Zago Stefano Et Al - Is Charcot and Bernard Case of Loss of Visual Imagery_neurological Impairment

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Is the Charcot and Bernard case(1883) of loss of visual imagery reallybased on neurological impairment?Stefano Zago

a, Nicola Allegri

a, Marta Cristoffanini

a, Roberta

Ferruccib, Mauro Porta

c& Alberto Priori

b

aDipartimento di Neuroscienze ed Organi di Senso, Universit

degli Studi di Milano, UOC di Neurologia Fondazione IRCCS CaGranda Ospedale Maggiore Policlinico, ItalybCentro Clinico per la Neurostimolazione, le Neurotecnologie

e i Disordini del Movimento, Dipartimento di Neuroscienze edOrgani di Senso, Universit degli Studi di Milano, ItalycCentro 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, MauroPorta & Alberto Priori (2011): Is the Charcot and Bernard case (1883) of loss of visual imageryreally 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 visualimagery really based on neurological impairment?

Stefano Zago1, Nicola Allegri1, Marta Cristoffanini1,

Roberta Ferrucci2, Mauro Porta3, and Alberto Priori2

1Dipartimento di Neuroscienze ed Organi di Senso, Universita degli

Studi di Milano, UOC di Neurologia Fondazione IRCCS Ca Granda

Ospedale Maggiore Policlinico, Italy2Centro Clinico per la Neurostimolazione, le Neurotecnologie e i

Disordini del Movimento, Dipartimento di Neuroscienze ed Organi di

Senso, Universita degli Studi di Milano, Italy3Centro 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 beenconsidered 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 ofanalogous 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:

[email protected]

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 visualinformation.

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 Progres Medicalwith the

title ofUn 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 Progres Medicalusually collected clinical cases examined

by Charcot at the prestigious Parisian hospital, the Salpetriere. It is thanks

482 ZAGO ET AL.



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to the written report by Desire 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 tounderstand 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 lessremarkable. 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, hestated:

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 havingreproduced the letters with his own finger was Monsieur X able to interpret

them, underlining, according to Charcot, a kind of compensation for mild

alexia (ceciteverbale).

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 Xused 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 calltechnical. 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 themwith 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 postmortemexamination*the only available method to locate cerebral lesions at the

time*was apparently not performed.

PUBLISHED CASES OF VISUAL IMAGERY LOSS AFTER THEMONSIEUR 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




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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 areasplay 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 particularlyvulnerable 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,

486 ZAGO ET AL.



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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 seehistorical 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 isproblematic 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 supposea 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




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TABLE 1

Summary of case reports of patients with a loss of visual imagery on a

Author/s Year Sex Age

Trauma/precipitating

stressful event

Neuropsychiatric

conditions

Brain

damage

Otherneurological

deficits

Visualperception

of dreams

Charcot & Bernard,

Case Monsieur X

1883 M (?) anxiety, depression,

depersonalisation (?),

derealisation (?)

* * loss of the visu

element of

dreaming

Cotard,

Case 1

1884 M 68 anxiety, depression, psychotic

disorder, depersonalisation,

derealisation

* * no informatio

Cotard,

Case 2

1884 M 40 anxiety, depression,

depersonalisation, derealisation

* * no informatio

Dugas,

Case M.

1898 M (?) apathy, depersonalisation,

derealisation

* * no informatio

Deny & Camus,

Case 1

1905 F 47 anxiety, psychotic disorder,


* * no informatio

Magalhaes Lemos,

Case 1

1906 F 36 anxiety, depression, psychotic


derealisation

* * preserved

Picard,

Case 1

1919 F 47 anxiety, depression

hypochondria, derealisation

* * no informatio

Downloadedby[189.170.4.149]at21:0921September2012


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TABLE 1 (Continued)


Trauma/

precipitating

stressful event

Neuropsychiatric

conditions

Brain

damage

Other

neurological

deficits

Visual

perception

of dreams

Wimmer,

Case 2

1919 F 55 anxiety, depression,


* * progressive

reduction of

visual imagery

Hartmann,

Case Auguste W

1922 M 35 anxiety, depersonalisation * facial

paresthesias

preserved

Ackner,

Case NP

1954 F 42 depression, depersonalisation,

derealisation

* * no informatio

Reda,

Case NF



* * no informatio

Reda,

Case RA


disorder (?), depersonalisation,

derealisation

* * no informatio

Reda,

Case NA

1960 F 27 anxiety, depersonalisation,

derealisation

* * no informatio

Reda,

Case BD



* * no informatio



12/26

TABLE 1 (Continued)


