Neuropathologies of The Self: A General Theory

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Neuropathologies of the Self: A General Theory

Todd E. Feinberg
Albert Einstein College of Medicine and the Yarmon Neurobehavior and Alzheimers Disease
Center, Beth Israel Medical Center, New York, U.S.A.
Published online: 09 Jan 2014.
To cite this article: Todd E. Feinberg (2010) Neuropathologies of the Self: A General Theory, Neuropsychoanalysis: An
Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 12:2, 133-158, DOI: 10.1080/15294145.2010.10773637
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Neuropsychoanalysis, 2010, 12 (2)
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Todd E. Feinberg (New York)
The neuropathologies of the self are a continuum of disorders of the self and identity that occur in the presence of identiable brain
pathology. They include perturbations of the bodily, relational, and narrative self. From the standpoint of neuropsychoanalysis, the
most interesting are those that display delusional and confabulatory aspects, especially the delusional misidentication syndromes.
Damage to the right, especially medial-frontal and orbitofrontal, sectors is particularly associated with these conditions. According to the ego-disequilibrium theory, in patients with neuropathologies of the self, right frontal damage creates a disturbance in
ego boundaries and a breakdown of the observing ego that also facilitates the emergence of developmentally immature styles of
thought and ego functioning and the return of psychologically primitive defenses such as denial, projection, splitting, and fantasy
characteristic of both the adult neurological patients and the child. It is hypothesized that in the course of normal brain development
between approximately the ages of 38 years there is a movement away from immature defensive functions and fantasies to mature
defenses and the inhibition of fantasy that critically depends on maturational processes within the right hemisphere. Once these
brain structures are established, the immature defenses and the use of fantasy typical of the child are inhibited and mature adult
defenses emerge. In the presence of right frontal damage, however, there is a reemergence of these primitive immature defenses.
The hypothesis posits that the preservation and activation of the verbal defenses in these cases, such as verbal denial, projection,
splitting, and fantasy, must be the result of the remaining, and presumably relatively intact, left verbal hemisphere and that it even
may be possible that the mature defenses are lateralized to the nondominant hemisphere. A four-tiered model of these syndromes
is proposed that can broadly account for the origin of all of these conditions. This model emphasizes a multifactorial approach that
includes both negative and positive, bottom up and top down, and neuropsychological and psychological factors and explains why any
given patient with one of these syndromes may lack a certain feature. Indeed, the model predicts that given that so many interacting
factors may play a role in the development of these disorders, we would expect that group studies that examine multiple factors will
vary in the presence, importance, and pattern of association and dissociation of any single one.
Keywords: neuropathologies of the self; delusional misidentication syndromes; delusional confabulation; anosognosia, asomatognosia; somatoparaphrenia; ego functions; psychological defense
Pathology has made us acquainted with a great number

of states in which the boundary lines between the ego
and the external world become uncertain or in which
they are actually drawn incorrectly. There are cases in
which parts of a persons own body, even portions of
his mental lifehis perceptions, thoughts, and feelings appear alien to him and as not belonging to his
ego; there are other cases in which he ascribes to the
external world things that clearly originate in his own
ego and that ought to be acknowledged by it. Thus,
even the feeling of our own ego is subject to disturbances, and the boundaries of the ego are not constant
(Freud, 1930).
The neuropathologies of the self are a group of
interrelated and extensively overlapping syndromes

(Table 1) (Feinberg, 2001, 2009a; Feinberg & Keenan,
2005). These conditions have in common the presence
of focal or diffuse brain lesions that create a transformation in an individuals sense of identity. Although
most of these conditions simultaneously impact more
than one aspect of the sense of self, we can roughly
identify a few specic self-related domains that are
most commonly affected. Disorders of the bodily self
transform the manner in which a person views or acts
upon the nature or limits of his or her physical being.
Disturbances of the relational self impact the manner in which the individual thinks about or interacts
with objects and persons and affect the personal and
Todd E. Feinberg: Albert Einstein College of Medicine and the Yarmon Neurobehavior and Alzheimers Disease Center, Beth Israel Medical Center,
New York, U.S.A.
Correspondence to: Todd E. Feinberg, Yarmon Neurobehavior and Alzheimers Disease Center, Beth Israel Medical Center, First Avenue at 16th Street,
New York, NY10003 (email: tfeinberg@bethisraelny.org).
2010 The International Neuropsychoanalysis Society
http://www.neuropsa.org
134
Todd E. Feinberg
Table 1.
Some of the more common neuropathologies of the self
Syndrome
Features
Delusional anosognosia
Persistent and refractory denial of paralysis, often accompanied by confabulation
Somatoparaphrenia
Delusional misidentication of part of the body, often accompanied by confabulation
DMS for the mirror image
Persistent and selective misidentication of the self in the mirror, often accompanied by
confabulation
Capgras syndrome
Persistent underrelated misidentication of a person, place, or thing
Frgoli syndrome
Persistent overrelated misidentication of a person, place, or thing
Phantom boarder syndrome
The delusional belief that a person(s) is living in the same house as, or close by to, the patient
Nurturing syndrome
The delusional belief that a deceased loved one (typically a spouse) is alive, and the patient
interacts with him or her
Delusional companion syndrome
The patient adopts a soft toy such as a teddy bear and treats it like a close companion or child
Note: The more delusional forms of these disorders are clinical endpoints on a multifactorial continuum that also includes less delusional
varieties of these conditions (see Table 3). A subset of these conditions most specically related to DMS have also been referred to as reduplicative paramnesia (e.g., Pick, 1903), delusional paramnesic misidentication (e.g., Burgess et al., 1996), content-specic delusions (e.g., Malloy &
Richardson, 1994), and monothematic delusions (e.g., Davies, Coltheart, Langdon, & Breen, 2001).
autobiographical signicance of the self in relation to

the world. Perturbations of the narrative self primarily
impact how one thinks about and describes personal
past and present circumstances.
Although the literature on these conditions extends
for over a hundred years, these syndromes are still
to an extent scientic orphans in that they are not
regarded as completely psychiatric or neurological in
origin, but, rather, as some yet-to-be-elucidated complex hybrid of the two. Nonetheless, the analysis of
these conditions is a particularly fertile source of information on the neurobiological underpinnings of the
self and the manner in which the brain creates personal
identity. In this review I provide a brief overview of
these conditions and then consider how they point
the way to a deeper and novel understanding of the
neurological basis of ego boundaries, ego functions,
and psychological defense. In particular, I will focus
on the most delusional and confabulatory varieties of
these disorders, which I place on a continuum with less
delusional subtypes (Tables 1 and 3).
Disorders of the bodily self
Anosognosia for hemiplegia
One of the rst disorders of the self and self-awareness
to be described in the neurological literature is anosognosia, literally lack of knowledge of the existence
of disease. Anosognosia is known to occur in a wide
variety of psychiatric, medical, and neurological conditions (Feinberg & Roane, 2003a), but here I will focus
on anosognosia for hemiplegia (AHP; for some recent
reviews and research see Fotopoulou et al., 2008; Marcel, Tegnr, & Nimmo-Smith, 2004; Orfei, Robinson,
Bria, Caltagirone, & Spalletta, 2008; Orfei et al., 2007;
Vallar & Ronchi, 2006; Vuilleumier, 2004).
Gabriel Anton (1893) presented what may be the rst
description of AHP, and Joseph Babinski (1914, 1918)
provided additional clinical examples and coined the
term anosognosia. In this syndrome, the patient typically has an acute lesion, most commonly a stroke in
the nondominant hemisphere, that leads to left hemiplegia, sensory loss, and hemispatial neglect. While the
diagnosis of anosognosia for hemiplegia requires only
a simple unawareness of hemiplegia, the actual clinical
syndrome is much more complex and variegated. In
some cases, patients may actually admit that the limb
does not move but attribute it to excuses such as laziness, fatigue, or a lack of effort. In other cases, patients
may confabulate that the limb has indeed moved when
in reality it lies motionless at their side (Feinberg,
Roane, & Ali, 2000). In the most extreme case, even
if the paralysis is demonstrated to the patient, and the
lifeless arm when lifted by the examiner drops inertly
on the bed, the patient still adamantly denies there
is anything awry. In these circumstances, the belief
takes on delusional proportions, a point we return to
later (Coltheart, 2007; Critchley, 1953; Davies, Aimola
Davies, & Coltheart, 2005; Feinberg & Roane, 1997;
Feinberg & Roane, 2003a; Feinberg, Roane, & Ali,
2000; Gerstmann, 1942; McKay, Langdon, & Coltheart, 2005). Thus, AHP is best conceptualized on a
continuum ranging from simple unawareness that may
be readily corrected by feedback from the examiner to
adamant and delusional denial and confabulation that
is resistant and relatively refractory to correction.
A typical example of AHP is patient P.M., a woman
in her sixties with a large right frontotemporal parietal
stroke, left hemiplegia, and neglect who demonstrated
profound denial of her paralysis and confabulation.
Throughout many weeks of hospitalization, and in
spite of having been repeatedly told that she had suffered a stroke and that her left side was paralyzed, P.M.
denied both her illness in general and her paralysis:
T.E.F.:
Ok. What are you doing here?

P.M.: Checking out why I fell over a coffee table.
T.E.F.: Is there anything wrong with you now?
P.M.: No.
T.E.F.: Nothing at all? Youre fine? Youre in the
picture of health?
P.M.: I would say that Im well enough to go home!
T.E.F.: Could you just get up and walk out of here?
P.M.: Yes I could.
T.E.F.: Are you having any difficulty walking?
P.M.: No.
T.E.F.: Ok. So what are you doing here?
P.M.: You all tell me I have a weak left side.
T.E.F.: Im sorry?
P.M.: You all say I have a weak left side.
T.E.F.: We all say you have a weak left side?
P.M.: And I dont agree!
T.E.F.: And you dont agree?
P.M.: No.
T.E.F.: Why?
P.M.: Because I know I dont!
T.E.F.: It feels fine?
P.M.: Yes.
T.E.F.: Theres no weakness over there?
P.M.: No [she is asked to raise her right arm, which
she does].
T.E.F.: Now raise the other arm for meraise your
left arm. Cant you do that for me? [Pause] Did
you do it? Did you raise it?
P.M.: I did now.
T.E.F.: You did now? Do you have any difficulty
raising it?
135
P.M.:
No
T.E.F.: Ok then. Why dont you touch your nose?
[Touches nose with right hand]
T.E.F.: Why dont you touch it with the other hand?
Can you touch it with the other hand?
P.M.: Yes.
T.E.F.: Could you do it for me? [No movement] Are
you doing it? [Again, no response] . . . You know,
it would seem to me that if you couldnt touch
your nose with your left hand, that there might be
some weakness over there. How does that sound
to you?
P.M.: No.
T.E.F.: You adamantly disagree? You are absolutely
certain theres no weakness over there? Could
you tell me why you wont touch your nose with
your left hand? Is there a reason for that?
P.M.: Because I think Im a comedian . . . and Id
probably make an obscene gesture.
T.E.F.: You know I cant help but notice it looks to
me like you have some degree of paralysis of
your left arm. Would you believe me if I told you
that you did?
P.M.: No . . . because I know I could drive to work
tomorrow and work with both hands! . . . I answer
the telephone and take messages constantly . . .
T.E.F.: And youd have no difficulty doing that?
P.M.: No.
This dialogue makes clear that P.M.s responses go
well beyond simple unawareness of her condition. In
fact, a more appropriate description is that she is in
denial not only of her left hemiplegia, but also of her
inability to walk, write, or use the telephone with both
hands. Additionally, she confabulates about her arm
movements or otherwise rationalizes its immobility.
There are a number of purely neurological and neurocognitive decits all or some of which may facilitate
AHP in any individual case, including proprioceptive
loss, hemispatial neglect, and generalized confusion,
as well as a host of others factors (for some of these,
see Critchley, 1953; Cutting, 1978; Feinberg & Roane,
2003a; Fotopoulou et al., 2008; Gerstmann, 1942; Heilman, 1991; Heilman, Barrett, & Adair, 1998; Levine,
Calvanio, & Rinn, 1991; Marcel, Tegnr, & NimmoSmith, 2004; McGlynn & Schacter, 1989; Orfei et
al., 2007, 2008; Vallar & Ronchi, 2006; Vuilleumier,
2004). However, there remain some important and
perplexing questions as to the nature and etiology of
AHP. For example, it has been demonstrated that one
136
can temporally reverse the neglect in some anosognosic

patients yet the anosognosia itself improves only in a
few of these (Bisiach, Rusconi, & Vallar, 1991; Cappa,
Sterzi, Vallar, & Bisiach, 1987). Also, some patients
deny their impairments whereas others with similar lesions and degrees of hemispatial neglect do not
(Weinstein & Friedland, 1977; for reviews see Bisiach
& Geminiani, 1991; Feinberg & Roane, 2003a). Furthermore, as noted above, there is a wide continuum of
anosognosic responses ranging from simple unawareness of the paralysis to obligate and adamant denial
of disability and the creation of delusional confabulations. This suggests that many cases of AHP cannot
be explained solely by the loss of certain faculties and
abilities that are known to occur in AHP, and that other
factorspositive factorsmust be involved. For these
and other reasons, there is a growing speculation that no
single factor or mechanism can account for AHP (Feinberg & Roane, 1997; Marcel Tegnr, & Nimmo-Smith,
2004; McKay, Langdon, & Coltheart, 2005; Orfei et al.,
2007); rather, a multiplicity of interacting factors must
be involved across a broad range of patients.
Asomatognosia and somatoparaphrenia
The term asomatognosia literally means lack of recognition of the body, but by far the most common
form of asomatognosia is the nonrecognition or denial
of ownership of the left arm in the setting of right(nondominant) hemisphere damage, left hemiplegia,
hemisensory decits, and hemispatial neglect (Baier
& Karnath, 2008; Critchley, 1953, 1955; Feinberg,
2009a; Feinberg, Haber, & Leeds, 1990; Feinberg,
Venneri, Simone, Fan, & Northoff, 2010; Gerstmann,
1942; Halligan, Marshall, & Wade, 1995; Meador,
Loring, Feinberg, Lee, & Nichols, 2000; Vallar &
Ronchi, 2009). As is the case with anosognosia, the
form and degree of the asomatognosic response varies
considerably among patients. Gerstmann (1942) distinguished autosomatamnesia and autosomatagnosia that
occurred as a consequence of unelaborated disturbances
of memory or consciousness, from somatoparaphrenia
that was characterized by elaborate delusional and
confabulatory features. Critchley (1953) later introduced the term asomatognosia to describe the more
general feature of a loss of awareness of one bodyhalf, without specifying the presence of delusional
features. Thus, as is the case with anosognosia, there is
a wide range of asomatognosic responses, from simple
unawareness or confusion regarding the ownership of
the limb to delusional denial and confabulation about
its identity (Feinberg et al., 2010).
Todd E. Feinberg
Both Gerstmann and Critchley noted that in these

