172 Neuropsychoanalysis, 2010, 12 (2)

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 to
engage 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

The need to fill (theoretical) gaps
A perhaps inevitable limitation in Feinberg’s proposi-
tion is the multiple meanings that can be attributed
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.
© 2010 The International Neuropsychoanalysis Society
to the notion of self. According to Feinberg’s Target
Article, 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 others
and him/herself. Feinberg also describes how the neu-
ropathologies of the self (NPS) might affect different
self-related domains, such as the bodily self, relational
self, and narrative self. This definition seems very
broad, conflating concepts that may belong to differ-
ent levels of analysis, or theoretical backgrounds—for
• http://www.neuropsa.org
Neuropathologies of the Self: A General Theory • Commentaries
example, when speaking about sense of self and iden-
tity. As we describe later, patients with purely cognitive
deficits often show transient disruptions in their sense
of self (coherence and continuity). However, they seem
to 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 psychoanalytic
definition of the self, especially given that psycho-
analysis has evolved into many schools, each with its
own account of the self (Westen, 1992). Implicitly,
Feinberg appears to use the notion of self consistent
with the ego psychology school, which underscores the
role 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 theory
Feinberg 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 derived
from the self-representation of the body and mental
life (Jacobson, 1964)? Also, is Feinberg suggesting an
affective nuclear self (Panksepp, 2002), constituted
on a moment-by-moment basis (Stern, 2002), or an
extended-representational self (Damasio, 1999)? These
theoretical affiliations generate rather diverse interpre-
tations of the clinical phenomena, and they need to be
made 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 that
the 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 experience
are not simply an exacerbation of primitive defense
mechanisms because of the loss of mature defenses.
Rather, they reflect the expression of a basic property
of the organism, which generates coherence and con-
tinuity regardless of reality constrains. Edelman and
Tononi (2001) address (in an appealing metaphor) the
implications of this basic tendency of the organism
toward coherence:
One is left with the impression that after a mas-
sive stroke or surgical resection, a conscious human
being is rapidly “resynthesized” or reunified within
the limits of a new, solipsistic universe that, to outside
appearances, is warped and restricted. The network
173
of relations that make up a conscious event is not left
broken and discontinuous; rather, the loose ends tend
rapidly to cohere again and bridge the rupture. The
drive to integration is so strong that often no empty
space is perceived where there is, in fact, a frightening
gap. Apparently, the feeling of an absence is far less
tolerable than the absence of a feeling. [p. 29]
“Cognitive” deficits and transient disruptions in
the sense of self
Feinberg appears to suggest that purely cognitive defi-
cits, such as amnesia, aphasia, apraxia, etc., may affect
thought 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 not
disturb 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’s
understanding of the impact caused by cognitive dys-
function in the relationship between organism and
environment, what he famously characterized as a
catastrophic reaction (Goldstein, 1956). According to
Goldstein, in a catastrophic reaction the individual
enters into a disorganized inner state because of not
being able to account for environmental demands.
Behavior is devoid of clear order, and it lacks a global
pattern 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 brain
injury 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 manifestation
of a threat to the person’s very existence” (p. 128). The
neuropsychiatric literature, however, has tended to use
the 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
tendency has neglected catastrophic reaction’s core
aspect, which may well be a discontinuity in the expe-
rience of the self. From a psychoanalytic background,
this discontinuity appears to be characterized as the
emergence of primitive anxieties (Salas, 2008a) or
“unthinkable anxieties,” such as profound falling anxi-
ety, fear of fragmentation (e.g., the patient Mr. L. in
Kaplan-Solms & Solms, 2000, p. 120), disorientation,
and psychosomatic dissociation (Winnicott, 1965).
Goldstein’s ideas seem to be supported by Arnold
Modell’s neuropsychoanalytic conceptualization of the
self (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 alignment
of the organism’s somatic and psychic components.
