 Blackwell Publishers Ltd.

1997, 108 Cowley Road, Oxford, OX4 1JF, UK

and 350 Main Street, Malden, MA 02148, USA.
Mind & Language, ISSN: 0268-1064
Vol. 12. No. 2 June 1997, pp 224–237.

Phenomenal Vision and Apperception:

Evidence from Blindsight
PETRA STOERIG

1. Introduction

Norton Nelkin, who taught at the University of New Orleans and had a
penchant for the city’s endemic jazz, was a philosopher who tried to under-
stand how things are. This distinguished him from those of his colleagues
who contemplated how they could be, or how they should be. Homing in
on perception, cognition, and consciousness, he would turn to neuropsycho-
logy, and test his ideas against its data and findings in patients with neuro-
logical disorders. In the context of perception, blindsight probably figures
largest in his arguments on the dissociability of conscious states.

2. Unconscious Vision: Perception Without Phenomena?

There is ample evidence that sensory information can be processed without

becoming conscious. In man, the lowest form of visual information pro-
cessing is exemplified in patients who are blind as a consequence of damage
to the eyes, the retinae, and the optic nerves. Such patients do not show a
pupil reflex and report not even the dimmest perception of light. Neverthe-
less, provided that a small sub-population of retinal ganglion cells survives
the damage and continues to project to the suprachiasmatic nucleus of the
hypothalamus, the patients’ melatonin secretion is suppressed when they
are exposed to bright light (Czeisler et al., 1995). This reaction is independent
of any conscious visual perception. Nevertheless, it is important for the
patient as well as for the normal observer, because it regulates the circadian
rhythm in accordance with the day and night cycle. Consequently, although
its absence cannot be noticed directly but requires measurements of mela-
tonin concentration, its effects are painfully noticeable in the form of sleep
disturbances. This is clearly an example of visual information being pro-

Address for correspondence: Institute of Physiological Psychology II, Heinrich-Heine-Uni-