latter cases the misidentication of the arm may have
considerable delusional elaboration wherein the patient
adamantly insists that the arm is not her own despite
irrefutable proof to the contrary, such as the demonstration of the arms attachment to the patients own
shoulder. In some extreme instances, the arm may even
be treated like a child or another person with a separate
identity, or given a nickname such as Little Monkey,
Toby, or Pet Rock (Critchley, 1953, 1955, 1974;
Feinberg, 2001, 2009a; Feinberg et al., 2010).
An example of the richness and complexity of the
somatoparaphrenic response is my patient J.K., a young
man who had been living in America for several years
while his family remained overseas in their homeland.
Following a tragic illness, he underwent surgery for an
abscess of his right hemisphere, after which he developed dense left-side paralysis and hemispatial neglect.
Holding up his arm, I asked him to identify it:
T.E.F.:
What is this?
J.K.: Its supposed to be my arm, but I think its my
brothers arm. I tell that to everyone but they
dont believe me. My brother was on the wrong
track for a while, and he got involved with some
gangsters. They chopped off his arms and threw
them in the river. I found this in my cofn [touching the left arm]. Some people thought I was dead
and it was there.
T.E.F.: Now what about, . . . you mentioned something about being in . . . you found it in your cofn. Tell me about that.
J.K.: I dont know why I was in a coffin . . . after I
was carried to the hospital . . . I was in a cofn
. . . thats what I remember . . . I was laying next
to this arm [pointing to left arm] . . . I was in a
cofn.
T.E.F.: And thats how you found it?
J.K.: Yeah, thats how I found it . . .
T.E.F.: Were you alive?
J.K.: I was alive . . . I didnt die . . . I found the arm
in the cofn.
J.K. not only misidenties his arm, he also gives it a
separate identity and confabulates about how it became
attached to his body. It is of interest to note how rich
in metaphor and meaning his statements are. Thus, as
is the case in the delusional anosognosic patients, the
degree of reality distortion and delusional and confabulatory elaboration go far beyond a rational explanation
of confusing circumstances.
Disorders of the relational self
Delusional misidentication syndromes

and delusional confabulation
The neuropathologies of the self as a group have
extensive overlap with the delusional misidentication
syndromes (DMS; Alexander, Stuss & Benson, 1979;
Capgras & Reboul-Lachaux, 1923; Christodoulou,
1976, 1977, 1986; Feinberg & Roane, 2005; Fleminger
& Burns, 1993; Vi, 1930, 1944). In these conditions
a person misidenties specic persons, places, objects,
or events in the world. Indeed, the neuropathologies of
the self most relevant to neuropsychoanalytic thought
are those in which the patient displays prominent delusions and delusional confabulation (Coltheart, 2007;
Critchley, 1953; Davies, Aimola Davies, & Coltheart,
2005; Feinberg & Roane, 1997, 2003b, 2005; Feinberg,
DeLuca, Giacino, Roane, & Solms, 2005; McKay,
Langdon, & Coltheart, 2005). It should be emphasized that we are addressing here a particular variety
of confabulation. Schnider (2008) has recently introduced a useful taxonomy that distinguishes the various subtypes of confabulation in which he describes
four categories of confabulation: intrusions or simple
provoked confabulations that occur during memory
tests; momentary confabulations that are prompted by
questions or occur in conversations, fantastic confabulations with no basis in reality and which tend
toward the nonsensical or bizarre; and behaviorally
spontaneous confabulations, which are the result of an
abnormal adaptation of thought to ongoing reality
and temporal-context confusions. To this grouping
Schnider also distinguishes mnestic confabulation,
which is due to memory failure, from non-mnestic
confabulations, which derive from false perceptions of
the body and the world. According to these criteria, the
elaborate confabulations in the delusional anosognosic
and somatoparaphrenia cases are primarily fantastic
and non-mnestic in type and are closer clinically to
delusional misidentication than they are to the other
varieties of confabulation.
One of the most commonly reported forms of delusional misidentication in neurological patients is Capgras syndrome (Capgras & Reboul-Lachaux, 1923),
in which the patient believes that persons, places, or
objects have been replaced by doubles or imposters.
A related type of misidentication is Frgoli syndrome
(Courbon & Fail, 1927), which involves the belief that
a person who is well known to the patient is really
impersonatingand hence taking on the appearance
ofa stranger in the patients environment. The delusional aspects of these conditions have been interpreted
137
along a dimension of personal relatedness based on the

pattern of identication between the self and other
persons, objects, events, or experiences. Capgras syndrome thus represents an underpersonalized response
and Frgoli syndrome an overpersonalized misidentication (Feinberg & Roane, 1997, 2003b, 2005).
This interpretation places emphasis on the emotional,
motivational, and self-related aspects of the condition.
It is consistent with the important feature that DMS
patients know who the misidentied entity should be,
but they experience a rift in, denial of, or transformation in their emotional relatedness and connectedness
to the misidentied entity.
Indeed, somatoparaphrenia also has been usefully
interpreted as a DMS in which patients misidentify in
a delusional and confabulatory fashion a part of their
body, and hence this condition can be interpreted as a
variant of Capgras syndrome for their arm (Vi, 1930,
1944; Feinberg & Roane, 1997, 2003b, 2005). The
most common version of the Capgras syndrome, however, is the misidentication of specic persons.
A typical patient with Capgras syndrome is F.P., a
woman in her eighties in the early stages of Alzheimers
disease. F.P. began to specically and selectively misidentify her sister whom she lived with, who was her
closest relation and friend, and whom she was becoming increasingly dependent upon as her caretaker. Her
sisters real name was Mary, but she was known to F.P.
as Paula. On most occasions F.P. referred to her sister
as Paula, but she began to assert that someone named
Marynot her sisterwas posing as Paula and trying to take her place in the house:
MARY/PAULA:
I would say nine times out of ten she

. . . Im the other person. I am not her sister
Paula. I am Paula someone else.
T.E.F.: But they both have same name though?
F.P.: No . . . she stole it [pointing to Paula] She
snitched it! Its not her real name . . . You remember you saidwhen we were on our way out
Heres the girl now and she was coming down
the steps, and you said which one is she? And
I said Well, I dont know which one but she is
always there, you know, . . . she is a lot of help to
me but sometimes she aggravates me and then I
cant see . . .
MARY/PAULA: Theres always a third person in the
room and it could be Mary, . . . its not her sister,
but its Mary this girl . . . its not Mary her sister,
its Mary a stranger, its somebody else that wants
to horn in and take Paulas place.
F.P.: You do that, dont you?
138
No, honey . . . I tried to tell you its

just a hallucination that you have . . .
F.P.: There are five Paulas now, and they have all
gone off the hook. Believe me. Five of them, yes.
And I think they are almost all in this room now!
And Im so aggravated with the whole bunch of
them . . . I call you Mary, I call you any other
name, but you will hang on to Paula. I said, why
would anyone want a rotten wily name that you
cant even bother about?
MARY/PAULA:
As in the other conditions I have discussed such as

anosognosia and somatoparaphrenia, F.P. had fundamental neurocognitive issues including memory and
visuospatial impairments, these two being common
accompaniments of the disorder. However, F.P.s misidentication was selective and exclusive to her sister,
and she never misidentied me or anyone else in her
environment. This selectivity is critical if one is to
appreciate the true nature of the disorder as it highlights
the delusional and self-related aspects of the condition.
Although some cases of Capgras syndrome may have
some degree of generalized difculty with face recognition (Silva & Leong, 1995; Young, Reid, Wright, &
Hellawell, 1993), the delusional misidentication in
Capgras syndrome is generally conned to one or a
few individuals whereas other family members, physicians, and neighbors are correctly identied. Furthermore, the patient with Capgras syndrome insists upon
the false identication in spite of being repeatedly
corrected, and he or she never uses extrafacial cues to
correct the error when it is pointed out. Thus, Capgras
syndrome cannot be explained solely on the basis of a
perceptual disorder, and other factors must be at play.
One feature I have repeatedly observed among Capgras patients is that the person who is misidentied is
often the person whom the patient is most dependent
on. For example, in dementia cases, in many instances
it is the son or daughter who has the greatest responsibility for the patients careand frequently the one
who must deal with the occasional abusive behavior
of the patientthat is misidentied. This suggests that
ambivalent feelings of the patient toward the patient
primary caretaker may be playing a role, a subject we
consider later.
A DMS of particular interest to neuropsychoanalysis
is delusional misidentication of the self in the mirror
(mirror-image DMS). The rst well-described example
of this syndrome was the case reported in the 1960s, a
61-year-old New Zealand woman of European descent
in the early stages of dementia (Gluckman, 1968). Her
major complaint was that there was a woman in her
home who was her double and who followed her about
Todd E. Feinberg
the house and imitated her in every way but could only
be seen when the patient was looking in the mirror:
She could only see her if she looked in the mirror. She
did not know what this woman was called, calling
her an old hag, an ugly hag or usually this thing. This
woman did not speak to her verbally but only in gesture or by mimicry. . . . The woman was there because
she wanted love and affection from the patient, but the
patient could not give her affection and she was very
much afraid of this double. . . she would say emphatically that it was not her but that terrible ugly old
woman who followed her everywhere and frightened
her. She could not escape, try as she would, from the
presence of this hag. . . . She had on occasion thrown
a bucket of water and other solid objects at her mirror image to try and persuade it to leave the house.
[Gluckman, 1968, p. 40]
Another example of this condition is my patient S.P.

(Susan), a woman in her sixties who had been hearing-impaired since the age of 5 years and communicated by speaking, lip reading, and sign language. S.P.
began to communicate in sign language with another
person she saw in the mirror also named S.P. who was
identical to her in appearance, age, and background.
Her neurological exam, brain MRI, and neuropsychological testing revealed evidence of right-hemisphere
dysfunction. This is how she described her double:
Well, shes all right . . . sounds funny for me talking
from one Susan to another, because you know she
was a new person to me, and Im surprised. She was
all right, but shes very nervous, she likes to do her
own ways . . . she never knew that she couldnt hear
so good, and shes not a very good lip reader. I had
to do mostly in sign language for her, to make her
understand . . . she copies every word I say like this,
like this motion . . . she doesnt even know the sign
language very well, and I was confused a little bit,
you know, because I wanted her . . . I thought she
knew the sign language very well, so I wont have
to repeat it twice, but then I found out that shes not
that bright. I hate to say that . . . I dont want to brag,
but shes a nice person; but one thing about her . . .
I see her everyday through a mirror, and thats the
only place I can see her. When she sees me through
the mirror, she looks a little then she comes over
and talks to me, and thats how we began becoming
friends through our sign language. She was very
nice.
As we shall see, S.P.s relationship with her mirror
image became in nearly every respect an imaginary
companion for her as occurs in childhood.
Delusions and fantasies about imaginary persons

Another neuropathology of the self that also may be
classied as a DMS (Hwang, Yang, & Tsai, 2003;
Rubin, Drevets, & Burke, 1988) involves individuals
who may or may not misidentify specic persons in
the environment but who hold a delusional belief about
an imaginary person. In some reported instances, the
ctitious individual is a duplication of an actual person, typically someone close to the patient, such as a
spouse or a sister. Weinstein Kahn, and Morris (1956)
described neurological cases who expressed delusional
beliefs about children. The most common delusion was
that the patient was the parent of a ctitious child. An
interesting self-referential aspect of these delusions
was that these patients often attributed to the phantom
child the same illness or disability that the patients
had themselves. For example, a women blind from a
brain tumor confabulated about a daughter child who
was sick and blind. Another woman who complained
how the nursing staff treated her claimed that she had
a baby that the nurses had harmed and even killed.
In essence, the phantom child served as an alter ego for
the patient (Feinberg, 2001).
My patient L.K. is a classic example of this sort of
delusional confabulation. She was 65 years old, with
a ruptured brain aneurysm, bifrontal cerebral damage, and signicant memory impairment. Although
divorced and childless, she claimed that she was in the
hospital to visit her niece, whom she described as a
child and a little girl. In extensive narratives that
reected her own her own difculties L.K. claimed that
the niece had an aneurysm, and she also insisted that
she had an aunt and six cousins all with aneurysms on
top of their heads:
T.E.F.:
So you came to visit somebody. Who did you

come to visit?
L.K.: I came to visit my aunt.
T.E.F.: You aunt . . . and what was wrong with her?
L.K.: She couldnt think straight.
T.E.F.: She couldnt think straight? Why?
L.K. [Patient now reaches up and feels the top of her
head, which was shaved and had a long line of
surgical staples]: Something was wrong on top
of her head . . . causing her . . . an aneurysm . . .
not to think straight.
T.E.F.: Your aunt had an aneurysm?
L.K.: Yeah. And an aneurysm is blood on top of your
head.
T.E.F.: What hospital was she in?
L.K.: This one.
139
T.E.F.:
Youre kidding? She was in the same hospital

