in self defense: disruptions in the sense of self, laterality and primitive defenses

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In Self-Defense: Disruptions in the Sense of Self, Lateralization, and Primitive

Defenses

Commentary by Christian Salas & Oliver H. Turnbull (Bangor, U.K.)

Perhaps the main appeal of Todd Feinberg’s proposal is his effort to undertake the study of one of the most avoided and controversial

topics in neuroscience and psychoanalysis: the self. The difficulties that this endeavor implies are multiple, and it is our intention toengage with Feinberg’s pursuit by constructively challenging and potentially enriching his theory. Our purpose here is to examine four

particular aspects of Feinberg’s argument. First, to point out the need to clarify how he understands the notion of self from a psycho-

analytic and neuroscientific perspective. Second, to review the evidence regarding how purely cognitive conditions (memory disorders,

aphasia, etc.) do affect the sense of self. Third, to examine his claim on how the neuropathologies of the self imply a regression to

earlier stages of development, characterized by a recrudescence of patterns of thought and psychological defenses. Fourth, to com-

ment on his theoretical suggestion that, because patients with right-sided lesions preserve immature defenses (denial, projection,

splitting, fantasy), those primitive defensive processes are somehow left-lateralized, while mature defenses are right-lateralized.

Keywords: catastrophic reaction; defense mechanisms; functional systems; lateralization; regression; sense of self

Christian Salas: Centre for Cognitive Neuroscience, School of Psychol-

ogy, University of Wales, Bangor, U.K., & Unidad Psicoterapia Dinámica,

José Horwitz Barak Psychiatric Institute, Santiago, Chile. Oliver H. Turn-

bull: Centre for Cognitive Neuroscience, School of Psychology, University

of Wales, Bangor, U.K.

The need to fill (theoretical) gaps

A perhaps inevitable limitation in Feinberg’s proposi-tion is the multiple meanings that can be attributed

to the notion of self. According to Feinberg’s TargetArticle, different aspects of a neuropathology of the

self might imply disturbances in the patient’s sense of self and of identity, and even the relation with othersand him/herself . Feinberg also describes how the neu-ropathologies of the self (NPS) might affect differentself-related domains, such as the bodily self, relational self, and narrative self. This definition seems verybroad, conflating concepts that may belong to differ-ent levels of analysis, or theoretical backgrounds—for

172 Neuropsychoanalysis, 2010, 12 (2)



Neuropathologies of the Self: A General Theory • Commentaries 173

example, when speaking about sense of self and iden-tity. As we describe later, patients with purely cognitivedeficits often show transient disruptions in their senseof self (coherence and continuity). However, they seemto preserve a global experience of identity. As a con-sequence, it seems necessary to make clear what we

mean by sense of self and identity.These issues of precision have previously been

raised in other fields where the self is the focus of study(e.g., Bukobza, 2007; Leary, 2004) and also in the neu-ropsychoanalytic debate (Panksepp, 2002). In addition,it is impossible to speak about a single psychoanalyticdefinition of the self, especially given that psycho-analysis has evolved into many schools, each with itsown account of the self (Westen, 1992). Implicitly,Feinberg appears to use the notion of self consistentwith the ego psychology school, which underscores therole of the ego as a mediator in the adaptation to real-ity, using defense mechanisms to cope with exigencies

of the external world, as well as drive demands (Freud,1936; Hartmann, 1958). However, although the theoryFeinberg proposes mainly relies on the disequilib-rium of the ego, he does not clarify the metapsycho-logical arrangement between ego and self. Is the self a substructure of the ego (Milrod, 2002)? Is it derivedfrom the self-representation of the body and mentallife (Jacobson, 1964)? Also, is Feinberg suggesting anaffective nuclear self (Panksepp, 2002), constitutedon a moment-by-moment basis (Stern, 2002), or anextended-representational self (Damasio, 1999)? Thesetheoretical affiliations generate rather diverse interpre-tations of the clinical phenomena, and they need to bemade explicit if we are to build a solid foundation for the NPS. For instance, if we adhere to a psychoanalyti-cally relational version of the self, we must accept thatthe self can be multiple, context-dependent, and dis-continuous, although always striving to sustain an illu-sory sense of unity and continuity (Bromberg, 1996;Mitchell, 1993). In this view, the efforts of anosog-nosic patients to preserve a coherent inner experienceare not simply an exacerbation of primitive defensemechanisms because of the loss of mature defenses.Rather, they reflect the expression of a basic propertyof the organism, which generates coherence and con-

tinuity regardless of reality constrains. Edelman andTononi (2001) address (in an appealing metaphor) theimplications of this basic tendency of the organismtoward coherence:

One is left with the impression that after a mas-sive stroke or surgical resection, a conscious humanbeing is rapidly “resynthesized” or reunified withinthe limits of a new, solipsistic universe that, to outsideappearances, is warped and restricted. The network

of relations that make up a conscious event is not leftbroken and discontinuous; rather, the loose ends tendrapidly to cohere again and bridge the rupture. Thedrive to integration is so strong that often no emptyspace is perceived where there is, in fact, a frighteninggap. Apparently, the feeling of an absence is far lesstolerable than the absence of a feeling. [p. 29]

“Cognitive” deficits and transient disruptions inthe sense of self

Feinberg appears to suggest that purely cognitive defi-cits, such as amnesia, aphasia, apraxia, etc., may affectthought and behavior but do not disrupt personal iden-tity, the sense of self, personal significance of self to others, or personal and autobiographical history.An alternative proposition would be that the sense of self, constituted by a sense of coherence and continu-ity, may be transiently disrupted after a brain injury

that compromises purely cognitive functions. In other words, the disruption to cognitive abilities might notdisturb the boundaries of the self (as Feinberg claims),but may well disrupt the experience of a cohesive self.

This proposition is aligned with Kurt Goldstein’sunderstanding of the impact caused by cognitive dys-function in the relationship between organism andenvironment, what he famously characterized as acatastrophic reaction (Goldstein, 1956). According toGoldstein, in a catastrophic reaction the individualenters into a disorganized inner state because of notbeing able to account for environmental demands.Behavior is devoid of clear order, and it lacks a globalpattern that aligns all the organism’s components— somatic and psychic—in the service of a particular task. The patient thus experiences a physical and men-tal “shock,” feeling “unfree, buffeted and vacillat-ing” (pp. 48–49). This shock, according to Goldstein,extends its impact beyond the patient’s person, provok-ing a collapse in his or her experience of the surround-ing world.

Goldstein’s conceptualization of catastrophic reac-tion is deeply rooted in the understanding of how braininjury shatters the coherence and continuity of the self.Contemporary authors, such as Ben-Yishay (2000),

have approached catastrophic reaction in a similar fashion, by defining it as the “behavioral manifestationof a threat to the person’s very existence” (p. 128). Theneuropsychiatric literature, however, has tended to usethe term in a much-reduced way, narrowing it to inad-equate outbursts of frustration, depression, or anger (Carota, Rossetti, Karapanayiotides, & Bogousslavsky,2001; Chemerinski & Robinson, 2000; Starkstein,Fedoroff, Price, Leiguarda, & Robinson, 1993). This



174 Christian Salas & Oliver H. Turnbull

tendency has neglected catastrophic reaction’s coreaspect, which may well be a discontinuity in the expe-rience of the self. From a psychoanalytic background,this discontinuity appears to be characterized as theemergence of primitive anxieties (Salas, 2008a) or “unthinkable anxieties,” such as profound falling anxi-

ety, fear of fragmentation (e.g., the patient Mr. L. inKaplan-Solms & Solms, 2000, p. 120), disorientation,and psychosomatic dissociation (Winnicott, 1965).

Goldstein’s ideas seem to be supported by ArnoldModell’s neuropsychoanalytic conceptualization of theself (Modell, 1993). He has suggested that the coher-ence and continuity of the self is a fundamental biolog-ical value that strives for the organism’s homeostasis.Coherence means, in Goldstein’s terms, the alignmentof the organism’s somatic and psychic components.Thus, a disturbance in the homeostasis of the self implies, to Modell (1993), a fragmentation and a senseof chaos (p. 172). The continuity of the self refers to

the continuous updating of the value-laden memorysystem, over time, in interaction with the environment(p. 163). Coherence and continuity are mutually rein-forcing loops: the “sticking together” of the self rein-forces its continuity, and vice versa (p. 202).

