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Is the Charcot and Bernard case
(1883) of loss of visual imagery really
based on neurological impairment?
Stefano Zago
a
, Nicola Allegri
a
, Marta Cristoffanini
a
, Roberta
Ferrucci
b
, Mauro Porta
c
& Alberto Priori
b
a
Dipartimento di Neuroscienze ed Organi di Senso, Universit
degli Studi di Milano, UOC di Neurologia Fondazione IRCCS Ca
Granda Ospedale Maggiore Policlinico, Italy
b
Centro Clinico per la Neurostimolazione, le Neurotecnologie
e i Disordini del Movimento, Dipartimento di Neuroscienze ed
Organi di Senso, Universit degli Studi di Milano, Italy
c
Centro Tourette e Malattie Extrapiramidali, IRCCS Ospedale
Galeazzi di Milano, Italy
Version of record first published: 23 May 2011.
To cite this article: Stefano Zago, Nicola Allegri, Marta Cristoffanini, Roberta Ferrucci, Mauro
Porta & Alberto Priori (2011): Is the Charcot and Bernard case (1883) of loss of visual imagery
really based on neurological impairment?, Cognitive Neuropsychiatry, 16:6, 481-504
To link to this article: http://dx.doi.org/10.1080/13546805.2011.556024
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Is the Charcot and Bernard case (1883) of loss of visual
imagery really based on neurological impairment?
Stefano Zago
1
, Nicola Allegri
1
, Marta Cristoffanini
1
,
Roberta Ferrucci
2
, Mauro Porta
3
, and Alberto Priori
2
1
Dipartimento di Neuroscienze ed Organi di Senso, Universita` degli
Studi di Milano, UOC di Neurologia Fondazione IRCCS Ca Granda
Ospedale Maggiore Policlinico, Italy
2
Centro Clinico per la Neurostimolazione, le Neurotecnologie e i
Disordini del Movimento, Dipartimento di Neuroscienze ed Organi di
Senso, Universita` degli Studi di Milano, Italy
3
Centro Tourette e Malattie Extrapiramidali, IRCCS Ospedale
Galeazzi di Milano, Italy
Introduction. The Charcot and Bernard case of visual imagery, Monsieur X, is a
classic case in the history of neuropsychology. Published in 1883, it has been
considered the first case of visual imagery loss due to brain injury. Also in recent
times a neurological valence has been given to it. However, the presence of
analogous cases of loss of visual imagery in the psychiatric field have led us to
hypothesise functional origins rather than organic.
Methods. In order to assess the validity of such an inference, we have compared the
symptomatology of Monsieur X with that found in cases of loss of visual mental
images, both psychiatric and neurological, presented in literature.
Results. The clinical findings show strong assonances of the Monsieur X case with
the symptoms manifested over time by the patients with functionally based loss of
visual imagery.
Conclusion. Although Monsieur Xs damage was initially interpreted as neurolo-
gical, reports of similar symptoms in the psychiatric field lead us to postulate a
functional cause for his impairment as well.
Correspondence should be addressed to Stefano Zago, PhD, Dipartimento di Neuroscienze ed
Organi di Senso, Universita` degli Studi di Milano, UOC di Neurologia, Fondazione IRCCS Ca
Granda, Ospedale Maggiore Policlinico, via Francesco Sforza 35, 20122 Milano, Italy. E-mail:
stefano.zago@unimi.it
We wish to thank David Noonan for help with the English text. Preliminary data were
presented at the eighth annual meeting of the American Academy of Clinical Neuropsychology
(AACN), Chicago, Illinois, 1719 June 2010.
COGNITIVE NEUROPSYCHIATRY
2011, 16 (6), 481504
#
2011 Psychology Press, an imprint of the Taylor & Francis Group, an Informa business
http://www.psypress.com/cogneuropsychiatry http://dx.doi.org/10.1080/13546805.2011.556024
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Keywords: Charcot and Bernard; Depersonalisation; Derealisation; Functional;
Loss of visual imagery; Monsieur X; Organic.
INTRODUCTION
Visual mental imagery is the ability to create, more or less faithfully, a similar
perceptual visual representation of environments, people, objects, symbols,
or scenes in absence of their physical presence. It is a function that plays an
important role in humans mental life and that is variously used in
representing for example the model of an organic molecule, a city route,
the appearance of places in our childhoods or the faces of our loved ones.
These examples reveal that visual imagery it is clearly a function that
involves both cognitive and emotional aspects even if there is not always an
emotional overlay in the acquisition and cognitive manipulation of visual
information.
Clinically, there is great evidence that visual imagery can be damaged by
neurological lesions which compromise the ability to describe and draw
familiar environments or objects from memory (e.g., Farah, 1984; Ganis,
Thompson, Mast, & Kosslyn, 2003; Trojano & Grossi, 1994). Less known,
but equally well documented, is the possibility that psychiatric patients
should result in a similar loss of visual imagery. This condition has been
documented in patients with depression and anxiety associated with
depersonalisation/derealisation and, more rarely, with psychosis (e.g.,
Reda, 1960; Schilder, 1928; Sierra & Berrios, 2001).
