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Neuropsychoanalysis: An Interdisciplinary Journal

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A Cognitive Neuroscience Perspective on

Confabulation: Commentary by Jorge Canestri
(Rome)
a

Jorge Canestri
a

Via Sesto Rufo 23, 00136 Rome, Italy, e-mail: . or

Published online: 09 Jan 2014.

To cite this article: Jorge Canestri (2000) A Cognitive Neuroscience Perspective on Confabulation: Commentary by
Jorge Canestri (Rome), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 2:2,
144-148, DOI: 10.1080/15294145.2000.10773297
To link to this article: http://dx.doi.org/10.1080/15294145.2000.10773297

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144
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Jorge Canestri
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Mark Blechner, Ph.D.

145 Central Park West
New York, NY 10023

A Cognitive Neuroscience Perspective on Confabulation

Commentary by Jorge Canestri (Rome)

DeLuca's paper presents the psychoanalyst with several interesting points: an accurate examination of a
pathological phenomenon (confabulation) whose
definition, uniqueness, and causality are still under
discussion; an alternative model constructed on the
cognitive neuroscience perspective emphasizing the
differences between the various forms of confabulation; and the possibility of comparison with psychoanalytic theories, specifically relative to this
phenomenon as well as in a wider sense concerning
the verisimilitude of certain statements of Freudian
metapsychology.
The neurosciences can offer to psychoanalysis
some tools that allow one to verify the biological plausibility of certain psychoanalytic hypotheses and to
find confirmation or refutation of them in the experimental field, while psychoanalysis can supply the neurosciences with a heuristic potential that cannot be
underestimated. In these brief notes I will try to illustrate this viewpoint.
My task in presenting these notes is greatly facilitated by Mark Solms's comment, which excuses me
from describing the fundamental principles of the
Freudian topographical model of the mind (Freud,
1900, 1911, 1915). With the addition of examples
taken from his clinical experience with bilateral ventromesial frontal lesioned patients, Solms highlights

what is essential to the Freudian task: the problem of

the psychoanalyst is not only to construct a causal
hypothesis, but above all to find meaning in the manifestations of psychic life. This is evidenced by the
different consideration that the symptoms merit in DeLuca's work and in the discussion by Solms. The latter
emphasizes the fact that behind the "positive" (or
"productive' ') manifestations of the organic lesions,
there are "underlying wishes," in consonance with
the Freudian model of the mind. It is therefore clear
that while DeLuca will put the accent on the deficit,
the psychoanalyst will also emphasize the "productive" aspect of the symptom and its meaning.
It might perhaps be useful to dwell for a while
on this difference in the general line of thinking, which
could be significant for the neurosciences also. As we
know, Freud constructed a hypothetical model of a
"mental apparatus." Setting aside for the time being
the verisimilitude of his construction, what is essential
is to note the implicit general concept: in a complex
system the global level of functioning of the system
cannot legitimately be explained by reference to the
"atomic" elements only. A deficit (in these cases due
to an organic lesion) must be interpreted also as a
function of the overall response of the system. This is
true at the physical level as well as at the level of
"mental life." If, for example, we consider the (some-

