Allan N. Schore, PhD

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Right Brain Affect Regulation: An Essential Mechanism Of Development, Trauma, Dissociation, And Psychotherapy

Allan N. Schore, PhD
UCLA David Geffen School of Medicine

Right Brain Processes in Psychotherapy: Enactments, Autonomic Arousal Dysregulation, and Dissociation

With an eye to the therapy process Dorpat asserts, “In normal awake adults, these two modes are integrated…although one or the other may predominate…The derivatives of the primary process system includes affects, imagery, metaphors, and nonverbal communication” (2001, p. 449).  Right brain primary process-to-right brain primary process transference-countertransference communications especially predominate in clinical enactments.  In a major contribution integrating clinical models and neurobiological data, Ginot (2007, p. 317) convincingly argues, “Increasingly, enactments are understood as powerful manifestations of the intersubjective process and as inevitable expressions of complex, though largely unconscious self-states and relational patterns” (my italics).

In line with earlier neuropsychoanalytic speculations (Schore, 1997) and in support of the central thesis of this chapter Ginot observes,

This focus on enactments as communicators of affective building blocks also reflects a growing realization that explicit content, verbal interpretations, and the mere act of uncovering memories are insufficient venues for curative shifts…As intense manifestations of transference-countertransference entanglements, enactments seem to generate interpersonal as well as internal processes eventually capable of promoting integration and growth (2007, p. 317-318).

She concludes that these “unconscious affective interactions” “bring to life and consequently alter implicit memories and attachment styles.”  Recall the hypothesis of Stern et al. (1998) that “implicit relational knowledge” stored in nonverbal domain is at the core of therapeutic change. 

In previous neuropsychoanalytic work (Schore, 1999) I offered interdisciplinary evidence which shows that the right hemisphere is the locus of implicit memory.  In discussing the role of the right hemisphere as “the seat of implicit memory” Mancia notes, “The discovery of the implicit memory has extended the concept of the unconscious and supports the hypothesis that this is where the emotional and affective - sometimes traumatic - presymbolic and preverbal experiences of the primary mother-infant relations are stored.” (2006, p. 83).  I further suggest that these implicit memories are encoded in high (hyperarousal) and low (hypoarousal) arousal states, marked by respectively bodily state-dependent memories of dysregulated sympathetic dominant energy-expending extreme increases of autonomic arousal (heart rate acceleration) as well as parasympathetic dominant energy-conserving extreme decreases of arousal (heart rate deceleration). The principle of state-dependent recall of implicit memories thus applies to each of these two domains: achieving a particular bodily state is necessary to access certain affects, behaviors and cognitions.

It is often overlooked that affects reflect an individual’s internal state and have an hedonic (valenced) dimension and an arousal (intensity) dimension.  In states of right hemispheric hyperarousal that generate a massive density of intense sympathetic dominant, energy-expending, high arousal negative affect, arousal levels are so extremely elevated that they interfere with the individual’s capacity to adaptively engage with the social (object relational, intersubjective) environment.  Bromberg (2006) links trauma, at any point in the life span, to autonomic hyperarousal, “a chaotic and terrifying flooding of affect that can threaten to overwhelm sanity and imperil psychological survival” (p. 33). 

In contrast, states of right hemispheric parasympathetic dominant, energy-conserving hypoarousal generate a massive density of intense low arousal negative affect.  In these latter affective states arousal levels are so extremely reduced that they interfere with individual’s capacity to adaptively disengage from  the social environment. Thus, early relational trauma, reactivated in transference-countertransference enactments, manifests in dysregulated autonomic hyperarousal associated with sympathetic-dominant affects (panic-terror, rage and pain), as well as dysregulated autonomic hypoarousal and parasympathetic-dominant affects (shame, disgust, and hopeless despair).

Visualizing this conception, in the following figure the central zone reflects operations of both the left and right hemispheres in states of moderate arousal.  Left hemispheric secondary process is dominant in states of neutral affect and autonomic balance.  This middle band of neutral affect is bounded by (1) an upper band of right brain sympathetic dominant energy-expending high arousal affects associated with tight engagement with the environment and (2) a lower band of right brain parasympathetic dominant energy-conserving low arousal affects and disengagement from the external environment (Recordati, 2003).

