Brain (1988). I l l , 1287-1297

PROSOPAGNOSIA AND AGNOSIA FOR
NONCANONICAL VIEWS
AN AUTOPSIED

CASE

by T. LANDIS, M. REGARD, A. BLIESTLE and P. KLEIHUES
{From the Department of Neurology and Neuropathology Laboratory, Institute of Pathology, University
Hospital, Zurich, Switzerland)

It has been postulated that for prosopagnosia to occur, bilateral lesions of the central visual system
are usually necessary. All but 1 of the 10 previously documented cases that came to autopsy showed
this pattern. However, the long survival period after the onset of prosopagnosia in most of these
patients limits the value of the autopsy findings for clinicopathological correlation. A patient is
presented who died 10 days after she had developed prosopagnosia, topographagnosia and an
agnosia for real objects seen from noncanonical views. These clinical symptoms corresponded
directly to the autopsy finding of a recent large occipitotemporal ischaemic infarct in the territory
of the right posterior cerebral artery. An additional right frontal infarct and a cortical microinfarct
in a deep left lateral parieto-occipital sulcus were both old lesions and had passed unnoticed
clinically. This first report of a direct clinicopathological correlation between a fresh right posterior
lesion and prosopagnosia demonstrates that bilateral involvement of the visual system is not a
prerequisite for prosopagnosia.

INTRODUCTION

Bodamer (1947), following the suggestion by Hoff and Potzl (1937), considered
the inability to recognize familiar faces as a specific agnosia which he named
prosop-agnosia. However, impaired recognition of familiar faces had been noted
long before in patients with disturbed visual recognition from cerebral lesions.
Wigan (1844), Quaglino (1867), Jackson (1876), Charcot (1883) and Wilbrand
(1887, 1892) were among the first to describe this symptom. Its anatomical
correlates, however, have become a matter for discussion. While Bodamer believed
that for prosopagnosia to occur the lesions must be bilateral, Hecaen et al. (1957)
emphasized the crucial role of the posterior right hemisphere lesion. Subsequent
reviews (Gloning et al., 1966; Meadows, 1974a; Benton, 1979; Damasio et al.,
1982) focused on the few pathology reports available (Wilbrand, 1892; Heidenhain,
1927; Arseni and Botez, 1958; Hecaen and Angelergues, 1962; Pevzner et al., 1962;
Gloning et al., 1970; Lhermitte et al., 1972; Benson et al., 1974; Cohn et al., 1977;
Correspondence to: Dr T. Landis, Neurologische Universitatsklinik, CH-8091 Zurich, Switzerland.
© Oxford University Press 1988

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SUMMARY

1288

T. LANDIS AND OTHERS

CASE

REPORT

A 75-yr-old right-handed woman was admitted for evaluation of a left homonymous hemianopia.
Apart from mild hypertension which had been treated for the last 10 years with diuretics, she had
always been well. Two days before admission, while working in her vineyard, she had had two brief
episodes of excessive sweating, nausea and tachycardia. Subsequently she had had difficulty in
finding the way back to her farmhouse. She could no longer recognize relatives visually but identified
them easily by their voices. This caused her no concern but she complained that she frequently
collided with obstacles to her left. On admission she had a complete left homonymous hemianopia,
and slowed optokinetic nystagmus to the left. Visual acuity was 0.8 in the right eye, 0.6 in the left;