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Commentary on Confabulation
times astonishing) cases of extensive malformations
of one hemisphere requiring early radical hemispherectomy (I recall a case with follow-up of left
hemispherectomy in a 2-year-old child), we can see
how the right hemisphere almost completely takes
over all the functions of the other hemisphere, privileging those higher functions that are essential from
the adaptive point of view.
Mental life operates no differently (and it could
not be otherwise). This justifies considering the gap
filling produced by the lesions in question as a function
of the mind (as a system), and not necessarily or only
as a response to embarrassment or feelings of inadequacy. Gazzaniga's observations (1998, quoted by DeLuca) can be viewed from the same angle: the point
is not so much in deciding whether this is confabulation from unawareness or not, but rather that in splitbrain patients the left hemisphere contains a mechanism (the Interpreter) that in any case tries to interpret
information in a plausible manner, even if it is not
correct. What I would say, if Gazzaniga is right, is
that this is a function of the system as a whole. Mental
life at the level of dreams (secondary elaboration),
the narrative rewriting of one's own history, regularly
works in the same way.
Solms insists on the fact that "mature cognitive
functions (like the function that DeLuca described as
'strategical retrieval'-which we would classify as an
executive 'ego' function) are built upon the foundations of more primitive mental functions." This leads
him to observe, rightly, that the symptomatology of
his patients is in consonance with the fundamental
principles of the Freudian topographical model of
the mind.
I would like to recall a Freudian concept that has
been somewhat forgotten (Canestri, 1989) and that
could prove useful in this context. The concept
emerges for the first time in Freud's analysis of the
Schreber case but reappears in other texts by Freud.
This is not the occasion for a detailed study of its uses
and applications, but I would only like to mention that
the concept in question-reconciliation (Versohnung)-was subsequently transformed by Melanie
Klein into reparation, thus modifying its original
meaning. What did Freud mean by reconciliation?
The Schreber case dealt with the fact that the patient
could "reconcile himself" with his homosexual fantasy because he was not able to eliminate it. Subsequently the concept broadened to include the
"reconciliation" of the three mental agencies (ego,
id, and superego) in Freud's structural model. In conclusion, through the deformations of the ego and the

145
use of different defense mechanisms, the entire system
seeks states of equilibrium (which mayor may not be
pathological) and this brings into consideration all the
elements of the system.
In my opinion, the general outline of Luria's
work (1973) in relation to confabulation is similar to
the one I have attempted to describe here. In fact,
whether he was analyzing attention disorders or memory disorders (in patients with ventromesial frontal lesions), Luria constantly emphasized that the classical
"basic concepts" of neuropsychology needed to be
reexamined. Thus, from the concept of "function" we
pass to the notion of whole "functional systems,"
from single abilities to "systemic organization," from
the cerebral zones to the articulation and hierarchical
organization of "complex functional systems," from
the symptom to the collapse of the system in its entirety. In the same way, Luria's conceptualizing of the
structures within the ventromesial frontal region of the
brain as being an executive system with the task of
organizing the available subroutines at lower hierarchical levels, are congruent with some central aspects
of Freudian metapsychology. This has already been
effectively pointed out by Solms when he quotes Luria, but I would like to return to some particular aspects, especially those concerning the function of
attention.
Freeman's (1992) paper "Psychiatric Perspectives on Freud's Metapsychology," is pertinent to our
topic. Even though DeLuca expressly leaves aside
confabulatory psychopathology of psychiatric origin,
many of Freeman's examples, including those of
schizophrenia and chronic brain syndrome, demonstrate the value in studying confabulation in a broad
rather than a narrow sense, as Solms also recommends.
In these disorders Freeman identifies a failure of selective attention (described by many authors, Luria in
particular) that, from a psychological point of view,
would result in the essential feature:
In the chronic brain syndrome reality has largely lost
its value.... The loss of reality has not occurred because it had become too frightening (Rosenfeld,
1952), too exciting (Katan, 1979), hated (Bion, 1959),
as is postulated in the case of schizophrenias. The
clinical phenomena suggest other causes for the break
with reality-namely the disorder of selective attention and the amnesic phenomena. Attention can no
longer be purposely directed to thoughts and percepts
although they have achieved mental registration [po
498].

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146

I will later return to the problem of the (associated)