versity, D-40225 Düsseldorf, Germany.
Email: petra.stoerigKuni-duesseldorf.de.
 Phenomenal Vision and Apperception 225
cessed and put to good use without being phenomenally represented. Is
that perception?
How about visual reflexes? To take only one example, the pupil light
reflex, which regulates the amount of light falling into the eye, is also inde-
pendent of a conscious representation of light levels. It can be elicited in a
sleeping person, and it persists in comatose patients (Keane, 1979). Like the
neuroendocrine responses, reflexes are important for the functional integrity
of the organism; they protect it from harm. While neuroendocrine responses
involve hormonal regulation, reflexes involve the autonomous motor system.
There are still more complex examples of visual information processing
in the absence of conscious perception. They are more complex because in
contrast to neuroendocrine and reflexive responses they require a voluntary
response and thus can only be elicited in patients who are conscious. The
patients who show these responses are cortically blind. Cortical blindness
results from (most commonly traumatic or vascular) lesions that destroy the
primary visual cortex and/or the optic radiation that provides its major thal-
amic input. The blindness reflects the lesion’s extent and position: it may
be confined to a small part of the visual half-field opposite to the lesioned
hemisphere; it may affect an entire half-field, or, in case the lesion destroys
the primary visual cortex bilaterally, it may affect the entire visual field and
thus cause a complete cortical blindness. Irrespective of the size of the defec-
tive field, its density may vary. If the blindness is absolute (as opposed to
relative), the patients do not consciously see any visual stimuli presented
within the blind field; they here lack ‘all and any sensation of light or colour’
(Wilbrand and Sänger, 1904).
Despite the absence of any conscious representation of visual stimuli in
absolute field defects, presentation of these same ‘unseen’ stimuli can influ-
ence the patients’ voluntary responses. When indirect paradigms are applied
to uncover the influence of an unseen stimulus, the responses required from
the patients are to stimuli presented in the normal visual field. Simultaneous
presentation of a second stimulus in the cortically blind field may render
these responses faster or slower (Corbetta et al., 1990), may improve the
detectability of the seen stimulus (Stoerig and Fahle, in preparation), or may
cause a change in the patients’ (conscious) perception of the seen stimulus
(Torjussen, 1976; Pöppel, 1986). In contrast to these indirect paradigms that
only request responses to seen stimuli (presented in the normal part of the
visual field), direct paradigms require the patients to respond to the unseen
stimulus presented in the blind field, either by moving the hand or the eyes
to the stimulus position, or by reporting its presence, or which one of a small
number of stimuli has been presented. Manual and saccadic localization,
detection, and discrimination of flux, size, motion, motion direction, orien-
tation and wavelength have been demonstrated with direct paradigms (see
Stoerig and Cowey, 1997, for recent review). As the patients cannot
(consciously) see the stimuli they respond to, forced-choice guessing para-
digms need to be used to reveal the direct responses. This is ‘blindsight’
(Weiskrantz et al., 1974).
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226 Mind & Language
The patients’ guessing performance can reveal remarkable sensitivity. For
instance, the threshold for orientation discrimination was found to be about
10° as compared to 2–3° at the corresponding position in the normal half-
field of patient DB (Weiskrantz, 1986). Wavelength discrimination thresholds
ranged between 20 and 30 nm, depending on the individual patient and the
part of the visible spectrum tested, as compared to only a few nm at the
corresponding control position in the normal hemifield, or in normal
observers (Stoerig and Cowey, 1992). Grating acuity was 15.8 c.p.d. as com-
pared to 20 c.p.d. (Weiskrantz, 1986), and increment threshold sensitivity
was reduced by 0.4 to about 1.5 log units maximally (Stoerig and Cowey,
1989; 1991). In addition to these small reductions in sensitivity, the patients’
detectability or discriminability may be as good as 100% correct (Perenin,
1991; Weiskrantz et al., 1991, 1995).
Blindsight is a complex form of vision: it makes use of a number of stimu-
lus dimensions, such as contrast, motion, size, length of contour, orientation,
wavelength. It can be demonstrated exclusively in conscious patients (or
monkeys) where it can be used to guide non-reflexive behaviour. The use it
can be put to has most impressively been demonstrated in the cortically
blind monkey Helen who in the course of eight years of testing learned
efficient navigation and prehension. Helen could even walk in the woods of
Madingley (Humphrey, 1974).
These features render blindsight superior to the visual reflexes. The
reflexes make use of fewer stimulus dimensions, mainly intensity and its
spatio-temporal distribution; they can be elicited in unconscious (comatose
or sleeping) people; and per definitionem they elicit only reflexive responses.
At the same time, blindsight is remarkably inferior to normal conscious per-
ception. The blindsight patients’ performance depends on a variety of vari-
ables that include retinal position, size, colour, onset time and type, speed
of the stimulus and level of adaptation. Together with the patients’ willing-
ness to play the guessing game, and with the amount of training that they
have had, those variables determine whether the performance is close to
perfect (Perenin, 1991), whether it is moderate but statistically significant
(e.g. Stoerig et al., 1985; Magnussen and Mathiesen, 1989), or whether it is
at chance level (e.g. Stoerig, 1987; Hess and Pointer, 1989). It is important
that even highly trained blindsight patients (and monkeys) fall to chance
level performance if condition are inadequate. Furthermore, it is necessary
that the patients and monkeys are relaxed; distraction and fear are detrimen-
tal to the performance. Even monkey Helen who seemed confident when
running around in familiar circumstances would lose her proficiency when
she was upset: ‘an unexpected noise, or even the presence of an unfamiliar
person in the room was enough to reduce her to a state of blind confusion’
(Humphrey, 1992, p. 89).
Conceivably, this is a consequence of blindsight’s being blind. Patients
with absolute cortical blindness insist that they do not see any stimulus in
the affected field. This has been confirmed in many reports on blindsight.
The patients ‘never reported seeing any targets during the experimental pro-
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 Phenomenal Vision and Apperception 227
cedure’ and, finding the task puzzling, one commented: ‘How can I look at
something that I haven’t seen?’ (Pöppel et al., 1973, p. 295). The patients
‘consistently, repeatedly and firmly said that they did not experience any-
thing’ that was related to stimulus presentation in the blind field (Stoerig
and Cowey, 1992, p. 431); ‘no form of visual impression was ever reported
in the hemianopic field’ (Magnussen and Mathiesen, 1989, p. 727); ‘none of
the patients exposed to visual rotation in the blind field was aware of any-
thing happening on this side’ (Pizzamiglio et al., 1984, p. 96); the patient
‘insisted that he saw nothing’ (Weiskrantz et al., 1974, p. 4); ‘none of the
subjects ever saw the bars when the stimuli were delivered into their blind
field’ (Richards, 1973, p. 338). The ample evidence from the patients’ reports
has been complemented by evidence from hemianopic monkeys (monkeys
with cortical blindness in one hemifield caused by unilateral ablation of pri-
mary visual cortex). Within the hemianopic field, they show a loss of sensi-
tivity that ranges between 0.4 and 1.5 log units, and can respond to supra-
threshold targets with close to 100% correct performance. Nevertheless, they
classified the same supra-threshold stimuli that they localized perfectly as
‘no-stimulus’ or ‘blank trials’ in a signal detection task (Cowey and Stoerig,
1995; Stoerig and Cowey, 1995).

