NOTE
RESIDUAL VISUAL CAPACITIES IN A CASE
OF CORTICAL BLINDNESS
M. T. Perenin, J. Ruel and H. Hecaen
(Laboratoire de Neuropsychologie Experimentale, et 'Unite de Recherches
Neuropsychologiques et Neurolingllistiqlles, INSERM)

In recent years, the use of a new methodology which comes mainly from
primate behavioral studies has contributed to the demonstration of the persistance
of some "residual vision" or "blindsight" within perimetricaIIy blind fields that
result from unilateral geniculostriate lesions in man (Poppel, Held and Frost,
1973; Weiskrantz, Warrington, Sanders and Marshall, 1974; Perenin and
Jeannerod, 1975, 1978). Such visual capacities were demonstrated, not by asking
the subject whether or not he had "seen" visual stimuli (such as in the perimetric technic) but rather by requiring him to make responses (mostly behavioral),
even in the absence of any perceptual awareness, using a forced-choice procedure.
Hence subjects with homonymous scotomatas or hemianopia were shown to be
able to localize visual targets which they could not see, either by shifting their
eyes or pointing with their hands. In a few cases, patients were even able to
discriminate line orientation or simple patterns.
These findings have been considered as an important argument for ascribing
a functional role to the extrageniculostriate visual pathways in humans. Such a
conclusion would logically predict similar residual vision in cases of bilateral
occipital lesions. In fact, most previous studies of apparently complete "cortical
blindness" have failed to find consistent visual capacities other than the pupillary
reaction to light. In accordance with some cases reported before, the two patients
of Brindley, Gautier-Smith and Lewin (1969) could only perceive sudden changes
of the surround illumination, whereas Ter Braak, Schenk and Van Vliet (1971)
reported the only case that exists in the literature of the reappearance of optokinetic nystagmus in a patient who did not recover any conscious visual perception.
In this latter case, the striate cortex appeared to be completely destroyed and
there was nearly total retrograde degeneration of both lateral geniculate bodies.
Apart from the possibility of these lesions extending as far as the secondary
visual cortical areas, a possibility which itself has not been given much consideration, these rather negative results might be explained by the method which
was used to test the patient's residual vision. Except for Ter Braak et a1. 's study,
previous investigations relied only on the "conscious" visual mode and the
majority of these studies were not performed systematically. If a methodology
similar to that which led to demonstrate "blind~ight" in hemianopic subjects
were to be used, one could expect that a greater visual capacity would be
demonstrated to remain in the case of cortical blindness.
Cortex (1980) 16, 605-612.

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M. T . Perenin, f. Ruel and H. Hecaen

This hypothesis was at least partially verified in the case reported below.
Indeed such an approach allowed the demonstration that some visual capacity
reappeared in a patient with apparently complete cortical blindness following
a dense lesion in both occipital lobes but which was largely restricted to their
medial side.

CASE REPORT

A 74 year-old left handed man, having suffered a left transitory hemiplegia
on 1975, woke up completely blind on February 28, 1978. Immediately, however, he totally denied any visual defect: he was only surprised that "there was
no light in the room" and asked repeatedly for the shutters to be opened and
for the light to be switched on. In addition, he was disoriented in time and
space and tended to forgot recent events. There was a good pupillar constriction
response to light. Ocular fundus was normal. The EEG showed intermittent
slow waves in the left temporal region.
When examined by us on March 14, 1978, the patient was still disoriented
and still denied that he was blind. He maintained that he was in the dark and,
at each concrete demonstration of his blindness, he failed to comprehend his
defect. For example, although he did not see his fingers waving before his
face, he persisted in saying "I am not blind". He was able to give a poor, but
correct, verbal description of his apartment and of the arrangement of the
rooms in it. There were no signs of speech disturbance, except for some impaired
naming of haptic and auditory stimuli. There were some difficulties in verbal
elicitation of the colors of specific objects. The tasks of writting his name, or
isolated words, or digits and numbers were all performed well. Neurological
examination showed only a bilateral Babinski sign.
On April 27, 1978, the temporospatial disorientation and denial of the
blindness were nearly unchanged. The patient claimed to be able to watch
television programs. However, he no longer felt as if he was in total darkness
as before, and during examination he mentionned that there was some light
in front of him (he was indeed just sitting in front of a window), but that he
could not see anything else. He now had been experiencing for several days
complex visual and auditory hallucinations (mostly, people and vehicles),
especially in the evening. He did not remember having dreamed recently (nor
ever in fact!). He was no longer able to describe his apartment, as he could
not visualize it mentally at that time. Denomination of haptic and auditory
stimuli had improved. Colors names were now elicited well.
In a latter examination, on September 28, 1978, the patient was still disoriented and his attention disorder was even more marked. Although he now admitted
a sight defect, he seemed to forget it sometimes, walking without caution and
colliding into furniture. At that time, memory was more impaired for past
events. He could talk about recent news he had heard on the radio, but he
did not remember the day's menu. Visualization of most of his relatives was
lacking and the patient could not give a verbal description of either of them.
Further examination was not possible, as the patient became confused and
tired rapidly.

