NOTE
PRESERVED IMAGERY FOR COLOURS IN A PATIENT
WITH CEREBRAL ACHROMATOPSIA
Paolo Bartolomeo1, 3, Anne-Catherine Bachoud-Lévi2, 3 and Gianfranco Denes4
(1 INSERM Unité 324, Paris, France; 2 LSCP, EHESS, CNRS, Paris, France; 3 Service de
Neurologie, Hôpital Henri-Mondor, Créteil, France; 4 Dipartimento di Scienze
Neurologiche e Psichiatriche, Università di Padova, Italy)

ABSTRACT
We report the case of a patient who, after sequential bilateral strokes in the occipital
regions sparing the primary visual cortex, developed a severe deficit of colour perception.
At variance with other reports of acquired achromatopsic patients, she showed a perfectly
vivid visual imagery for colours. These findings, together with similar data in domains other
than colour processing, challenge the theories which posit that the same cognitive processes
are involved in both the perception and the retrieval from memory of a given stimulus.

INTRODUCTION
Cerebral achromatopsia is an uncommon disorder of colour perception resulting from
lesions in the anterior inferior part of the occipital lobe (Meadows, 1974). Patients typically
complain that they cannot see colours anymore, and the world appears uniformly grey or
brown. In the case of unilateral lesion achromatopsia is confined to the contralateral visual
hemifield (see Zeki, 1990, for review).
According to some authors (Farah, 1988; Damasio, 1989), this perceptual deficit is always
associated with an inability to recall the colour of common objects from memory (e.g., a
tangerine, a poppy), a task which is often solved by imagining the relevant object in colour.
Farah (1988) reviewed several case studies of acquired achromatopsic patients. She found
a consistent association between impaired colour vision and impaired colour imagery, and
concluded that the same neural representations are involved in seeing colours and imagining
them. Additional evidence of the association between perception and imagery deficits in
colour processing was provided by Damasio, Yamada, Damasio et al. (1980, case 2), Gomori
and Hawryluk (1984), Levine, Warach and Farah (1985, patient 1), Rizzo, Smith, Pokorny
et al. (1993), Goldenberg (1992), and Shelton, Bowers, Duara et al. (1994). These findings
obtained in single-case studies are corroborated by the results of De Renzi and Spinnler
(1967), who found a consistent association between “colour amnesia” (i.e., the inability to
retrieve from memory the colour of an object) and perceptual colour processing deficits in
an unselected group of unilaterally brain-damaged patients. The authors concluded that a
deficit of colour revisualization was almost always present in patients with impaired colour
perception.
However, this association of deficits is far from being the rule. Patients have been
described with impaired mental colour imagery and preserved colour perception, thus
suggesting a possible image generation deficit (see Goldenberg, 1993, for review). Possible
instances of the opposite dissociation, namely colour perceptual deficit with intact colour
imagery, have also been reported. The patient described by Meadows (1974, appendix;
Pearlman, Birch and Meadows, 1979) was able to name the colours of common objects
either spoken by the examiner or presented as black and white images. Also other
Cortex, (1997) 33, 369-378

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achromatopsic patients had no difficulty in naming the colours of common objects from
memory (Green and Lessell, 1977; Heywood, Wilson and Cowey, 1987; Scarpatetti, Ketz
and Jung, 1983). It must be noted, however, that in these studies the results of colour imagery
tests are only cursorily reported, and all details on the questions are not given. This is a
crucial point, since these patients’ good performance could rely on a verbal association strategy
rather than on the inspection of centrally generated images. Indeed, the colour of the items
provided as examples by Meadows (grass, banana, fire-engine, London bus) may be recalled
using verbal semantic knowledge. That achromatopsic patients can use a verbal strategy to
answer colour-from-memory questions is strongly suggested by the report of a Belgian
achromatopsic patient of Italian origin (Dumont, Griggio, Dupont et al., 1981). She enumerated
in Italian the colours of the Italian flag, but was not able to say the colours of the Belgian
flag, although she had been living in Belgium for decades. A more direct demonstration of
the use of different strategies in these tasks was provided by Beauvois and Saillant (1985),
whose patient R.V. was better in retrieving colour names using verbal strategies than using
visual imagery, even when the same colour was concerned (e.g., R.V. was better on question
like “what do people say when asked what colour snow is?” than answering questions like
“imagine a beautiful snowy landscape... Can you see it? Well, now tell me what colour the
snow is”). A similar dissociation was described by De Vreese (1991, case II).
Unequivocal evidence of a dissociation between perceptual colour processing and colour
imagery abilities is provided by the present case study1.
CASE REPORT
Madame D is a 74-year-old right-handed housewife who had worked as a secretary and
loved painting in oils as a hobby. She suffered in May 1995 from a haematoma located
across the left temporo-occipital sulcus, involving the middle occipital gyrus and the inferior
temporal gyrus (Brodmann areas 18, 19 and 37). She presented with a right homonymous

