c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

Available online at www.sciencedirect.com

ScienceDirect
Journal homepage: www.elsevier.com/locate/cortex

Special issue: Historical paper

The construction of anosognosia: History and

implications

a and German E. Berrios b,*
Ivana S. Markova
a
b

Centre for Health and Population Sciences, Hull York Medical School, University of Hull, UK
Department of Psychiatry, University of Cambridge, UK

article info

abstract

Article history:

The construction of anosognosia as a clinical disorder resulted from the convergence (in

Received 5 February 2014

the work of various writers and culminating in Babinski) of a name, a concept, and a

Reviewed 4 April 2014

clinical phenomenon. During the early stages of this convergence, unawareness of

Revised 16 June 2014

neurological dysfunction was not considered as an independent clinical phenomenon.

Accepted 12 September 2014

Started in the work of Anton, the process of separating it as a differentiable clinical state is

Published online 30 September 2014

completed by Babinski who reaffirmed the semiological independence of unawareness.

The history of the construction of anosognosia parallels the late 19th century debate on

Keywords:

the nature and brain inscription of the concept of consciousness.

Anosognosia

2014 Elsevier Ltd. All rights reserved.

Unawareness
Neurological dysfunction
Anton
Babinski
von Monakow
Insight
Neuropsychology

1.

Matters historiographical

The celebration of the centenary of anosognosia (Babinski,

1914) provides an opportunity to revisit the history of its
construction.1 This is no easy task for from its inception
anosognosia2 has: 1) shown permeable boundaries allowing
for the accumulation of all manner of clinical descriptions and
explanatory hypotheses; 2) been definitionally reliant upon
concepts such as awareness, consciousness, and knowledge
whose definition, structure and content are known to have

changed during the last century; 3) included clinical phenomena3 with vague ontology4 (i.e., are they best defined as
events or as natural kinds?) and; 4) made use of explanatory
mechanisms ranging from agency to passivity (is anosognosia
the result of denial, self-deception,5 disconnection or
disruption of brain pathways?).
To deal with the historiography of such a nebulous clinical
notion the historian needs to resort to categories borrowed
from the sociology of knowledge6 and make use of a
convergence model. According to the latter, clinical categories result from the conjunction, at a given historical time,

* Corresponding author. Department of Psychiatry, University of Cambridge, Cambridge CB215DL, UK.

E-mail address: geb11@cam.ac.uk (G.E. Berrios).
http://dx.doi.org/10.1016/j.cortex.2014.09.011
0010-9452/ 2014 Elsevier Ltd. All rights reserved.

10

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

of a behaviour, a term, and a concept (Berrios, 2011).7 This

approach is adopted here and examples of illustrative clinical
cases8 are summarised under each of these headings. Convergences are historical events and hence a historical context
will be briefly provided.

2.

The historical background

Anton, Babinski and the other writers who were involved in

the construction of anosognosia thought and wrote during a
specific historical period. Their work can only be understood if
something is known about their conceptual milieu. Twentyfirst century views on awareness and consciousness are not
helpful in this regard.9
Scholars agree on the view that the concept of consciousness (in the sense in which this notion is understood
nowadays) is absent in Plato and Aristotle (Cancrini, 1970;
Ellrodt, 1983). This claim can be variously interpreted. If it is
assumed that consciousness is a thing or state necessarily
generated by the brain (and on the assumption that brains
have not changed since Classical times) then, it could be asked
why was it not possible for Plato or Aristotle to discover it or
describe it. If, on the other hand, it is posited that consciousness is a construct then it has to be asked what mind
concepts and other cultural factors were present in Classical
Greek thinking that made the concept of consciousness either
redundant or impossible.
The history of the construction, or invention (as it has
been aptly called by Balibar, 2013) of the concept of consciousness in Europe since the 17th C is long and tortuous
(Brain, 1958; Clarke & Jacyna, 1987; Williams, 1958). In Descartes and Locke the term consciousness refers to that act
whereby man gets to know (becomes aware of) the world
around and himself. Hence, it is used in a predominantly
epistemological sense. It was not meant to refer to a mental
faculty or power, to a circumscribed thing which in the
fullness of time might be considered as the specific function
of a brain structure or network.
The concept of consciousness was fully psychologized
only during the 19th century. In practice, this meant that in
addition to being a metaphysical or epistemological notion
(Shepherd, 1915) consciousness started to be considered as a
central component of the mind and hence of the brain. This
made possible the development of germane notions such as
self-reflexion (Janzen, 2008) and of research methodologies
such as introspection (Danziger, 1980). This process reached
its culmination in the work of Laycock (1845; 1869) who
expressed the view that consciousness was sited in the cranial
ganglia, was a mere accompaniment of perception and hence
had no causal role.
In conceptual terms, the 19th century entertained a
reworded version of the old Aristotelian dilemma (Caston,
2002) about the nature of consciousness. Was it: a) an independent mental function (Consciousness Type1) and hence
needed to be inscribed in a dedicated region of the brain or b)
just a secondary feature, an epiphenomenon that appears
associated with each mental function or sensory organ (Consciousness Type2)10 (Hamilton, 1877). The fact that C1 could
lead to an infinite regress,11 convinced some to opt for C2. Both