There is a significant literature that supports Gold-stein claims, in opposition to Feinberg’s argument thatpurely cognitive deficits cannot disrupt the continu-ity and coherence of the self. For example, patientswith amnesic disorders describe interruptions in theexperience of continuity, relating episodes where their mind is in a state of “blankness” (Tulving, 1985; Turn-bull, Zois, Kaplan-Solms, & Solms, 2007). PatientN.N. (Tulving, 1985), who suffers both retrograde andanterograde amnesia, portrays this state of mind whentrying to think: “It’s like being in a room with nothing there and having a guy tell you to go find a chair, andthere is nothing there . . . or it’s like swimming in themiddle of a lake. There is nothing to hold you up or do anything with” (p. 4). These memory deficits mayalter the survivor’s relationship with his or her environ-ment. For instance, patient KC (Tulving, 1993), withanterograde amnesia, showed a profound change in hispersonality: “whereas he used to be outgoing, adven-turous, and gregarious, he is now passive, cautious and

reticent . . . he does not typically initiate interactionswith people around him, although he does ask ques-tions from time to time” (p. 150). In a similar trend,patient Jack (Wilson, 1999), again with anterogradeamnesia, described how he avoided situations wherehis memory difficulties would leave him lost and dis-orientated (p. 42). To him, memory deficits also causeda loss of continuity in interpersonal relationships(p. 42).

On the basis of a similar argument, and contraryto Feinberg’s claim to exclude cognitive functionsfrom the realm of the self, one must take into accountlanguage disorders and their impact on the coherenceand continuity of the self. On rare occasions, languagedisorders have been associated with disruptions in the

sense of self, where there is a widespread recognitionof their emotional and interpersonal impact (Gainotti,1997; Wilson, 1999). A possible reason to neglect therelevance of language to the sense of self is the dif-ficulty in establishing accurately the patient’s subjec-tive experience in such cases, because a central tool of communication is compromised. Nevertheless, Moss(1972), an experimented clinical psychologist who hadsuffered a stroke, offers a rare account of the subjec-tive experience of having aphasia. Moss had an initialglobal aphasia, which later evolved into an expressiveaphasia, and he describes his experience as follows:initially it was like “living in a vacuum of self produced

concepts . . . with absolutely no words to express whatwas happening to me, not even to myself . . . I was ren-dered concrete in terms of my thinking . . . I could dealonly with the immediate present in terms of concreteactions” (pp. 76–79). As regards his interpersonal life,he explains: “trying to follow each person’s contribu-tion, to integrate the various topics, and also attemptingto formalize what I might say in response was just tootaxing, and after a while I inevitably lapsed back intoa semiconscious reverie” (p. 91). Although Moss’sreport suggests that language deficits might underminethe continuity and time-traveling quality of thoughtprocesses, in other aphasic patients such capacitiesseemed to be preserved, suggesting a possible dissocia-tion between thinking and language (Kapur, 1996, pp.111–113; Varley & Siegal, 2000).

The psychotherapeutic exploration of aphasicpatients offers an opportunity to disentangle howspecific language deficits might impact differentiallythe patient’s sense of self. In a neuropsychoanalyticaccount, Kaplan-Solms and Solms (2000) compare thepsychic transformations after Broca’s aphasia (Mr. J)and Wernicke’s aphasia (Mrs. K). In the case of Mr. J,the damage to the motor element of speech (Broca) didnot compromise his capacity to think, to relate to others,

or to test reality. In fact, they conclude that the motoriclanguage areas lie at the sensorimotor “periphery” of the ego (p. 89). The case of Mrs. K was quite different.Her main difficulty lay in her inability to retain audio-verbal material in working memory, which generated a“perforation in her consciousness, and therefore in thefabric of her being” (p. 107). Mrs. K complained aboutbeen unable to think, experiencing regular gaps in her sense of continuity, as if the ongoing awareness of her