as this one? Is she here now?
L.K.: I think so.
T.E.F.: Where is she?
L.K.: You got me! I dont know exactly where, but I
know she is in this hospital.
Shanks and Venneri (2002) have described a group
of patients with delusional companions who imbue
an inanimate object with a human identity. In many
respects these cases resemble those with mirror companions. They reported three women with a predominantly right parietal, temporal, or frontal hemisphere
dysfunction, who treated teddy bears, soft toys, or
dolls as if they were alive. One case claimed a large
teddy bear was alive and a super person very interested in what is going on and was a very attractive
little youngster. She conversed with it and encouraged it to have meals with her and read the newspaper.
Another case called a teddy bear Doreen and gave
her an allowance. Interestingly, the wishful nature of
the belief emerged when she was asked if Doreen
was really alive, to which she responded No, she does
not breathe or anything like that, I sometime wonder
myself whether she is alive, I wish she were, she would
make a lovely companion! All three of these cases had
right-hemisphere dysfunction, and in all three the delusional companions were an important source of emotional comfort and companionship, a point to which we
return later.
Venneri and coworkers have also described a similar disorder they call nurturing syndrome (Venneri,
Shanks, Staff, & Della Sala, 2000). They reported two
casesinterestingly both women as wellin the early
stages of dementia. These women claimed after the
deaths of their husbands that the spouses were in reality
still alive. One patient claimed the husband would visit
her, and she became obsessively morbidly attached
to a photograph of him, which she tried to feed. The
second also denied the husbands death and talked to
and also tried to feed his photograph. On single photon
emission computed tomography (SPECT) scans, both
patients showed frontal dysfunction, right greater than
left.
Disorders of the narrative self
Symbolic representations of personal experiences
In delusional or personal confabulation an individual
produces a narrative in the form of a delusion or
140
recurring confabulation in which he or she ostensibly

discusses veridical events about the self or others but
is implicitly, unconsciously, metaphorically, or symbolically expressing his or her feelings about his/herself and his or her current situation (Feinberg, 2009b).
Weinstein described this variety of confabulation in
the case of a 42-year-old army ofcer who sustained
a brain injury in a jeep accident while stationed in
Korea. As a result of the accident, he suffered from
right hemiparasis, dysarthria, alexia, and agraphia.
Although he would explicitly admit his impairments,
he seemed indifferent to them. When he was asked to
describe his accident, he produced the following narrative:
I had a big job overseas. I was an intelligence ofcer
in the Air Force. The man I relieved was a captain and
his assistant a rst lieutenant. I was sent to check on
their security. They were just as Commie as if painted
with a red brush. I had to write out everything I found
so that it could be read at court in a courtmartial for
these men some day. I wrote it out and turned it into
headquarters. I had enough written so that any jury in
its right senses would give those guys 20 years in jail
apiece, they were just that Commie. Those two were
riding with me on the day the shell exploded in my
jeep. I can remember now that I stopped to look at
my road map over there in Korea. [Weistein, Kahn, &
Malitz, 1956, p. 387]
Weinstein and coworkers suggested that the use of the

words intelligence, reading, writing, and right senses
(I would add remembering, head, checking, and looking) are implicit references to the patients neurological impairments. More recently Feinberg et al.
(2005) described patient L.A., who, after a ruptured
arteriovenous malformation, denied his neurological
decits although he was conned to a wheelchair and
had signicant memory and cognitive impairments.
When we asked him to describe what had happened,
he repeatedly produced a variant of the following confabulation:
L.A.:
A couple of days ago people been telling me

the things that happened to me and its possible
that something happened to me . . . People been
telling me that they think there was a big explosion in one place I was at and that destroyed my
mind. And that is one of the reasons Im having
now . . . What do you call a person that is sleeping and starts to walk?
T.E.F.: Sleepwalking.
L.A.: Yeah, I started to do that . . . and that is causing all the disturbances in my mind . . . People
are saying, somebody said I was in a room like
Todd E. Feinberg
next door, a big explosion in there and I was in

there, and that was going to destroy my mind,
my personality. That might be what it is . . . They
said also that I was going to be sleeping and I was
going to awake. But I didnt wake up and I started
to walk [starts to cry] I never had it before . . .
The doctor said I was going to be sleeping and
start walking in my sleep, and I dont understand
because I never had it.
T.E.F.: Are you sleepwalking now?
L.A.: Not according to my parents and not according
to me.
T.E.F.: How is your actual walking?
L.A.: My actual walking is good.
T.E.F.: Fine? So you can run and dance and jump?
L.A.: No problem . . .
At the same time that L.A. denies his severe ataxia, he
is preoccupied with the idea that he is sleepwalking,
and although he denies his cognitive decits he admits
that the professionals have told him that an explosion had destroyed his mind. In this metaphorical,
symbolic, or personal confabulation, L.A.s personal
concerns are expressed in terms of a substitute for the
actual experiences of the self.
Explaining the neuropathologies of the self:
negative and positive factors
Most neurological hypotheses regarding the mechanisms of these disorders can be roughly categorized
according to Jacksonian terminology as emphasizing
negative or positive symptoms or factors. Hughlings
Jacksons model of the nervous system posits that in
the presence of neurological dysfunction, the nervous
system may revert to developmentally earlier or hierarchically lower stages of neurological functioning.
Jackson referred to this process as dissolution, and it
has certain predictable effects on behavior and neurological functions. In order to describe these patterns,
Jackson (1884) introduced the distinction between
negative and positive neurological symptoms. Negative symptoms are the result of a destructive lesion of
the nervous system that creates a loss of neurological
function. A positive symptom occurs when there is
destruction of a brain region that normally regulates
or inhibits another brain region. When this occurs, the
dissolution of the suppressing area releases from inhibition the normally suppressed region. This can lead
to overactivity of the normal functions of the remaining systems.
We have already noted the numerous decit

statesnegative symptomsthat often accompany
AHP, asomatognosia, and DMS. However, many of
the original writers on theses syndromes had suspected for decades that negative features of these conditions cannot fully explain these disorders (e.g., see
Goldstein, 1939). So, for instance, we need to explain
why the misbeliefs and misidentications are generally very selective. In DMS, only particular individuals are misidentied, while other persons also close to
the affected individual are accurately identied. There
is also the question of the delusional nature of these
beliefs. In spite of the apparent illogical nature of the
misbeliefs, and the repeated correction by examiners
and family members, some patients hold to their delusional misbeliefs and misidentications. This suggests
that there is an impediment or resistance to the truth.
Indeed, these patients may have explicit or implicit
knowledge regarding their true location, illnesses, and
other issues that they seem to be unaware of or confabulate about. Furthermore, the misidentications in
these syndromes reect specic alterations in personal
signicance. This indicates that one of the salient features of this particular variety of confabulation is that
the misidentications, reduplications, and fantasies
that these patients display are almost wholly with
reference to entities of emotional signicance, such as
ones body, family, or personal possessions. Finally, it
has been observed by many clinicians and researchers
that the delusions, confabulations, and misidentications in these cases may be wish-fullling (Conway
& Tacchi, 1996; Feinberg & Roane, 1997, 2003b;
Feinberg et al., 2005; Fotopoulou, Conway, & Solms,
2007; Fotopoulou, Solms, & Turnbull, 2004). Thus a
unied theory must address these positive, adaptive,
and motivational aspects.
Ideally, in order to develop a comprehensive
theory of the origin of the neuropathologies of the
self as a group, we would like a unifying and parsimonious hypothesis that takes all these factors into
account. The theory should be as general as possible
and explain the common features of the conditions,
as opposed to an account that is selectively tailored
to explain one or another syndrome. We would like
the theory to explain the aforementioned positive
symptoms that are not explained solely by a loss of
neurological dysfunction. Finally, we would like the
theory to be consistent with a common neuropathology across these conditions. One hypothesis that is
an attempt to satisfy these three constraints and unify
many different points of view on these conditions
I call ego dysequilibrium theory (Feinberg, 2009a,
2009b ; Feinberg et. al., 2005).
141
A proposed synthesis:
the ego-disequilibrium theory
The ego-dysequilibrium theory posits that the unique
features of the adult neuropathologies of the self result
from (1) a neurologically derived alteration in the
self-boundaries, (2) a regression to a developmentally
earlier, hierarchically lower, or more primitive stage
of psychological functioning, and (3) a recrudescence
of the patterns of thought and defense typical of theses
earlier periods. The primitive defensive patterns in
question include but are not limited to denial, projection, splitting, fantasy, and paranoiafunctions that
were dormant in the normal adult brain but are now
activated by the neurological lesion
In order to understand the dynamic, psychoanalytic,
and developmental aspects of the theory, we can again
refer to Jacksons concept of negative and positive
symptoms, his emphasis upon the hierarchical organization of the nervous system, and the central role that
disinhibition could play in symptom formation. Indeed,
Jacksons conceptualization on these points had a profound impact on Freuds thinking about the structure
and function of the psyche. In applying the notion of
dissolution to psychoanalysis, Freud introduced the
concept of regression, in which pathology causes a
return to a developmentally earlier, less mature, and
hierarchically lower stage of psychological functioning (Freud, 1900).
The meaning of the term regression has evolved
since the time of Freud, and the concept now encompasses a number of interrelated constructs. For a general
denition of regression that emphasizes the hierarchical and developmental aspects, Arlow and Brenner
suggest the following:
Regression is the re-emergence of modes of mental
functioning which were characteristic of the psychic
activity of the individual during earlier periods of
development. Viewed descriptively, regression may
be regarded as a primitivization of function. . . . It
stresses the importance of maturational and developmental processes in shaping the form and function
of the psychic apparatus. [Arlow & Brenner, 1964, p.
71]
According to this account, regression in general followsin reverse orderthe patterns of maturation
of the cognitive and ego functions in the child. And
just as the nervous system, as emphasized by Jackson,
displays a hierarchical arrangement, the psychological
defenses also display functional characteristics that
suggest they also possess a hierarchical organization.
According to George Vaillant (1977, 1992, 1993), who
has lent considerable empirical support to the con-
142
Todd E. Feinberg
cept of the hierarchical organization of ego functions

and defenses, the concept of ego defenses entails two
important concepts. The rst is the theoretical notion
of ego itself:
The modern psychoanalytic use of the term ego

encompasses the adaptive and executive aspects of the
human brain: the ability of the mind to integrate, master, and make sense of inner and outer reality. Or, in
Freuds words, We have formed the idea that in each
individual there is a coherent organization of mental
processes; and we call this his ego (Freud, 1923). The
term ego addresses the capacity of the integrated mind
to accommodate and assimilate the world. [Vaillant,
1997, p. 3]
The other relevant theoretical concept is that of ego

defense. Based on Freuds analysis, Vaillant provides
the following description:
In more formal terms, ego mechanisms of defense
describe unconscious, and sometimes pathological,
mental processes that the ego uses to resolve conict
among the four lodestars of our inner life: instincts,
the real world, important people, and the internalized
prohibitions provided by our conscience and our culture. [Vaillant, 1977, p. 9]
According to Vaillants model, denial, delusional projection (including delusional paranoia), and distortion
are the most primitive and pathological defenses, and
therefore they are ranked at the lowest rung on the
Level IV
Level III
Level II
Level I
defensive hierarchy (see Figure 1). Vaillant refers to

these as psychotic defenses because they tend to
distort reality to the greatest degree. However, Vaillant
points out that these defenses may also be present in
normal individuals in dreams as well as during development in children under the age of 5 years. Therefore,
these defenses are considered the hierarchically lowest and the most psychologically primitive, both with
reference to the degree of ego dysfunction and with
regard to the level of developmental maturity.
The next hierarchical level in Vaillants scheme is a
group of defenses that includes projection and fantasy.
These are considered immature defenses because they
make their appearance early in development, but they
are ranked hierarchically higher than the aforementioned psychotic defenses because they are less realitydistorting and require more mental and psychological
development than the psychotic levels of defense.
Level III and Level IV defenses (neurotic and mature
defenses) make their appearance later in life and are
considered less pathological than Level I and Level II
defenses.
The maturation of the defenses
Although Freud suggested that the defenses followed
some developmental evolution, his daughter Anna
Freud (1936) discussed this progression in children
Mature Mechanisms
Common in healthy adults

Sublimation, Altruism, Suppression, Anticipation, Humor
Neurotic Mechanisms
Seen in everyone
Intellectualization, Repression, Reaction formation, Displacement,
Dissociation
Immature Mechanisms
Seen in depression, personality disorders, adolescence