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Nardelli et al., 1982). These cases all showed a right medial occipitotemporal
lesion and in all but 2 cases (Hecaen and Angelergues, 1962; Pevzner et al., 1962)
the corresponding area of the left hemisphere was also damaged. It is held
therefore (Damasio et al., 1982) that functionally symmetric damage to the medial
occipitotemporal region is generally necessary for prosopagnosia to occur and
that exceptions to this rule must be rare (Damasio et al., 1986). There is, however,
an increasing number of reports of patients with prosopagnosia who have clinical
as well as radiological evidence only of right posterior cerebral damage (Hecaen
et al., 1956; Assal, 1969; Meadows, 1974a; Lhermitte and Pillon, 1975; Whiteley
and Warrington, 1977; Torii and Tamai, 1985; De Renzi, 1986; Landis et al.,
19866; Michel et al., 1986). Moreover, for most of the cases with prosopagnosia
who came to pathology there was a long delay between the onset of the symptom
and death. Because of the possibility that the lesion on one side may have occurred
after the onset of prosopagnosia such autopsy findings are of only limited
value for clinicopathological comparison and a close temporal correlation seems
necessary for the definitive association of symptom and lesion.
Comparing 22 patients with retrorolandic lesions with prosopagnosia to
393 patients with retrorolandic lesions but without prosopagnosia, Hecaen and
Angelergues (1962) found aphasic defects and alexia less frequently in prosopagnosic patients than in those without prosopagnosia. While alexia and aphasia
are seen with left posterior lesions, prosopagnosia occurs most often with
topographagnosia, dressing apraxia, unilateral spatial agnosia or neglect and poor
nonverbal learning, all of which are associated with right posterior lesions (Hecaen
et al., 1956; Tzavaras et a!., 1970; Meadows, 19746; Landis et a!., 1986a). This
finding emphasizes the importance of right posterior lesions for the manifestation
of prosopagnosia. Patients with right posterior lesions may also have difficulty
recognizing objects photographed from an unconventional angle, but recognize
pictures of objects presented in a canonical view (Warrington and Taylor, 1973,
1978; Riddoch and Humphreys, 1986; Warrington and James, 1986).
We report a patient with an acute onset of prosopagnosia, topographagnosia
and an agnosia for real objects shown in a noncanonical perspective, in whom the
short survival period of only 10 days after a right posterior vascular lesion allowed
a reliable clinicopathological correlation.

PROSOPAGNOSIA

1289

ocular movements were full. The remaining cranial nerves were intact. Primary and cortical sensory
modalities were intact and there was no extinction on double simultaneous tactile stimulation. Gait,
motor strength and coordination were normal. On mental status examination she was alert,
orientated, interested and cooperative, but she showed little concern about her illness. Although
she occasionally cned and scored 10 points on the Hamilton Depression Scale she did not appear
generally depressed. She denied visual hallucinations. Throughout the examination she was
hemianopic and neglected the left half of her visual space. She could no longer recognize relatives
or other familiar persons when she saw their faces, but immediately identified them when they
spoke. She could learn to recognize the hospital staff only by voice, not by face. She was usually
unable to recognize photographed faces of famous people; occasionally, however, she demonstrated
a strange 'paradoxical knowledge' (e.g., confronted with a photograph of J. F. Kennedy she said
'this man could be a relative of Kennedy', or to the Mona Lisa 'this cannot possibly be Mona
Lisa'). Neither in real life situations nor on photographs did she have difficulty in identifying a face
as a face and she never saw faces as distorted. However, she was incapable of putting a face together
from its single features (fig. 1), although she correctly named the parts and knew they should make

a face. She was also accurate in labelling emotional facial expressions on people and photographs.
Thus she labelled an angry face 'a person who is not in the mood to talk", and imitated the
appropriate expression. In a facial sorting test (Regard and Landis, 1986) she identified only
'friendly/unfriendly' out of five possible concepts (emotion, gender, headgear, age, fame). Control
subjects found more than three concepts according to which they can sort these faces. Along with
her prosopagnosia, she also suffered from severe topographagnosia. To find the way back to her
room on the ward, the door had to be marked; she would usually deposit a personal object on the
right side of the door. To find her bed she placed her pillow in the vertical position; if the position
of the pillow was changed in her absence, she did not find her bed. She also confused her glasses
with those of the examiner and insisted on exchanging them.
When shown objects or pictures she always took considerable time for visual inspection and, as
an initial response, usually denied knowing what they represented. However, she correctly named
most of the objects presented in a canonical view, that is in a prototypical representation (fig. 2).
When shown real objects and small-scale models she was unable to identify the noncanonically
presented items (Palmer et ai, 1981) but identified them correctly when the same objects were
presented in a canonical view. When shown, for example, a folded pair of glasses (fig. 2, upper) she
said 'something made of glass'; shown the same glasses in a more canonical perspective (fig. 2,

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FIG. I. Right, correct solution of a face
puzzle. I.cfi, ihe patient's attempt despite
correct recognition of the single parts.