The main aim of this paper is to revisit, in a critical vein, the Monsieur X
case reported in 1883 by Charcot and Bernard, considered by neurological
and neuropsychological literature as the first case of loss of visualisation and
considered a standard citation in case reports or reviews of loss of visual
imagery. In particular, on the basis of evidence of past and present
psychiatric and neurological literature, we aim to assess if it is possible to
put forward an alternative hypothesis to the neurological origins explanation
which has been commonly and indeed recently posed (see Bartolomeo, 2008;
Della Sala & Young, 2003; Goldenberg, 1993; Zeman et al., 2010).
THE RENOWNED CASE OF MONSIEUR X
The Monsieur X case was published in 1883 on Le Progre`s Medical with the
title of Un cas de suppression brusque et isolee de la vision mentale des signes
et des objets (formes et couleurs) [A case of sudden and isolated suppression of
the mental vision of signs and objects (forms and colours)] (Charcot &
Bernard, 1883). Le Progre`s Medical usually collected clinical cases examined
by Charcot at the prestigious Parisian hospital, the Salpetrie`re. It is thanks
482 ZAGO ET AL.
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to the written report by De`sire` Bernard, an apprentice within his entourage,
that the description of this patient has reached us.
From the short account, Monsieur X was an entrepreneur born in
Vienna, with good business acumen and was a cultured person, able to
understand and express himself in his German mother tongue, Spanish,
and French, and with a good knowledge of Latin and Greek (both ancient
and modern), so much so that he was able to do business in the latter. He
would read the works of Virgil and Homer, whose first books he knew very
well and could finish lines from these when prompted with the beginnings.
According to the same Monsieur X, before the onset of the symptomatol-
ogy that led him to see professor Charcot, he enjoyed a formidable visual
memory in recalling the features of faces, shapes, and the colours of
objects, so as to use this ability as a mnemonic technique. However, by his
own admission, his auditory-verbal and musical memory skills were less
remarkable. A year and a half before visiting Charcot, Monsieur X had
presented a marked and persistent mood disturbance with states of
agitation and restlessness linked to the possible risk of losing huge sums
of money. In addition to the psychopathological symptomatology, there
was sudden appearance of the well-known loss of the ability to recognise
and to visualise both recent and past shapes and colours. Prodromic
symptoms, which were somatic in nature, had not been noted during the
visit to Charcot nor were other neurological signs present besides the visual
imagery and recognition deficits. An ophthalmological examination carried
out at the clinic by Dr. Parinaud had indicated significant myopia (7
dioptres), but ocular lesions or defects of the visual field were excluded.
The only meaningful data was represented by a light weakening of
chromatic sensitivity in relation to the entire spectrum of colours. The
onset and development of Monsieur Xs disturbance, over an 18 month
period, are described both in the article and in a letter sent personally
by Monsieur X to Charcot, dated 11 June 1883, attached to the
original article. Charcot and Bernard described the onset of the disorder
as follows:
About a year and half ago he was assailed by a strong concern related to the
payment of considerable credits of which seemed to him to be uncertain. He lost his
appetite and was unable to sleep despite the fact that the problems were not serious
enough to justify the disorders which manifested themselves. The disturbance had
been very intense and showed no signs of diminishing, until one day Monsieur
X was abruptly shaken at noticing in himself a deep change. At first he felt a
complete loss and a violent contrast between the old and the new state that had
taken place. For a moment Monsieur X believed he was threatened by a mental
alienation, so much so that things around him appeared strange and new. He
became anxious and irritable . . .
CHARCOT AND BERNARD AND VISUAL IMAGERY LOSS 483
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Monsieur X himself noticed that he had become less sensitive to loss and
suffering confessing he had not felt sadness at the death of a beloved relative.
He recognised a strong change in his own personality and, as he himself
pointed out:
I think my existence has completely changed and obviously also my personality.
Before, I used to be much more emotional and enthusiastic and I had a fervent
imagination. Today, instead, I am calm, cold and my imagination does not allow me
any more representation . . .
Everything Monsieur X perceived seemed as though it were being observed
for the first time, including monuments, streets and houses familiar to
him. When he went down the streets of his native town, this gave him a
strange feeling as if everything had assumed new forms. To the request to
provide a description of his native citys main public square from memory, he
stated:
I know that it exists, but I am unable to imagine it nor can I tell you anything about
it, I can tell you no more.
Also the ability to recognise faces seemed to be disturbed. As Charcot and
Bernard noted:
Recently, in a public gallery, someone crossed his path to whom he immediately
apologised but it was nothing more than his own image reflected in a mirror.
Monsieur X was scared of finding himself in always new situations on a daily
basis, pointing out:
No longer being able to form images of what I see and having completely preserved
my abstract memory, I feel every day a great astonishment in seeing for the first
time things which should be very familiar for me.
The visual recognition impairment, was apparently also extended to
graphical signs. When he was asked to write the Greek alphabet, he omitted
certain letters (u, w, s, z, 8, c, l) that he was not then able to recognise and
read when Charcot traced the form of these with his finger. Only after having
reproduced the letters with his own finger was Monsieur X able to interpret
them, underlining, according to Charcot, a kind of compensation for mild
alexia (cecite verbale).
He was not able to visualise his wifes or his childrens features, but the
thing that depressed him most was the inability to visualise colours. All in
all, Monsieur X described his loss of visual imagery as follows:
. . . if you ask me to represent the towers of Notre-Dame, a sheep that is grazing or a
ship that is sinking into the sea, I would answer that, even distinguishing perfectly
484 ZAGO ET AL.
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the three things and knowing very well what it concerns, they do not have any
meaning for me from the point of view of inner vision.
