknown, as well as for which target populations or types of tasks administration would be most efficacious.

Color version available online

Social functioning

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Fig. 1. Baseline social cognition/mentaliza-

tion. SPD = Schizoid personality disorder; SCZ = schizophrenia; ASD = autism spectrum disorder; HC = healthy control.

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Fig. 2. Interactionist model after oxytocin

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Fig. 3. Optimizing model after oxytocin (OXT) administration. For abbreviations, see figure 1.

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Hypermentalization


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(OXT) administration. For abbreviations, see figure 1.

treatment. Rather than using regressive countertransference states as a source of information about the patient’s internal world, the therapist encourages the capacity for explicit mentalization through identification with the therapist’s mode of thinking. TFP, in contrast, was not designed initially to target mentalization per se but to address the borderline patient’s identity diffusion and the split polarized mental representations [111]. The path to mature mentalization was a multistage process involving ‘transformations in cognitive and affective ego and superego structures’, a development which reflects ‘the building up, modulation and integration of object relations’ [107, p. 175]. Interpretation is central to the process; the mutative factor is the evocation in the transference and subsequent interpretation of self/object configurations including the accompanying fantasies that remained unconscious because of maladaptive defensive strategies such as splitting and denial. The focus on containment and supportive techniques in MBT is seen as potentially driving split off affect states further from consciousness. Unlike MBT, in TFP countertransference states which, at times, involve the evocation of SR networks with their attendant fusion of self and object images are seen as involving a primitive form of identification which allows for increased empathic understanding of the patient’s internal world. Thus, the model of TFP involves more integration of SR and MSA networks, while MBT is directed primarily at the suppression of SR reactivity. Which model is more successful is an empirical question complicated by the use of different measures to define successful outcome, the difference in training required of therapists in the two models and the length of the treatment. Several studies [112, 113] note that, when paradigms are used which more clearly reflect complex real-world social situations, the neural systems involved in SR processing and MSA coactivate. Thus, the suppression of SR-based activity may ultimately decrease the capacity for reflection. Experiences associated with utilization of SR networks, specifically the loss of self/object differentiation may also allow the therapist a palpable experience of the patient’s inner world, supporting a form of containment that will (as in early development) gradually help the patient develop through a noncontingent marking of emotional states, a feeling for his own affect states which allows a distinction from the feelings of others. Attachment research suggests that the templates which determine our expectations about interpersonal scenarios are others and are internalized, unconscious and not easily subject to reclassification.



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pending on the underlying personality configuration and extant conflicts, increases in oxytocin can be experienced as pleasurable, prompting approach, or as stressful, engendering avoidance and regression. The reaction depends on several factors – the characteristics of the internalized narrative constructed around attachment, the current relational context, the intensity of stimulation, and the person’s capacity to mentalize about themselves and others. As the most potentially mutable factor, and one which can potentially mediate the negative effects of insecure or disorganized attachment [6], it is not surprising that both of the two evidence-based psychodynamic treatments for BPD, transference-focused psychotherapy (TFP) [106, 107] and mentalization-based therapy (MBT) [108, 109], see the development of the capacity for mature mentalization as a goal. As interpersonal dysfunction is increasingly seen as part of all personality disorders, the use of these treatments has spread to other clinical populations. The basic principles of MBT have been used to structure treatment for antisocial personality disorder, substance abuse, eating disorders, at-risk mother-infant pairs, and family groups [109]. Similarly, the tenets of TFP were judged applicable to the treatment of a broad range of personality disorders organized at the borderline level [110]. Although development of mature mentalization is viewed in both models as a goal and as an instrument through which transformation can take place, the therapeutic techniques believed to best serve the aim of developing mature mentalization differ. In MBT, the therapist aims to kindle the patient’s attachment while simultaneously helping the patient to consistently maintain access to controlled mentalization. As intense attachment is seen as disabling the mentalizing system, the intensity of the therapeutic relationship is continually titrated in order to avoid a precipitous regression to more primitive, concrete SR modes of cognition with their propensity to action [108]. In an effort to stabilize the patient’s internal world prior to considering their internal life, as well as to mimic maternal behaviors which foster the development of secure attachment in early development, treatment is structured and predictable so that the patient can begin to ascertain regularities in the object, and differentiate their affect state from that of the object. MBT focuses primarily on conscious or preconscious material with a concomitant de-emphasis on the unconscious and the genetic roots of past relationship configurations, with a concomitant move away from the use of interpretation and an examination of the transference, particularly early in

The findings on oxytocin suggest a more nuanced way to think about the therapy relationship. While some may experience an increase in oxytocin as a spur to engagement, others may find this disorganizing. A similar mechanism may take place within the therapeutic relationship so that moment-to-moment shifts in attachment need to be a focus of attention lest an overzealous approach precipitate a premature termination. The patient’s history of attachment needs to be factored into treatment choices as well as diagnostic category. One can assume that what is experienced as support is different for every patient. Careful assessment of the patient’s attachment style, capacity for mentalization, as well as the state of the transference relationship may help to guide one’s interven-

tions and clinical stance. A patient might experience an overt effort to be closer as threatening, while a distant relationship may allow for continued contact. Attachment patterns can mediate the patient’s willingness to engage with the therapist or the likelihood of dropout, as well as influence the therapist’s response to the patient. By breaking the attachment process down into component parts that can be more closely tied to neurobiology, a more differentiated and potentially testable picture emerges of the interactions between current context, levels of endogenous and exogenous stimulation, the stability of internalized models of behavior and the influence of each of these factors on the success or failure of therapy.

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