self, and thought, kept disappearing (p. 98). The senseof estrangement from herself is clearly depicted in her disjointed account: “now I can’t think . . . I don’t knowwhat is going on . . . it is too terrible. I can’t remember the simplest things, it is just not me . . . I’m so mixedup, sometimes I remember things and sometimes they

are gone . . . I’m in bits and pieces through my mind. . . often I just want to sit down on my own so I don’thave to talk, because I can’t remember things . . .when things go, everything goes” (pp. 99–102).

In yet another cognitive domain, lesions to the leftparietal cortex typically produce spatial disorders, con-structional apraxia, and impairment of quasi-spatialsynthesis (Luria, 1973). In Luria’s The Man with aShattered World (1972), the patient Zazetsky describeshis inner experience after an injury, which has a pro-foundly fragmented quality: “whatever I do remember is scattered, broken down into disconnected bits andpieces . . . I’m in a kind of fog all the time, like a

heavy half sleep. My memory is blank” (pp. 23–25).Zazetsky’s sense of continuity in time was also dis-rupted: “I remember nothing! Just separate bits of information that I sense have to do with one field or another. But that’s all! I have no real knowledge of anysubject. My past has been just wiped out!” (p. 116). Thecoherence between recognizing objects and using themalso appears to have been altered, as was his bodilyself-experience. Similar to this is Kaplan-Solms andSolms’s (2000) patient with damage to the left parietalcortex. The impact of a lack of quasi-spatial synthesisto “glue” experience together is seen in Mr. L, whohas transcortical aphasia and Gertsmann syndrome (p.118). He showed an almost complete absence of men-tal activity, apparently without being able to realizeany kind of associative thinking. Although he exhib-ited extreme anxiety and panic, and his mood was thatof someone whose world was entirely devastated, hewas not able to do anything with those preoccupations,besides having them (pp. 120–124).

In sum, we would offer a mixed conclusion onFeinberg’s account of the role of cognition in the main-tenance of the self. Fundamentally, we endorse hisoverall claim that a break in the boundaries of the self can be catastrophic after focal brain lesion, especially

involving midline (and perhaps right-lateralized) brainstructures. Such a breakdown in the boundaries of theself is indeed often associated with the deployment of defenses, often of the most primitive type. Our com-mentary serves primarily to better clarify the preciserole of cognitive deficits in producing disruptions onthe self. In contrast to Feinberg’s position—that theyare neutral with reference to the patient’s personalrelatedness to self—it appears that a variety of cogni-

tive impairments (in the domain of memory, language,and visuospatial skills) do indeed disrupt the sense of self.

Lateralization and primitive defenses

A further issue of note raised by Feinberg is that of defenses and their neuroanatomical basis. First, wenote that Feinberg draws on the idea of regression, anargument that has long been suggested in the brain-injury literature (Jackson, 1884), and also related to theidea of defenses (Freed, 2002; Kaplan-Solms & Solms,2000; Lewis, 1999). Notably, Feinberg observes thatpatients with right-sided lesions exhibit immaturedefenses, further suggesting that these mechanisms aretypically lateralized to the left hemisphere). Further-more, he hypothesizes the existence of a “left-brainto right-brain defensive shift” during development,

between 3 and 8 years, such that the right hemispheretakes over, inhibiting immature defenses and allowingthe development of mature ones.

Feinberg’s suggestion that different forms of defenses may be related to different neuroanatomi-cal substrates has some merit. Indeed, the discrimina-tion between mature and immature defenses is wellestablished on clinical grounds (Cramer, 2006, 2008;Vaillant, 1994), and there is a small literature offeringopinions on laterality and defense mechanisms (i.e.,Gainotti, 2006; Ramachandran & Blakeslee, 1998;Stern, 1997; Tucker, 1981). We would like to offer afurther analysis of the problem, which we hope willallow us to understand the neuropsychological basis of defense, from first principles.