His graphical abilities were also changed. Before the illness, Monsieur X
used to reproduce meticulous drawings of the things that he observed,
imprinting them in his memory. After the appearance of the disorder he was
able to draw environments, objects, and faces using only notions that one
might call technical. Invited to draw a minaret, Monsieur X reported that
he knew that this constituted a high and quadrangular tower and traced a
schematic design formed by a few vertical and horizontal lines on the sheet.
He added:
Do you want an arcade? I am about to trace it because I am aware that a round arch
is a circumference, an ogive is formed from two arches that intersect one another at
an acute angle. In spite of that I cannot imagine them at all and I cannot see them
with my mind.
Monsieur X reported he had also changed his way of dreaming:
. . . now I dream only words, where once instead, I had above all a visual perception
of my dreams.
The diminished ability of visual memory led him to have to rely on other
kinds of memory in order to continue carrying out his own work activities.
He was forced to read words and phrases aloud several times, resorting to
repetition in order to memorise:
Today I am forced to say to myself the things that I want to keep in my memory,
whereas before I only needed to photograph them with my vision.
After having widely described Monsieur Xs inability to conjure up mental
visual images, Charcot and Bernard provided an explanation in neuropsy-
chological terms of this deficit, assuming that the case represented an
example of selective loss of visual memory linked to a hypothetical
circumscribed cerebral lesion. This conception derives from the componen-
tial memory theory proposed at the time by Theodule Ribot (1881). There is
no information available about aetiology or lesion site, as the postmortem
examination*the only available method to locate cerebral lesions at the
time*was apparently not performed.
PUBLISHED CASES OF VISUAL IMAGERY LOSS AFTER THE
MONSIEUR X CASE
Since Charcot and Bernards pioneering study at the turn of the twentieth
century, a number of cases similar to Monsieur X with an inability to
CHARCOT AND BERNARD AND VISUAL IMAGERY LOSS 485
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visualise absent objects in their thoughts were reported in France, among
whom the clinical contexts suggest a psychopathologic basis. In these
patients, impaired visual images fall within a complex medical history in
which a depressive and anxious symptomatology coexist with depersonalisa-
tion and derealisation (Cotard, 1884; Deny & Camus, 1905; Dugas, 1898;
Magalhaes Lemos, 1906; Picard, 1919; Wimmer, 1919).
Depersonalisation and derealisation are both dissociative disorders
having a strong affiliation with anxiety and depression and consist of a
change of self-awareness or experience of the environment in clinical settings
(Sierra, 2009). Both the disorders occur in healthy subjects as a response to
stress, fatigue, or drug use and in those with psychiatric disorders where
symptoms can persist for lengthy periods (Senior et al., 2001). From a
neurobiological standpoint, depersonalisation has been characterised in
terms of inhibitory and excitatory processes in which three cerebral areas
play a critical role: bilateral prefrontal cortex, amygdala, and cingulated
cortex (Sierra & Berrios, 2001).
From the 1950s and 1960s, a series of single cases began to appear in
neurological/neuropsychological literature, in which the inability to generate
visual mental images was linked to various neurological conditions such as
head injury, vascular disorders, postsurgical complications, etc. Often, in
these cases, visual imagery disorder is associated with visual recognition
deficits due to focal lesion to the posterior cortical damage. Moreover, it
should be noted that, although clearly organically damaged, an additional
functional component is sometimes also invoked in some of these patients
(e.g., Brain, 1954). However, the organic/functional question has never been
explicitly raised either in the psychiatric or neurological fields.
The same situation recurs subsequently in psychiatric literature starting
from the 1960s where a series of cases of sudden loss of mental visual
imagery appear again, apparently only in Italy (e.g., Amabile & Rizzo, 1966;
Giacheddu, Amabile, & Sanarelli, 1968; Giannini & Loprieno, 1964;
Giovanardi Rossi & Muscatello, 1968; Muscatello & Giovanardi Rossi,
1967; Reda, 1960). In particular, Reda (1960) observed that visual imagery is
a faded and vanishing copy of perception, a weakened and veiled reliving of
sensations mainly characterised by fragility and uncertainty and particularly
vulnerable in states of poor affectivity and loss of emotion. The images, such
as the faded copy of perception, underwent further opacity to the point of
appearing even more distant and hazy, so distant to convince them they have
lost the capacity for imagination. The patients who complained of loss of
visual imagery had, according to Reda, anxiety attacks, different levels of
depressive states, and, above all, depersonalisation and derealisation. These
latter two aspects will be the key elements of the syndrome.
To our knowledge, after the end of the 1960s no single case studies of
selective visual imagery loss have been reported in psychiatric literature,
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excluding among other things, an evaluation with modern neuropsycholo-
gical tools. It is difficult to give an explanation for this gap but it should be
remembered that, after the first group of French patients, over forty years
passed before the publication regarding the Italian cases. You can see
historical phases in which the attention on a phenomenon is strong, then
reduces and fades from memory.
Many years later, a new series of neurological cases of loss of visual
imagery with confirmed focal cerebral lesions and a visual imagery
psychometric evaluation were reported (e.g., Basso, Bisiach, & Luzzatti,
1980; Deleval, de Mol, & Noterman, 1983; Riddoch, 1990).