2.1 Blindsight and Hue

The evidence indicates that blindsight is blind in the sense that the blindsight
patient does not see a phenomenal image of the stimulus although he can
‘guess’ its presence and, again in a guessing mode, even discriminate its
wavelength. Nelkin repeatedly comes back to this ‘hue’ discrimination,
because it has been argued (for instance by Hardin, 1988) that colours are
essentially phenomenal. If blindsight is non-phenomenal, the discrimin-
ability of red and green stimuli must be based on their difference in wave-
length or on an ensuing difference in physiological processing, but not on
colour which is the phenomenal counterpart of wavelength in conscious
vision. The colour words (for instance ‘red’ and ‘green’) that we asked the
patients to use during the two-alternative forced-choice guessing procedures
could easily be replaced with ‘1’ and ‘2’ or with ‘630’ and ‘550 nm’ (Stoerig,
1987; Stoerig and Cowey, 1992, Brent et al., 1994), and should thus not be
seen as indicating an underlying phenomenality of hue. Nelkin acknowl-
edges this possibility (p. 178) but nevertheless holds on to the view that it
is colours and not wavelengths (or physiological indices of chromaticity) that
are being discriminated.
To stress this point, he accumulates several additional hypotheses
(pp. 178–9):

(1) Extrastriate visual cortical areas are involved in monkey blindsight

colour discrimination, in particular area V4 where cells are known to
respond in a colour-constant fashion (Wild et al., 1985).
(2) An involvement of these cells renders it ‘reasonable to think that for
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228 Mind & Language
the blindsight monkeys ‘color’ = ‘hue’, because constancy correlates
more strongly to hue than to wavelength’ (p. 178).
(3) A similar human extrastriate cortical colour area containing colour-
constant cells could be involved in human blindsight, and thus there
may be colour constancy in blindsight wavelength discriminations.
(4) If hemispherectomized patients, like patients with destruction of the
visual cortex, succeed at blindsight wavelength discrimination as
well, and in a manner that implies colour rather than wavelength
discrimination, this ability cannot depend on extrastriate cortical col-
our areas.

Let us examine these hypotheses:

(1) Monkeys with striate cortex ablations have been reported to discrimi-
nate stimuli of different colour (Keating, 1979), and indeed extrastriate
cortical areas may well be involved in their discriminability. How-
ever, the existing evidence shows that while the occipitoparietal vis-
ual areas retain visual responsivity when primary visual cortex is
inactivated, the occipitotemporal areas do not, or to a minimal extent
(Bullier et al., 1993). V4 is part of this ventral processing stream and
therefore less likely a candidate for wavelength discrimination.
(2) Similarly, there is no evidence available that would show an area with
colour-constancy coded cells to be involved. More to the point, neither
is there evidence for colour-constancy in monkey blindsight.
(3) Several areas in human extrastriate cortex respond selectively to col-
our (Gulyàs and Roland, 1991). Whether any, some, or all of these are
involved in blindsight wavelength discrimination is an open issue.
As in the monkeys, there is presently only evidence for visual respon-
sivity in the dorsal (occipitoparietal) cortical processing stream of
blindsight patients.
(4) Hemidecorticated patients who do not retain any extrastriate cortex
in the hemisphere contralateral to their hemianopic field, do not show
blindsight as demonstrated with direct (guessing) methods (King et
al., 1996; Stoerig et al., 1996), let alone wavelength discrimination. The
descriptions ‘blue as the sky’ or ‘like a sunset’ that the patients uttered
appropriately in response to light blue and orange stimuli, and that
I mentioned to Nelkin (see p. 179) were indeed evidence of a phenom-
enal perception, only we could in the end not find any evidence that
this was mediated by the hemianopic field. Instead, statistically sig-
nificant detection and colour identification only occurred when the
stimuli were intense enough to be detected by the unaffected hemi-
retina on the basis of intraocular light reflection and diffusion (Stoerig
et al., 1996).

It is clear that the latter finding does not preclude the possibility that
patients and monkeys with damage confined to the visual cortex demon-
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 Phenomenal Vision and Apperception 229
strate wavelength discriminability indicative of colour constancy. If there
was colour constancy in blindsight—and it would not matter in this context
which part of the remaining visual system was responsible for it—then its
presence would provide a (still very controversial) argument in favour of a
phenomenal representation of chromatic information in blindsight (see Stoe-
rig, 1997). However, so far there is no answer to this empirical question.
Indeed, the related evidence from a dyschromatopsic patient (a patient with
a central colour vision deficit) demonstrated that colour vision and colour
constancy were affected in tandem (Kennard et al., 1995). Although colour
constancy may well turn out to be a composite of several mechanisms,
encompassing retinal as well as extrastriate cortical stages, what little empiri-
cal evidence there is indicates that constancy is lost along with colour vision.
It follows that at least for now there is no empirical reason to think that
there are phenomenal images involved in blindsight. The patients claim they
do not have them, the monkeys appear to claim something similar, and the
chromatic discriminations that blindsight patients can perform do not sup-
port a divergent view: blindsight, like purely reflexive visual processing,
appears to be an instance of non-phenomenal vision.
Although Nelkin concedes that this straightforward reading of the avail-
able evidence—that blindsight patients lack the phenomenal representation
of visual stimuli—is at least ‘empirically and theoretically possible’, he does
not share this view: ‘Actually, I don’t think that the right interpretation of
these cases is that no phenomena are experienced. Rather, it is only that the
clinical subjects are not apperceptively conscious of their phenomenal states’
(p. 57). This brings us to apperception, another kind of consciousness.

3. Blindsight: Phenomena Without Apperception?

Apperception is not a simple term. That I am apperceptively aware of my

watch means more than that I have a phenomenal image of it. It can mean
that I know I have this image because I looked at the watch, i.e. I know that
it is through my vision that the watch is given to me. It can mean that I can
introspect the image of the watch, and thus know that I have it even if I do
not know that it is through my eyes that I do. In addition to ‘I know that I
have an image’ it can also imply that ‘I know what I see’, i.e. a watch. In a
still broader sense, it can mean that some visual (or in general sensory) infor-
mation is available for conscious manipulation. In that sense, it is roughly
similar to information being consciously accessible. In the words of Block,
‘a representation is access-conscious if it is poised for direct control of
reasoning, reporting, and action’ (1996, p. 457).
In my opinion, blindsight patients have lost apperception in all these
meanings.