We begin with the assumption of Luria’s functionalsystem concept, which suggests that all complex psy-chological processes, presumably including defensemechanisms, have multiple component parts (Luria,1973). This approach is also congruent with contempo-rary efforts to understand defenses as complex modesof emotion–cognitive interaction, where neural activitybetween distant and remote brain regions is adjusted,coordinated, and harmonized (Northoff & Boeker,2006). The classic psychoanalytic literature on defense

mechanisms has, for example, long suggested that thedefensive process implies: (1) an undesirable thoughtor impulse, (2) the emergence of anxiety as the thoughtor impulse approaches consciousness, (3) the use of a“counterforce” that allows the diminution of the driveor drive derivate (Freud, 1894).

If we consider this classical—and broad—definitionof the defensive process, we might suggest a neuropsy-chological translation of the possible component parts.




First, there is an increase in arousal of negative valencecaused by an aversive mental representation and/or external event. There is an active modulation (perhapsinhibiting or buffering) of this elevated level of arousalby exercising a set of cognitive–affective processes,which might vary according to the defense mechanism

used. In the case of mature defenses (rationalization,intellectualization, sublimation, repression, etc) thiswould require the use of more complex mental opera-tions (Cramer, 2008), or higher order psychologicalfunctions (voluntary orienting of attention, language,executive functions, etc.), which allow anxiety mini-mization and flexible adaptation to the environment(Clarkin, Lenzenweger, Yeomans, Levy, & Kernberg,2007). In contrast, immature defenses (denial, projec-tion, splitting) might require the use of more automaticand bodily based operations (Hofer, 2005; Schore,2003, pp. 59), which are more rigid and inflexible inadapting to external reality (Clarkin et al., 2007).

At this point we might find our first disagreementwith Feinberg’s argument. If mature defenses requirethe use of “higher order” psychological processes, itseems reasonable to suggest that some of their neuro-psychological components might be left-lateralized,considering the reported laterality of language (Binder et al., 1997; Gazzaniga & Sperry, 1967), determinate(as opposed to indeterminate) reasoning (Gazzaniga,2000; Gazzaniga & Smylie, 1984; Goel & Dolan,2004; Goel et al., 2007), verbal working memory(D’Esposito & Postle, 2002; Paulesu, Frith, & Frack-owiak, 1993), or verbal memory retrieval (Buckner,1996). The field of emotion regulation offers further evidence that might support the participation of left-hemisphere structures in mature defenses. Individualswith high levels of baseline left-prefrontal activationare particularly skilled in the down-regulation of neg-ative emotions (Davidson, 2000a, 2000b). Further-more, in reducing negative affect by reappraisal (thevoluntary language-based self-regulatory process thatresembles rationalization), the left prefrontal cortexstructures activate (Goldin, McRae, Ramel, & Gross,2008; Ochsner, Bunge, Gross, & Gabrieli, 2002). Insum, many of the complex processes that would logi-cally appear to underpin mature defenses depend on

left-sided neural structures. However, Feinberg sug-gests that mechanisms of mature defenses in their entirety are right-lateralized.

The idea that immature defenses are cognitivelyless complex seems supported by two main arguments.First, primitive defenses (projection/identification)appear early on in development, as psychological pro-cesses that allow the building of a primary sense of self (Freud, 1925; Klein, 1946) and the communication

of states of mind between child and caregiver (Bion,1959). This early appearance of primitive defensesmight fit with the proposed early development of theright hemisphere (Chi, Dooling, & Gilles, 1977; Chironet al., 1997; Crowell, Jones, Kapuniani, & Nakagawa,1973; Geschwind & Galaburda, 1987) and its role in

the generation of an image of the body in space andtime (Benton & Silvan, 1993) and the sense of agency(Farrer & Frith, 2002; Farrer et al., 2003). Moreover,primitive defense mechanisms are less sophisticated inpart because their main function is to rapidly regulatebodily based states (Schore, 2003, p. 59) of intensenegative affect (Kernberg, 1986, p. 148) in a rigid andinflexible fashion (Clarkin et al., 2007), addressing sur-vival situations presumably to avoid the fragmentationof the self (McCarthy, 2004). In particular, immaturedefenses appear to deal with negative arousal “spa-tially” (by placing it outside the body), nonverbally(by doing something concrete with the affect instead