Fantasy Projection Hypocondriasis Passive-aggressive, Acting out
Psychotic Mechanisms
Seen in psychosis, dreams, and childhood up to approximately

age 5 years
Denial of external reality
Delusional projection (including paranoid delusions)
Distortion (includes wish-fullling delusions)
Figure 1. A hierarchical/developmental arrangement of ego functions (based on scheme proposed by Vaillant, 1993).
more explicitly in her book The Ego and the Mechanisms of Defense. More recently Phoebe Cramer (1991,
2006) has provided good evidence for a hierarchy of
defenses along a chronological timetable in which psychological defenses occur as a necessary and adaptive
part of normal development, a view that both Sigmund
and Anna Freud endorsed.
Cramers hierarchy runs for the most part parallel to
the hierarchy proposed by Vaillant. Her research indicates that the earliest defense to develop is psychological denial, and this remains the predominant defense
until about age 7 years. The next defense to emerge is
projection, in which the individual deals with unacceptable and unwanted emotions or thoughts by attributing
them to others. Projection markedly increases as the
child develops, and by about age 7 denial and projection are approximately equally. Projection ultimately
takes the place of denial as the predominant defense.
Cramer suggest that the shift from denial to projection
is the result of the childs increased cognitive ability
that enables him or her to see the self-deceptive nature
of the more primitive defense, making it less available
as a self-protecting mechanism.
At about the same time, the use of fantasy is undergoing a transformation as it interacts and supports the
immature defenses. Fantasy serves many purposes, but
Anna Freud noted that children commonly use fantasy
to support denial. In a similar way, Cramer points out
the way that denial through fantasy enables the child to
cope with unpleasant or unacceptable realities:
Such fantasies serve denial in several ways. If the
unreal can be made to appear true, then the real may
be delegated to the realm of the untrue. In this case,
the fantasies, uninuenced by external events, acquire
a salience that rivals external reality. Eventually these
fantasies come to exist as an alternative reality. The
denial function of this personally constructed alternative reality is manifest when it is imposed on the
external world. Real events are then recognized only
insofar as they conform to the fantasy. The occurrence
of unfounded optimism and elation in the face of
objective failure may be understood as a result of the
substitution of a personal fantasy for objective reality,
and is a manifestation of this component of denial.
[Cramer, 1991, p. 38]
Therefore, denial may be related to wishful fantasy

in several ways. A wishful substitute can serve in the
place of the void left by a signicant emotional loss,
such as when one fantasizes that a deceased loved one
is still alive (Lindemann, 1945). Alternatively, in the
presence of an unfullled motive such as loneliness,
a need or desire may be satised through a pleasant, wish-fullling substitute (Breznitz, 1983; Dorpat,
1985; Feinberg et al., 2005).
143
Children commonly display the use of fantasy in the

creation of imaginary companions. Taylor (1999) suggests that imaginary companions serve a host of functions in the psychological life of the child, including
alleviating loneliness, coping with trauma, conquering
fears, and achieving feelings of mastery and competence, and also as a vehicle for avoiding blame via
scapegoating. As we shall see, all of these functions are
relevant to the coping strategies and defenses of adults
with neurological injury and dementia.
Splitting is another primitive defense that has relevance to the creation of imaginary companions in
children and is also associated with the adult neuropathology cases. Although there are many different denitions of the term, the DSM-IV-TR (APA, 2000) denes
splitting as occurring when the individual deals with
emotional conict or internal or external stressors by
compartmentalizing opposite affect states and failing
to integrate the positive and negative qualities of the
self or others into cohesive images. In some cases, the
positive aspects of the self remain internalized while
the negative aspects of the self are externalized and
projected. Fraiberg (1959) observed that in the presence of intense ambivalence, the child might attribute
negative characteristics to the imaginary companion
and keep positive attributes for the self. In these cases,
the child appears to be coping with conicting aspects
of the self-image. Taylor also reported splitting in children with imaginary companions who described the
existence of two imaginary companions, one deemed
good and the other bad. Again, these patterns of
defense are virtually indistinguishable from some of
the adult neurological cases.
Regression and the adult neuropathologies
of the self
In summary, the defenses are hierarchically organized, with denial, projection, splitting, and the use
of fantasy among the earliest and most primitive psychological defenses and operations. The patterns of
defense and denial we see in children do not simply
disappear, however; they evolve and are replaced by
hierarchically more mature methods of thought and
emotional defense. The ego-disequilibrium theory
posits that certain neurological lesions promote dissolution and regression of ego functions that cause the
adult to revert to more primitive cognitive operations
and defenses.
A similar mechanism was proposed by Semrad
(1967) with reference to the evolution of psychosis.
He observed that, after an unbearable loss, the patient
144
responded to the threat of psychological disintegration with the processes of denial, delusional projection, and distortion, which Semrad interpreted as a
regression to pathological defenses. Furthermore, as
the patient recovered from psychosis, progressively
less pathological, less psychotic, and more normal
defenses were reinstituted. In a similar way, when we
consider the ego disturbances and defensive operations
seen in the neurological patients we have discussed, it
becomes apparent that the psychotic and immature
defenses characteristic of these adult patients extensively overlap with the immature defenses of the
child.
Indeed, there has been past speculation on the relationship of some of these neuropathological disorders
individually to certain psychological defenses. Kurt
Goldstein (1939) was among the rst to emphasize the
potential role of psychological denial in anosognosia.
He argued that anosognosia, rather than being solely
due to neurological or psychotic disruption, is the result
of the normal mechanisms of psychological defense
and the product of brain regions that remained intact in
the wake of neurological injury. Paul Schilder (1950)
proposed that in anosognosia the patient uses organic
repression to exclude the unpleasant aspects of illness
and neurological impairment from consciousness:
What makes these patients neglect their paralysis?
What makes them disown one half of their bodies? . . .
We may want to forget a defectiveness. We may want
to suppress the thought that we are disabled, but the
tormenting consciousness of the defect will still come
back again and again. We may speak of the conscious
psychic level. It is clear that in the cases mentioned
this mechanism does not take place. But if we continue
in our efforts, we may nally forget the difculty, and
then we shall be dealing with a mechanism in which
the conscious attitude has found support from the
unconscious. But then we nd also a clear-cut psychic motive, which is fully understandable. [p. 31]
In their monograph Denial of Illness (1955), Weinstein

and Kahn also emphasized the motivational, defensive,
and adaptive mechanisms that were operative in their
anosognosic patients, and Dorpat (1985) provided an
extensive analysis of anosognosia from a Freudian perspective. He argued that denial and other anosognosic
behaviors are subjectively meaningful and can be interpreted psychodynamically. In this respect anosognosia
behaviors are no different from psychiatric symptoms
in patients who do not have brain damage (p. 257).
With reference to the relationship between denial
and wish-fulllment that we have already discussed,
more recent investigators have provided further evidence that psychological defenses, motivations, and
Todd E. Feinberg
wish-fulllment play an important role in the production of anosognosia, asomatognosia, and delusions
and confabulation in brain-damaged subjects (Conway
& Tacchi, 1996; Feinberg, 1997, 2001; Feinberg &
Roane, 1997; Fotopoulou, Solms, & Turnbull, 2004;
Fotopoulou et al., 2007; Joseph, 1986; Kaplan-Solms
& Solms, 2000; McGlynn & Schacter, 1989; Turnbull,
Berry, & Evans, 2004; Ullman, 1960).
Finally, Berson (1983) pointed out that patients with
Capgras syndrome who claim there are good and
bad versions of a single person may be using the psychological defense of splitting to deal with ambivalent
feelings about someone by psychologically dividing the person in two. This enables the individual to
express dissatisfaction with the bad version yet still
maintain an emotional relationship with the good
one. Finally, when we consider paranoia, there is abundant evidence that patients with Capgras syndrome
and phantom boarder syndrome often display paranoia
(e.g., see Alexander, Stuss, & Benson, 1979; Berson,
1983; Feinberg et al., 2005; Fleminger & Burns, 1993;
Hwang, Yang, & Tsai, 2003).
Testing the theory
In order to further explore the hypothesis that the adult
neuropathologies of the self are indeed representative
of the immature patterns of defense and thought in the
child, I analyzed a representative series of patients with
imaginary others in a series of published reports as
well as in personal cases and judged the predominant
psychological defense(s) and mechanisms that were
utilized in each case (see Table 2; for details and narratives of these cases, see Feinberg, 2009a).
In support of the present hypothesis, many of the
characteristic defensive patterns in these cases were
immature defenses that have their parallels in the child.
For instance, in some of the mirror DMS, delusional
companion, and nurturing syndrome cases, many of
the defenses were straightforward wishful fantasies
in that the delusion provided for the patient a desired
companion. The fantasy of the adopted child in Case
S.C. (Table 2, Phantom child) provided a means for
the patient to imagine reuniting with his wife. Paranoia
was particularly common in the mirror DMS cases. In
patient R.D. (Table 2, Mirror DMS 9), who screamed
at the whore in the mirror, both paranoia and projection were evident. This is apparent in the following
dialogue with the patient and her husband, in which
although R.D. complains that the mirror image calls
her a whore, R.D. asserts that in fact this is actually
true of the mirror self:
Table 2.
145
Analysis of the psychological mechanisms in a representative sample of neurological cases with

imaginary others (N = 21)
Syndrome
Patient
Description of behavior
Source
Mirror DMS 1
61-year-old
woman
The mirror double followed her around the house and mocked and insulted
her. She was afraid of the double, and she attacked the mirror image with a
bucket of water and other objects. (p)
Gluckman, 1968
Mirror DMS 2
64-year-old
woman
The patient was frankly paranoid in general and feared being raped, robbed, Cummings, 1985
or killed. The mirror double followed her and stole her possessions. (p)
Mirror DMS 3
Case S.P.,
77-year-old
woman
A woman with deafness conversed with her mirror double via sign language. Feinberg & Shapiro,
1989
The double was a friend to her and often kept her company and served as
a companion. (wf) She was nearly identical to the patient in every way,
although the patient felt superior to her in intelligence and in the ability to
use sign language. (wf)
Mirror DMS 4
Case MH,
82-year-old
woman
The mirror-other wanted to move into her home and drain her resources.
She was described as a little girl tormenting her. (p)
Mirror DMS 5
Case HT,
61-year-old
woman
The patient was chased out of her home by the woman in the mirror, who
Molchan, Martinez,
was hostile to the patient, became tearful and upset upon seeing her, and hid Lawlor, Grafman, &
from her. (p)
Sunderland, 1990
Mirror DMS 6
Case L.B., 55- Patient described as suspicious of, and became angry and accusatory toward, Molchan et al., 1990
year-old man the image, although at other times talked and laughed with it. The patient
uctuated from being mildly suspicious to frankly paranoid. (p)
Mirror DMS 7
Case 2,
83-year-old
woman
Increasing paranoia for several years. The mirror-other interfered with

her activities and stole her possessions. The mirror-other was described
as crude and unpleasant. (p) Actual characteristics true of herself were
denied and were attributed to the mirror-other. (proj)
Mirror DMS 8
Case EF,
80-year-old
woman
The mirror-other was described as a friend. She became anxious when she Phillips, Howard, &
couldnt look in the mirror and was noticeably reassured when able to see David, 1996
her reection once again. (wf)
Mirror DMS 9
Case R.D.
Became extremely angry and upset with the mirror-other, thought she called Feinberg, 2001, 2009b
her names, spied on her, followed her, and bothered her. The mirror-other
called her a streetwalker. The patient says she wants to kill her. (p)
Mirror DMS 10
Case FE, 87year-old man
Patient did not seem to have much emotional reaction to the mirror-other.
(n)
Mirror DMS 11
Case TH, 77- Patient did not seem to have much emotional reaction to the mirror-other.
year-old man: (n)
Breen et al., 2001
Delusional
companion 1
Case A.S.
A teddy bear is a companion, appeared to derive pleasure and company

from her new friend. (wf)
Shanks & Venneri,

2002
Delusional
companion 2
Case A.L.
Treated a teddy bear as if she were a live companion with a dearly loving Shanks & Venneri,
heart. (wf)
2002
Delusional
companion 3
Case S.T.
Bought 30 dolls and soft toys whom she claimed she could speak to. She sat Shanks & Venneri,
them on her coffee table so they could watch television. (wf)
2002
Phantom other
Case G.T.
A malevolent amoeba-like entity entered his body and tortured him. (p)
Feinberg, 2009a
Phantom child
Case S.C.
A patient with extensive frontal brain damage denied his

neuropsychological impairments and hospitalizations (d) but claimed he
was adopting a child with impairments that in reality were like his own.
(proj). He was separated from his wife but claimed they were doing the
adoption together. (wf)
Feinberg, 2009a
Spangenberg, Wagner,
& Bachman, 1998
Mendez, 1992
Breen, Caine, &

Coltheart, 2001
continued
146
Todd E. Feinberg
Table 2.
Analysis of the psychological mechanisms in a representative sample of neurological cases with

imaginary others (N = 21) (continued)
Syndrome
Patient
Description of behavior
Source
Delusional
reduplication 1
Case R.J.
The patient minimized a serious auto accident and head injury. (d) He
claimed he had two brothers (he actually had one) both named Martin
(spl) one of whom was killed in a car accident. (proj)
Baddeley & Wilson,

1986
Delusional
reduplication 2
Case I.P.
The patient had sustained a serious traumatic brain injury and claimed he
had another self . He was in the body of one self who was in an accident,
but he himself would wake up later in good health when he would be in
the body of the healthy double. (spl, d, wf)
Bouvier-Peyrou,
Landis, & Annoni, 2000
Delusional
reduplication 3
Case 6
The patient claimed she had a good daughter and a bad daughter. (spl)
Mendez, 1992
Nurturing
syndrome
Case C.S.
The patient claimed her deceased husband was alive and came to visit her
most evenings and this provided comfort. (d, wf) She suspected he was
having an affair with a very young woman. (p)
Venneri et al., 2000
Nurturing
syndrome
Case K.C.
Denied her husbands death. (d) Talked to and fed his photographs. (wf)
Venneri et al., 2000
Note:
(n = 2).
d = denial (n = 5); proj = projection (n = 3); p = paranoia (n = 9); spl = splitting(n = 3); wf = wishful fantasy (n = 9); n = neutral
HUSBAND:
She calls her names . . .