A

B
Fig. 1 – T1 weighted MRI showing a left-sided lesion tying across the temporo-occipital sulcus
and a right-sided lesion centred on the middle occipital gyrus.

1 Since submission of this paper, an achromatopsic patient has been described (Shuren, Brott, Schefft et al., 1996)
with an unquestionable preservation of mental imagery for colours.

Colour imagery in cerebral achromatopsia

Fig. 2 – Goldmann perimetry showing a central scotoma with II/4 testing.

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Fig. 3 – Mme D’s performance on the Farnsworth (1947) dichotomous test. Normal subjects’ diagram follows the contours. Colour-blind subjects’ performance is characterised by two or more lines
crossing the diagram. The lack of any definite confusion axes is a frequent feature in cerebral, as
opposed to congenital, achromatopsia (see, e.g., McCarthy and Warrington, 1990; Meadows, 1974).

Colour imagery in cerebral achromatopsia

373

hemianopia and showed a mild anomia, without any comprehension or repetition deficit, that
subsided after some weeks. No other linguistic deficits were present, apart from a pure alexia
(which will be the focus of a subsequent article). After some weeks, her visual field defect
had resolved on confrontation testing. Goldmann perimetry showed a residual right paracentral
scotoma, which disappeared with IV/4 test. She named correctly and without hesitation 20
colours (see below, Colour Naming, for description of the test material). Colour identification
in the right visual hemifield was also flawless on clinical testing: The colour of 4 × 4 cm
colour patches presented at about 30° to the right of fixation on the horizontal midline was
identified rapidly and without errors. At that time, Mme D’s only complain was her reading
difficulty. Since she could not enjoy reading anymore, Mme D occupied herself almost
exclusively by painting. At that time, she never complained about problems with colours or
colour mixtures.
In December 1995 she suffered from a second, right-sided haematoma, almost symmetrical
to the first. The lesion was centred to the middle occipital gyrus, just posteriorly to the
temporo-occipital sulcus. It involved area 19 and the white matter underlying area 18 (Figure
1). After the occurrence of the second stroke, Mme D found herself unable to recognise
familiar faces and common objects by sight, and complained of seeing the world in shades
of grey. She had full visual field on confrontation testing. Goldmann perimetry showed a
central scotoma with II/4 test (Figure 2). Visual evoked responses with black and white
pattern were normal for latency and amplitude. Mme D obtained a verbal IQ of 109 on the
WAIS-R. She performed at chance level on a modified version of the Efron test (Warrington
and James, 1988) and on the shape detection screening test of the Visual Object and Space
Perception Battery (Warrington and James, 1991). She was unable to name any black-andwhite realistic drawings. When asked to name real objects presented by the examiner, she
was 13/35 correct on visual presentation, claiming that she was unable to recognise the other
items. Examples of wrong responses in this task include ring → “coin”, telephone → “wall
diary”, glass → “alarm clock”. She correctly named the same objects when they produced
some noise (e.g., jiggling keys) or on tactile presentation.
Formal colour testing began on February, 1996. By that time, Mme D claimed that her
visual world had changed from grey to a reddish-brownish appearance, and reported to have
occasionally perceived bright, saturated colours (e.g., she correctly identified the red of a
truck moving on the road).
PERCEPTUAL COLOUR TESTING
Colour Discrimination
The Farnsworth D-15 test (Farnsworth, 1947) was administered on two different occasions.
The patient’s performance was grossly defective (Figure 3). Mme D was well aware of her
difficulties, and looked at each patch for a long time before arranging it. She never attempted
to name the colours of the patches.
Mme D correctly identified the first and last items of the Ishihara (1974) plates, as colourblind subjects can do. She was permitted to follow the targets’ contour of the other items
with her index finger, on account of her alexia. She found the task difficult, and outlined
correctly 7 targets (items 2, 3, 9, 15, 16, 17). This result indicates a pathological performance.
Colour Matching
The patient was presented with a 16 × 20 cm board composed of 20 4 × 4 cm different
colour patches and 20 separate 4 × 4 cm colour patches that she had to match with the
corresponding colours on the board. Again she looked puzzled and performed the test slowly
and hesitantly. She was 6/20 correct, when matching the orange, white, sky blue, dark green,
royal blue and light brown patches.
Colour Pointing
Mme D was asked to point to the colours spoken by the examiner. The same plate was
used as in the preceding test. The patient was 8/20 correct, when pointing to the green,
black, orange, chestnut brown, white, dark green, royal blue and pink patches.