options, however, generated different models of anosognosia.

In normal functioning, according to C1, the brain region where
consciousness was sited required to be connected with each
other sensory region (this connectionism is typical of Wernicke's model). Hence anosognosia was to be explained as a
disconnection syndrome.12 In the case of C2, anosognosia
required a different explanation and soon enough various
were marshalled such as partial lesion, sensory disorder,
memory disorder; and after the advent of Freud, concepts
such as denial and suppression (illustrations for these
explanatory models are provided below).

3.

Anosognosia: the behaviours

Descriptions of patients showing unawareness of neurological dysfunction (e.g., blindness, Redlich & Dorsey, 1945) can
be found before Babinski coined anosognosia in relation to
hemiplegia. Amongst others, unawareness was reported in
relation to blindness (Anton, 1899; Dejerine & Vialet, 1893; von
Monakow, 1885; Redlich & Bonvicini, 1911), deafness (Anton,
1899) and alexia (Bonhoeffer, 1903).
In the context of searching for correlations between clinical findings and brain lesions von Monakow (1885) described
4 patients with cortical blindness.
Case 1.
70 year old man who had been well until 4 years prior to
admission when he developed severe nose bleeds followed
by a left sided facial paralysis, left hemiplegia and mild
dysphasia. He had visual hallucinations and some visual
impairment. He recovered but was left with mild gait unsteadiness, mild visual impairment and subtle intellectual
impairment. The next year, following an epileptic seizure
he developed mild left sided facial and limb pareses and his
visual impairment became more obvious. Again he
improved and remained relatively well for 2 years. He then
began complaining that his eyesight was worsening and he
was experiencing difficulty with writing. At that time, he
complained of a thick fog in front of his eyes e blaming this
on bad weather. Ophthalmological examination was
normal. The next month following another apoplectic
attack he became completely blind as well as suffering
visual hallucinations, mobility problems and speech
problems (he could not understand the spoken word). His
mobility improved quickly. However, his blindness
remained and from this point on he was not aware of his
blindness. Initially he thought that he was in a dark pit or
cellar and shouted for light and fire. Later, he appeared to
have got accustomed to the visual hallucinations and so
the notion that he could not actually see anything did not
reach his awareness. He complained that he was old, stupid and weak e but he never articulated that he was blind.
This, together with the speech problem, gave the impression that he was totally confused and disorientated and
robbed him of the possibility of making sense of his environment. He often believed that he was outside the home
and demanded to go home. Although remaining well
kempt, empathic, and at times able to speak coherently,