1290

T. LAND1S A N D O T H E R S

lower) she recognized them. When presented with a toy trumpet from the front or from the top she
said 'something made of metal'; when it was shown in a more canonical view from the side she
identified it as a trumpet.
Although she could not identify an object presented noncanonically, she almost always identified
the material out of which it was made and sometimes misidentified it as an object of the same
material, such as a key lying flat in the examiner's hand as tweezers. Similar problems occurred
with photographed objects taken from noncanonical angles, such as those presented by Warrington
and Taylor (1973). When presented, for example, with the picture of a bucket seen from above, she
described it as something which is empty inside and has the shape of a cylinder, but identified it as
a bucket only when seen from the side. She immediately identified all objects by touch. As with the
pictures of famous faces, she occasionally identified the object in a paradoxical way. When, for
example, shown a pen she commented 'this is clearly not a pen', or for an eggbox she said 'a box
made out of cardboard, but not one to put eggs in'. She was unable to identify Swiss currency
unless she touched the coins. Clock reading was impossible and she wore her wrist watch upside
down. From letters made up of small other letters she only identified the small letters; however, in
pictures of overlapping drawings of highly stylized objects (Poppelreuter, 1917) she outlined and
named all objects correctly. Another striking defect was her inability to recognize 'negative shape'.
When shown a newspaper advertisement, where the picture of a car had been cut out, and asked
to guess the missing part, she concentrated on the written legend, read and understood the text
correctly, but was unable to recognize the missing shape as a car. The same happened, for example,
with the advertisements for a hiking boot and bottle. Again she was unable to recognize the cutout shape, despite verbal cues gathered from reading the accompanying text, but recognition
improved when she followed the contours with her finger or when given the positive shape. She
guessed 'foot' or 'hand' for the boot, and the negative shape of the bottle she named 'container
made of glass, to drink out of it'. When the examiner enquired whether she meant a bottle, she
denied it. However, when shown 12 assorted halves of 6 highly stylized canonical views she assembled
and named them correctly. Colour perception was normal; she named and matched colours correctly
and had no problems with the Farnsworth 16 hues test. She matched letters and words written in
various typefaces with ease, had no alexia, and she understood words spelled out loud to her.
However, she was unable to read mirror writing. Her spontaneous speech, repetition, auditory
comprehension and prosody were intact. Naming of definitions, tactile naming and naming of

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FIG. 2. Upper, noncanonical presentation of glasses.
Lower, canonical presentation of the same glasses.

PROSOPAGNOSIA

1291

environmental sounds were normal. Writing was normal except for a left hemispatial neglect. Verbal
memory was good: out of 10 words she learned 9 in 3 trials and recalled 8. She had a severe
constructional apraxia. She was unable to copy or to draw a cube, a bicycle, a clock or a geometric
figure with either hand. She had no buccolinguofacial, ideomotor or ideational apraxia.
The patient died of a pulmonary em bolus 10 days after the onset of symptoms.
Postmortem findings
Massive recent pulmonary embolism was identified as the cause of death. There was an extensive
subacute myocardial infarct in the region of the interventricular septum. The foramen ovale was
patent. Both cardiac ventricles were dilated and the coronary arteries showed a nonstenosing

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FIG 3. Serial drawings of the parietal and occipital lobes. The hatched areas correspond to the recent infarct
in the territory of the right posterior cerebral artery. The arrow indicates an old microinfarct in the left parietooccipital region ( xO.ti).