In our opinion, there are two categories of patients, functional and
organic, with a visual imagery deficit but with distinctive clinical and
pathophysiological features (see Tables 1 and 2).
However, for a small number of patients a dichotomic framework is
problematic due to the overlapping of organic and functional factors (see
Table 3). Once again we see, for the visual imagery function the same old
organic/functional debate, that for over a century has been concerned with
the loss of retrograde amnesia (Barbarotto, Laiacona, & Cocchini, 1996; de
Renzi, Lucchelli, Muggia, & Spinnler, 1997; Serra, Fadda, Buccione,
Caltagirone, & Carlesimo, 2007). Moreover, it has been demonstrated that
in patients with retrograde amnesia, there can be a substantial overlap in
terms of neuroanatomic dysfunctional locus noticeable when they undergo
examinations using functional neuroimaging techniques (Markowitsch,
2003). This is an observation that makes us reflect on the need to suppose
a dichotomy on a lesional basis rather than using the simple organic/
functional distinction. In other words, it may be more correct to assume that,
apart from structural neurological alterations which can be identified
through traditional neuroradiological methods (CT, NMR), there are also
others consisting in anomalous focal reactions of brain metabolism that can
be documented only through neurofunctional imaging methods (PET, fMRI,
or others). In this sense, the organic or functional disorders represent two
sides of the same coin as highlighted by Markowitsch (1996).
MONSIEUR X: AN ORGANIC OR FUNCTIONAL CASE?
As seen in Table 1, in our opinion Monsieur X must be included among
those patients with a functional disturbance. Such positioning finds
justification after comparing the symptomatology of this patient with those
cases of a neurological and functional nature presented in literature, and also
through critical rereading of the symptoms he complained of.
From Table 1 it can be clearly deduced that patients identified with a
functional origin constantly present a symptomatology characterised by
CHARCOT AND BERNARD AND VISUAL IMAGERY LOSS 487
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TABLE 1
Summary of case reports of patients with a loss of visual imagery on a functional basis
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions
Brain
damage
Other
neurological
deficits
Visual
perception
of dreams
Typology
of visual
imagery
deficit
Evolution
of visual
imagery
deficit
Other
neuropsychological
deficits
Charcot & Bernard,
Case Monsieur X
1883 M (?) anxiety, depression,
depersonalisation (?),
derealisation (?)
* * loss of the visual
element of
dreaming
objects, places,
faces
none mild
achromatopsia,
visual agnosia (?),
prosopagnosia (?),
alexia (?)
Cotard,
Case 1
1884 M 68 anxiety, depression, psychotic
disorder, depersonalisation,
derealisation
* * no information objects, places,
faces
(?) (?)
Cotard,
Case 2
1884 M 40 anxiety, depression,
depersonalisation, derealisation
* * no information objects, faces (?) *
Dugas,
Case M.
1898 M (?) apathy, depersonalisation,
derealisation
* * no information faces none *
Deny & Camus,
Case 1
1905 F 47 anxiety, psychotic disorder,
depersonalisation, derealisation
* * no information objects, places,
faces, own
image
none *
Magalhaes Lemos,
Case 1
1906 F 36 anxiety, depression, psychotic
disorder, depersonalisation,
derealisation
* * preserved objects, places,
faces, colours,
own image
complete
recovery
*
Picard,
Case 1
1919 F 47 anxiety, depression
hypochondria, derealisation
* * no information objects, places,
faces
none *
4
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TABLE 1 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions
Brain
damage
Other
neurological
deficits
Visual
perception
of dreams
Typology
of visual
imagery
deficit
Evolution
of visual
imagery
deficit
Other
neuropsychological
deficits
Wimmer,
Case 2
1919 F 55 anxiety, depression,
depersonalisation, derealisation
* * progressive
reduction of
visual imagery
objects, places,
faces
none *
Hartmann,
Case Auguste W
1922 M 35 anxiety, depersonalisation * facial
paresthesias
preserved objects, places,
faces, own
image
none *
Ackner,
Case NP
1954 F 42 depression, depersonalisation,
derealisation
* * no information objects, places none *
Reda,
Case NF
1960 F 33 anxiety, depression,
depersonalisation, derealisation
* * no information faces, own
image
complete
recovery
*
Reda,
Case RA
1960 F 57 anxiety, depression, psychotic
disorder (?), depersonalisation,
derealisation
* * no information object, places,
faces, own
image
complete
recovery
*
Reda,
Case NA
1960 F 27 anxiety, depersonalisation,
derealisation
* * no information object, places,
faces, own
image
complete
recovery
*
Reda,
Case BD
1960 F 37 anxiety, depression,
depersonalisation, derealisation
* * no information object, places,
faces, own
image
complete
recovery
*
C
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D
V
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U
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TABLE 1 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions
Brain
damage
Other
neurological
deficits
Visual
perception
of dreams
Typology
of visual
imagery
deficit
Evolution
of visual
imagery
deficit
Other
neuropsychological
deficits
Giannini & Loprieno,
Case FJ
1964 F 42 anxiety, depression,
depersonalisation, derealisation
* * no information object, places,
faces, own
image
(?) *
Amabile & Rizzo,
Case 1
1966 M 37 anxiety, depression,
depersonalisation, derealisation