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

his nights became disturbed and his agitation increased

such that he needed admission. On admission he appeared
friendly, with normal mood and was cooperative. He
expressed some correct phrases but had no idea where he
was. When questioned, he answered readily and in a correct form e except that his answers did not relate at all to
the questions. He walked into the admission room without
bumping into anything and was able to find the door. On
examination his left pupil was larger than the right and
only weakly reactive. His right pupil was of average size
with some impairment of reactivity but better than the left.
He had left ptosis and drooping of the left side of mouth.
Ophthalmological examination was impossible because of
his agitation. His gait was slightly unsteady and he was
dragging his left foot. He seemed to retain good sensation.
His word deafness limited the examination. He recognised
objects by touch and his wife by handshake and stroking.
He had good vocabulary and used words correctly. His
hearing was good. When spoken to, he was aware of this
and made the effort to try to understand e but his answers
betrayed the fact that he had not understood one word. It
was as if one spoke in a foreign tongue to him. He seemed
to still hear voices but it was not possible to establish this
with certainty. He did not react or blink when a fist was put
close to his eyes in a threatening way. When a flame was lit
in a dark room, his right pupil reacted but he did not fix his
gaze on the light. He could not eat by himself e he tapped
the spoon next to the plate and food in an aimless fashion.
When given food in his hand, he would eat it. His facial
expression was that of a blind person but not unintelligent.
What he saw e did not enter his awareness or had only a
general meaning for him. Whilst he would complain of
clumsiness or stupidity, his blindness never entered his
awareness. Until his death, he continued to show warm
interest in people around him, would worry about his
family and enter into their concerns. He retained a good
memory for events in the past. He showed good reasoning
and had no delusions. He did not lose all insight (Einsicht)
into his psychological weaknesses.
Following the patient's death, von Monakow carried out an
extensive post-mortem study of the brain describing in detail
the macroscopic and microscopic results and relating these to
the clinical findings. Whilst clinically highlighting the fact that
the patient showed unawareness of his blindness, this was
not viewed as a separate phenomenon as such, but as part of
the pathology relating to the blindness (that is, the C2 model
was followed).
Case 2.
60 year old man, had dementia with cortical blindness
[but no mention was made concerning whether or not he
had awareness of his blindness].
Case 3.
48 year old woman, developed cortical blindness in the
context of multiple pathologies including psychosis,

11

dementia and tumour. She had an apoplectic attack, lost

consciousness and subsequently went blind. Perhaps she
was able to recognise light. She did not fix her gaze on
things. When someone reached something out to her, she
would grasp next to it. She appeared not to be aware of her
blindness but it was not possible to establish this with
certainty. She answered all questions with I don't know or
there is a fog. Again lesions in both occipital lobes.
[von Monakow concluded that she probably lacked insight
(Einsicht) into her state]
In contrast to cases 1e3, the fourth patient developed
blindness not as a result of occipital lesions but in the context
of long standing degeneration of the optic nerves.
Case 4.
42 year old man, previously fit, admitted to hospital in
January 1884. Eight years ago he had experienced a strange
attack awaking one night with pressure on his chest, acute
fear and dizziness. He did not lose consciousness. The next
morning he complained of reduced acuity in his right eye
and had a right ptosis. His vision slowly got worse. In 1879
he saw the ophthalmologist who diagnosed optic atrophy
and chorioretinitis in the macula. He was psychologically
well at this time. In 1881 he became irritable, forgetful and
had disturbed sleep. One year later, his speech tone altered
and became laboured. He developed motor weakness in his
legs and an ataxic gait. Six months prior to hospital
admission, he became manic, overactive, buying useless
things, burning money, etc. His vision deteriorated,
extending to his left eye and he became totally blind in the
right eye. He could only dimly recognise objects around
him. He had vivid visual and auditory hallucinations,
hearing the police, believing he was being poisoned and
that his legs and head were stolen, etc. Six weeks prior to
hospital admission, he became totally blind, sustained an
apoplectic attack causing left sided weakness of facial
nerve and tongue. This improved but he remained
confused and his ataxia was so bad that he was completely
uncoordinated. Whilst initially he complained of his eyes
being covered or that he was stuck in fog, shouting for light
and fire, later he did not worry about his blindness and
appeared not to be aware of it. On admission, he was
confused, disorientated, agitated and talking nonsense.
Occasionally he was able to answer correctly. He expressed
delusions. He recognised his family by voice and was able
to talk some sensible things with them. He had a right
sided ptosis and both pupils were fixed and dilated with no
reaction to light. His lower limbs were ataxic and he
couldn't stand or walk. He died soon afterwards e fluid in
the lungs.
Thus of the 4 cases of cortical blindness, two patients were
unaware of their blindness and one was possibly unaware.
The clinical descriptions were detailed and hence the unawareness was described as part of the clinical presentations.
The anatomico-pathological associations that were described
related to the cortical blindness and there was no indication in