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Colour Naming
Mme D was shown the same colour board and asked to name the colour pointed by the
examiner. The test was administered twice on different days. As with the previously described
tests, she was slow and hesitant in responding, carefully examining the patches and often
expressing doubts about her responses. Occasionally, she remarked that colours changed in
hue before her eyes. The overall correct performance was 8/40. In half of the cases the
patient perseverated on some colour names (beige nine times, green seven times, yellow and
brown four times). Names of the colour stimuli and patient’s responses on the two test
sessions are reported in the Appendix.
Mme D showed the same degree of impairment on naming, matching and pointing to
colours (x2 = 2.76, d.f. = 2, p n.s.). A qualitative comparison among the results of colour
perceptual tests does not seem to suggest any consistent patterns of impairment on particular
colours. For example, while green appeared to be relatively spared in some tests (it was
correctly pointed at, it was named two times out of four, and it was present in all the
identified items of the Ishihara plates), green patches were also erroneously arranged next to
ochre, blue and violet in the Farnsworth test.
Colour Imagery Tasks
Colour Verbal Memory
Mme D was asked to say the appropriate colour of 20 objects indicated verbally by the
examiner (De Renzi and Spinnler, 1967). She named quickly and correctly all the 20 colours,
sometimes employing expressions that suggested the use of visual imagery rather than a
verbal association strategy (e.g., wheat → “cream-coloured, pale yellow”). Equally flawless
was the patient’s performance on 15 items of the “verbo-visuo-verbal test” devised by
Beauvois and Saillant (1985, appendix 3, experiment 2). Analysis of Mme D’s responses
suggested that she again relied on a mental imagery strategy (e.g., interior part of a radish
→ “white, with pale red streaks”; champagne wine → “it can be either pink or golden”;
pastis → “opaline”).
Colour-object Fluency (De Vreese, 1988)
The patient was asked to produce the name of as many objects as possible which are
typically red, green, yellow and black. A time limit of 60 sec was allowed for each colour.
Her score, 23 according to De Vreese’s procedure, was largely higher than normative data
(controls’ mean score: 14.07 ± 3.98).
Colouyr Name Fluency (De Vreese, 1991)
Although this test does not necessarily require imagery abilities, it was administered to
our patient in order to confirm the integrity of her colour lexicon. Mme D was asked to
produce as many colour names as possible in 60 sec. She produced 14 colour names (controls’
mean score: 10.41 ± 2.15).
Mental Hue Comparison
A modified version of a test devised by De Vreese (1991) was developed. Twenty-five
pairs of items were proposed verbally by the examiner. Each pair was composed of objects
of the same colour with a different hue (e.g., French bean/bay leaf, interior of a pineapple/
interior of a potato, cherries/strawberries, Paris metro ticket/pine). The patient was asked to
say which of the items within a pair was darker in colour. Mme D was 24/25 correct. The
only response that was considered as wrong was “potatoes are darker than chestnuts”. On
subsequent questioning, the patient explained that chestnuts are shiny, while potatoes are
brown with a dull grey appearance.