Thus, a disturbance in the homeostasis of the self
implies, to Modell (1993), a fragmentation and a sense
of chaos (p. 172). The continuity of the self refers to
the continuous updating of the value-laden memory
system, 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 that
purely cognitive deficits cannot disrupt the continu-
ity and coherence of the self. For example, patients
with amnesic disorders describe interruptions in the
experience of continuity, relating episodes where their
mind is in a state of “blankness” (Tulving, 1985; Turn-
bull, Zois, Kaplan-Solms, & Solms, 2007). Patient
N.N. (Tulving, 1985), who suffers both retrograde and
anterograde amnesia, portrays this state of mind when
trying to think: “It’s like being in a room with nothing
there and having a guy tell you to go find a chair, and
there is nothing there . . . or it’s like swimming in the
middle of a lake. There is nothing to hold you up or
do anything with” (p. 4). These memory deficits may
alter the survivor’s relationship with his or her environ-
ment. For instance, patient KC (Tulving, 1993), with
anterograde amnesia, showed a profound change in his
personality: “whereas he used to be outgoing, adven-
turous, and gregarious, he is now passive, cautious and
reticent . . . he does not typically initiate interactions
with 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 anterograde
amnesia, described how he avoided situations where
his memory difficulties would leave him lost and dis-
orientated (p. 42). To him, memory deficits also caused
a loss of continuity in interpersonal relationships
(p. 42).
Christian Salas & Oliver H. Turnbull
On the basis of a similar argument, and contrary
to Feinberg’s claim to exclude cognitive functions
from the realm of the self, one must take into account
language disorders and their impact on the coherence
and continuity of the self. On rare occasions, language
disorders have been associated with disruptions in the
sense of self, where there is a widespread recognition
of their emotional and interpersonal impact (Gainotti,
1997; Wilson, 1999). A possible reason to neglect the
relevance 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 had
suffered a stroke, offers a rare account of the subjec-
tive experience of having aphasia. Moss had an initial
global aphasia, which later evolved into an expressive
aphasia, 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 what
was happening to me, not even to myself . . . I was ren-
dered concrete in terms of my thinking . . . I could deal
only with the immediate present in terms of concrete
actions” (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 attempting
to formalize what I might say in response was just too
taxing, and after a while I inevitably lapsed back into
a semiconscious reverie” (p. 91). Although Moss’s
report suggests that language deficits might undermine
the continuity and time-traveling quality of thought
processes, in other aphasic patients such capacities
seemed to be preserved, suggesting a possible dissocia-
tion between thinking and language (Kapur, 1996, pp.
111–113; Varley & Siegal, 2000).
The psychotherapeutic exploration of aphasic
patients offers an opportunity to disentangle how
specific language deficits might impact differentially
the patient’s sense of self. In a neuropsychoanalytic
account, Kaplan-Solms and Solms (2000) compare the
psychic 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) did
not compromise his capacity to think, to relate to others,
or to test reality. In fact, they conclude that the motoric
language 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 the
fabric of her being” (p. 107). Mrs. K complained about
been unable to think, experiencing regular gaps in her
sense of continuity, as if the ongoing awareness of her
Neuropathologies of the Self: A General Theory • Commentaries
self, and thought, kept disappearing (p. 98). The sense
of estrangement from herself is clearly depicted in her
disjointed account: “now I can’t think . . . I don’t know
what is going on . . . it is too terrible. I can’t remember
the simplest things, it is just not me . . . I’m so mixed
up, 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’t
have to talk, because I can’t remember things . . .
when things go, everything goes” (pp. 99–102).
In yet another cognitive domain, lesions to the left
parietal cortex typically produce spatial disorders, con-
structional apraxia, and impairment of quasi-spatial
synthesis (Luria, 1973). In Luria’s The Man with a
Shattered World (1972), the patient Zazetsky describes
his inner experience after an injury, which has a pro-
foundly fragmented quality: “whatever I do remember
is scattered, broken down into disconnected bits and
pieces . . . 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 any
subject. My past has been just wiped out!” (p. 116). The
coherence between recognizing objects and using them
also appears to have been altered, as was his bodily
self-experience. Similar to this is Kaplan-Solms and
Solms’s (2000) patient with damage to the left parietal
cortex. The impact of a lack of quasi-spatial synthesis
to “glue” experience together is seen in Mr. L, who
has transcortical aphasia and Gertsmann syndrome (p.
118). He showed an almost complete absence of men-
tal activity, apparently without being able to realize
any kind of associative thinking. Although he exhib-
ited extreme anxiety and panic, and his mood was that
of someone whose world was entirely devastated, he
was not able to do anything with those preoccupations,
besides having them (pp. 120–124).