12

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

the descriptions that the unawareness was viewed as a

separate phenomenon, one that could be studied clinically or
localised to brain/neuronal systems.
Similarly, Dejerine and Vialet (1893) reported:
Case 5.
^tre, had become blind
64 year old man, in-patient at the Bice
5 years previously. Information about his background was
given by his wife. His father had been fit and died at 70
years. His mother was alcoholic and died in a mad state

ne

e) at 37 years. The patient was an ex-soldier and had
(alie
always been active. His memory was intact and he was of
high intelligence. He married at 30 and his wife said that
ever since she knew him he had been a heavy drinker.
Seven years previously e since 1883 e he suddenly became
suspicious of his wife, accusing her of being unfaithful and
would not allow her to talk to or even see visitors. At this
time he was suffering frequent falls. He complained of
having a spot in his eye and had to stop working as a tailor.
In 1885, he suffered two apoplectic attacks. Loss of consciousness was not longer than half an hour. Following
these, his gait became unsteady but no hemiplegia. The left
side was weaker. He never developed aphasia. He retained
memory for people and objects. He wanted news of his cat,
his hens etc. each time his wife came to see him. He led a
^tre, even working in his old trade of a
peaceful life in Bice
tailor. In 1888, whilst in the middle of sewing he suddenly
lost his vision. This happened without any paralysis or loss
of consciousness. He was transferred to the chronic ward
for repeated examinations. His last complete examination
was in 1890. At this time he was lying in bed, his eyes open,
gaze vague. He directed his eyes from side to side without
fixing on anything. The strange thing was that even though
he no longer could distinguish anything, he did not want to
admit to his blindness. When presented with an object and
asked to name it, he did not hesitate and gave it a name
which bore no relation with the object he was shown, e.g.,
an inkwell was a diamond. He took the course of not
admitting that he could not see. When told of his error in
naming things, he excused himself on the grounds that he
had a tear in his eye which prevented him from distinguishing things properly. He was unable to distinguish
the door, the window, but was able to use his hearing and
touch to compensate for his lack of vision. When given a
quill in his hand with the request to dip it into the inkwell
he could only find this after a long time of tapping around
on the table as if in complete darkness. If asked to write his
name, pressing his hand on the paper, he wrote the words
superimposed on one another and when he came to the
edge of the paper he continued to write on the table itself.
Detailed examination of his vision showed his pupils to be
dilated and reacting normally to light. It was not possible to
test accommodation because all types of fixation were
abolished but there was constriction on convergence when
he was asked to look at his nose. The retina was anaesthetic apart from a small upper section on the left which
retained weak sensation. Corneal and conjunctival sensations were preserved. Ophthalmological examination was
normal. He had bilateral mild hearing loss and normal

taste and smell. He had normal speech and no word

deafness or problems with writing. His gait was that of a
blind man, walking carefully with his arms in front and the
slightest shove would make him stumble.
Again the clinical description was detailed and his unawareness of blindness was viewed almost as an incidental
albeit curious finding. As with von Monakow's cases, the unawareness was not viewed as an independent phenomenon
for which brain localisation was sought. Instead the focus was
on localising the lesion causing the cortical blindness as a
whole (bilateral lesions in the occipital lobes and degeneration
of association fibres).
Such case descriptions provide evidence that clinical states
or behaviours which now would be termed unawareness of
dysfunction or Anton's syndrome or anosognosia were being
observed and described. They were not however singled out
from the rest of the clinical observations but were simply part
of the general descriptions of patients with specific neurological diseases. Hence, they were not conceptualised as independent phenomena and focus instead was on determining
the neuro-pathological lesions relating to the neurological
disease as a whole. The historico-scientific context is relevant
in this regard. In the 1880s through his experiments with
cortical lesions on dogs, Hermann Munk, professor of physiology in Berlin had developed the notion of Seelenblindheit
(psychic blindness) e a visual agnosia where as a result of
occipital cortical lesions, visual images or memories were lost
(Finger, 1994). This concept soon became a focus of much
debate (e.g., Freund, 1889; von Monakow, 1885; Muller, 1892;
Hahn, 1895). Later on, Anton used the phrase seelenblind fur
ihre erblindung (Anton, 1899, p104) (psychically blind [visual
agnosia] for her blindness) to describe his patient with cortical
blindness.

4.