role that certain defense mechanisms-denial or disavowal (Verleunung)-----ean also play in these pathologies.
What is specifically interesting in this case is that
Freeman (and also Solms) resorts to the Freudian theory of attention, another metapsychological concept
not always taken sufficiently into account. Freeman's
synopsis of the Freudian theory of attention highlights
the fact that' 'selective attention is a function of the
ego system Pcpt-Cs which acts as a sense organ" (p.
499). This implies that unconscious mental processes
(wishes) have to make contact with preconscious verbal representations to find conscious expression, and
this, in turn, requires that the Pcpt.-Cs. system should
have an adequate "cathexis" (activation). What happens with pathology of the vetromesial frontal region
of the brain? Luria and others emphasize that the
"voluntary" or selective attention-arousal systems of
the brain are defective, adding that the frontal lesion
disturbs only the higher cortical forms of such activation, formed with the help of language, while the elementary forms not only remain intact but may actually
be increased. Returning to the Freudian hypothesis;
on the one hand, we are brought back to what Solms
clearly explained when he writes that:
[A] defining property of the deficit in question must
be that it deprives the mental apparatus of something
that is fundamental to the whole mode of functioning
of the system Pcs.-Cs.-and therefore to the secondary process (and the reality principle) in general. This
implies that structures within the ventromesial frontal
region of the brain subserve functions that are prerequisite for the secondary process mode of functioning
that characterizes the system Pcs.-Cs.

On the other hand, there also appears to be a

deficit in the' 'filtering" of information and in its regulation, as Luria describes (i.e., an increase in elementary forms of arousal). In Freudian language, this is
attributed to absence of the' 'countercathectic barrier"
that protects the operations linked to voluntary attention from undesirable interference (or restated in terms
of primary and secondary processes: protects thought
from continuous invasion by the procedural forms of
the primary process).
In the same way as the functioning of the mental
apparatus presupposes the constant and simultaneous
presence of "primitive functions," it also implies an
adequate control and filtering of these functions in the
development of higher cognitive capacities.

Jorge Canestri

In Freeman's words:
As the Pes contents are hypercathected, a countercathectic barrier arises simultaneously to insulate directed thinking and perceiving from extraneous and
internal stimuli ... In terms of Freud's theory (1900),
patients suffering from chronic brain syndrome cannot voluntarily recall preconscious ideas and percepts
because the system Pcpt-Cs is deprived of that
(bound) cathexis which would enable it to bring these
representations to consciousness. The accompanying
distractibility occurs because of the cathectic depletion of the barriers which protect consciousness from
excessive stimuli ... the loss of functions served by
the system Pcpt-Cs leads to the appearance of an elementary form of cognition (primary process) [po 499].

This is consistent with Luria's observations

(quoted by Solms) concerning a "sharp decrease in
cortical tone" and with the statements of Solms (and
psychoanalysis in general) on the importance of considering not only the deficit but also the' 'productive"
aspects of pathology. If what I briefly mentioned
above, regarding the brain and the mental apparatus
as a complex system, is plausible, then these aspects
simultaneously reveal the work of the primary process
in terms of wishful states; but they also reveal the
striving toward a "reconciliation" with the new condition of the entire mental apparatus.
One of my patients with severe cyclical pathology, at a certain point in the analysis, had a partial
occlusion of the carotid. The excessive deficits that
ensued led to the suspicion of a second pathology.
Radiological investigations revealed diffuse atrophy
of the cortex, the extent of which amazed everybody
as it was difficult to imagine how the patient could
have led quite a "normal life" (at least from the neurological point of view) considering the extent of the
cortical atrophy. A surgical intervention to clear the
carotid (endartorectomy) brought the situation back to
the stato quo ante, but the following months of analysis provided a good opportunity to observe a complex
and articulated assemblage of productive symptoms,
deficits, and compensatory efforts by the patient
(pseudo-explanations, confabulations, rationalizations, etc.) to reconcile himself to his state. The psychiatric pathology did not disappear, rather it was
enriched by the intersection of organic symptoms and
psychiatric symptoms. The definition of denial by Prigatano and Klonoff (1998, quoted by DeLuca) could
be applied to some manifestations of this point: "denial after brain injury reflects the individual's attempt