Who does she say it is? Who does she think
it is?
HUSBAND: A streetwalker, a tramp, a whore.
R.D.: Thats what she called me! Those are all
her names . . . all her names. I cannot stand it! I
just cannot stand it at all . . . Shes like a streetwalker.
T.E.F.:
Denial, projection, and splitting were most directly

implicated in the delusional reduplication cases. Case
S.C in Table 2 denied his neurological impairments and
personal history but at the same time attributed them to
a phantom child. Case R.J (Table 2, Delusional reduplication 1) denied the seriousness of his accident and
injury but claimed a reduplicated brother was killed
in a car accident. Splitting was apparent when two
versions of a single entity were imagined, only one of
which was bad (Case 6: Table 2, Delusional reduplication 3) or injured (Case I.P: Table 2, Delusional
reduplication 2).
Finally, it is of related interest that many cases of
somatoparaphrenia, in which a limb or other object is
personied, show many of the same patterns we have
uncovered in the cases of the imaginary others. My
patient J.K. discussed above revealed quite clearly the
role of fantasy and motivation in creating the somatoparaphrenic delusion:
T.E.F.:
You have told me that all your family is overseas, and that you miss them very much. How
does it feel to have your brothers arm here?
J.K. [begins to cry profusely; he holds his left arm
in his right hand]: It makes me happy. It makes
me very happy. It makes me feel closer to my
brother. Emotionally it makes me happy. [He
remains very tearful] I feel sad to not be able to
see my friends and family. I have to wait for them
to come see me. I am learning so much. This is
a sort of rebirth. It was so sad. But now Im not
sad, because I can now correct my mistakes.
[Crying]
T.E.F.: How did it make you feel that it was your
brothers?
J.K.: I thought it was a little funny . . . like a little
gross.
T.E.F.: A little funny and a little gross? But you also
said . . .
J.K.: But now it makes me a little comforted.
T.E.F.: A little what?
J.K.: Comforted . . . because I have my brother here
[pointing to left arm, begins to cry]. Its a little
comfort for me now . . .
T.E.F.: A little comforting for you?
J.K.: But now it makes me a little comforted.
T.E.F.: Ok, so why? You said it kept you company?
J.K.:
Yes.
T.E.F.: How did it make you feel emotionally?
J.K.: I felt stronger . . .
T.E.F.: Because . . . you missed your family?
J.K.: Yeah . . . I missed my brother. [I lift the arm
toward his right side and ask him how he feels
about it]
J.K.: I feel good. I feel good about this . . . It feels
good. I dont know. Just because.
T.E.F.: [I lift his right hand] How about this?
J.K.: This is my hand . . . my right hand.
T.E.F.: How do you feel about this?
J.K.: This is ok . . .
T.E.F.: This one is ok . . . You just feel ok about this
one?
J.K.: This one doesnt have a story like this one
[pointing to his left hand] . . . it has a story. Like
the one I told you . . . this hand has a background
that makes me feel closer to my brother.
When we consider cases of asomatognosia such as
J.K.s, there are signicant parallels with the personication fantasies and defenses that we see in childhood and in the cases with imaginary others described
above. The arm in these cases may take on an identity
independent from the patient, a companion fantasy
that for some patients provides comfort. This motivation was so powerful that J.K. actually claimed he
preferred his paralyzed arm over his real one. Others patients claim that the paralyzed arm belongs to
an absent spouse. Parallels are clear between cases
where patients display nurturing behaviors toward the
paralyzed arm, in which it is treated like a baby, petted,
fed, or sung to, and the nurturing cases of women with
deceased husbands.
A four-tiered model
of the neuropathologies of the self
It is apparent, given the complexity of the issues we
have already covered in this brief review, that there is
panoply of intersecting and interacting issues and factors that come into play when we attempt an analysis of
these syndromes. Nonetheless, I believe we have sufcient information regarding the factors that contribute
to these conditions that a parsimonious account of their
origin is possible. It is essential, however, that we keep
the levels of analysis clear when we attempt to explain
the impact of all the disparate elements that make a
147
contribution in any given case and syndrome. In Table

3, I offer a roughly hierarchical four-tiered model that
can serve as a template for the analysis of most if not
all instance of these syndromes.
Tier 1.
Cognitive decits
The column on the far left of Table 3 indicates the

various basic cognitive decits that potentially make a
contribution to these conditions. Depending on the particular condition, some are more essential than others.
In the development of asomatognosia and somatoparaphrenia, for example, sensory loss and neglect play a
prominent role, while in delusional confabulation and
misidentication, memory and executive dysfunction
are among the most important variables. In Jacksonian
terms, these are among the numerous negative factors
that alone or in combination are essential in the creation of these syndromes. However, as argued earlier,
there is more to these conditions than can be explained
by basic cognitive decits alone.
Tier 2.
Self-related decits
The second column in Table 3 lists the specically selfrelated decits that may play a role in the production of
these disorders. These factors include a perturbation in
the normal relatedness to a part of the body such as an
arm, as in asomatognosia, or loss of awareness of ones
physical integrity, as occurs in anosognosia. I refer to
these negative factors as self-related decits. Like the
rst group of factors, these are negative factors within
a Jacksonian framework, but they are more specically
linked to the sense of self and self-awareness.
With reference to AHP and asomatognosia, I characterize this level of impairment as unawareness
as opposed to adamant and delusional denial. For
instance, in our study of asomatognosia (Feinberg et
al., 2010) we found that there were clear differences
both clinically and anatomically between patients with
simple asomatognosia, who did not display prominent
delusions and confabulations about the arm (unawareness of ownership), and somatoparaphrenia cases with
prominent delusions and confabulation (delusional
denial of ownership; see section below, Ego Boundaries and Neuroanatomy). At this midlevel on the
continuum, the patient may be more amenable to feedback from the examiner, and there is less consistency
regarding how often and under what circumstances the
patient makes the misidentication.
Another self-related negative factor that is well
148
Todd E. Feinberg
Table 3.
A hierarchical four-tiered model of representative factors contributing to the neuropathologies

of the self
Negative factors
Positive factors
Cognitive decits
Self-related decits
Reaction/adaptation/defense
Syndromes
Spatial disorientation
Anosognosia (unawareness)
Denial
Delusional anosognosia
Visuoperceptual disturbances
Asomatognosia (unawareness)
Projection
Somatoparaphrenia
Hemispatial neglect
Loss of personal identity
Paranoia
Delusional misidentication
Sensory loss
Dissociationc
Splitting
Delusional confabulation/
reduplication
Retro- and anterograde amnesia
Disturbed ego boundariesd
Fantasy
Delusional companion
syndrome
Temporal context confusion
Autobiographical memory loss
Restitution of identity
Phantom child/others
Nurturing syndrome
Executive dysfunction
Reality monitoring decit
Confabulation
Anatomical disconnectiona
Anomaly detector decitf
Wish-fulllment
Feedforward dysfunctionb
Belief evaluation decitg
Note: Specic cognitive decits may only be relevant to certain conditions, while self-related decits and positive features may be applied
to all syndromes. The most delusional varieties of these conditions are represented in the fourth column.
a
With reference to Capgras syndrome, see Ellis & Young (1990); with reference to asomatognosia, see Geschwind (1965) and Gazzaniga
(2000). b Heilman (1991), Heilman, Barrett, & Adair (1998). c Christodoulou (1977, 1986). d Feinberg et al. (2005), Feinberg (2009a, 2009b),
Feinberg et al. (2010). e Johnson (1991). f Ramachandran (1995). g Coltheart (2007), Davies, Aimola Davies, & Coltheart (2005), McKay, Langdon,
& Coltheart (2005).
established is the failure of self-monitoring that is

known to occur as part of the dysexecutive syndrome
after frontal damage. For instance, a signicant feature
of the delusional confabulation cases is its irrationality
and its resistance to correction. To account for this feature, Johnson (1991; Johnson, Hayes, DEsposito, &
Raye, 2000) suggested that some confabulations result
from a reality-monitoring defect that causes a failure to discriminate between memories and internally
derived thoughts. With reference to AHP, Ramachandran (1995) posits an abnormality in an anomaly detector localized in the right hemisphere that
prevents the patient from appreciating the disparity
between ctions generated by the left hemisphere and
reality. Davies, Aimola Davies, and Coltheart (2005),
Coltheart (2005, 2007), and McKay, Langdon, and
Coltheart (2005) posit that a primary neurological dysfunction is accompanied by a disruption in a belief
evaluation system lateralized to the right hemisphere
that prevents the patient from realizing the illogical
nature of their delusions.
I suggest, however, that among the self-related decits, the most parsimonious explanation for the neuropathologies of the self as a group is a disturbance
in a rm and stable sense of personal identity and
a perturbation in ego boundaries. The key negative
feature is that in these cases, bilateral or right frontal

pathology (see section below, Ego Boundaries and
Neuroanatomy) causes an alteration in the permeability of the ego boundaries. For instance, some clinical conditions, such as Capgras syndrome, suggest a
profound underrelatedness on the part of the patient to
signicant aspects of the self. In these circumstances,
personally signicant incoming information may lose
a feeling of emotional relatedness. Perhaps the most
obvious transformation of the self of this type occurs in
somatoparaphrenia when the patient mentally excises
the paralyzed limb from the limits of the self. However, as noted by Freud in the quotation at the start
of this article, there are other aspects of these conditions in which the patient inappropriately incorporates
relatively neutral aspects of the environment into the
self. For instance, in the Frgoli syndrome, the patient
is overinclusive, and relatively neutral aspects of the
environment are incorporated into the self. The present theory proposes that in both these instances there
is an ego dysequilibrium that produces a two-way
disturbance between the self and the environment specically with regard to personal relatedness. This could
potentially lead to disorders of both under- and overrelatedness between the self and the world (Feinberg,
2009a, 2009b; Feinberg et al., 2005, 2010).
Tier 3.
Reaction/adaptation/defense
Some cases of, for example, anosognosia (simple

unawareness of decit) or asomatognosia (confusion
regarding limb ownership) or neutral confabulation are
amply explained by the various negative decits outlined in Table 3. However, we still need to explain the
numerous positive features we have outlined above, as
well as the additional mechanisms that contribute to
the etiology of the neuropathologies of the self listed in
Table 1. It is here that ego dysfunction and regression
complete the picture. These aspects of these syndromes
are best explained by the way the damaged brain
adaptsin a positive fashionto various psychological stresses and loss, but does so in a psychologically
regressed fashion. These considerations lead us to the
third column of Table 3, where we see the role that the
positive adaptive and defensive functions play in the
creation of these conditions.
There are number of factors that could encourage
the emergence of these defenses in the presence of
brain dysfunction. For one, the primitive defenses are
understood to be largely unconscious and automatic in
comparison to the mature defenses, which are held to
be more conscious and voluntary (Cramer, 1991). This
conception of hierarchically lower defenses as less
conscious and voluntary than the hierarchically higher
defenses is congruent with the Jacksonian model of a
hierarchical organization of the nervous system as outlined above in which dissolution of higher order centers
would encourage the reemergence of lower level functions. Some authors have also noted that the progression from primitive and immature to mature defenses
is in part the result of brain maturation and increasing
cognitive skills (Cramer, 1991, 2006; Elkind, 1976;
Laughlin, 1970; Lichtenberg & Slap, 1972; Wallerstein, 1985). According to these accounts, the simple
process of denial would emerge at an earlier stage
of cognitive development than would more sophisticated defenses such as intellectualization, sublimation,
and humor, based on the greater degree of intellectual sophistication required for the mature defenses
to come on-line. Once again, the loss of higher order
abstraction and cognitive skills necessary for the more
advanced defenses would encourage the release of
lower order defenses.
The variable I wish to emphasize as most important
in the genesis of the neuropathologies of the self is the
relationship between primitive and immature defenses
and ego boundaries. As Cramer (1991) points out,
immature or hierarchically lower defenses are more
likely to violate the boundary between self and nonself,
while hierarchically higher defenses deal with internal
149
boundaries such as that between ego and superego.

Indeed, the manifestations of both denial and projection involve treating that which actually pertains to the
self as if it were only relevant to the external world. In
this sense, both defenses involve the externalization
of self-related material, a primitive defensive process
made possible by poorly differentiated ego boundaries.
We may see the effects of a loss of self-boundaries
and projection in certain instances of personal confabulation in which patients erroneously displace their personal concerns into the environment. This was nicely
demonstrated by a patient, L.K., with ruptured cerebral
aneurysms, bilateral frontal lesions, and anterograde
amnesia. During her examination, I asked L.K. to listen
to and repeat what we call the King Story, which is
used to check not only the patients memory but also a
tendency to deny illness:
T.E.F.:
Im going to tell you a story, and I want

you to tell it back to me as best you can. Once
there was a king who was very ill and his doctors
couldnt cure him. But his Wisemen told him,
Oh King! You will be well, if you would wear
the shirt of a happy man. So the King sent his
messengers all over the Kingdom, and they found
a happy man, but he didnt own a shirt. Now you
tell the story to me.
L.K: There was a King who . . . had an aneurysm or
something on his head [at this point the patient
lifted her left hand on top of her head feeling her
own surgical scar]. He could be cured forever if
he found a man with a happy shirt. He went all
over. The man with a happy shirt did not have a
happy shirt. So, nothing was done. He never had
an operation. There was no . . . nothing done for
this unhappy man, and nothing was done for him!
So, he was hanging around the hospital unhappy.
T.E.F.: So, how do you feel about whats going on?
L.K.: I feel that if Im so unhappy, I should get an
operation and be happy.
L.K.s version of the King Story shows the permeability between her recall of the narrative and her own
self-related concerns. She readily inserts her personal
concerns, wishes, and feelings into the story, in much
the same way that a neurologically intact adult inserts
his or her personal feelings and concerns in his or her
interpretation of a projective exam like the Rorschach
test. Although L.K. thinks she is reproducing a veridical version of the King Story, what she is in actuality doing is creating an idiosyncratic narrative about
150
herselfa process that occurs without her conscious

awareness. A perturbation in ego boundaries, in which
the patient under- or overrelates the balance between
internal and external circumstances, could help explain
the disequilibrium between the patients idiosyncratic
concerns and motivations and external reality. The
breakdown between the personal and the extrapersonal
is also clear in the cases of delusional or personal
confabulation described above, in which the individual
produces a narrative in the form of a delusion or recurring confabulation in which the patient ostensively
discusses veridical events about the self or others but is
implicitly, unconsciously, metaphorically, or symbolically expressing his or her feelings about him/herself
and his or her current situation (Weinstein, 1996).
Indeed, all the primitive and immature psychological mechanismsdenial, projection, splitting, fantasy,
and paranoiareect a distorted relationship between
the inner needs of the individual, the margins of the
self, and the constraints of external reality. In denial,
the signicance of the external is excluded from the
self; in projection, the personal is rejected and displaced into the environment; in splitting, one aspect
of the self is preserved while another is externalized;
in fantasy, inner wishes or the need to deny a painful
reality take precedence over the constraints of external
reality; and in paranoia, personal unwanted feelings are
experienced as coming from another person. In fact,
in these cases there appears to be a general tendency
for the patient to externalize unwanted and disturbing aspects of reality, and therefore the emergence of
theses defenses is dependent on the dedifferentiation
between inner and outer reality that facilitates the
deployment of primitive defenses (i.e., denial, projection, splitting, fantasy, paranoia). Therefore, we see
that the same distortion in ego boundaries that creates the perturbations of under- and overrelatedness
between the self and world could also facilitate the
activation of the defenses that are characteristic of the
immature and underdeveloped ego. As noted in Table
3, most patients actually employ an admixture of these
psychological devices, but all of these have in common
the externalization of the personal, a tendency that is
facilitated by impaired ego boundaries.
In addition to the externalization of the negative
is the externalization of the positive wish via fantasy.
Some fantasies are in the service of denial, such as the
severe traumatic brain injury cases of Staton, Brumback, and Wilson (1982) and Bouvier-Peyrou, Landis,
and Annoni (2000) with frontal damage who believed
that they were in a dream and would eventually wake
up and be well. Other fantasies in the adult cases, as we
have seen, serve to fulll a need, such as for compan-
Todd E. Feinberg
ionship or to replace a lost spouse. Still others are in