In sum, we would offer a mixed conclusion on
Feinberg’s account of the role of cognition in the main-
tenance of the self. Fundamentally, we endorse his
overall claim that a break in the boundaries of the self
can be catastrophic after focal brain lesion, especially
involving midline (and perhaps right-lateralized) brain
structures. Such a breakdown in the boundaries of the
self is indeed often associated with the deployment of
defenses, often of the most primitive type. Our com-
mentary serves primarily to better clarify the precise
role of cognitive deficits in producing disruptions on
the self. In contrast to Feinberg’s position—that they
are neutral with reference to the patient’s personal
relatedness to self—it appears that a variety of cogni-
175
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, we
note that Feinberg draws on the idea of regression, an
argument that has long been suggested in the brain-
injury literature (Jackson, 1884), and also related to the
idea of defenses (Freed, 2002; Kaplan-Solms & Solms,
2000; Lewis, 1999). Notably, Feinberg observes that
patients with right-sided lesions exhibit immature
defenses, further suggesting that these mechanisms are
typically lateralized to the left hemisphere). Further-
more, he hypothesizes the existence of a “left-brain
to right-brain defensive shift” during development,
between 3 and 8 years, such that the right hemisphere
takes over, inhibiting immature defenses and allowing
the 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 well
established on clinical grounds (Cramer, 2006, 2008;
Vaillant, 1994), and there is a small literature offering
opinions on laterality and defense mechanisms (i.e.,
Gainotti, 2006; Ramachandran & Blakeslee, 1998;
Stern, 1997; Tucker, 1981). We would like to offer a
further analysis of the problem, which we hope will
allow us to understand the neuropsychological basis of
defense, from first principles.
We begin with the assumption of Luria’s functional
system concept, which suggests that all complex psy-
chological processes, presumably including defense
mechanisms, have multiple component parts (Luria,
1973). This approach is also congruent with contempo-
rary efforts to understand defenses as complex modes
of emotion–cognitive interaction, where neural activity
between 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 the
defensive process implies: (1) an undesirable thought
or impulse, (2) the emergence of anxiety as the thought
or impulse approaches consciousness, (3) the use of a
“counterforce” that allows the diminution of the drive
or drive derivate (Freud, 1894).
If we consider this classical—and broad—definition
of the defensive process, we might suggest a neuropsy-
chological translation of the possible component parts.
176
First, there is an increase in arousal of negative valence
caused by an aversive mental representation and/or
external event. There is an active modulation (perhaps
inhibiting or buffering) of this elevated level of arousal
by 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) this
would require the use of more complex mental opera-
tions (Cramer, 2008), or higher order psychological
functions (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 automatic
and bodily based operations (Hofer, 2005; Schore,
2003, pp. 59), which are more rigid and inflexible in
adapting to external reality (Clarkin et al., 2007).
At this point we might find our first disagreement
with Feinberg’s argument. If mature defenses require
the use of “higher order” psychological processes, it
seems 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. Individuals
with high levels of baseline left-prefrontal activation
are particularly skilled in the down-regulation of neg-
ative emotions (Davidson, 2000a, 2000b). Further-
more, in reducing negative affect by reappraisal (the
voluntary language-based self-regulatory process that
resembles rationalization), the left prefrontal cortex
structures activate (Goldin, McRae, Ramel, & Gross,
2008; Ochsner, Bunge, Gross, & Gabrieli, 2002). In
sum, 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 cognitively
less 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
Christian Salas & Oliver H. Turnbull
of states of mind between child and caregiver (Bion,
1959). This early appearance of primitive defenses
might fit with the proposed early development of the
right hemisphere (Chi, Dooling, & Gilles, 1977; Chiron
et al., 1997; Crowell, Jones, Kapuniani, & Nakagawa,
1973; Geschwind & Galaburda, 1987) and its role in
the generation of an image of the body in space and
time (Benton & Silvan, 1993) and the sense of agency
(Farrer & Frith, 2002; Farrer et al., 2003). Moreover,
primitive defense mechanisms are less sophisticated in
part because their main function is to rapidly regulate
bodily based states (Schore, 2003, p. 59) of intense
negative affect (Kernberg, 1986, p. 148) in a rigid and
inflexible fashion (Clarkin et al., 2007), addressing sur-
vival situations presumably to avoid the fragmentation
of the self (McCarthy, 2004). In particular, immature
defenses 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). All
these cognitive abilities have typically been attrib-
uted to the right hemisphere (Borod, 2000, p. 7),
as has the association of the right hemisphere with
withdrawal-related emotions (Davidson, 1984; Heller,
1 990; Kinsbourne & Bemporad, 1984), sympathetic
arousal (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 et
al., 1982; Silberman & Weingartner, 1986), and the
processing of somatic information (Damasio, 1994).