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Commentary on Confabulation
to use previous coping strategies to deal with impairments that are only partially recognized." This definition coincides with the above hypothesis on the
function of "reconciliation." But how do we trace a
clear dividing line between denial of illness and unawareness of illness?
Although it may be reasonable to try to differentiate between anosognosia and functional "denial of
illness," as DeLuca does in the section of his paper
entitled "Confabulation and Awareness," to me it
seems unsatisfactory to state (following the American
Psychiatric Association's definition) that the difference must be sought in the fact that denial of illness
presupposes merely altered self-awareness rather than
actual unawareness. Here we must take account of the
fact that denial (in the Freudian sense of disavowal,
i.e., Verleunung or Verweifung) is a very powerful
defense mechanism, the effects of which can produce
total unawareness (rather than mere altered awareness). Denial involves a cognitive alteration that can
be very serious, including substitution of one reality
with another. Theo Dorpat (1983), in hypothesizing
four phases of denial; (1) preconscious appraisal of
danger or trauma, (2) painful affect, (3) cognitive arrest, and (4) screen behavior, describes how "cognitive arrest concerning the painful object and the need
to adapt to the dangerous or traumatic situation stimulates the need to create a cover story or screen to hide,
as it were, the gap caused by the preceding phase. The
cognitive arrest is usually followed by some kind of
screen behaviour the content of which is often the
opposite from what has just been negated" (p. 54).
Moreover, this operation clearly shows how the
needs of the primary process (realization of a desire
through its opposite, screen behavior, etc.) are articulated alongside those of the entire system (' 'need to
adapt," neutralization of the trauma, consequent distortion of the perception of reality, misidentification,
misrecognition); in other words, alongside distortions
of the ego and alteration of its functions.
I think it will seem obvious to DeLuca that all
these observations invite a "nuancing" of the differences, while his approach is to emphasize them-to
consider only neurogenic confabulation and to set
aside psychiatric pathology, to differentiate unawareness from denial of illness, to discriminate confabulation in a narrow sense from that in a broad sense.
This different orientation partly reflects a disparity between the disciplines. It is difficult, and would be contradictory from the analyst's point of view, not to take
into account the premobid personality features, the
productive aspects of the illness, and the fact that they

147
express unconscious tendencies. From the DeLuca's
viewpoint, on the other hand, the search for clarity in
definitions and for precision in delimiting the field is
paramount. I do not think, however, that these two
orientations need necessarily be incompatible. From
the neurologist's viewpoint, the proposal DeLuca illustrates in Figure 1 could be useful, provided that
DeLuca also accepts that although it is useful in neurological practice, it probably is not really accurate when
one deals with confabulatory phenomena as a whole.
Moreover, a radical separation between all these phenomena can risk impoverishing our understanding of
the overall functioning of the mental apparatus as well
as of the brain itself.
In his section reviewing the "Neurobehavioral
Models of Confabulation," DeLuca adheres to the
third model, hypothesizing that the expression of confabulation requires "both amnesia and executive dysfunction. " Solms on the other hand thinks that the
memory disorder is an executive disorder, that a "special type of executive disorder .... necessarily produces a confabulatory amnesia," thus associating
himself with the second model. From this point of
view, Ptak and Schnider's (1999) observations
(quoted by DeLuca in support of the third model) seem
to lead in the direction proposed by Solms; in fact
Ptak and Schnider attribute a core role to the orbitofrontal cortex in the maintenance of temporal order in
memory, and it is mainly this (temporal order) that is
altered in memory confabulation, rather than memory
content itself. We could therefore hypothesize that the
maintenance of temporal order is one of the executive
functions of the frontal cortex and that the "amnesia,"
as Solms says, is only the inevitable consequence.
However, some contradictory cases could be found;
for example, the case reported by Wheatly and
McGrath (1997, quoted by DeLuca) of confabulation
in a non-ACoA patient with executive dysfunction and

impaired memory secondary to a diencephalic lesion,

and others. Such cases indicate that other nearby structures, connected to the ventromesial portion of the
frontal lobes, are compromised (Damasio, Graff-Redford, Eslinger, Damasio, and Kassel, 1985). In my
opinion the argument remains open to further study
and is of considerable interest from the neuroscientific
and psychoanalytic point of view.
I have already mentioned how psychoanalysis
can have heuristic value for the neurosciences. Psychoanalysis, of necessity, works with a wider vision
of subjective phenomena, with a perspective that must
continuously take into consideration the phenomena
of meaning as well as the phenomena of deficit, and
with a viewpoint that must confront the mental apparatus in its totality alongside each of its manifestations.