Visual capacities in cortical blindness

607

Computerized axial tomography

A CAT scan was performed on March 23, and once again on July 28, 1978
(Dr. Cabanis). As shown on Figure 1, a large ischemic lesion which had evolved
to a porencephaly of both occipital lobes was observed. The topography of

A

8

Fig. 1 - Pictures of CAT Scans performed respectively one month (A) and five months
(B) after the illness onset. In A, extensive lesion, undergoing reabsorption of both medial occipital regions. In B, marked hypodensity in the same territory.

the lesion remained nearly unchanged from March until September. The lesion
lay the length of the medial side of both occipital lobes, including both occipital
poles. It was a little larger on the left side where it extended close to the
occipital horn. In addition, a trace of the first stroke was seen as a slight
hypodensity in the right temporo-occipital region. There was also diffuse cortical
atrophy.
Visual evoked potentials

Visual evoked potentials were checked on three occasions (M. Leblanc).
On March 22, no specific response could be recorded, but only a late wave
(200 ms latency) in response to flashes. On May 3 and July 5, responses of
abnormally low amplitude and long latency were sometimes observed mainly
in the left occipital region when checkerboards with 1 20 elements were shown.
Flashing patterns with smaller elements did not evoke responses.
0

Residual visual capacities

Sparing and recovery of visual capacities were examinated on several
occasions until the seventh month of the illness, even though the patient still
behaved completely blind in everyday life, and the QAT aspect of the calcarine
lesion remained as extensive as it was first seen. Various types of visual
stimulations were performed, most of them were in total darkness. These will

608

M. T. Perenin, J. Ruel and H. Hecaen

be described at a later point, along with their results. Both informal and formal
investigations were done, depending on the state of attention or fatigue of the
subject. But a forced choice procedure was used as soon as possible, which
required the subject to make a behavioral response, mostly pointing to one of
the stimuli, or choosing verbally between two items. This procedure was used
irrespective of the patient's conscious visual experience, i.e. even if he did
not really see anything. Of course, he often took some time to be persuaded
to do so.
The first experimental session was carried out on March 16, 1978, i.e. 17
days after the illness onset. It included three main types of visual investigations:
Stationary lights

Bright flashed patterns (70 joules, 1,5 ms), which induces a long-lasting
afterimage in normal subjects (8° of visual angle cross), could be switched on
at six different positions (from 15 to 165° with a 30° interval) at 57 cm in
front of the subject. The click produced by the flash bulb was masked with
white noise. At the beginning of each trial the subject was required to direct
the eyes straight ahead and, after the stimulus was presented, to point with
his arm fully extended (right or left, depending on the side of the response)
in the direction where he guessed the flash had come from, irrespective of
whether he "saw" something or even had any conscious idea of where the
light source was. Responses were recorded (with about a 5 ° precision) on a
radial scale which was drawn on the table at which the subject was seated. Thus,
two sessions of 30 trials each were performed at that time . It was striking
that the patient could not "see" any of the 60 flashes switched on in complete
darkness during these two sessions. Blink reflex to flashes was absent. In addition,
pointing responses were not correlated with the flashes location : in most trials,
the patient pointed to about the same region, in front of him. But, he could
perceive and localize the "clicks" of the flashes quite well in one of the two
sessions where no masking noise was used.
Flickering lights

A spot of maximum size and luminance (116', 318 cd/m2) of the Tubingen
perimeter was used with a flicker frequency of 5 to 8 Hz, with a background
luminance set at 3,18 cd/m2 • Thus, the contrast was much weaker than in the
previous test. In this condition, when examined clinically the patient did not
orient his eyes in the direction of the flickering spot nor did he follow it when
it was displaced on the screen.
Moving visual stimuli

When placed inside a rotating optokinetic drum (57 cm radius, 0.04
cycler) the patient had the feeling on several occasions, that something was
moving around him and at those times he indicated correctly the direction and
stopping place of the movement. No optokinetic nystagmus could be seen,
but there was a frequent deviation of the eyes toward the direction of the drum
rotation.
Return of some visual capacities could be stated on further examinations