of symbolizing), and holistically (pars pro toto). Allthese cognitive abilities have typically been attrib-uted to the right hemisphere (Borod, 2000, p. 7),as has the association of the right hemisphere withwithdrawal-related emotions (Davidson, 1984; Heller,1 990; Kinsbourne & Bemporad, 1984), sympatheticarousal (Craig, 2010), physiological arousal (Eidelberg& Galaburda, 1984; Heilman, Schwartz, & Watson,1978; Heller, 1993; Heller, Nitschke, & Lindsay, 1997;Liotti & Tucker, 1992; Tucker & Williamson, 1984),negative emotional states (Heller, 1990; Sackeim etal., 1982; Silberman & Weingartner, 1986), and theprocessing of somatic information (Damasio, 1994).Such findings offer further support for the rightwardlateralization of many or most of the likely componentparts of primitive defenses.

A consequence of the argument presented in theprevious paragraph would be that patients with right-sided lesions should somehow lose immature defenses,leaving only the left hemisphere and its respectivemature defenses. This argument not only runs counter to Feinberg’s proposal, it may also be oversimplistic,appearing inconsistent with a substantial body of lit-erature on the dynamic nature of defense mechanismsin the brain-injured population. First of all we must

acknowledge that the psychoanalytic notion of defenseitself has changed in recent decades, moving from anintrapsychic process whose goal is the preservation of internal equilibrium toward a psychological processhighly dependent on context and shaped by interper-sonal settings (i.e., Cooper, 1998; Stolorow & Atwood,1992). This contextual feature of defense mechanismshas also been stressed by Cramer (2008) when suggest-ing that the use of defense mechanisms varies accord-




ing to exposure to situations that trigger excessiveanxiety or threaten self-esteem. Finally, as regards thedynamic nature of defenses in psychoanalysis, it seemsappropriate to keep in mind the meaning of the Klei-nian idea of “positions” (Klein, 1935), which entails a(normal) oscillation of the ego in relation to anxieties,

defenses, and object relations.In the brain-injured population, a similar claim

has been suggested, specifically regarding the waythat patients reduce their defensiveness when proper contextual support is offered (Fiegelson, 1993; Salas,2009; Ylvisaker & Feeney, 2000), or maintain it whendenial stabilizes an interpersonal system (Clarici &Giuliani, 2008). The fluctuation in the use of defensemechanisms has also been reported in patients withright-brain damage and anosognosia, where varia-tions seem to appear spontaneously (Moss & Turn-bull, 1996), are sensitive to sensory manipulations(Ramachandran & Blakeslee, 1998), or depend on the

self-referential quality of the interview questions (Mar-cel, Tegnér, & Nimmo-Smith, 2004). This dynamicapproach does not deny the recrudescence of primitivedefense mechanisms (à la Feinberg), after right-braindamage, but challenges the idea that brain injury gen-erates a static regression to a previous developmentalstage, abolishing the possibility of a more complexfunctioning. Even in psychoanalysis itself, regressionis a functional , not a structural, clinical concept. Aview like this also ignores the complex relationshipbetween context and brain functioning, a point stressedby so-called cultural neuropsychology (i.e. Ylvisaker & Feeney, 1998), which has been progressively incor-porated in the neuropsychological rehabilitation litera-ture (Salas, 2008b; Yeates et al., 2008).

A dynamic approach toward defense mechanismsalso raises other questions regarding Feinberg’sproposal. Is the recrudescence of primitive defensemechanisms restricted to the awareness of post-injurydisabilities? Are primitive defenses present in other domains, such as interpersonal conflicts? Do other contextual situations elicit, or facilitate, the use of mature defenses in the same patients? Clarificationof this point is crucial for the understanding of theneural basis of defense mechanisms. If we find that

after right-sided lesions patients still use both types of defense, then the hypothesis that each defense mecha-nism is lateralized to a specific hemisphere cannot besustained. If we approach the problem from our pointof view, acknowledging the dynamic nature of defensemechanisms used in brain-injury patients, the questionseems to be: which are the components that, after right-brain damage, generate the so-called recrudescence of primitive defense mechanisms?