* * no information object, places,
faces
partial
recovery
*
Muscatello &
Giovanardi Rossi,
Case R Anna
Maria
1967 F 35 anxiety (?), depression,
psychotic disorder,
depersonalisation, derealisation
* * dream feeling
without visual
images
object, places,
faces
(?) *
Muscatello &
Giovanardi Rossi,
Case P Renata
1967 F 23 anxiety (?), depression,
psychotic disorder,
depersonalisation, derealisation
* * dream feeling
without visual
images
object, places,
faces
none *
Muscatello &
Giovanardi Rossi,
Case C Elvira
1967 F 31 anxiety, depression, psychotic
disorder (?), depersonalisation,
derealisation
* * restriction of
visual dream
imagery
object, places,
faces
(?) *
Muscatello &
Giovanardi Rossi,
Case M Corinna
1967 F 60 anxiety, depression, psychotic
disorder, depersonalisation,
derealisation
* * no information faces none *
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TABLE 1 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions
Brain
damage
Other
neurological
deficits
Visual
perception
of dreams
Typology
of visual
imagery
deficit
Evolution
of visual
imagery
deficit
Other
neuropsychological
deficits
Giacheddu et al.,
Case DV Matilde
1968 F 43 anxiety, depression, psychotic
disorder, depersonalisation,
derealisation
* * no information object, places,
faces, own
image
complete
recovery
*
Giacheddu et al.,
Case 2 C. Pierina
1968 F 37 anxiety, depression,
depersonalisation, derealisation
* * no information faces complete
recovery
*
Giacheddu et al.,
Case 3 P Santina
1968 F 68 anxiety, depression, psychotic
disorder, depersonalisation,
derealisation
* * no information object, places,
faces, own
image
complete
recovery
*
Giovanardi Rossi
& Muscatello,
Case Katia
1968 F 19 depression, psychotic disorder,
depersonalisation, derealisation
* * no information object, places,
faces
no
information
*
Giovanardi Rossi
& Muscatello,
Case Ivonne
1968 F 17 psychotic disorder,
depersonalisation
* * no information faces no
information
*
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TABLE 2
Summary of case reports of patients with a loss of visual imagery on a neurological basis
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions Brain damage
Other neurological
deficits
Visual
perception of
dreams
Typology of
visual imagery
deficit
Evolution of
visual imagery
deficit
Other neuro
psychological
deficits
Stengel,
Case 1
1948 M 63 (?) * (?) right hemianopia no
information
colours, letter
or word
blindness
no information alexia, anosognosia
Stengel,
Case 2
1948 M 68 (?) depression (?) right hemianopia no
information
colours no information alexia,
achromatopsia,
aphasia
Boyle & Nielsen,
Case ES
1954 M 31 * bilateral occipital (?) left hemiparesis,
papilledema
no
information
objects, faces,
colours, self
image
no information anosognosia, visual
agnosia, retrograde
amnesia
Macrae & Trolle,
Case 1
1956 M 32 * bilateral parietal (?) none preserved (?) animals, places,
faces
no information prosopagnosia; post
traumatic amnesia,
visual agnosia, alexia
agraphia, anomia
Beyn and Knyazeva,
Case Ch
1962 39 * bilateral occipital right hemianosia,
right superior
quadrantopia
no
information
objects, places,
people, colours
partial recovery anomic aphasia,
visual agnosia,
prosopagnosia,
achromatopsia
Basso et al.,
Case MG
1980 M 63 * left mesial occipital
lobe, part of left
temporal
juxtaventricular
structures, possible
inclusion of the
hippocampus, upper
left cerebellar
hemisphere
decreased density
right hemiparesis,
slight right motor,
right homonymus
hemianopia
loss of the
visual
element of
dreaming
animals, places,
faces
no information anomic aphasia,
mild
achromatopsia,
alexia, agraphia
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TABLE 2 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions Brain damage
Other neurological
deficits
Visual
perception of
dreams
Typology of
visual imagery
deficit
Evolution of
visual imagery
deficit
Other neuro
psychological
deficits
Deleval et al.,
Case Ch. T
1983 M 35 aphaty parieto-occipito-
temporal with left
occipital lesion
penetrating into deep
posterior angular
gyrus
right homonymous
hemianopia, right
hemiparesis
mentioned
absence of
imagery even
prior to
neurological
damage
objects,
animals, places
no information visual agnosia,
right neglect,
global aphasia,
temporal
disorientation,
agraphia, alexia,
acalculia
Levine et al.,
Case 1
1985 M 18 * right anterior
temporal, right
inferior frontal, left
temporo-occipital
superior left
homynimous
quadrantopia,
partial right
homonymus superior
quadrantopia
no
information
animals,
colours, faces
no information visual agnosia,
prosopagnosia,
achromatopsia
Levine et al.,
Case 2
1985 M 43 * bilateral parieto-
occipital
right homonymous
hemianopia, right
hemiparersis, right
hemianesthesia
no
information
places,
geographic
location
no information optic ataxia, right
left disorientation,
constructional
apraxia, agraphia,
visual disorientation
Grossi et al.,
Case AP
1986 M 56 * left temporo-
occipital
right hemiparesis,
right superior
quadrantopia
no
information
objects, places,
people
no information anterograde
amnesia, short-term
memory deficit,
unusual prospective
agnosia
Chiacchio et al.,
Case BL
1987 M 58 * left occipital right homonymus
hemianopia
no
information
objects, places no information temporal
disorientation, short-
term visual memory
deficit,
constructional
apraxia, mild oral
comprehension
impairment
C
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C
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T
A
N
D
B
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N