Visual capacities in cortical blindness

609

performed two (April 27), four (June 22) and seven (Septemb~r 28) months
after the onset of the illness.
Stationary lights

At first, the patient could again detect some of the flashes (11 of 30 on the
second month) and then from the 4th month on, he could perceive all the
flashes that were presented in the 30 trial sessions. In the 2nd month, four
exact and three approximate responses were obtained following stimulation on
the right side, but the patient refused to point when he did not "see" anything.
Afterwards, he did point at each trial, but there was no relationship between
the pointing and the position of the flashes: the responses tended to be localized
around the center (Figure 2A).

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Fig. 2 - Average hand paintings to targets presented in front of the subject, at different
positions, from the extreme left (J 5°) to the extreme right (J 65°). In A, where targets are
bright flashed patterns, there is no relationship between hand pointing and target position. In
B instead, where targets are flickering spots, there is a significant correlation between pointing
responses and target positions. Both sessions were performed (In the fourth month after the
illness onset.

In the seventh month, stationary spots of light (116', 318 cd/m2) of the
perimeter were still infrequently detected when presented in total darkness
and they could not be localized even if the choice was only between two
positions: right or left (at 20° from the center). Thus the scores remained at
chance level (23/40).
When asked whether he was in a dark or in an illuminated room, the
patient still made numerous errors (and sometimes answered "light" instead
of "dark") although some improvement was noticed after the second month.
Finally, only large and sudden changes of surround luminance such as flashes
could be discriminated without error.

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M. T. Perenin, f. Ruel and H. Hecaen

Flickering lights

Unlike the case of stationary spots, the ability to locate flickering spots (not
tested at the second month) became very clear on the fourth month: there was a
rather good correlation indeed (R = 0.558, P < 0.01) between the pointing
responses of the patient and the six possible positions of the target (5°, 46 cd/m2 ,
2 Hz spot provided by a projectoscope, same procedure, as for flashes), even
though he did not "see" any light on every trial nor did he have any conscious
idea of where was its source (fig. 2B). On the seventh month however, the value
of R failed to reach significance on the same test, although the patient was
still able to make choices above chance level (scores: 25 and 27/40) between
two different positions (top or bottom and right or left) of the flickering spot
of the perimeter, presented in complete darkness.
Moving visual stimuli

Movement perception inside the optokinetic drum became the most constant
finding from the second month on: the patient indicated the correct direction
of the movement in 100% of cases on the three occasions where this ability
was checked. On the seventh month the same precision was obtained during a
session of 40 trials with random alternation of clockwise and counterclockwise
rotations. Each time, the patient also indicated with quite good precision the
onset and offset of the rotation. Although he claimed he could "see" something
moving, he could either not tell at all what it was that was moving or he gave
curious responses such as "people", "pictures". These responses correspond
most likely to hallucinations. When black and white stripes were projected to
only part of the visual field, or when the patient was placed in front of a
vertical wheel with rotating random .black and white patterns, the subject could
only perceive the movement from time to time and then he was mostly wrong
in his indication of the direction. In none of these situations did he report a
sensation of self-motion. Oculomotor behavior remained the same as on the
first examination, i.e. no optokinetic nystagmus could be observed.
Colors

In the second month, when he was asked to name the colors of spots of
the perimeter (green, red, orange or blue, 11°, 318 cd/m2), the patient gave
6 correct (for the red and blue spots) and 4 approximate responses on 16
different presentations. On the seventh month, these spots were, for the most part,
not even perceived as light and when a forced-choice task was imposed between
red and green, the score was at chance level (21/40).

DISCUSSION

Thus, in a patient with a very extensive (if not complete) ischemic necrosis
of both calcarine cortices, we were able to demonstrate that some visual
functions reappeared. At first, moving stimuli could be detected, and then
bright lights, especially when they had sudden onsets such as flashes. Responses
improved with time to 100% detection of moving stimuli and flashes. At last,