In our opinion, a possible key to understandingthe deployment of primitive defense mechanisms isthe role of the right hemisphere in the regulation of arousal. A recrudescence does not imply that maturedefenses are abolished, but that immature defensesare exacerbated . If we have a patient who previously

tended to use mature defenses, what might cause theshift to using immature defenses more often? We sug-gest that in order to use mature defenses, we need to becapable of tolerating an amount of negative arousal, asa means of generating psychological conflict, but not ina survival situation that requires immediate discharge.Freed (2002) has stressed this point before, by sug-gesting that brain-injury patients have difficulties inusing signal anxiety, experiencing automatic anxietyinstead. In other words, anxiety cannot be used by theego as an anticipatory reaction that signals danger, thusmobilizing ego-defensive capacities. On the contrary,the ego is overwhelmed by excessive stimulation that

the organism is incapable of modulating (Freed, 2002,p. 63).

Our hypothesis, in contrast to Feinberg’s, suggeststhat the recrudescence of primitive defense mechanismsmay be caused by a failure in the capacity to regulate theintensity of arousal and negative emotional states. Thiselevated arousal would imply a dampening of higher cognitive processes (needed for mature defenses), anda “survival” situation, activating primitive defensesthat are able to restore the organism’s homeostasis bydifferent means. In consequence, we propose that it isnot that primitive defenses (left-lateralized accordingto Feinberg) “take over” because of damage to the righthemisphere, but that damage to the right hemisphereimpairs the arousal regulation capacity, which formsone component of mature defenses. This then producesa setting in which left-lateralized components (e.g.,determinate reasoning) operate in a primitive fashion (e.g., delusional, promoting discharge and immediatealleviation of negative affect). In this sense, Feinberg’slateralization argument appears limited by suggestingthat primitive defense mechanisms are largely basedon verbal mechanisms. Verbal mechanisms, or a verbalcomponent thereof, can collaborate in the generation of both mature (e.g., rationalization) and immature (e.g.,

delusional rationalization) defense mechanisms. Theyare not the exclusive province of primitive maturedefenses. In our view, the capacity to tolerate a certainamount of negative arousal is the key factor that per-mits the use of mature defense mechanisms.

We believe that this hypothesis can accommodate toFeinberg’s observation that primitive defenses are morecommon after right-sided lesions (by virtue of disrup-tion to emotional regulation), but it also adds complex-




ity by considering the dynamic nature of defenses froma functional system perspective (Luria, 1973). We havecited a significant literature that supports the relation-ship of the right hemisphere with negative valenceemotions, physiological arousal, and the processingof somatic information. We would like to take this

hypothesis further by pointing to some studies thathave associated left-hemisphere activity with anxietyapprehension, and righthemisphere activity with anx-ious arousal or somatic anxiety (Engels et al., 2007;Nitschke, Heller, & Miller, 2000).

A further exploration of this dynamic hypothesis of defense mechanisms, specifically in relation to primi-tive defenses, would potentially disentangle the preciserole of the right anterior and posterior zones. Feinbergdemonstrated that right frontal damage is related tohigher levels of delusional pathology and to somato-paraphrenia. This claim is congruent with the psycho-analytic exploration of patients with right convexity

lesions by Kaplan-Solms and Solms (2000), wherelarger lesions that involved anterior structures gener-ated more pervasive delusional symptoms and failurein reality testing (Mr. D and Mr. E). However, patientswith more posterior lesions (Mr. A, Mr. B, and Mr. C)also exhibited primitive defense mechanisms (projec-tion, splitting, and abrupt dissociation of affect). Of special interest, in the context of the right hemisphereand negative arousal, these posterior-lesioned patientsalso showed a significant difficulty in tolerating their negative emotional states, and they even lacked thecapacity to bring them to full conscious awareness,though reality testing was not as severely impaired asin the frontal cases. For Kaplan-Solms and Solms, thesymptoms observed after lesions to the right convexityare caused by a diminution in whole-object relation-ships, which generates the emergence of primitivedefenses (p. 197). If we take Feinberg’s and Kaplan-Solms & Solms’s evidence together, it is possible tosuggest: (1) right-hemisphere damage to posterior andanterior regions generates a recrudescence of primi-tive defense mechanisms; (2) right frontal-lobe lesionsgenerate more delusional symptoms than do posterior lesions, where external reality is obliterated; (3) pos-terior lesions generate an impairment in the capacity