Anosognosia: the concept

Studying the embedded concept helps the historian to date

the convergence and to understand intellectual undercurrents.13 In this regard, it was Anton who conceptualised
the clinical phenomenon under study as a lack of selfawareness (Selbstwahrnehmung) of the neurological dysfunction. In his 1899 paper he reported two patients with cortical
deafness and one with cortical blindness.
Case 6.
64 year old man who developed deafness and psychological / personality changes following a head injury several
years previously. On admission to hospital he was agitated
and over-talkative. He was orientated in place and
recounted his general background spontaneously and
correctly but jumped from topic to topic. It was immediately obvious that the patient did not react to sounds, even
very loud noise next to his ear. It was also apparent that he
was not putting any effort into trying to hear or understand
the questions put to him. He did not react to questions but
related to gestures. When the ear was pointed at or a
listening gesture performed, he explained that he was

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

hearing bells from his home and that he heard people

shouting loudly at him. He had auditory hallucinations and
responded angrily to these. He believed that enemies
outside heard everything that he said. He repeated words
and sentences and sometimes he used newly created
words. Instead of naming objects, he used circumlocutions. It was possible to communicate with him by writing.
He claimed that he could write in German and Latin and
that he had read many books. In fact, he read badly and
mis-read words. When asked, by writing, about his deafness he insisted vehemently and irritably that he was not
deaf and that he heard everything well. When his attention
was drawn, through writing or through listening gestures,
his auditory hallucinations came immediately and vividly
to the fore. He was never aware, however, of noises that
were deliberately produced around him. He managed to
copy but spontaneous writing often produced nonsensical
or incorrectly written words. He blocked his ears with
cotton wool, tying bandages around them and became
distressed when attempts were made to remove these.
With fellow patients it was also obvious that he never
reacted to their comments but was constantly talking, not
allowing any interruption to his flow of thoughts. It never
occurred to him that he was not taking anything in when
other patients were talking to him. He constantly reiterated
that he was not deaf, that he heard everything and that he
understood well and that if he were deaf then he would not
hear all the abuse (auditory hallucinations). Examination
showed him to have normal eardrums but he was
completely deaf. He was oversensitive to examination e
even a light puff of air caused him to resist and demand
that people did not shout so much in his ear. He knew how
long he had been at the clinic, he recalled previous examinations, he knew that he was in a mental illness unit and
knew that people thought he was mentally unwell. He
insisted that he was not confused, that he was much
cleverer than the attendants. He spontaneously expressed
delusional ideas that people wanted to steal his inheritance; that people could hear his thoughts, and that even in
Vienna people knew his name.
Case 7.
56 year old lady with cortical blindness. She had a 4 year
history of personality change and had been unable to work
for the last 2 years. She had poor mobility on account of
pain. At interview, it was obvious that she was having
difficulty in remembering words and used circumlocutions. She noticed that she used wrong words and became
upset and agitated. She was better with spontaneous
speech following her own thread of thought. She became
completely blind and could not distinguish between darkness and light. She did not react to intense light or to objects placed close to her. Her gaze was directed into the
distance and she did not fix onto objects. What was striking
was that she took no notice of her blindness and was not
bothered by her visual loss. She identified objects by touch
and made no effort to visualise them. When asked directly
about her vision, she would answer vaguely and in generalities e.g., it is just so, one sees better in one's youth. She