Visual capacities in cortical blindness

611

the patient could estimate, by pointing with his hand, the position of flickering
spots, but he could not do so when the lights were stationary. In the two
partial examinations for color discrimination, he did not surpass chance level.
It may be noted that this recovery was first clearly observed at the time when
the patient began to have visual hallucinations, i.e. in the second month of
the illness, even though he still denied that he was blind. Wether this is only
a coincidence or whether some relationship indeed exists between these two
facts is debatable. Perhaps this kind of visual experience, even though it is
abnormal, might have rendered the subject more able to attend to visual stimuli.
Of course, hallucinations and confabulations (e.g. when he responded "light"
even though it was dark) make it difficult sometimes to rely on the subjective
responses for the evaluation of the patient's perceptual awareness, in the different conditions of visual stimulation. However, according to most of these
responses on numerous trials, he seemed to be able to detect moving stimuli
and flashes by "seeing": he probably could "see" weakly something moving
or some amount of light. Instead only rarely did he report to have seen the
flickering spots, yet he could localize them approximately, in a forced-choice
situation. In this respect, at least some of the residual capacities of our patient
were quite similar to "blindsight" (in the sense of this term was used by
Weiskrantz et aI., 1974, for describing unconscious visual capacities observed
in their patient with a unilateral occipital lesion).
If we reconsider the types of visual stimuli that the patient could perceive
(whatever the nature of this perception), his visual capacities can be compared
to those of destriated monkeys: bright flashes, moving objects, flickering lights
are all stimuli for which such animals reestablish an ability to detect or to
localize, whereas, at least during the first months of postoperative training,
they remain quite insensitive to stationary stimuli (Humphrey and Weiskrantz,
1967). However, according to these experimental results, we might have expected
that our patient would also recover optokinetic nystagmus, as did in fact occur
in the case of Ter Brack et al.'s (1971) patient. Although we frequently
observed a deviation of the gaze in the direction of the movement on the part
of our patient, no nystagmus could be seen.
In spite of the fact that we have no anatomical proof that the whole striate
cortex has been affected by the lesion, the analogy with animal results together
with the previous data in subjects with unilateral occipital lesions serve to
support the view that such residual vision would be subsumed by extra-geniculostriate visual pathways. The superior colliculus and/or its ascending projections via the pulvinar on the secondary visual cortical areas (presumably
left intact by the lesion) could thus be the structures responsible for this
crude residual vision, as was argued in cases of unilateral occipital lesions.
Transient functional changes such as those known the occur at the midbrain
level following striate cortex ablation (Sprague, 1966) might well be one of
the factors responsible for the delayed recovery.

ABSTRACT

A case of cortical blindness resulting from a dense ischemic lesion of both
calcarine cortices (as seen on CAT Scan) was studied up till the seventh
month after the initial stroke. By using mainly forced-choice procedures, similar
to those previously used for testing hemianopic subjects, we were able to

M. T. Perenin, f. Ruel and H. Hecaen

612

demonstrate the reappearance of some visual capacities, even though the patient
still behaved as if completely blind in everyday life and the lesion remained as
it was first seen. First, an ability to detect moving stimuli reappeared then
bright flashes could be detected. At last, the patient could localize flickering spots
approximately, by pointing with his hand, despite the fact that he did not really
see them. As was hypothezised in cases of unilateral occipital lesions, such
residual vision would likely to be sub served by extrageniculostriate pathways.

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functions of the non-geniculate fibres of the optic tracts, J. Neurol. Neurosurg. Psychiat.,

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HUMPHREY, N. K., and WEISKRANTZ, L. (1967) Visioll in monkeys after removal of the striate
cortex, Nature, 215, 595-597.
PERENIN, M. T., and JEANNEROD, M. (1975) Residual vision in cortically blind hemifields,
Neuropsychologia, 13, 1-7.

-, - (1978) Visual function within the hemianopic field following early cerebral hemidecortication in man. I. Spatial localization, Neuropsychologia, 16, 1-13.
POPPEL, E., HELD, R., and FROST, D. (1973) Residual visual fUllction after brain wounds
involving the central visual pathways in man, Nature, 243, 295-296.
SPRAGUE, J. M. (1966) Interaction of cortex and superior colliculus in mediation of visually
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TER BRAAK, J. W. G., SCHENK, V. W. D., and VAN VLIET, A. G. M. (1971) Visual reactions in
a case of long-lasting cortical blindness, J. Neurol. Neurosurg. Psychiat., 34, 140-147.
WEISKRANTZ, L., WARRINGTON, E. K., SANDERS, M. D., and MARSHALL, J. (1974) Visual
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M. T. Perenin, Laboratoire de Neuropsychologie Experimentale, INSERM U 94, 16 Avenue du Doyen Lepine 69500 Bron, France.
r. Ruel, H. Hecaen, Unite de Recherches Neuropsychologiques et Neurolinguistiques INSERM, Unite 111,
21e , rue d'Alesia 75014 Paris, France.