Downloaded by [Gazi University] at 22:50 18 August 2014

148

Neill Graff-Radford

Moreover, I do not believe it is useful, or epistemologically correct, from the neuroscientific point of
view, to reject as nonscientific the descriptive data
resulting from subjective experience. First, they are
not in themselves less scientific by definition than experimental data. Many disciplines-psychoanalysis
among them-are based on the accurate, programmed, and intersubjectively controlled collection
of empirical data, and this does not exclude them from
the field of empirical science. The neurosciences could
receive useful information from psychoanalysis relative to the complexity of the phenomena to be studied,
for the reason that it possesses an overarching model
of the mental apparatus still lacking in neuroscience.
Psychoanalysis in its turn could receive valuable help
from the neurosciences in order to test the empirical
and experimental probity of its hypothetical and sometimes speculative concepts, derived from a particular
experience in the treatment of mental illness.
From this point of view, DeLuca's work provides
an excellent opportunity for reconsidering some basic
concepts of Freudian metapsychology, such as the difference between bound and freely mobile energy, primary process and secondary process, and the entire
Freudian concept of attention, and the like. But Solms
has already commented on these aspects.

Damasio, A. R., Graff-Radford, P. J., Eslinger, H., Damasio,

H., & Kassel, N. (1985), Amnesia following basal forebrain lesions. Arch. Neurol., 42:263-271.
Dorpat, T. L. (1983), The cognitive arrest hypothesis of
denial. Internat. J. Psycho-Anal., 64:47-57.
Freeman, T. (1992), Psychiatric perspectives on Freud's
metapsychology.
Internat.
Rev.
Psycho-Anal.,
19:497-502.
Freud, S. (1900), The Interpretation of Dreams. Standard
Edition, 4&5. London: Hogarth Press, 1953.
- - - (1911), Formulations on the two principles of mental function. Standard Edition, 12:213-226. London: Hogarth Press, 1958.
- - - (1915), The unconscious. Standard Editon,
14: 159-204. London: Hogarth Press, 1957.
Gazzaniga, M. S. (1998), The Mind's Past. Berkeley: University of California Press.
Luria, A. R. (1973), The Working Brain: An Introduction
to Neuropsychology. Harmondsworth, U.K.: Penguin
Books.
Prigatano, G. P., & Klonoff, P. S. (1998), A clinician's
rating scale for evaluating impaired self-awareness and
denial of disability after brain damage. Clin. Neuropsychol., 12:56-67.
Ptak, R., & Schnider, A. (1999), Spontaneous confabulation
after orbitofrontal damage: The role of temporal context
confusion and self-monitoring. Neurocase., 5:243-250.
Wheatly, J., & McGrath, J. (1997), Co-occurrence of executive impairment and amnestic syndrome following subarachnoid haemorrhage: A case study. Cortex,
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References

Jorge Canestri
Via Sesto Rufo 23
00136 Rome, Italy
e-mail: canestri@mclink.it.ormc4958@mclink.it

Canestri, J. (1989), Restauro, Riparazione, Riconciliazione.

In: 11 Piccolo Hans, Vol. 61. Milan: Media Press.

A Cognitive Neuroscience Perspective on Confabulation

Commentary by Neill Graff-Radford (Jacksonville, FL)

Dr. John DeLuca has written a scholary review of the

cognitive neuroscience perspective of confabulation,
while Dr. Mark Solms has made a compelling case
that many of the features characterizing confabulation
are found in Freud's model of the unconscious mind.
With these articles in mind, and from a pragmatic
point of view, it is important to ask the following questions about confabulations: What are they? What are
Professor Graff-Radford is Chair, Department of Neurology, Mayo
Clinic, Jacksonville, Florida.

the known causes? Do we know the anatomy of the

lesion(s) causing them? Why do they occur? What are
the associated features?

What Are They?

Dr. DeLuca has used the Moscovitch and Melo (1997)
definition of "statements or actions that involve unintentional but obvious distortions." This is an all-inclusive definition and fits with the model in his Figure 1,