the service of the restitution of identityfor example,
a college professor who, after a ruptured cerebral aneurysm while in the rehabilitation hospital, produced
extended confabulations about how he was there to
give lectures and conduct a research study.
Lastly, the primitive defenses of dissociation, derealization, and depersonalization are also commonly
reported among the neuropathologies of the self. The
DSM-IV-TR denes dissociation as A disruption
in the usually integrated functions of consciousness,
memory, identity, or perception of the environment
(APA, 2000), and its occurrence certainly depends
in large measure upon integrative ego functions as
dened earlier by Vaillant and Freud. Christodoulou
(1986) and Berson (1983) both note the high frequency
of reports of depersonalization and derealization in
the DMS (Christodoulou, 1986), and derealization has
been noted in cases of reduplicative paramnesia in
association with Capgras symptoms (Bouvier-Peyrou,
Landis, & Annoni, 2000; Staton, Brumback, & Wilson,
1982). Among the neurological patients I have examined, the case of R.D., who saw a persecutor reected
in the mirror, comes closest to representing a dissociative disorder. While in the early stages of dementia, whenever R.D. viewed her mirror reection, she
became agitated and claimed that a hostile persecutor
was following her. Although R.D. was a church-going
prim and proper wife and mother, the mirror-other
called her a whore:
R.D.:
Did you hear the story? Eh? Did you hear it?
Now you get out . . . get home where you belong.
You dont belong here . . . you dont live here.
Out! . . . Thats her, thats her. Yeah, thats her
. . . sure thats her. She has no name . . . I never
heard her name . . . never, never! I never! She
never told me her name. No, no . . . you cant go
in the house! No, you cant go in the house! She
never let me know, had a lot of problems with
her . . . Yeah, not this here one. Then she starts
calling me these kind of names, streetwalker . . .
cannot stand her . . . I dont know, shes just an
old bag . . . shes a bag. Yeah, and you, and you.
Heh, Im not afraid of you. Go ahead . . . I dont
know shes just an old bag. Yeah, shes a bag . . .
yeah, afraid to say it . . . You want to know who
she is? You want to know who she is? Because
youre a . . . thats what you are. We know where
you live. Where do you live? You know what?
Youre a good for nothin . . . You know what?
Youre a good for nothin . . . Yeah, where you
walk . . . yeah, you little bitch . . . yeah. Now
you know where youre gonna go? Youre gonna

go home . . . and when we get home, you know
what? Were gonna nd her right around the . . .
well nd her walkin right around the windows.
In the windows where she watches . . . listens to
what we do. I cant stand her . . . shes been walking around the house, around the area for a long
time . . . you know that? All the time she bothers
everybody. I always wanted to hit her! Im gonna
kill her
Although R.D. did not experience a loss of her own
personal identity, and the person in the mirror was
implicitly recognized (since only her own reection
was misidentied), she treated her mirror image as if
it had an entirely separate identity dissociated from her
own personal identity.
Tier 4.
Syndromes
Using Table 3 as a template, I believe that we can determine the probable contributing factors, both positive
and negative, as well as trace the lines of development,
for any given disorder of the self I have discussed in
Table 1. In the development of somatoparaphrenia,
for instance, moving from left to right in Table 3, the
brain lesion(s) establishes typical generalized cognitive decits such as sensory loss, neglect, and anatomical disconnection. To these are added specic
self-related decits such as disturbed ego boundaries
and self-monitoring defects. These also set the stage
for the development of asomatognosia (lack of feeling of ownership), a self-related decit that still falls
within the negative impairments or losses. Moving
toward the positive contributing factors, the disturbed
ego boundaries and self-monitoring defects promote
the mobilization of certain specic adaptations and
defensesnamely, the immature defenses such as
denial, projection, fantasy, or splitting. Ultimately, if
a sufcient number of these interacting factors are
operative, the entire picture results in the full clinical
syndrome of somatoparaphrenia.
A similar analysis would apply to the development
of delusional anosognosia and the DMS. In the strikingly similar cases mentioned above, one described by
Staton, Brumback, and Wilson (1982) and another by
Bouvier-Peyrou, Landis, and Annoni (2000), young
men had sustained major head injuries with bifrontal
damage and a period of coma followed by executive
and short-term memory dysfunction on neuropsychological testing. Several months after their injuries, both
cases experienced feelings of dissociation (feelings of
151
unreality or living in a dream, respectively.). This

was associated with delusions that their current lives or
selves were not real, and that eventually they would
return to their real selves. Both patients developed
DMS and claimed their parents were not the real
ones.
Both Staton et al. and Bouvier-Peyrou et al. suggest
that the combined executive and memory impairments
(rst column, Table 3) led to a failure to integrate current experience with their past sense of who they were.
Alexander, Stuss, and Benson (1979) posit a similar
tempero-limbic-frontal disconnection in their case of
Capgras/reduplication. This disconnect between past
and present selves created feelings of depersonalization, derealization of their experience, and loss of
personal identity, all suggestive of a disturbance in
ego boundaries and functions (second column in Table
3). Their adaptation to this experience (third column)
is interesting. In the presence of the neurologically
derived perturbation in ego boundaries, the adaptation reects the emergence of the primitive defenses
of denial and projection (this cant be happening;
its the world that isnt real; its my parents who are
fake, not me) and fantasy (another version of me will
wake up from this nightmare and Ill be better). The
ultimate syndromes in the fourth column of Table 3 we
call delusional misidentication and reduplication. The
essential point is that lacking the perturbation in ego
boundaries that sets up the mobilization of the primitive and immature defenses, the nal clinical syndrome
would not emerge.
This form of analysis also allows for the inuence
of top-down factors in the creation of the syndrome.
For instance, in Case S.P. with the mirror companion,
I would argue that her deafness and resulting social
isolation was the chief factor in promoting the fantasy
of the mirror double. Her right-hemisphere pathology
set the stage for the permeability of her ego boundaries
and the release of unbridled fantasy, but the motivation
for companionship in this case was critically important
in the development of her condition. In Case R.D., who
screamed at the mirror, her paranoia and dissociation
were certainly paramount and in excess to her primary
cognitive defects in determining her DMS for her mirror image.
Finally, one strength of this multifactorial approach
that identies an array of negative and positive, bottom-up and top-down, and neuropsychological and
psychological factors is that we no longer need to be
concerned that any single patient lacks a particular
feature. Indeed, given that so many individual factors
are at play, we would expect that group studies of a particular syndrome that examine many of these potential
152
Todd E. Feinberg
variables will necessarily vary in the presence, degree,

and strength of any single one, and multiple dissociations between variables will inevitably emerge (on this
point see, e.g., Marcel, Tegnr, & Nimmo-Smith, 2004;
Orfei et al., 2007; Vallar & Ronchi, 2006).
Ego boundaries and neuroanatomy

There is accumulating evidence that cases of DMS,
reduplication, and imagined others are specically
associated with frontal pathology, especially involving the right hemisphere (Burgess, Baxter, Martyn, &
Alderman, 1996; Feinberg & Shapiro, 1989; Fleminger
& Burns, 1993; Frstl, Burns, Jacoby, & Levy, 1991;
Malloy, Cimino, & Westlake, 1992; Spangenberg,
Wagner & Bachman, 1998). For instance, Feinberg &
Shapiro (1989) examined the neuroanatomical ndings
in previously reported cases of Capgras syndrome (CS,
n = 26) and reduplication syndrome (RS, n = 69), in
which brain pathology was implicated and reported.
We found that in CS bilateral hemispheric pathology was the most common nding, but there was a
clear trend toward a right- greater than left-hemisphere
pathology (p = .06). In RS, although bilateral hemispheric dysfunction was also common, there was a
powerful bias toward greater right-hemisphere pathology (p = .0000) (Table 4).
Burgess et al. (1996), in a literature review of cases of
confabulation, paramnesias, reduplicative phenomena,
and various DMS, found similar laterality but noted that
there was a predilection for specically frontal lesions.
They found that of 41 cases reviewed, the highest percentage of case had right frontal hemisphere (44%) or
bilateral frontal (39%) lesions, whereas only 9.7% had
left frontal lesions. We analyzed a series of published
cases of DMS or delusional reduplication (Feinberg &
Keenan, 2005; Feinberg et al., 2005) and included in
this series patients with stable misidentication(s) or
reduplication(s) of the Capgras or Frgoli type or delusional reduplication in which sufcient neuropathology was reported to determine the site of the pathology
Table 4.
(Table 5). These included patients with Capgras syndrome for persons or the environment, asomatognosia,
Frgoli syndrome for persons or the environment, or
delusional doubling of the self or other persons. While
bilateral cerebral pathology was a common nding
(14/29, 48%) we found that all 29 observations (100%)
suffered right-hemisphere damage, whereas only 15
(51.72%) suffered from left-hemisphere damage. Signicantly, in 28 out of 29 of the observations (96.6%),
right frontal damage was present. Regarding the location of the lesion, 10 (34.48%) cases had exclusively
frontal damage. There were no cases of any other brain
region exclusively affected, suggesting that the frontal
cortex is highly related to these disorders of the self
and personal relatedness. Therefore, the anatomical
ndings were surprisingly clear-cut. First, there was
an overwhelming predominance of patients across all
categories of self-disorders with damage in the right
(nondominant) hemisphere. Second, it appeared that
within the right hemisphere the lesions were much
more likely to be within the right frontal lobe.
In a subsequent investigation of the neuroanatomy
of asomatognosia and somatoparaphrenia (Feinberg
et al., 2010), we studied patients with right-hemisphere strokes and left hemiplegia. We initially analyzed the anatomy of three groups of patients with
unilateral right-hemisphere lesions: G1: asomatognosia + neglect; G2: non-asomatognosia + neglect; and
G3: hemiplegia only. The asomatognosic group was
further subdivided into somatoparaphrenia (G1-SP:
asomatognosia + delusions/confabulation) and simple
asomatognosia (G1-SA: asomatognosia without delusions/confabulation). We found that patients with all
forms of asomatognosia (G1) had larger lesions than
did non-asomatognosic patients in all regions. Patients
in the asomatognosia group as well as the control groups
had signicant temporoparietal involvement, but we
found that the subgroup of patients with somatoparaphrenia had the largest lesions overall and signicantly
more frontal involvement when compared to patients
with simple asomatognosia. All patients with asomotognosia (G1-SP and G1-SA) had more medial frontal
The neuropathology of Capgras syndrome and reduplication syndrome in cases in whom neuropathology
was implicated and reported (based on Feinberg & Shapiro, 1989)
Right-hemisphere lesion(s)
Left-hemisphere lesion(s)
Syndrome
n (%)
n (%)
n (%)
Capgras (n = 26)
8 (32)a
2 (7)
16 (62)
Reduplication (n = 69)
36 (52)b
5 (7)
28 (41)
Right- vs. left-hemisphere lesion, p = .06; b right- vs. left-hemisphere lesion, p = .0000
Bilateral lesions

Table 5.
153
Neuroanatomical ndings in delusional misidentication/reduplication after focal brain lesions

Frontal
Temporal
Parietal
Occipital
Frontal
Temporal
Parietal
Occipital
Capgras for persons( N = 6)
Capgras for environment

(N= 2)
Capgras for arm

(asomatognosia) (N = 3)
Frgoli for persons(N = 7)
Frgoli for environment
Delusional reduplication
(without misidentication) of
self or other persons:
Grand total (N = 29)a
28
13
14
Syndrome
Note: See Feinberg et al. (2005)

a
There were 27 cases reviewed and 29 instances recorded.
damage when compared to control groups, indicating

a role for medial frontal damage in the development
of all forms of asomatognosia. However, somatoparaphrenia cases also had greater orbitofrontal damage
than did simple asomatognosia cases, suggesting an
additional role for an orbitofrontal lesion in the development of somatoparaphrenia. These ndings indicated that asomatognosia results from large lesions that
involved multiple sectors including temporoparietal
lobes, but that the addition of medial frontal involvement appeared to be important for the development of
asomatognosia. Additionally, orbitofrontal dysfunction
was implicated in the development of somatoparaphrenia and distinguished this syndrome from simple
asomatognosia. The latter nding could be the result of
the role that orbitofrontal damage plays in the development of confabulation (Deluca & Diamond, 1995; Ptak
& Schnider, 1999; Schnider, 2008).
Based on the cases of delusional and imaginary others from Table 2, I reviewed the neuroanatomy of those
cases in which structural or functional brain imaging
was reported. This series had a much higher percentage
of dementia cases than the series described in Table 5,
but in spite of this we nd a similar pattern of results
(see Table 6). If cases in which the scans showed diffuse cerebral atrophy are counted as instances of bilateral pathology, then bilateral cerebral dysfunction was
the most common pattern. However, when we consider
whether there was a right- or left-hemisphere bias, we
again nd a signicant bias toward right-hemisphere
pathology. Of 14 cases, 4 (29%) had exclusively righthemisphere lesions, while no case had exclusively
left-hemisphere lesions, and 8/14 cases (57%) showed