Trauma/

precipitating

stressful event

Neuropsychiatric

conditions

Brain

damage

Other

neurological

deficits

Visual

perception

of dreams

Giannini & Loprieno,

Case FJ



* * no informatio

Amabile & Rizzo,

Case 1

1966 M 37 anxiety, depression,


* * no informatio

Muscatello &

Giovanardi Rossi,

Case R Anna

Maria

1967 F 35 anxiety (?), depression,

psychotic disorder,


* * dream feeling

without visual

images

Muscatello &

Giovanardi Rossi,

Case P Renata

1967 F 23 anxiety (?), depression,

psychotic disorder,


* * dream feeling

without visual

images

Muscatello &

Giovanardi Rossi,

Case C Elvira


disorder (?), depersonalisation,

derealisation

* * restriction of

visual dream

imagery

Muscatello &

Giovanardi Rossi,

Case M Corinna



derealisation

* * no informatio



13/26


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TABLE 2

Summary of case reports of patients with a loss of visual imagery on a


Trauma/

precipitatingstressful event

Neuropsychiatricconditions Brai n damage

Other neurologicaldeficits

Visual

perception ofdreams

Stengel,

Case 1

1948 M 63 (?) * (?) right hemianopia no

information

Stengel,

Case 2

1948 M 68 (?) depression (?) right hemianopia no

information

Boyle & Nielsen,

Case ES

1954 M 31 * bilateral occipital (?) left hemiparesis,

papilledema

no

information

Macrae & Trolle,Case 1

1956 M 32 * bilateral parietal (?) none preserved (?)

Beyn and Knyazeva,

Case Ch

1962 39 * bilateral occipital right hemianosia,

right superior

quadrantopia

no

information

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



15/26

TABLE 2 (Continued)


Trauma/

precipitating

stressful event

Neuropsychiatric

conditions Brain damage

Other neurological

deficits

Visual

perception of

dreams

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

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

Levine et al.,

Case 2

1985 M 43 * bilateral parieto-

occipital

right homonymous

hemianopia, right

hemiparersis, right

hemianesthesia

no

information

Grossi et al.,

Case AP

1986 M 56 * left temporo-

occipital

right hemiparesis,

right superior

quadrantopia

no

information

Chiacchio et al.,Case BL 1987 M 58 *

left occipital r ight homonymushemianopia noinformationDownloadedby[189.170.4.149]at21:0921September2012


16/26

TABLE 2 (Continued)


Trauma/

precipitating

stressful event

Neuropsychiatric

conditions Brain damage

Other neurological

deficits

Visual

perception of

dreams

Farah et al.,

Case RM

1988 M 64 * left occipital and

medial temporal

regions

right homonymus

hemianopia

no

information

Riddoch,

Case DW

1990 M 71 * left temporo-parietal right-sided

hemiplegia, right

homonymus

hemianopia

no

information

Goldenberg,

Case K. Qu


occipital

right homonymus

quadrantopia

no

information

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

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



17/26

TABLE 2 (Continued)


Trauma/

precipitating

stressful event

Neuropsychiatric

conditi ons Brain damage

Other neurological

deficits

Visual

perception of

dreams

Zago & Policardi,

Case ZB

1996 M 67 * left fronto-temporo-

parieto-occipital,

cortical, and

subcortical

slight right

hemiparesis

no

information

o

Zago et al.,

Case

Michelangelo

1997 M 44 * temporal bilateral none no

information

a

Moro et al.,

Case 1

2008 F 29 * left middle and

inferior temporalgyrus

none no

information

o

ac

Moro et al.,

Case 2


occipital, left medial

and superior parietal

lobe

none no

information

o

a

c



18/26

TABLE 3

Summary of case reports of patients with a loss of visual imagery with u


Trauma/

precipitatingstressful event

Neuropsychiatricconditions Brain damage

Other

neurologicaldeficits

Visual perceptionof dreams

Typ

visuad

Brain,

Case 1

1954 M 36 nevrotic traits (?) probably frontal

damage

none loss of the visual

element of

dreaming

objects

faces

Brain,

Case 2

1954 M 50 depression frontal none no information objects

faces

Botez et al.,

Case 1

1985 M 38 none right hemisphere (?),

corpus callosum (III

posterior) (?),

dysgenesis (?)

none restriction of

visual dream

imagery

objects

faces

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

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

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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 congruentwith 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 withdepersonalisation 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 BB I 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 toexplain 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 thatshe 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




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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 interferewith 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 ImageryQuestionnaire (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 areatraditionally 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 inliterature 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 themajority 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

Salpetriere 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 THEORGANIC/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.




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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 staticneuroradiological 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

500 ZAGO ET AL.



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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. Thecomparison 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 2010Revised manuscript received 7 January 2011

First published online 23 May 2011

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Zago Stefano Et Al - Is Charcot and Bernard Case of Loss of Visual Imagery_neurological Impairment