to experience, and sustain, a negative affective statebut preserve reality testing. This suggests a regula-tory role of right frontal cortex, supported by studiesthat propose a role of this brain region in social skills(Bach, Happe, Fleminger, & Powell, 2000), emotionalprocessing (Bechara, 2004; Tranel, Bechara, & Den-burg, 2002), “hot” executive functioning (Zelazo &Cunningham, 2007), decision making (Manes et al.,2002), evaluation of beliefs (Davies, Aimola Davies, &

Coltheart, 2005; Coltheart, 2005, 2007; McKay, Lang-don, & Coltheart, 2005), reasoning under uncertainty(Goel & Vartanian, 2005), and maintaining on-lineambiguous representations (Goel, Stollstorff, Nakic,Knutson, & Grafman, 2009; Goel et al., 2007). In sum,the role of the posterior zones in assembling subjective

emotional experience seems supported by studies thatrelate this area to interoceptive feelings (Craig, 2009),corporeal awareness (Berlucchi & Aglioti, 1997), self-relatedness to the body (Tsakaris, 2009), attribution of action to the self (Blakemore & Decety, 2001; Farrer & Frith, 2002; Frith & Frith, 1999; Ruby & Decety,2001), the experience of emotion from “secondaryinducers” (Damasio, Bechara, Tranel, & Damasio,1997), and imagining other peoples’ feelings (Adolphs,2001; Adolphs, Damasio, Tranel, Cooper, & Damasio,2000).

Closing remarks

Perhaps it is necessary to conclude this commentaryby addressing Feinberg’s core proposal of what a neu-ropathology of the self is. For Feinberg, neuropatholo-gies of the self appear to have three main features: (1)there is a disturbance in the sense of self, identity, andrelatedness to others and the world; (2) they are associ-ated with confabulation; (c) they are related to braininjury. A possible limitation of Feinberg’s proposal ishis emphasis on syndromes that include confabula-tions, with less emphasis on other cases where there isno sign of confabulation but changes in the experienceof the self are evident. It would be helpful if a surveyof changes in the NPS were undertaken based on lesionsite, but focused more broadly than on confabula-tion. Along this line, we have expanded Feinberg’sunderstanding of the NPS by describing disturbancesin the sense of self that are related to pure cognitivedeficits. One might take this argument further, con-sidering instances where only the bodily self appearsabnormally changed, with no signs of confabulation,as is observed after left parietal lesions (Luria, 1972,1973; cf. cases of supernumerary phantom limbs after stroke—McGonogle et al., 2002; Miyazawa, Hayashi,

Komiya, & Akiyama, 2004). Our final point is thus thatFeinberg’s emphasis seems to be centered on the delu-sional component, which seems likely to be merelya subgroup of the NPS, albeit containing the mostextreme cases. An all-encompassing account of the NPSshould then include syndromes where the self may bemodified, by either cognitive or somatic changes. Fur-thermore, an inclusive account should even consider modifications of the self that are not exclusively caused




by brain injury to the central nervous system, as in thecase of phantom limbs after amputation (Chen, Cohen,& Hallett, 2002; Giummarra, Gibson, Georgiou-Karis-tianis, & Bradshaw, 2007), changes in body schemaafter quadriplegia (Salas, 2010), or peripheral injury(Sacks, 1998). In sum, we believe that Feinberg’s pro-

posal of the neuropathologies of the self would increaseits value if, as a theoretical framework, it were capableof incorporating the many different ways by which theself can change after a neurological insult.

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