exclusively or predominantly right-hemisphere dysfunction; only one case showed more lesions in the left
hemisphere than in the right (L>R, 7%).
These results taken collectively support the role that
the frontal lobes play more generally in a host of other
self-related functions (Stuss, 1991; Stuss, Picton, &
Alexander, 2001; Stuss, Rosenbaum, Malcolm, Christianna, & Keenan, 2005), and nondominant frontal
lobe damage appears to play a particular role in the
origin of the neuropathologies of the self (Feinberg,
2009a; Feinberg et al., 2005). The medial and orbitomedial prefrontal cortices are heteromodal association
regions that are situated between the paralimbic zones
most allied with the limbic functions of the maintenance of homeostasis and the conditions of the internal
milieu and the unimodal zones that represent the most
abstract aspects of sensorimotor processing (Mesulam,
2000). These regions serve as a convergence zone
(Damasio, 1999) for the integration of the other two
systems. It has been proposed that an integrative self
system serves to assimilate and mediate the organisms
internal needs and self-representation with the external environment (for a neurological model of the self
systems, see Feinberg, 2009a). Since this region is
intimately concerned with distinguishing the self from
the world, damage to this system could cause confusion between the internal representation of the self and
external stimuli and contribute to the breakdown of ego
boundaries. Our ndings indicate that the right frontal
zones are even more important in the regulation of
these ego functions.
154
Table 6.
Todd E. Feinberg
Neuroanatomical ndings in selected adult cases with imaginary others in which imaging was reported
Syndrome
Age
Sex
M DMS 1
61
CA
CA
M DMS 2
64
CA
CA
M DMS 3
77
CA R>L
M DMS 4
82
CA R>L
CA
DC 1
81
CA SPECT R>L
CA
DC 2
85
SPECT parietal
DC 3
74
frontoparietal
PO 1
73
frontotemporal parietal
PO 2
76
CA
CA
PC
63
frontal
frontal
DR 1
42
frontal
frontal
DR 2
16
frontal
L>R
NS 1
78
CA SPECT R>L
CA
NS 2
71
CA SPECT R>L
CA
R>L = 8
L>R = 1
Total = 14
Note: M DMS, mirror delusional misidentication syndrome; DC = delusional companion; PO, phantom other; PC = phantom child; DR =
delusional reduplication of self, friends, or relatives; NS = nurturing syndrome; CA, cerebral atrophy; SPECT = single photon emission computed
tomography.
Conclusions: the right hemisphere and ego

disequilibrium
In summary, there are several syndromes that I group
together under the rubric of neuropathologies of the
self in which brain damage causes signicant and
profound disturbances of ego boundaries and ego functions. The evidence suggests that the critical underlying neuropathology in these cases involves frontal
regions especially within the right hemisphere and that
these regions must play a central role in establishing
the margins of the psychological self. It is further conjectured that the critical regions for these functions lie
within the right frontal heteromodal association cortices (integrative self system), and these structures play
a special role in mediating the relationship between the
self and the world.
Second, I have argued that the neuropathologies of
the self have a profound and previously unrecognized
relationship with the thought and defensive style of
the normal child. The immature defenses including
denial, projection, splitting, and wishful fantasy that
play such an important role in the origin of the adult
neuropathologies of the self are also among the primi-
tive defenses in the normal child. I suggest that the

disturbance of ego boundaries caused by a (right) frontal lesion also causes the activation or release of these
immature defenses.
A strength of the current hypothesis is that it provides an explanation for one of the most common criticisms of the proposed role that psychological denial
might play in the development of AHP. If psychological denial is important in the development of AHP, why
wouldnt patients with left-hemisphere lesions and right
hemiplegia be just as likely to utilize the psychological
defense of denial as do patients with right-hemisphere
lesions and left hemiplegia? (For a discussion of this
point see, e.g., Heilman, 1991; McKay, Langdon, &
Coltheart, 2005.) It is argued, therefore, that psychological denial cannot account for the greater frequency
of AHP after right-hemisphere lesions. The proposed
disequilibrium account provides a parsimonious explanation for why patients with right-hemisphere lesions
might have both neglect and psychological denial more
commonly after right- as opposed to left-hemisphere
lesions.
Lastly, I hypothesize that, in the course of brain
maturation between the ages of 3 and 8 years, there is
a developmental shift away from immature defensive

functions and fantasies toward mature defenses and
the inhibition of fantasy and that this shift critically
depends on maturational process within the right hemispherea left-brain to right-brain defensive shift.
Once this occurs and the mature pattern of brain structures is established, the immature defenses and the use
of fantasy typical of the child are inhibited and mature
adult defenses may emerge. In the adult, right frontal
damage creates both a disequilibrium in ego boundaries as well as a breakdown of the observing egothe
ability to take an outside perspective on ones experiencethat facilitates the emergence of developmentally immature styles of thought and ego functioning.
Finally, according to this hypothesis, the preservation and activation of the verbal defensessuch as
verbal denial, projection, splitting, and fantasymust
be the result of the remaining, and presumably relatively intact, left verbal hemisphere. The evidence suggests that given the fact these immature defenses and
fantasies are preserved in the presence of right-hemisphere damage, they may be normally lateralized to the
intact left hemisphere. It is possible that given that the
primitive defenses are largely based on verbal mechanismswhat people say to themselves and others
about themselves and the worldit is conceivable that
the neural structures that the mature defenses depend
on may be lateralized to the nondominant hemisphere.
REFERENCES
Alexander, M. P., Stuss, D. T., & Benson, D. F. (1979). Capgras syndrome: A reduplicative phenomenon. Neurology,
29: 334339.
Anton, G. (1893). Beitrage zur klinischen Beurthelung und
zur Localisation der Muskelsinnstorungen im Grosshirne.
Zeitschrift Heilk, 14: 313348.
APA (2000). Diagnostic and Statistical Manual of Mental Disorders (4th edition, text revision). Washington, DC: American Psychiatric Association.
Arlow, J. A., & Brenner, C. (1964). Psychoanalytic Concepts
and the Structural Theory. New York: International Universities Press.
Babinski, J. (1914). Contribution to the study of mental disturbances in organic cerebral hemiplegia (anosognosia). Revue
Neurologique, 12: 845848.
Babinski, J. (1918). Anosognosia. Revue Neurologique, 25:
365367.
Baddeley, A. D., & Wilson, B. (1986). Amnesia, autobiographical memory, and confabulation. In: Autobiographical Memory, ed. D. C Rubin. Cambridge: Cambridge University
Press.
Baier, B., & Karnath, H.-O. (2008). Tight link between our
sense of limb ownership and self-awareness of actions.
Stroke, 39: 486488.
155
Berson, R. J. (1983). Capgras syndrome. American Journal of
Psychiatry, 140: 969978.
Bisiach, E., & Geminiani, G. (1991). Anosognosia related to
hemiplegia and hemianopia. In: Awareness of Decit after
Brain Injury, ed. G. P. Prigatano & D. L. Schacter. New
York: Oxford University Press, pp. 1739.
Bisiach, E., Rusconi, M. L., & Vallar, G. (1991). Remission of
somatoparaphrenic delusion through vestibular stimulation.
Neuropsychologia, 29: 10291031.
Bouvier-Peyrou, M., Landis, T., & Annoni, J.-M. (2000). Selfduplication shifted in time: A particular form of delusional
misidentication syndrome. Neurocase, 6: 5763.
Breen, N., Caine, D., & Coltheart, M. (2001). Mirrored-self
misidentication: Two cases of focal onset dementia. Neurocase, 7: 239254.
Breznitz, S. (Ed.) (1983). The Denial Of Stress. New York:
International Universities Press.
Burgess, P. W., Baxter, D., Martyn, R., & Alderman, N. (1996).
Delusional paramnesic misidentication. In: Method in
Madness: Case Studies in Cognitive Neuropsychiatry, ed.
P. W. Halligan & J. C. Marshall. Hove: Psychology Press,
pp. 5178.
Capgras, J., & Reboul-Lachaux, J. (1923). Lillusion des sosies dans un delire systematize. Bulletin de Socit Clinique
de Mdicine Mentale,11: 616.
Cappa, S., Sterzi, R., Vallar, G., & Bisiach, E. (1987). Remission of hemineglect and anosognosia during vestibular stimulation. Neuropsychologia, 25: 775782.
Christodoulou, G. N. (1976). Delusional hyper-identications
of the Fregoli type. Acta Psychiatrica Scandinavica, 54:
305314.
Christodoulou, G. N. (1977). The syndrome of Capgras. British
Journal of Psychiatry 130: 556564.
Christodoulou, G. N. (1986). Role of depersonalizationderealization phenomena in the delusional misidentication syndromes. Bibliotecha Psychiatrica, 164: 99104.
Coltheart, M. (2005). Delusional belief. Australian Journal of
Psychology, 57: 7276.
Coltheart, M. (2007). The 33rd Bartlett Lecture: Cognitive
neuropsychiatry and delusional belief. Quarterly Journal of
Experimental Psychology, 60: 10411062.
Conway, M. A., & Tacchi, P. C. (1996). Motivated confabulation. Neurocase, 2: 325339.
Courbon, P., & Fail, G. (1927). Syndrome dillusion de Frgoli
et schizophrnie. Bulletin de Socit Clinique de Mdicine
Mentale, 15: 121124.
Cramer, P. (1991). The Development of Defense Mechanisms:
Theory, Research, and Assessment. New York: SpringerVerlag.
Cramer, P. (2006). Protecting the Self: Defense Mechanisms in
Action. New York: Guilford Press.
Critchley, M. (1953). The Parietal Lobes. New York: Hafner
Press.
Critchley, M. (1955). Personication of paralyzed limbs in
hemiplegics. British Medical Journal, 30: 284287.
Critchley. M. (1974). Misoplegia or hatred of hemiplegia.
Mount Sinai Journal of Medicine, 41: 8287.
Cummings, J. L. (1985). Organic delusions: Phenomenology,
156
anatomical correlations, and review. British Journal of Psychiatry, 146: 184197.
Cutting, J. (1978). Study of anosognosia. Neurology, Neurosurgery, and Psychiatry, 41: 548555.
Damasio, A. R. (1999). The Feeling of What Happens: Body
and Emotion in the Making of Consciousness. New York:
Harcourt Brace.
Davies, M., Aimola Davies, A., & Coltheart, M. (2005).
Anosognosia and the two-factor theory of delusion. Mind &
Language, 20: 209236.
Davies, M., Coltheart, M., Langdon, R., & Breen, N. (2001).
Monothematic delusions: Towards a two-factor account.
Philosophy, Psychiatry & Psychology, 8: 133158.
Deluca, J., & Diamond, B. J. (1995). Aneurysm of the anterior
communicating artery: A review of the neuroanatomical and
neuropsychological sequelae. Clinical and Experimental
Neuropsychology; 17: 100121.
Dorpat, T. L. (1985). Denial and Defense in the Therapeutic
Situation. New York: Jason Aronson.
Elkind, D. (1976). Cognitive development and psychopathology: Observations on egocentrism and ego defense. In:
Psychopathology and Child Development. Research and
Treatment, ed. E. Schopler & R. J. Reichler. New York: Plenum Press, pp. 167183.
Ellis, H. D., & Young, A. W. (1990). Accounting for delusional misidentications. British Journal of Psychiatry, 157:
239248.
Feinberg, T. E. (1997). Some interesting perturbations of the
self in neurology. Seminars in Neurology, 17: 129135.
Feinberg, T. E. (2001). Altered Egos: How the Brain Creates the
Self. New York: Oxford University Press.
Feinberg, T. E. (2009a). From Axons to Identity: Neurological
Explorations of the Nature of the Self. New York: W. W.
Norton.
Feinberg, T. E. (2009b). Confabulation, the self, and ego functions: The ego dysequilibrium theory. In: Confabulation:
Views from Neuroscience, Psychiatry, Psychology and Philosophy, ed. W. Hirstein. New York: Oxford University
Press, pp. 91107.
Feinberg, T. E., DeLuca, J., Giacino, J. T., Roane, D. M., &
Solms, M. (2005). Right hemisphere pathology and the self:
Delusional misidentication and reduplication. In: The Lost
Self: Pathologies of the Brain and Identity, ed. T. E. Feinberg & J. P. Keenan. New York: Oxford University Press,
pp. 100130.
Feinberg, T. E., Haber, L. D., & Leeds, N. E. (1990). Verbal
asomatognosia. Neurology, 40: 13911394.
Feinberg, T. E., & Keenan, J. P. (2005). Where in the brain is the
self? Consciousness and Cognition,14: 661678.
Feinberg, T. E., & Roane, D. M. (1997). Anosognosia, completion and confabulation: The neutral-personal dichotomy.
Neurocase, 3: 7385.
Feinberg, T. E., & Roane, D. M. (2003a). Anosognosia. In:
Behavioral Neurology and Neuropsychology (2nd edition),
ed. T. E. Feinberg & M. J. Farah. New York: McGraw-Hill,
pp. 345362.
Feinberg, T. E., & Roane D. M. (2003b). Misidentication
syndromes. In: Behavioral Neurology and Neuropsychology
Todd E. Feinberg
(2nd edition), ed. T. E. Feinberg & M. J. Farah. New York:
McGraw-Hill, pp. 373381.
Feinberg, T. E., & Roane, D. M. (2005). Delusional misidentication syndromes. Psychiatric Clinics of North America:
Neuropsychiatry, 28: 665683.
Feinberg, T. E., Roane, D. M., & Ali, J. (2000). Illusory limb
movements in anosognosia for hemiplegia. Journal of Neurology, Neurosurgery and Psychiatry, 68: 511513.
Feinberg, T. E., & Shapiro, R. M. (1989). Misidentication
reduplication and the right hemisphere. Neuropsychiatry,
Neuropsychology, and Behavioral Neurology, 2: 3948.
Feinberg, T. E., Venneri, A., Simone, A. M., Fan, Y., & Northoff, G. (2010). The neuroanatomy of asomatognosia and
somatoparaphrenia. Journal of Neurology, Neurosurgery
and Psychiatry, 81 (3): 276281
Fleminger, S., & Burns, A. (1993). The delusional misidentication syndromes in patients with and without evidence
of organic cerebral disorder: A structured review of case
reports. Biological Psychiatry, 33: 2232.
Frstl, H., Burns, A., Jacoby, R., & Levy, R. (1991). Neuroanatomical correlates of clinical misidentication and misperception in senile dementia of the Alzheimers type. Journal
of Clinical Psychiatry, 52: 268271.
Fotopoulou, A., Conway, M. A., & Solms, M. (2007). Confabulation: Motivated reality monitoring. Neuropsychologia, 45:
21802190.
Fotopoulou, A., Solms, M., & Turnbull, O. (2004). Wishful
reality distortions in confabulation: A case report. Neuropsychologia, 42: 727744.
Fotopoulou, A., Tsakiris, M., Haggard, P., Vagopoulou, A.,
Rudd, R., & Kopelman, M. (2008). The role of motor intention in motor awareness: An experimental study on anosognosia for hemiplegia. Brain, 131: 34323442.
Fraiberg, S. (1959). The Magic Years. New York: Scribners.
Freud, A. (1936). The Ego and the Mechanisms of Defence.
London: Hogarth Press and The Institute of Psycho-Analysis.
Freud, S. (1900). The Interpretation of Dreams. Standard Edition, 4/5.
Freud, S. (1923). The Ego and the Id. Standard Edition, 19.
Freud, S. (1930). Civilization and Its Discontents. Standard
Edition, 21.
Gazzaniga, M. S. (2000). Cerebral specialization and interhemispheric communication: Does the corpus callosum enable
the human condition? Brain; 123: 12931326.
Gerstmann, J. (1942). Problem of imperception of disease and
of impaired body territories with organic lesions. Archives of
Neurology and Psychiatry, 48: 890913.
Geschwind N. (1965). Disconnexion syndromes in animals and
man. Brain, 88: 585644.
Gluckman, L. K. (1968). A case of Capgras syndrome. Australian and New Zealand Journal of Psychiatry, 2: 3943.
Goldstein, K. (1939). The Organism: A Holistic Approach to
Biology Derived from Pathological Data in Man. New York:
American Book Company.
Halligan, P. W., Marshall, J. C., & Wade, D. T. (1995). Unilateral somatoparaphrenia after right hemisphere stroke: A case
description. Cortex, 31: 173182.