A
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D
A
N
D
V
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U
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M
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G
E
R
Y
L
O
S
S
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TABLE 2 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions Brain damage
Other neurological
deficits
Visual
perception of
dreams
Typology of
visual imagery
deficit
Evolution of
visual imagery
deficit
Other neuro
psychological
deficits
Farah et al.,
Case RM
1988 M 64 * left occipital and
medial temporal
regions
right homonymus
hemianopia
no
information
places no information mild achromatopsia
(?), anterograde
amnesia, short-term
memory deficit,
alexia
Riddoch,
Case DW
1990 M 71 * left temporo-parietal right-sided
hemiplegia, right
homonymus
hemianopia
no
information
objects, animals no information nonfluent aphasia,
mild comprehension
deficit, mild alexia,
bucco-facial apraxia
Goldenberg,
Case K. Qu
1992 M 83 * left temporo-
occipital
right homonymus
quadrantopia
no
information
objects, colours no information achromatopsia,
anomic aphasia,
alexia
Mehta et al.,
Case MS
1992 M 42 * bilateral temporo-
occipital, enlarged
ventricles,
parahippocampal
gyrus and fourth
temporal gyrus, left
mesial temporo-
occipital
left-sided
homonymus
hemianopia
no
information
animals no information visual agnosia,
achromatopsia,
prosopagnosia,
tactile agnosia,
semantic deficit for
animal category
Ogden,
Case MH
1993 M 24 * medial bilateral
occipital lobes,
dilatation of both
occipital horns
transitory cortical
blindness
loss of the
visual
element of
dreaming
objects, colours,
familiar places,
familiar people
(persone
familiari)
no information visual agnosia,
achromatopsia,
prosopagnosia,
anterograde and
retrograde memory
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TABLE 2 (Continued)
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions Brain damage
Other neurological
deficits
Visual
perception of
dreams
Typology of
visual imagery
deficit
Evolution of
visual imagery
deficit
Other neuro
psychological
deficits
Zago & Policardi,
Case ZB
1996 M 67 * left fronto-temporo-
parieto-occipital,
cortical, and
subcortical
slight right
hemiparesis
no
information
objects, animals no information temporal
disorientation, mild
aphasia, mild
apraxia bucco facial
and ideomotor,
acalculia
Zago et al.,
Case
Michelangelo
1997 M 44 * temporal bilateral none no
information
animals no information anterograde and
retrograde amnesia
Moro et al.,
Case 1
2008 F 29 * left middle and
inferior temporal
gyrus
none no
information
objects,
animals, places,
colours
no information no information
Moro et al.,
Case 2
2008 M 23 * left temporo-
occipital, left medial
and superior parietal
lobe
none no
information
objects,
animals, places,
colours
no information anomia, alexia tactile
imagery
C
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C
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D
B
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N
A
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D
A
N
D
V
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U
A
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I
M
A
G
E
R
Y
L
O
S
S
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TABLE 3
Summary of case reports of patients with a loss of visual imagery with uncertain diagnosis
Author/s Year Sex Age
Trauma/
precipitating
stressful event
Neuropsychiatric
conditions Brain damage
Other
neurological
deficits
Visual perception
of dreams
Typology of
visual imagery
deficit
Visual imagery
deficit evolution
Other neuropsychological
deficits
Brain,
Case 1
1954 M 36 nevrotic traits (?) probably frontal
damage
none loss of the visual
element of
dreaming
objects, places,
faces
no information mild aphasia,
anterograde verbal
amnesia
Brain,
Case 2
1954 M 50 depression frontal none no information objects, places,
faces
no information none
Botez et al.,
Case 1
1985 M 38 none right hemisphere (?),
corpus callosum (III
posterior) (?),
dysgenesis (?)
none restriction of
visual dream
imagery
objects, places,
faces
no information mild achromatopsia,
leftright disorientation,
finger agnosia, visual
anterograde amnesia
Solms,
Case 1
1997 F 26 depersonalisation
(?)
arterio-venous
malformation in the
right parietal lobe
left
hemiparesis,
somotosensory
defect, left
field visual loss
loss of the visual
element of
dreaming
objects, animals no information conduction aphasia,
alexia, prosopagnosia,
visual agnosia,
topographical
disorientation,
anosodiaphoria,
constructional praxis
Zeman et al.,
Case MX
2010 M 65 none mild hypodensity of
the white matter, slight
fronto-temporal
atrophy estimated
within normal limits
none initial loss of the
visual element of
dreaming with
partial recovery
after 1 year
subjective loss of
visual imagery
not confirmed by
psychometric
tests
partial recovery
(fleeting
involuntary
images)
none
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anxiety, depression, depersonalisation with derealisation and sometimes
psychotic features. Some of these features are clearly present in Monsieur X.
In fact, financial worries caused in him a state of anguish leading to obvious
symptoms of depression, anxiety, and an unreal view of the world congruent
with derealisation and probable depersonalisation. In particular, the
derealisation feature can in itself justify the subjective sense of strangeness
and unfamiliarity in the external visual perception manifested by him.