Such findings offer further support for the rightward
lateralization of many or most of the likely component
parts of primitive defenses.
A consequence of the argument presented in the
previous paragraph would be that patients with right-
sided lesions should somehow lose immature defenses,
leaving only the left hemisphere and its respective
mature 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 mechanisms
in the brain-injured population. First of all we must
acknowledge that the psychoanalytic notion of defense
itself has changed in recent decades, moving from an
intrapsychic process whose goal is the preservation of
internal equilibrium toward a psychological process
highly dependent on context and shaped by interper-
sonal settings (i.e., Cooper, 1998; Stolorow & Atwood,
1992). This contextual feature of defense mechanisms
has also been stressed by Cramer (2008) when suggest-
ing that the use of defense mechanisms varies accord-
Neuropathologies of the Self: A General Theory • Commentaries
ing to exposure to situations that trigger excessive
anxiety or threaten self-esteem. Finally, as regards the
dynamic nature of defenses in psychoanalysis, it seems
appropriate 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 way
that patients reduce their defensiveness when proper
contextual support is offered (Fiegelson, 1993; Salas,
2009; Ylvisaker & Feeney, 2000), or maintain it when
denial stabilizes an interpersonal system (Clarici &
Giuliani, 2008). The fluctuation in the use of defense
mechanisms has also been reported in patients with
right-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 dynamic
approach does not deny the recrudescence of primitive
defense mechanisms (à la Feinberg), after right-brain
damage, but challenges the idea that brain injury gen-
erates a static regression to a previous developmental
stage, abolishing the possibility of a more complex
functioning. Even in psychoanalysis itself, regression
is a functional, not a structural, clinical concept. A
view like this also ignores the complex relationship
between context and brain functioning, a point stressed
by 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 mechanisms
also raises other questions regarding Feinberg’s
proposal. Is the recrudescence of primitive defense
mechanisms restricted to the awareness of post-injury
disabilities? 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? Clarification
of this point is crucial for the understanding of the
neural 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 be
sustained. If we approach the problem from our point
of view, acknowledging the dynamic nature of defense
mechanisms used in brain-injury patients, the question
seems to be: which are the components that, after right-
brain damage, generate the so-called recrudescence of
primitive defense mechanisms?
177
In our opinion, a possible key to understanding
the deployment of primitive defense mechanisms is
the role of the right hemisphere in the regulation of
arousal. A recrudescence does not imply that mature
defenses are abolished, but that immature defenses
are exacerbated. If we have a patient who previously
tended to use mature defenses, what might cause the
shift to using immature defenses more often? We sug-
gest that in order to use mature defenses, we need to be
capable of tolerating an amount of negative arousal, as
a means of generating psychological conflict, but not in
a survival situation that requires immediate discharge.
Freed (2002) has stressed this point before, by sug-
gesting that brain-injury patients have difficulties in
using signal anxiety, experiencing automatic anxiety
instead. In other words, anxiety cannot be used by the
ego as an anticipatory reaction that signals danger, thus
mobilizing 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, suggests
that the recrudescence of primitive defense mechanisms
may be caused by a failure in the capacity to regulate the
intensity of arousal and negative emotional states. This
elevated arousal would imply a dampening of higher
cognitive processes (needed for mature defenses), and
a “survival” situation, activating primitive defenses
that are able to restore the organism’s homeostasis by
different means. In consequence, we propose that it is
not that primitive defenses (left-lateralized according
to Feinberg) “take over” because of damage to the right
hemisphere, but that damage to the right hemisphere
impairs the arousal regulation capacity, which forms
one component of mature defenses. This then produces
a setting in which left-lateralized components (e.g.,
determinate reasoning) operate in a primitive fashion
(e.g., delusional, promoting discharge and immediate
alleviation of negative affect). In this sense, Feinberg’s
lateralization argument appears limited by suggesting
that primitive defense mechanisms are largely based
on verbal mechanisms. Verbal mechanisms, or a verbal
component thereof, can collaborate in the generation of
both mature (e.g., rationalization) and immature (e.g.,
delusional rationalization) defense mechanisms. They
are not the exclusive province of primitive mature
defenses. In our view, the capacity to tolerate a certain
amount of negative arousal is the key factor that per-
mits the use of mature defense mechanisms.