Heilman, K. M. (1991). Anosognosia: Possible neuropsychological mechanisms. In: Awareness of Decit after Brain
Injury: Clinical and Theoretical Issues, ed. G. P. Prigatano
& G. L. Schacter. New York: Oxford University Press, pp.
5362.
Heilman, K. M., Barrett, A. M., & Adair, J. C. (1998). Possible
mechanisms of anosognosia: A defect in self-awareness.
Philosophical Transactions of the Royal Society London, B.
Biological Sciences, 353: 19031909.
Hwang, J.-P., Yang, C.-H., & Tsai, S.-J. (2003). Phantom boarder
symptom in dementia. International Journal of Geriatric
Psychiatry, 18: 417420.
Jackson, J. H. (1884). Evolution and dissolution of the nervous
system [Croonian Lectures delivered at the Royal College
of Physicians]. In: Selected Writings of John Hughlings
Jackson, Vol. 2, ed. J. Taylor. New York: Basic Books, 1958,
pp. 4575.
Johnson, M. K. (1991). Reality monitoring: Evidence from confabulation in organic brain disease patients. In: Awareness of
Decit after Brain Injury: Clinical and Theoretical Issues,
ed. G. P. Prigatano & G. L. Schacter. New York: Oxford,
University Press, pp. 176197.
Johnson, M. K., Hayes, S. M., DEsposito, M., & Raye, C. L.
(2000). Confabulation. In: Handbook of Neuropsychology
(2nd edition), ed. J. Grafman & F. Boller. Amsterdam: Elsevier Science, pp. 383407.
Joseph, R. (1986). Confabulation and delusional denial.: Frontal lobe and lateralized inuences. Journal of Clinical Psychology, 42: 507518.
Kaplan-Solms, K., & Solms, M. (2000). Clinical Studies in
Neuro-Psychoanalysis. London: Karnac.
Laughlin, H. P. (1970). The Ego and Its Defenses. New York:
Appleton-Century-Crofts.
Levine, D. N., Calvanio, R., & Rinn, W. E. (1991). The pathogenesis of anosognosia for hemiplegia. Neurology, 41:
17701781.
Lichtenberg, J. D., & Slap, J. W. (1972). On the defense mechanism: A survey and synthesis. Journal of the American Psychoanalytic Association, 20: 776792.
Lindemann, E. (1945). Symptomatology of acute grief. American Journal of Psychiatry, 101: 141148.
Malloy, P., Cimino, C., & Westlake, R. (1992). Differential
diagnosis of primary and secondary delusions. Neuropsychiatry, Neuropsychology, and Behavioral Neurology, 5:
8396.
Malloy, P., & Richardson, E. D. (1994). The frontal lobes and
content-specic delusions. Journal of Neuropsychiatry and
Clinical Neurosciences, 6: 455466.
Marcel, A. J, Tegnr, R., & Nimmo-Smith, I. (2004). Anosognosia for plegia: Specicity, extension, partiality and disunity of bodily unawareness. Cortex, 40: 1940.
McGlynn, S. M., & Schacter, D. L. (1989). Unawareness of
decits in neuropsychological syndromes. Clinical and
Experimental Neuropsychology, 11: 143205.
McKay, R., Langdon, R., & Coltheart, M. (2005). Sleights of
mind: Delusions, defences and self-deception. Cognitive
Neuropsychiatry, 10: 305326.
Meador, K. J., Loring, D. W., Feinberg, T. E., Lee, G. P., &
157
Nichols, M. E. (2000). Anosognosia and asomatognosia
during intracarotid amobarbital inactivation. Neurology, 55:
816820.
Mendez, M. F. (1992). Delusional misidentication of persons
in dementia. British Journal of Psychiatry, 160: 414416.
Mesulam, M.-M. (2000). Principles of Behavioral and Cognitive Neurology (2nd edition). New York: Oxford University
Press.
Molchan, S. E., Martinez, R. A., Lawlor, B. A., Grafman, J. H.,
& Sunderland, T. (1990). Reections of the self: Atypical
misidentication and delusional syndromes in two patients
with Alzheimers disease. British Journal of Psychiatry,
157: 605608.
Orfei, M. D., Robinson, R. G., Bria, P., Caltagirone, C., & Spalletta, G. (2008). Unawareness of illness in neuropsychiatric
disorders: Phenomenological certainty versus etiopathogenic
vagueness. The Neuroscientist, 14: 203222.
Orfei, M. D., Robinson, R. G., Prigatano, G. P., Starkstein,
S., Rsch, N., Bria, P. C., et al. (2007). Anosognosia for
hemiplegia after stroke is a multifaceted phenomenon: A
systematic review of the literature. Brain, 130: 30753090.
Phillips, M. L., Howard, R., & David, A. S. (1996). Mirror,
mirror on the wall, who . . . ? Towards a model of visual
self-recognition. Cognitive Neuropsychiatry, 1: 153164.
Pick, A. (1903). On reduplicative paramnesia. Brain, 26: 260
267.
Ptak, R., & Schnider, A. (1999). Spontaneous confabulations
after orbitofrontal damage: The role of temporal context
confusions and self-monitoring. Neurocase; 5: 243250.
Ramachandran, V. S. (1995). Anosognosia in parietal lobe syndrome. Consciousness and Cognition, 4: 2251.
Rubin, E. H., Drevets, W. C., & Burke, W. J. (1988). The nature
of psychotic symptoms in senile dementia of the Alzheimer
type. Journal of Geriatric Psychiatry and Neurology, 1:
1620.
Schilder, P. (1950). The Image and Appearance of the Human
Body. New York: International Universities Press.
Schnider, A. (2008). The Confabulating Mind: How the Brain
Creates Reality. New York: Oxford University Press.
Semrad, E. (1967). The organization of ego defenses and object
loss. In: The Loss of Loved Ones, ed. D. M. Moriarity.
Springeld, IL: Charles C Thomas, pp 126134.
Shanks, M. F., & Venneri, A. (2002). The emergence of delusional companions in Alzheimers disease: An unusual
misidentication syndrome. Cognitive Neuropsychiatry, 7:
317328.
Silva, J. A., & Leong, G. B. (1995). Visual-perceptual abnormalities in delusional misidentication. Canadian Journal
of Psychiatry, 40: 68.
Spangenberg, K. B., Wagner, M. T., & Bachman, D. L. (1998).
Neuropsychological analysis of a case of abrupt onset mirror
sign following a hypotensive crisis in a patient with vascular
dementia. Neurocase, 4: 149154.
Staton, R. D., Brumback, R. A., & Wilson, H.(1982). Reduplicative paramnesia: A disconnection syndrome of memory.
Cortex, 18: 2336.
Stuss, D. T. (1991). Disturbances of self-awareness after frontal
system damage. In: Awareness of Decit after Brain Injury,
158
ed. G. P. Prigatano & D. L. Schacter. New York: Oxford
University Press, pp. 6383.
Stuss, D. T., Picton, T. W., & Alexander, M. P. (2001). Consciousness, self-awareness, and the frontal lobes. In: The
Frontal Lobes and Neuropsychiatric Illness, ed. S. P. Salloway, P. F. Malloy, & J. D. Duffy. Washington, DC: American
Psychiatric Publishing, pp. 101109.
Stuss, D. T., Rosenbaum, R. S., Malcolm, S., Christianna, W., &
Keenan, J. P. (2005). The frontal lobes and self-awareness.
In: The Lost Self: Pathologies of the Brain and Identity, ed.
T. E. Feinberg & J. P. Keenan. New York: Oxford University
Press, pp. 5064.
Taylor, M. (1999). Imaginary Companions and the Children
Who Create Them. New York: Oxford University Press.
Turnbull, O. H., Berry, H., & Evans, C. E. Y. (2004). A positive
emotional bias in confabulatory false beliefs about place.
Brain and Cognition, 55: 490494.
Vaillant, G. E. (1977). Adaptation to Life. Boston, MA: Little,
Brown.
Vaillant, G. E. (1992). Ego Mechanisms of Defense: A Guide
for Clinicians and Researchers. Washington, DC: American
Psychiatric Press.
Vaillant, G. E. (1993). The Wisdom of the Ego. Cambridge, MA:
Harvard University Press.
Vallar, G., & Ronchi, R. (2006). Anosognosia for motor and
sensory decits after unilateral brain damage: A review.
Restorative Neurology and Neuroscience, 24: 247257.
Vallar, G., & Ronchi, R. (2009). Somatoparaphrenia: A body
delusion. A review of the neuropsychological literature.
Experimental Brain Research, 192: 533551.
Venneri, A., Shanks, M. F., Staff, R. T., & Della Sala, S. (2000).
Todd E. Feinberg
Nurturing syndrome: A form of pathological bereavement
with delusions in Alzheimers disease. Neuropsychologia,
38: 213224.
Vi, J. (1930). Un trouble de lidentication des personnes.
Lillusion des sosies. Annales Mdico-Psychologiques, 88:
214237.
Vi, J. (1944). Les meconnaissances systematiques. Annales
Mdico-Psychologiques (Paris), 102: 410455.
Vuilleumier, P. (2004). Anosognosia: The neurology of beliefs
and uncertainties. Cortex, 40: 917.
Wallerstein, R. S. (1985). Defenses, defense mechanisms, and
the structure of the mind. Journal of the American Psychoanalytic Association, 31S: 201225.
Weinstein, E. A. (1996). Symbolic aspects of confabulation
following brain injury: Inuence of premorbid personality.
Bulletin of the Menninger Clinic, 60: 331350.
Weinstein, E. A., & Friedland, R. P. (1977). Behavioral disorders associated with hemi-inattention. In: Hemi-Inattention
and Hemispheric Specialization. Advances in Neurology,
Vol. 18, ed. E. A. Weinstein & R. P. Friedland. New York:
Raven Press, pp. 5162.
Weinstein, E. A., & Kahn, R. L. (1955). Denial of Illness.
Springeld, IL: Charles C Thomas.
Weinstein, E. A., Kahn, R. L., & Malitz S (1956). Confabulation as a social process. Psychiatry,19: 383396.
Weinstein, E. A., Kahn, R. L., & Morris, G. O. (1956). Delusions about children following brain injury. Journal of the
Hillside Hospital, 5: 290298.
Young, A. W., Reid, I., Wright, S., & Hellawell, D. J. (1993).
Face-processing impairments and the Capgras delusion.
British Journal of Psychiatry, 162: 695698.

Neuropathologies of The Self: A General Theory

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Neuropsychoanalysis: An Interdisciplinary Journal for

Neuropathologies of the Self: A General Theory

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Neuropsychoanalysis, 2010, 12 (2)

Neuropathologies of the Self: A General Theory

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Todd E. Feinberg (New York)

Pathology has made us acquainted with a great number

interrelated and extensively overlapping syndromes

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Some of the more common neuropathologies of the self

Persistent and refractory denial of paralysis, often accompanied by confabulation

Delusional misidentication of part of the body, often accompanied by confabulation

DMS for the mirror image

Persistent underrelated misidentication of a person, place, or thing

Persistent overrelated misidentication of a person, place, or thing

Phantom boarder syndrome

Delusional companion syndrome

autobiographical signicance of the self in relation to

Neuropathologies of the Self: A General Theory

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Ok. What are you doing here?

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can temporally reverse the neglect in some anosognosic

Both Gerstmann and Critchley noted that in these

Neuropathologies of the Self: A General Theory

Disorders of the relational self

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Delusional misidentication syndromes

along a dimension of personal relatedness based on the

I would say nine times out of ten she

No, honey . . . I tried to tell you its

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As in the other conditions I have discussed such as

Another example of this condition is my patient S.P.

Neuropathologies of the Self: A General Theory

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Delusions and fantasies about imaginary persons

So you came to visit somebody. Who did you

Youre kidding? She was in the same hospital

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recurring confabulation in which he or she ostensibly

Weinstein and coworkers suggested that the use of the

A couple of days ago people been telling me

next door, a big explosion in there and I was in

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Neuropathologies of the Self: A General Theory

We have already noted the numerous decit

cept of the hierarchical organization of ego functions

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The modern psychoanalytic use of the term ego

The other relevant theoretical concept is that of ego

defensive hierarchy (see Figure 1). Vaillant refers to

Common in healthy adults

Seen in depression, personality disorders, adolescence

Seen in psychosis, dreams, and childhood up to approximately

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Neuropathologies of the Self: A General Theory

Therefore, denial may be related to wishful fantasy

Children commonly display the use of fantasy in the

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