Therefore, although he seems to reflect a dysfunctional pattern, widely
documented in neurological literature, of a deficit of visual mental imagery
accompanied by visual recognition disturbances (visual agnosia, proso-
pagnosia, alexia), an alternative hypothesis is that the misrecognitions of
Monsieur X can be justified by a disorder of derealisation with depersona-
lisation.
In fact, it is worth noting that certain cases of loss of mental vision with
depersonalisation present this disorder. Again, Reda (1960), in relation to a
patient of his stated: RA goes to the market and everything appears to her
new and artificial; the houses of cardboard, the chalk fruit; she takes in her
hand a tomato, she looks at it curiously, and even recognising it perfectly
says to herself: BB How strange these tomatoes are . BB Do you see
that house before us? the same patient says to me BBI see it as if were
of cardboard, according to me it is only the facade without anything in it
. A patient studied by Giacheddu et al. (1968) states that: objects no
longer have any shape or defined colours; it is as if things were made of wood
and the people were statues. Everything has changed . . . I am unable to
explain to myself why.
Also the deficits of recognition of faces and letters, present in Monsieur
X, can be interpreted as the consequence of a functional reaction. In the very
brief passage describing the face recognition disorder (see earlier), there is a
clear resemblance to some patients with depersonalisation (e.g., Ackner,
1954; Mayer-Gross, 1935). For example, Mayer-Grosss patient stated that:
When looking in a mirror I have to keep telling myself the reflection is
mine. Its like looking at another person. Likewise, Ackner (1954) wrote:
Miss P; aged 28, suffering from depressive state, was so struck by her
strange reflection in the mirror that for short while she was convinced that
she appeared peculiar and that other people must be laughing at her and
talking about her.
Similarly, the same argument could be extended to Monsieur Xs
recognition disorder regarding the letters of the Greek alphabet. Despite
not having been described in the depersonalisation context, it is worth noting
that reading disorders have been reported in a psychopathological context
(e.g., Dinshaw & Lishman, 1984; Saunders & Barker, 1972).
It is important to state that Monsieur X continued to carry out his
commercial transactions profitably, even if resorting to alternative strategies
CHARCOT AND BERNARD AND VISUAL IMAGERY LOSS 497
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to that of visual mental imagery. This appears unusual as if effectively an
agnosic/prosopagnosic impairment with an associated mild reading disorder
were present.
The proposal that depersonalisation/derealisation disorders can interfere
with the visual imagery process is also supported by some group studies.
Schilder (1928) had observed that patients with a depersonalisation
condition: characterize their imagery as pale, colourless and some complain
they have altogether lost the power of imagination. Shorvon, Hill, Burkitt,
and Halstead (1946) mentioned a study in which imagery tests were made on
16 cases of depersonalisation and reported that a few patients complained of
genuine loss of visual imagery. More recently, Lambert et al. (2001), based
on the examination of 28 patients with depersonalisation/derealisation,
found a significant level of complaints of imagery deficit in this group,
compared to the healthy subjects on the Vividness of Visual Imagery
Questionnaire (VVIQ; Marks, 1973) and the Vividness of Movement
Imagery Questionnaire (VMIQ; Issac, Marks, & Russell, 1986). Sierra and
Berrios (2001), in a historical analysis of the 200 cases of depersonalisation
disorder in the medical literature since 1898, showed that complaints about
inability to evoke images occurred with a frequency of 52.6% in the pre-1946
cases (phenomenological period) and 18.8% in the post-1946 cases (empirical
period).
It is also of interest that Simeon et al. (2000) in a PET study with subjects
with depersonalisation found a pattern of altered metabolic activity,
primarily in the posterior cortex including left occipital area 19, an area
traditionally considered critical for image generation process (Farah, 1984;
Nielsen, 1946). Left temporo-occipital activation in visual imagery has also
been demonstrated in a series of SPECT, PET, and fMRI studies (e.g.,
DEsposito et al., 1997; Goldenberg et al., 1989; Goldenberg, Steiner,
Podreka, & Deecke, 1992; Roland & Guylas, 1994).
An additional element that characterises psychiatric patients with
depersonalisation/derealisation is the emphatic self-reporting of the loss of
mental vision, an element present in Monsieur X but rare in neurological
patients (e.g., Nielsen, 1955: for a loss of visual imagery in dreaming and,
partially, Case K. Qu of Goldenberg, 1992: for drawing from memory).
Interestingly, in some patients the reporting of mental imagery deficit does
not seem to correspond to a deficit found in nonsubjective measure of
imagining capacity (e.g., drawing from memory, description from memory).
This is an intriguing aspect already highlighted by Shorvon et al. (1946), and
reported in some single case reports (Amabile & Rizzo, 1966; Giannini &
Loprieno, 1964; Reda, 1960; Zeman et al., 2010).
Another discordant aspect in the case of Monsieur X is the absence of
deficit of the visual field*which can usually be found in neurological
patients with posterior lesions*while only an undefined slight decrease
498 ZAGO ET AL.
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in colour perception was detected. Also Monsieur Xs dream abnormality
appears unusual in that he lost only the visual aspects of dreaming. Solms
(1997), in his personal examination of a series of 361 neurological cases,
found only two cases of nonvisual dreams, and another 15 cases reported in
literature from 1883 to 1991 (including the Charcot & Bernard case). It is
worth noting that in one case, personally observed by Solms, he suspected a
depersonalisation disorder (included in Table 3, doubtful cases). Of the 15
cases found in literature we have considered three as doubtful and have
included them in Table 3.