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375

DISCUSSION
Here we have reported the case of a patient who developed full-field achromatopsia
following sequential bilateral occipital lesions. In fact, the symptom was not present following
the first, left-sided occipito-temporal lesion, but it appeared when a second, symmetrical
lesion in the right occipital cortex occurred. This puzzling sequence of events is difficult to
reconcile both with the well known case descriptions of hemiachromatopsia due to unilateral
lesion and with PET studies reporting a response to colour stimuli larger on the left than on
the right side (Corbetta, Miezin, Dobmeyer et al., 1990; Lueck, Zeki, Friston et al., 1989;
Zeki, Watson, Lueck et al., 1990). A subclinical hemi- or free field achromatopsia after the
first left-sided occipital lesion cannot be excluded, but it would be surprising, given the
pleasure that Mme D found in painting at that tirne. More in general, our data could support
the notion of a critical role of the right hemisphere in colour processing (see, e.g., De Renzi
and Spinnler, 1967; Davidoff, 1991).
Our patient’s pattern of performance is relevant as concerns the relationship between
perceptual and imagery processes. Visual imagery deficits often parallel visual perceptual
deficits in the same domain. This observation led some authors (Damasio, 1989; Farah, 1988,
1989; Kosslyn, 1994) to postulate a common neural substrate for perception and imagery,
i.e., specialised, domain-specific cortical areas would be used to process the same kind of
information (e.g., colours) in perception and retrieval from memory.
However, perceptual and imagery deficits can dissociate one from another in several
domains. Visual imagery can be spared in cases of cortical blindness (Chatterjee and
Southwood, 1995; Goldenberg, Mullbacher and Nowak, 1995) and object agnosia (Behrmann,
Moscovitch and Winocur, 1994; Servos and Goodale, 1995), and Behrmann et al.’s metanalysis
of previous reports makes the case for a double dissociation between perceptual and imagery
deficits of objects. Perri, Bartolomeo and Silveri (1996) described a pure alexic patient who
showed a perceptual deficit of letter identification in the absence of any deficit of visual
imagery for letters. Also prosopagnosic patients can be able to imagine faces (Hécaen,
Ajuriaguerra, Magis et al., 1952).
Moreover, dissociations between performance on visual and imagery tasks can be observed
in patients with unilateral spatial neglect (Anderson, 1993). In a group study, Bartolomeo,
D’Erme and Gainotti (1994) found that only a minority of visual neglect patients showed
signs of neglect on description from memory of familiar places (a task devised by Bisiach
and Luzzatti, 1978). Moreover, the possibility exists of an imaginal neglect in the absence
of, or after recovery from, visuospatial neglect (Bartolomeo et al., 1994; D’Erm, Bartolomeo
and Gainotti, 1994; Guariglia, Padovani, Pantano et al., 1993).
In Kosslyn’s (1994) and Farah’s (1984) models, colour perception and colour imagery
share a common visual buffer, in which both mental and physical colour percepts occur.
Through a generation process, the content of long-term memory is transferred onto the visual
buffer, where it can be inspected for further processing. According to this model, a selective
deficit of the generation process should result in impaired imagery coupled with intact
perception (recognition would be possible through a direct access to long-term memory
representations) (Farah, 1984).
The opposite dissociation, namely impaired perception and intact imagery, should occur
following a deficit of perceptual access to intact visual representations. In Kosslyn’s words,
“problems in perceptual organization or in matching input to stored visual representations
in the pattern activation subsystems can impair perception but leave imagery relatively intact
(1994, p. 329)”. In our patient, however, visual imagery for colours was not only “relatively”
spared, but perfectly vivid, despite a striking impairment of colour perception. The hypothesis
of a problem of matching between visual input and stored visual representations does not
fit with the clinical reality of Mme D’s perception of the world as drained of colours, and
her inability not only to identify but also to discriminate between colours. According to
Kosslyn (1994), the visual buffer is a structure in the occipital lobe, composed of
retinotopically organised areas from V1 to V4. An impairment of early sensory analysis (i.e.,
from the retina to V1) can be reasonably ruled out in our patient, given the lack of clinical,
neuroradiological and neurophysiological evidence of damage to the visual system prior to
the extrastriate areas (apart from the small visual field deficit, which obviously cannot account