1293

T

LAND1S A N D

OTHERS

atherosclerosis. The brain weighed 1,231 g. It was fixed in 4% formaldehyde and cut in 4-5 mm
thick coronal sections. Following paraffin embedding, whole brain sections (7 fim) were prepared
using a Jung Tetrander microtome. Sections were stained with haematoxylin and eosin and luxolNissl. Morphological analysis revealed a large recent infarct in the territory of the right posterior
cerebral artery (fig. 3), extending from the level of the splenium of the corpus callosum to the
occipital pole. The rostral portion of the infarct involved the parahippocampal gyrus. The infarct
largely corresponded to the anatomical distribution of the right posterior cerebral artery. There was
no evidence of collateral blood supply via meningeal anastomoses from the anterior or middle
cerebral artery. The entire visual cortex (areas 17 and 18) was therefore included in the infarction.
Histologically, there were typical features of a recent infarction with eosinophilic neurons, loss of
Nissl staining and a spongy demarcation from adjacent brain structures. The border zone showed
marked vascular proliferation and macrophages as early indicators of resorption of the necrotic
tissue. These changes were compatible with the clinical observation of a stroke 10 days before the
patient's death.

FIG 4. Coronal section through the cerebral hemisphere at the level
of the anterior commissure. The old infarct in the right inferior frontal
gyrus is marked black.

DISCUSSION

The patient described had an acute onset of prosopagnosia, topographagnosia,
agnosia for objects presented noncanonically and paradoxical visual knowledge.
Autopsy 10 days after the event revealed a recent large ischaemic infarct in the
territory of the right posterior cerebral artery. The short time lapse between the
onset of these symptoms and autopsy and the absence of other recent lesions in
this case make the correlation between the right posterior lesion and the
symptomatology highly probable. In the previous cases of prosopagnosia which
came to autopsy a causal connection could not be established directly because of
a long delay between onset of symptoms and autopsy. This is perhaps best
illustrated by the second patient described by Cohn et al. (1977). They state
'following the first episode, there were several other insults that left him blind'
(p. 180). Clearly, the bilateral posterior lesions which were present at the time of

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In addition to this large recent infarct there were two circumscribed old vascular lesions. A Ushaped infarct was located in the right inferior frontal gyrus at the level of the anterior commissure
(fig. 4). Histology revealed an old lesion with almost complete resorption of the necrotic tissue. A
cortical microinfarct (diameter approximately 2 x 5 mm) was present in a deep lateral panetooccipital sulcus of the left cerebral hemisphere (fig. 3, arrow). This lesion, too, was old, appearing
as a small glial scar.

PROSOPAGNOSIA

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autopsy in this case cannot be taken as proof that functionally symmetric medial
occipitotemporal lesions in the visual system are necessary for prosopagnosia to
occur.
In addition to the recent large right posterior symptomatic infarct, we found in
our case two additional old lesions, which were apparently clinically silent. One
was a cortical microinfarct in the left lateral parieto-occipital area, the other a
right frontal infarct. The left hemisphere microinfarct was much smaller than, but
in a similar location to the lesion in the case described by Pevzner et al. (1962).
Their patient showed at autopsy (4 years after the event), in addition to the typical
right posteromedial infarct, a clinically silent left hemisphere posterolateral lesion
in the middle of the inferior parietal lobule, angular gyrus, and upper part of the
superior temporal sulcus. In their case the lesion was described as slight atrophy,
gliosis and rarefaction of cells. Whether this left posterolateral pathology, however
small and clinically silent, is a necessary prerequisite for prosopagnosia to occur
or is just an incidental finding must remain open. It is, however, certain that in
these 2 cases the lesions, though bilateral, are not symmetric. Benson et al. (1974)
and Meadows (1974a), from their analysis of the few available pathology reports,
emphasized the role of the right inferior longitudinal fasciculus, and Benson et al.
(1974) envisaged a combination of a lesion of this structure with a lesion of the
splenium of the corpus callosum as the possible neuroanatomical basis of
prosopagnosia. As our case demonstrates, a single large lesion in the territory of
the right posterior cerebral artery can damage both of these crucial fibre tracts.
This view is supported by the increasing number of clinical reports of prosopagnosia
subsequent to right posterior cerebral lesions without clinical or radiological
evidence for additional left posterior damage (Whiteley and Warrington, 1977;
Christen et al., 1985; Torii and Tamai, 1985; De Renzi, 1986; Landis et al., 19866;
Michel et al., 1986).
The detailed pathological analysis of the posterior brain in our case shows
virtually complete destruction of the right striate and peristriate cortex. The entire
remaining visual recognition, therefore, was carried out by the primary and
associative visual areas of the left hemisphere. Our patient was able to read and
to recognize objects as long as they were presented from prototypical views. She
was not, however, able to recognize faces (prosopagnosia), or places (topographagnosia) well known to her, nor was she able to recognize objects presented
noncanonically. The isolated left hemisphere visual areas were thus not able to
analyse the entire visual world. They appeared capable of visual categorization
(e.g., to recognize a face as a face) but were unable to detect individuality (e.g.,
whose face) within a category. Moreover, they were only capable of categorizing
objects within the narrow range of a canonical representation. Both phenomena,
namely, impaired recognition of identity within a category (Lhermitte et al., 1972;
Whiteley and Warrington, 1977; Damasio et al., 1982), and impaired identification
and matching of common objects photographed from noncanonical views (Warrington and Taylor, 1973, 1978; Warrington and James, 1986) have previously