In our review of the seven psychiatric cases in which dream loss is
reported, four presented a nonvisual dream loss and two had normal dream
recall. Out of the four neurological cases, in which dreams recall is
mentioned, two showed a global loss, one preserved it, and one indicated
an absence of dream recall before neurological damage. Unfortunately, in the
majority of the other cases, both psychiatric and neurological, there is no
mention of dreaming.
Finally, a functional origin (hysterical) of Monsieur Xs deficit had
been suggested by Sigmund Freud who, on having the opportunity to
personally examine Monsieur X during the months spent at the
Salpetrie`re with Charcot, suspected a neurosis (Schilder, 1951). More
recently, Young and van de Wal (1996), in the first volume of Classic
Cases in Neuropsychology, also raised doubts about the aetiology of this
case, being surprised at the fact that Charcot had not taken into account
the hypothesis of a hysterical form, despite being the greatest expert at
the time in the field.
UNSOLVED ASPECTS WITH REGARD TO THE
ORGANIC/FUNCTIONAL DISTINCTION
Undoubtedly, the organic/functional distinction is a difficult subject both for
the researchers of the past and for those today (Goldenberg, 2002). This is
particularly true in cases in which organic and functional aspects are
combined or when the structural and functional imaging examinations are
difficult to interpret. Examples regarding the loss of visual mental imagery
are found among cases described by Botez, Olivier, Vezina, Botez, and
Kaufman (1985), Brain (1954), and Zeman et al. (2010). In particular, Case
MX, reported by Zeman et al. (2010), who abruptly lost the ability to form
visual images, showed the absence of a relevant organic cause on MRI but a
significantly reduced activity within the posterior region network on a visual
imagery fMRI task, as opposed to an increased frontal activation compared
to controls.
CHARCOT AND BERNARD AND VISUAL IMAGERY LOSS 499
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To further complicate this framework, there is evidence of disorders
classically interpreted in psychopathological terms which can also occur as
secondary to neurological conditions such as epilepsy or head injuries. This
is precisely the case of the phenomena of depersonalisation and derealisation
(Kenna & Seldman, 1965; Sierra, Lopera, Lambert, Phillips, & David, 2002).
Moreover, it must be pointed out that the advent of refined functional
imaging techniques have radically changed the approach to dysfunctional
neural mechanisms of psychopathologic disorders. From indications of a
vague and imprecise organicism we have moved to a clear physiopathological
orientation. This aims to define brain metabolic-functional modifications
also in functional cases, traditionally considered lacking in documentable
structural or neurochemical brain correlate (Markowitsch, 1996, 2003;
Tramoni et al., 2009). This deals with functional alterations, potentially of
a reversible nature, that mimic true organic damage.
Despite the above specifications and limitations, we believe it is possible
to help the clinician to position patients in a functional or organic form of
loss of visual imagery. Table 4 summarises the main discriminating
TABLE 4
Criteria for distinguishing between a functional or an organic loss of visual imagery
Main features in patients with loss of visual imagery
Psychogenic basis Organic basis
Emphatic complaint about visual imagery
deficits
Rare complaint about visual imagery deficits
Psychological stressors and/or traumas in past
or recent medical history
Lack of relevant psychological stressors and/or
traumas in past or recent medical history
Relevant depressive and anxious
symptomatologies
Lack of relevant depressive and anxious
symptomatologies or, at the most, presence of
reactive symptomatology of neurological
disorder
Presence of depersonalisation/derealisation Lack of depersonalisation/derealisation
Psychotic disorders Lack of psychotic symptoms
Lack of structural alterations as seen by static
neuroradiological examination (CT, NMR)
Neuropsychological deficits of visual recognition
(visual agnosia, prosopagnosia,
achromatopsia, alexia)
Possible presence of metabolic-functional
modifications as detected by functional
examinations (PET, fMRI, and others)
Presence of structural alterations (commonly
involving posterior areas) as detected by
neuroradiological examination (CT, NMR)
Evidence of metabolic-functional
modifications as per functional
examinations (PET, SPECT, fMRI, and
others) congruent with detected neurological
lesions
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characteristics that in our opinion can help modern clinicians to differentiate
functional or organic forms of loss of visual imagery.
CONCLUSIONS
The Charcot and Bernard case of visual imagery loss is a classic in clinical
neuropsychology. Although a neurological valence has been attributed to
this case for more than a century, the presence of analogous unknown
European cases of loss of mental imagery in the psychiatric field, has led us
to consider the hypothesis of a functional origin rather than organic. In
order to assess the validity of such inference, we compared the symptoma-
tology of Monsieur X with that found in cases of loss of visual mental
images, both psychiatric and neurological, presented in the literature. The
comparison highlights strong assonances of Monsieur X with those
symptoms manifested by the patients with functionally based loss of visual
imagery, and provides support to the hypothesis of a psychogenic base origin
of the disorder. Such an assumption is formulated in the awareness that the
gap between organic and functional closes when we consider functional
neuroimaging evidence. This demonstrates that both conditions are able to
alter*even if in a qualitatively different way*circumscribed cerebral areas
selectively, hence causing specific cognitive deficits.
Manuscript received 12 July 2010
Revised manuscript received 7 January 2011
First published online 23 May 2011
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