Figure 5. Affect associated with right brain sympathetc hyperarousal and parasympathetic hypoarousal

Figure 5. Affect associated with right brain sympathetc hyperarousal and parasympathetic hypoarousal

 

In terms of Porges (1997) polyvagal model (Figure 6), the sympathetic hyperarousal zone processes states of danger (fight/flight), while the dorsal vagal hypoarousal system is dominant in states of life survival-threat (see Schore, in press).  Recall the early development of these two stress-responsive psychobiological domains is directly impacted by dysregulated (abuse and neglect) attachment experiences.  These right brain imprinted implicit memories of the hyperarousal and dissociative-hypoarousal responses to early relational trauma are re-activated in the transference-countertransference.

 

Figure 6. Porges polyvagal model

Figure 6. Porges polyvagal model

Kalsched (2003) articulates the accepted clinical principle:

For our early trauma patients to get well again, they will have to suffer through a re-traumatization in their transferences. This repetition in the transference will be the person’s way of remembering, and may actually lead to the potential of healing of trauma, provided that the therapist and patient can survive the furor therapeuticus that such transformation requires.

Such work implies a profound commitment by both therapeutic participants and a deep emotional involvement on the therapist’s part (Tutte, 2004). In these enactments the therapist’s affect tolerance is a critical factor determining the range, types, and intensities of emotions that are explored or disavowed in the transference-countertransference relationship and the therapeutic alliance (Schore, 2003b). 

A general principle of this work is that the sensitive empathic therapist allows the patient to re-experience dysregulating affects in affectively tolerable doses in the context of a safe environment, so that overwhelming traumatic feelings can be regulated and integrated into the patient’s emotional life. In agreement with Ogden et al. (2005), Bromberg (2006) also points out that the therapeutic relationship must “feel safe but not perfectly safe. If it were even possible for the relationship to be perfectly safe, which it is not, there would be no potential for safe surprises…” (p. 95).  This affect-focused work occurs of at the edges of the regulatory boundaries of affect tolerance (Figure 7), or what Lyons-Ruth describes as the “fault lines” of self-experience where “interactive negotiations have failed, goals remain aborted, negative affects are unresolved, and conflict is experienced” (2005, p. 21).

Figure 7. Regulatory boundaries at the edges of windows of affect tolerance

Figure 7. Regulatory boundaries at the edges of windows of affect tolerance

In the above figure note the term “windows of affect tolerance.”  This differs from the usual concept of “window of tolerance” which describes the range of optimal level of arousal to sustain secondary process cognition (conscious, verbal, explicit) and striatal motor activities (voluntary action; controlled overt behavior). These “cognitive and behavioral” functions are dependent upon a moderate rather than high or low arousal range, represented by a classical “inverted U.” This window of optimal verbal processing and overt behavioral expression thus reflects arousal levels optimal for left hemispheric functions. Current cognitive-behavioral insight-driven clinical models operate in this arousal range and focus on these left hemispheric functions. 

On the other hand the right brain has a different range of arousal tolerance to sustain its unique nonconscious psychobiological functions, and can operate at very high or very low arousal levels. The “windows of affect tolerance” thus refers to an optimal range of arousal for different affects and motivational states, which vary in arousal intensity.  This affect tolerance is severely restricted in the emotional deadening defense of pathological dissociation.  An expansion of both negative and positive affect tolerance is a goal of the affectively focused psychotherapy described in this chapter.

In such work, at some point the threatening dissociated affect must be activated, but in trace form, and regulated sufficiently so as not to trigger new avoidance.  “The questions of how much and when to activate or to permit this activation, so as to repair the dissociation rather than reinforce it, must be addressed specifically for each patient.” (Bucci, 2002, p. 787).  According to Bromberg (2005), “Clinically, the phenomenon of dissociation as a defense against self-destabilization…has its greatest relevance during enactments, a mode of clinical engagement that requires a [therapist’s] closest attunement to the unacknowledged affective shifts in his own and the patient’s self-states” (p. 5).   This self-destabilization of the emotional right brain in clinical enactments can take one of two forms: high arousal explosive fragmentation vs. low arousal implosion of the implicit self (see Figure 8).

Figure 8. Psychobiology of high and low arousal enactments

Figure 8. Psychobiology of high and low arousal enactments