1294

T. LANDIS AND O T H E R S

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been associated with right posterior lesions. Our case not only confirms these
findings, but also demonstrates that when there is complete destruction of the
primary and associative visual system of the right hemisphere, the isolated visual
structures of the left hemisphere are unable to provide this analysis. However, the
present patient on several occasions explicitly denied knowing the correct item.
This phenomenon, which we termed 'paradoxical knowledge', indicates that in
some instances the left hemisphere visual system was even capable of analysing
perceptually and categorizing faces of well-known people, but not with sufficient
subjective certainty. We conjecture that the processing of faces or unusual objects
by the left hemisphere visual structures, that is, those 'nondominant' for this
analysis, lacks some specific features which estrange the percept from the inner
model sufficiently to provoke active denial. The visual gnostic abilities of this
patient are virtually the reverse of those seen in cases of major damage to the
posterior left hemisphere. Since Lissauer's (1890) description of a patient with
associative visual agnosia who subsequently came to pathology (Hahn, 1895), we
know that a large lesion in the territory of the left posterior cerebral artery can
render a patient unable to recognize visually-presented objects despite a visual
capacity sufficient to copy objects. The intact visual system of the right hemisphere
in these patients is apparently not capable on its own of providing object
recognition. However, recognition of well-known faces, emotional facial expressions, familiar places and spatial orientation was relatively spared in most of
the patients with visual associative agnosia due to isolated left posterior damage
(Scheller, 1966; Lhermitte et al., 1973; Hecaen el al, 1974; Pillon et ai, 1981;
Ferro and Santos, 1984; Larrabee et al., 1985).
De Renzi et al. (1969) and Warrington and Taylor (1973, 1978), who compared
the performance of patients with left or right hemisphere lesions on a variety of
visual tasks, suggested 'apperception' (i.e., the identification and discrimination
of complex pattern) (De Renzi et al., 1969) or 'perceptual categorization'
(Warrington and Taylor, 1978) to be impaired with right hemisphere damage; and
'association' or 'semantic categorization' to be deficient in patients with left
hemisphere lesions.
Our patient had prosopagnosia, topographagnosia and an agnosia for noncanonical views, but could read and recognize prototypical objects easily. On the
other hand, patients with similarly large lesions in the territory of the opposite
(left) posterior cerebral artery have been reported to suffer from associative visual
object agnosia and cannot read, but usually recognize well-known faces and
places.
This pattern of double dissociation of function which emerges when comparing
patients with large posterior lesions that isolate the visual areas of the opposite
hemispheres, suggests that homologous areas of the visual systems of the right
and the left hemispheres are specialized differently in the analysis of visual
information.

PROSOPAGNOSIA

1295

ACKNOWLEDGEMENTS
We thank Ms B. Walker for her assistance and Drs Jane Casey, Roger Graves and Joe Bogen for
their suggestions and editorial help. This study was supported by the Swiss National Science
Foundation grant 3.884.0.83. Part of this study was presented to the 15th Annual International
Neuropsychology Society meeting held in Washington, DC, in February, 1987.

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