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for the achromatopsia). Assuming Kosslyn’s model, the functional locus of impairment in
our patient should be at the level of the visual buffer, challenging the claim (Farah, 1984;
Kosslyn, 1994) that a single visual buffer constitutes the common “screen” for perceptual
and imagery processes.
From the anatomo-functional point of view, our patient’s pattern of spared colour
memories in the absence of colour perception does not easily accommodate with Damasio’s
(1989) hypothesis that memory contents are retrieved through the retroactivation of the very
same cortical areas that had processed the revelant information during perception. These
“early cortices” include the primary and first-order associative sensory cortices. According
to Damasio, “no other cortices, and certainly no other higher order, integrative cortices, are
capable of supporting the recall of the perceptually impaired feature (1989, p. 33)”. Our
patient’s achromatopsia can be explained either by direct damage to a cortical area specialised
for colour processing (possibly the human homologue of V4, located in the prestriate cortex
[Corbetta, Miezin, Dobmeyer et al., 1990; Zeki, Watson, Lueck et al., 1990]), or by a
disconnection of V4 from the primary visual areas (V 1). In the first case, Damasio’s
hypothesis is directly disconfirmed. As for the hypothesis of a disconnection between intact
V4 and V1 areas, it explains Mme D’s pattern of impairment. But even in this case a difficulty
arises with Damasio’s hypothesis. According to Damasio, Mme D’s vivid visual memories
should depend on the retroactivation of V1, but this would be an implausible mechanism if
this area were disconnected from more anterior areas, such as V4.
Our case can be explained in a much easier way by postulating different cortical
implementations of perceptual and imagery colour processing. In a PET experiment (Martin,
Haxby, Lalonde et al., 1995), subjects had to generate the name of colours associated with
an achromatic line drawing of an object, or with its written name. In both conditions, a
region was activated in the ventral temporal lobe, 2 to 3 cm anterior to the region of the
fusiform gyrus activated by colour perception (Corbetta et al., 1990; Zeki et al., 1993).
Provided that subjects used a colour-imagery strategy to perform the task, the data would
suggest that distinct cortical regions are implied in perceptual analysis and imagery of colours.
The fact that these cortical areas lie close to one another would make them liable to be
damaged at the same time, thus accounting for the frequent observation of an association
between perceptual and imagery deficits in colour processing.
Additional support for this interpretation of our patient’s pattern of performance comes
from the report (Luzzatti and Davidoff, 1994) of two patients with the opposite dissociation
to the one showed by Mme D. These two patients had preserved colour perception and
impaired retrieval of knowledge concerning the colours of objects. Interestingly, their lesions,
caused by herpes simplex encephalitis, appeared to affect regions anterior to the location of
Mme D’s lesions.
The possibility that perception and imagery are implemented in distinct cortical areas is
a disappointing one for those of us who followed with interest the attempts to establish a
neural equivalence between the two processes. Nevertheless, this possibility is reassuring in
that it seems to confirm common experience: That seeing something for real is quite different
from imagining it – unless, of course, one suffers from hallucinations.
Acknowledgements. This work was supported by the European Union grant n.
ERBCHBGCT930344 to P.B. and by an INSERM grant to G.D. We are grateful to Madame
D and her husband for their good humour and friendly attitude, and to J.-D. Degos for
permission to study the patient and for helpful discussion. Thanks are also due to M. Magne
and M.-F. Boissé for standard neuropsychological testing, to P. Brugières for evaluation of
MRI data, and to A. Petrov for reviewing the English.

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Paolo Bartolomeo, INSERM Unité 324, Centre Paul Broca, 2ter rue d’Alésia, 75014 Paris, France.
E-mail: paolo@broca.inserm. fr.

(Received 28 April 1996; accepted 13 July 1996)

APPENDIX
Responses Produced by Mme D on the Colour Naming Test
Stimulus

1st session

2nd session

Green
Red
Black
Orange
Mauve
Chestnut brown
Pale yellow
Violet
Ochre
White
Crimson
Yellow
Golden yellow
Pastel green
Sky blue
Dark green
Royal blue
Dark grey
Light brown
Pink

Beige
Pink, not red
Grey or brown
Light beige
Dark beige
Green
Beige
Light brown
Dark yellow
Light yellow
No answer
Yellow (+), beige
Beige
Blue
Blue-green
Green (+)
Green
Green
Beige (+)
Beige

+
+
Brown
Red
Brown
Grey
Pink
Red
Brown
Pink
Dark red (+)
Yellow, grey, yellow (+)
Ochre
Blue
Green
Grey
+
Grey-beige
Orange
Green