13

insisted that she did see the objects in front of her (despite
daily examinations disproving this). She also claimed that
she saw objects not presented to her. She was not aware of
her visual loss and this did not cause her concern or
distress or preoccupation. Her word finding difficulties
however did cause her obvious distress. She had lack of
spatial orientation but was able to localise touch, pain and
own body parts. She recognised people by voice and touch
but made no attempt to build up a visual image.
Case 8.
69 year old lady with cortical deafness. She was admitted to
the psychiatric unit because of confusion and agitation. At
that time she experienced a strong feeling of illness
(Krankheitsgefuhl) which later disappeared. She soon
became more settled. Upon admission it was evident that
she did not understand the spoken word and neither by
turning her head nor by answering did she react to this. Nor
did she react to clapping or loud noises or to shouting close
to her ears. Likewise she did not respond to bone conduction. She showed no understanding or interest in the examination. Her spontaneous speech was and remained
significantly impaired. She frequently chose wrong words
to express herself though sometimes she would start with
the right beginning of a word. Her speech showed
abnormal grammatical construction. She could read relatively well and this together with gesturing was the only
way communication could occur. She frequently repeated
syllables and words. She recognised people around her by
sight and named objects put before her mostly correctly.
She was also able to find the right name for touch and body
sensation. She complained frequently of her bronchitis as
well as her short-sightedness. Concerning her hearing loss
however she never complained and remained completely
indifferent to it. During conversations she was also never
aware that she could not hear nor understand the questions put to her. What she answered was nothing other
than a continuation of her own thoughts. She was
repeatedly asked (by writing) whether she could hear and
she firmly answered that she could hear well. It was
remarkable that despite the severe unawareness of her
hearing loss, she was aware of her problem with using
wrong words and tried to correct this.
Anton tried to relate these clinical states to detailed postmortem findings in an attempt to determine the relationship
between unawareness of the neurological dysfunction and
damaged brain areas. In contrast to the earlier descriptions
found in von Monakow or Dejerine, he differentiated the
unawareness of dysfunction as an independent symptom or
state and conceptualised it as a phenomenon in its own right.
This, he sought to understand clinically, by exploring in more
detail patients' descriptions and behaviours, as well as pathologically by seeking to link these with neuro-anatomical
changes. He emphasised the selective nature of the unawareness, that is, patients were unaware of their hearing or
visual loss but were distressed by relatively minor problems
such as word finding difficulties; and observed that the unawareness might encompass more than the hearing or visual

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c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

function. For example, in the cases of hearing loss, it was not

just that the raw material of hearing was lost but that the
patients seemed to have lost the memory of having been able
to hear before, and all associations with hearing from the past
(e.g., she did not behave like a deaf person but like a person
who had never heard in her life, differentiating this from
auditory agnosia [Seelentaubheit], p115). Hence, patients did
not appreciate that they had a lack of hearing. He pointed out
that this was different from patients with peripheral hearing
loss where they missed not being able to hear. Interestingly,
this same point was made by Bonhoeffer (1903, p594) in relation to a patient with unawareness of his alexia: [he] did not
behave like someone who could not read he did not have
the awareness that he could not read.
This broader conceptualisation of the phenomenon guided
his interpretation of post-mortem findings. Because the unawareness of dysfunction involved other psychological processes it could not be caused by a single cortical lesion (e.g., of
the auditory centre) but association fibres to other parts of the
cerebrum had to be damaged resulting in disconnections between peripheral and central tracts.
Why did Anton focus specifically on this aspect of the
clinical presentation, differentiating it from the other behaviours, and conceptualising it as an independent phenomenon? In contrast to the cases described earlier where the
unawareness of dysfunction was simply a behaviour/clinical
state that was noted along with the other clinical observations
around a particular neurological condition (e.g., von
Monakow, 1885), Anton singled out the unawareness of
dysfunction as a phenomenon in itself e to be localised in the
neuronal system.
Gabriel Anton (1858e1933) studied medicine in Prague and
under the influence of Anton von Hans Chiari and Arnold Pick
he developed early on an interest in the anatomical investigation of the brain. This was consolidated further when he
moved to Vienna in 1887 to work in the psychiatric clinic with
Theodor Meynert. In 1894 he took up the chair at the University of Graz, and as director of the psychiatric and neurological
clinic before being called to the University of Halle in 1905
following the death of Carl Wernicke. Anton's focus on finding
neuro-anatomical concomitants of clinical presentations can
thus be understood in the drive at the time to determine the
neuro-pathological bases to neurological/psychiatric syndromes (Lanczik & Keil, 1991; Marx, 1970; Seitelberger, 1997).
It is possible that Anton's conceptualisation of unawareness of dysfunction as an independent phenomenon might
have been influenced by Pick's earlier ideas on awareness and
insight into madness (Pick, 1882). At this time in 1882, Anton
was working as Pick's assistant in Prague before moving to
Vienna in 1887 (Kumbier, Haack, & Herpetz, 2005). Indeed,
Anton's use of the term feeling of illness (Krankheitsgefuhl) in
case 8 above may have come directly from Pick. Pick had
explicitly focused on awareness of illness (Krankheitsbewubtsein) in relation to mental illness and conceived of
this as a broad concept constituted by i) a feeling of illness
(Krankheitsgefuhl) and ii) insight into illness (Krankheitseinsicht).
Pick viewed the former concept as an alteration in the feeling
or sense of well-being e which he related to the disturbance of
Gemeingefuhl.14 On the other hand, insight into illness was the
product of reason and reflection (Pick, 1882).