We believe that this hypothesis can accommodate to
Feinberg’s observation that primitive defenses are more
common after right-sided lesions (by virtue of disrup-
tion to emotional regulation), but it also adds complex-
178
ity by considering the dynamic nature of defenses from
a functional system perspective (Luria, 1973). We have
cited a significant literature that supports the relation-
ship of the right hemisphere with negative valence
emotions, physiological arousal, and the processing
of somatic information. We would like to take this
hypothesis further by pointing to some studies that
have associated left-hemisphere activity with anxiety
apprehension, and right- hemisphere 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 precise
role of the right anterior and posterior zones. Feinberg
demonstrated that right frontal damage is related to
higher 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), where
larger lesions that involved anterior structures gener-
ated more pervasive delusional symptoms and failure
in reality testing (Mr. D and Mr. E). However, patients
with 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 hemisphere
and negative arousal, these posterior-lesioned patients
also showed a significant difficulty in tolerating their
negative emotional states, and they even lacked the
capacity to bring them to full conscious awareness,
though reality testing was not as severely impaired as
in the frontal cases. For Kaplan-Solms and Solms, the
symptoms observed after lesions to the right convexity
are caused by a diminution in whole-object relation-
ships, which generates the emergence of primitive
defenses (p. 197). If we take Feinberg’s and Kaplan-
Solms & Solms’s evidence together, it is possible to
suggest: (1) right-hemisphere damage to posterior and
anterior regions generates a recrudescence of primi-
tive defense mechanisms; (2) right frontal-lobe lesions
generate 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 state
but preserve reality testing. This suggests a regula-
tory role of right frontal cortex, supported by studies
that propose a role of this brain region in social skills
(Bach, Happe, Fleminger, & Powell, 2000), emotional
processing (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, &
Christian Salas & Oliver H. Turnbull
Coltheart, 2005; Coltheart, 2005, 2007; McKay, Lang-
don, & Coltheart, 2005), reasoning under uncertainty
(Goel & Vartanian, 2005), and maintaining on-line
ambiguous 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 that
relate 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 “secondary
inducers” (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 commentary
by 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, and
relatedness to others and the world; (2) they are associ-
ated with confabulation; (c) they are related to brain
injury. A possible limitation of Feinberg’s proposal is
his emphasis on syndromes that include confabula-
tions, with less emphasis on other cases where there is
no sign of confabulation but changes in the experience
of the self are evident. It would be helpful if a survey
of changes in the NPS were undertaken based on lesion
site, but focused more broadly than on confabula-
tion. Along this line, we have expanded Feinberg’s
understanding of the NPS by describing disturbances
in the sense of self that are related to pure cognitive
deficits. One might take this argument further, con-
sidering instances where only the bodily self appears
abnormally 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 that
Feinberg’s emphasis seems to be centered on the delu-
sional component, which seems likely to be merely
a subgroup of the NPS, albeit containing the most
extreme cases. An all-encompassing account of the NPS
should then include syndromes where the self may be
modified, by either cognitive or somatic changes. Fur-
thermore, an inclusive account should even consider
modifications of the self that are not exclusively caused
Neuropathologies of the Self: A General Theory • Commentaries
by brain injury to the central nervous system, as in the
case of phantom limbs after amputation (Chen, Cohen,
& Hallett, 2002; Giummarra, Gibson, Georgiou-Karis-
tianis, & Bradshaw, 2007), changes in body schema
after quadriplegia (Salas, 2010), or peripheral injury
(Sacks, 1998). In sum, we believe that Feinberg’s pro-
posal of the neuropathologies of the self would increase
its value if, as a theoretical framework, it were capable
of incorporating the many different ways by which the
self can change after a neurological insult.
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