5.

Anosognosia: the term

Of the three components of a convergence, terms are probably

the least interesting. This is because by then the structure of
the phenomenon in question is already, more or less, formed.
It matters little whether the new convergence is called by a
neologism, a recycled term, an eponym or a number.15 In his
1914 paper Babinski drew attention to a mental disturbance
(trouble mental) occasionally seen in cerebral hemiplegia in
which patients ignored or appeared to ignore the existence of
the paralysis affecting them.
Case 9.
Woman affected by left hemiplegia for several months. Her
intellectual and affective faculties were mostly preserved
and she had no difficulty remembering past events. She
expressed herself correctly and was interested in people
around her and in current events and had no hallucinations or confusion. She related to her family in the same
way as she had prior to her stroke. However, in contrast to
the preserved intellect she appeared to ignore the existence of her hemiplegia. She never complained of it or
alluded to it. If she was asked to move her right arm, she
did so immediately. If she was asked to move her left arm,
she stayed immobile and quiet and behaved as if the
question was addressed to someone else. Sensation in her
paralysed limbs was impaired but not abolished. She could
feel passive movements and sometimes complained of
pain in her left shoulder.
Case 10.
Woman with a left-sided hemiplegia following a stroke
who presented similarly. She also had no confusion, hallucinations or confabulation. However, she was apparently
slightly over-excited and, according to her maid who had
known her for years, would make some inappropriate
comments. Her memory was excellent and conversation
was lively and interesting. When she was asked what was
bothering her, she would respond that she had back pain or
was suffering from an old phlebitis e but she did not
complain at all of her paralysed upper limb. When asked,
she carried out all movements in her right arm but when
asked to move her left arm she either did not answer or
said simply that it was done. Electrotherapy was discussed
in front of her and she later asked the doctor why electrotherapy was being suggested for her e as she was not
paralysed. This patient also had loss of sensation in her
limb and did not appear to perceive passive movements.
Babinski (1914) proposed the term anosognosia to refer to
the lack of knowledge patients had concerning their hemiplegia; and anosodiaphoria to name the indifference or lack
of concern shown by other patients who appeared to
acknowledge the existence of their paralysis. Due to the
persistence of the phenomenon he ruled out as unlikely the
possibility that the phenomenon was feigned,16 as might
happen in patients who through pride hid or disguised their

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

disability. He believed that anosognosia was linked to right

cerebral lesions and that sensory impairment might be an
important factor in its development.
In the debates that followed Babinski's presentations (1914,
1918) it was suggested (e.g., by Pierre Marie and Gilbert Ballet)
that this phenomenon, anosognosia, also occurred in other
neurological dysfunction such as blindness and the role
played by sensory impairment was discussed.17 Quoting from
his 1905 paper, Henry Meige reported that in some patients
there was a lack of memory for movement (terming these
functional motor amnesias) and argued for a broader conceptualisation of the phenomenon. Evocative of Anton's and
Bonhoeffer's descriptions he emphasised that it was as if the
paralysed limb had never existed (our emphasis).
Whilst the eponym Anton's syndrome is often used to
refer to unawareness in relation to blindness (Albrecht, 1918)
and Anton-Babinski syndrome for unawareness in hemiplegia (Kumbier et al., 2005), anosognosia in general has
come to signify the state of unawareness of a neurological
impairment including aphasia (Rubens & Garrett, 1991),
hemiballismus (Roth, 1944), amnesic syndromes (McGlynn &
Schacter, 1989), dementia (Reed, Jagust, & Coulter, 1993), tardive dyskinesia (Myslobodsky, 1986) and deficits following
head injury (Prigatano, 1991), etc.
The coining of the term thus represents the culmination of
a convergence that began with the differentiation of particular
behaviours or mental states, their conceptualisation into a
distinct clinical phenomenon and lastly their naming as
anosognosia. Whilst the term contributes little to the original
concept, it can serve to consolidate and stabilise it as a phenomenon. That anosognosia has survived these hundred
years and continues to be a source of much research is evidence of this. How might the naming of the phenomenon thus
help to achieve this stability? In the case of anosognosia, there
are at least two factors to consider. In the first place, Babinski's
role is important. A contemporary of Anton, Joseph Babinski
(1857e1932) lived and worked all his life in Paris. In 1885 he
^trie
re, working
became chief resident to Charcot at the Salpe
with him until Charcot's death in 1893. From 1895 until his
retirement in 1922, Babinski was Head of internal medicine at

. Although like Anton, Babinski had started his career
La Pitie
in pathological anatomy, his residency under Charcot seemed
to mark a turning point where he changed both direction, to
become a pure clinician interested by semiology, and purpose, to find clinical means of distinguishing organic pathology from hysteria (Philippon & Poirier, 2009, p 133e135).
His focus thus was on detailed clinical examinations with a
view to identifying features or signs that were associated with
organic pathology (but not with localisation of brain function).
This semiological perspective is important here. By focussing
on the fact that there was a relationship between the clinical
observation and the associated organic meaning, it also
emphasised that the clinical sign and the organic association
were separable. In the second place and related to this was the
choice of anosognosia as the name for the phenomenon.
Referring to lack of knowledge of disease, it not only again
emphasised the potential to separate out lack of knowledge
from disease but also suggests a generic use for the term
since disease can refer to other disabilities and not just
hemiplegia.

15

These two factors, namely the semiological perspective

(facilitating the separation between lack of awareness/
knowledge from the pathology) and the generic implication
inherent to the term (allowing reference to disabilities other
than hemiplegia) have likely been crucial for the stability of
the phenomenon. Anton had delineated unawareness of
dysfunction as a distinct clinical phenomenon. Babinski's
anosognosia had implicitly split this into unawareness and
dysfunction. In turn, this has allowed for future research to
focus on unawareness as an object of inquiry e not just as
something in association with different neurological impairments but as a phenomenon to be explored in its own right.

6.

Summary and conclusions

Although the cases reported above all fall within the broad
category of anosognosia they also show a great deal of difference in regards to their background complaints such as
confusion, cognitive impairment and psychotic symptoms. It
is the case that most of these patients seemed unaware of one
of their disabilities, usually a dramatic sensory or motor
disability. Although more than one clinician participated in
the construction of anosognosia, Babinski seems to be the one
celebrated in this context. This may be due to the fact that in
addition to coining the name he offered a semiological
perspective that emphasized the separation of unawareness
as a phenomenon. This has driven much of subsequent
research in this area (Prigatano, 2010) and contributed to its
stability.
The idea that failures of awareness can be an independent
condition has had various consequences. For example, it has
legitimized the idea that awareness (the entity that fails in
unawareness) can be conceptualized and studied as an independent function in neuropsychology (Bisiach, Vallar, Perani,
Papagno, & Berti, 1986; McGlynn & Schacter, 1989). Focussing
attention on unawareness is also likely to have encouraged
detailed clinical observation and this has led to identifying a
host of anosognosia-like phenomena (Cutting, 1978). In the
same vein, the view that unawareness may be an independent phenomenon has opened the door to all manner of accounts including denial (Weinstein & Kahn, 1955) which
radically changes the old meaning of anosognosia by introducing a participatory agency on the part of the person.
There has not been the space here to consider the historical
construction of awareness (or insight) into madness. Debates
concerning the question of patients' awareness or their
madness were already taking place some fifty years earlier

, 2004). Constructed in parallel and arising
(Berrios & Markova
from a different direction and perspective, the phenomenon
of awareness into madness carried a very different structure

, 2005; Markova

& Berrios, 2011). In recent years there
(Markova
has however been a convergence of these approaches with the
assumption that the clinical phenomena of anosognosia and
lack of insight are equivalent (e.g., Mullen et al., 1996). In the
light of the analysis here, the validity of such a convergence
has to be questionable. However, it is only through understanding how a new clinical condition is constructed and
what factors are involved in such construction that sense can
be made of its structure and meaning. For that reason an

16

c o r t e x 6 1 ( 2 0 1 4 ) 9 e1 7

epistemological (a combination of historical, philosophical

and empirical methods) approach to the exploration of clinical
phenomena is essential to understand them and to develop
the right tools for their management.

Supplementary data
Supplementary data related to this article can be found at
http://dx.doi.org/10.1016/j.cortex.2014.09.011.

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