(1) The patients have lost the direct conscious knowledge of their seeing.
The patients certainly know that they are performing in a test, but
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230 Mind & Language
their commentaries indicate that they do not know that they see and
cannot judge the quality of their performance. ‘When shown his
results he [patient DB] expressed great surprise, and reiterated that he
was only guessing’ (Weiskrantz et al., 1974, p. 4); the patients ‘actually
believed their performance was completely random’ (Pöppel et al.,
1973, p. 296); the patient ‘had no awareness of her above-chance per-
formance’ (Magnussen and Mathiesen, 1989, p. 727); the patient
‘claimed he was only guessing, and could hardly believe that his per-
formance was above chance’ (Stoerig et al., 1985, p. 596). Blindsight
patients know not that they see; they may know that indirectly, for
instance because the experimenter tells them, but they have no direct
knowledge of the fact. This is comparable to the normally sighted
subjects’ ignorance of their pupil responses; you can acquire that
knowledge indirectly, for instance by watching your eyes in a mirror,
but you have no direct conscious access to the response.
Furthermore, the patients cannot even distinguish between the
highly significant performance which they show in response to visual
stimuli in their blind field and the chance level performance which
they show in response to stimuli confined to their blind spot, a recep-
tor-free zone of the retina used for control experiments (own
observation). As a consequence, without feedback, blindsight patients
do not know how they fare in their responses, just as the normally
sighted observer does not know of his pupil responses and their
variability.

(2) The patients do not consciously know what they see.

The watch in front of the blindsight patient’s eyes cannot be identified
as a watch; its meaning as an object, let alone as an individual object
(‘the one I received as a graduation present’), defies visual recog-
nition. Cortical blindness includes a dense agnosia; neither patients
nor monkeys show any evidence of recognizing objects. This intrinsic
connection was already apparent to William James who said: ‘total
blindness, sensorial as well as psychic, [comes] from destruction of
both [occipital lobes]’ (1890, p. 47). Similarly, Humphrey described
the cortically blind Helen as ‘a monkey who in a sense sees everything
but recognises nothing’ (Humphrey, 1970, p. 334). That cortical blind-
ness (Rindenblindheit) would encompass psychic blindness
(Seelenblindheit, agnosia) is an empirical finding; there’s no logical
necessity for object vision and recognition to depend on phenomenal
vision. However, there may be a biological necessity (Stoerig, 1997),
with a lack of phenomenal vision entailing an inability to see and
recognize objects.

(3) The patients cannot explicitly access the ‘blindseen’ visual information.
The patients cannot use the visual information they have processed
for direct control of reasoning or reporting. Control of action, another
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 Phenomenal Vision and Apperception 231
use visual information can be put to, is slightly more complicated an
issue because visually guided movements such as pointing and grasp-
ing are less affected than verbal responses and matching motor
responses in both blindsight (Perenin and Rossetti, 1996) and agnosia
(Goodale et al., 1991). It seems that motor control can to some extent
be executed in response to unconsciously processed visual infor-
mation while this same information cannot be used for conscious
planning of actions, reporting, reasoning, and remembering.

It is in principle possible that the loss of apperception and conscious access

is the primary deficit of blindsight; if you lose all access, you could still have
phenomenal images, but you would not have any means to use them, let
alone report them to others. Nelkin champions this possibility, and I agree
that this is a possible phenomenon. We have no way of knowing whether
someone has consciously inaccessible phenomenal images because we have
no means to directly access someone else’s phenomenal images. Indeed, I
think that phenomenal images in the absence of apperception are a distinct
possibility, and may even be a phase in our normal development. The first
conscious visual experiences of an infant are likely to be of colour and bright-
ness; apperceptions, concepts, thoughts seem to come much later. I therefore
agree with Nelkin that phenomenal images can occur in the absence of
apperception. I should even concede that this situation could be a clinical
symptom. In analogy to a locked-in syndrome, a state in which the patient
is self-aware but unable to communicate, to talk, or to move anything other
than his eyes and eye-lids, such a pathological state would be a visual
locked-in syndrome in which the visual information is phenomenally rep-
resented but the patient cannot use it in any way. The patient could still
show evidence for blind visual functions such as neuroendocrine responses
and reflexes, but his visual images would remain private in a sense stronger
than any one in which it is commonly used in philosophical essays.
While I agree that phenomena can exist and not be apperceived, I do not
share Nelkin’s view that this is likely to be the case in blindsight. Why?

3.1 The Phenomenal Image Is the First Stage of Conscious Vision

A review of the acquired disturbances of conscious vision demonstrates that

the phenomenal representation of visual information can be preserved in the
absence of any object vision and recognition. Patients with lesions in extra-
striate visual cortex can suffer from an inability to segregate the visual image
into foreground, background, and objects which renders them incapable to
copy, draw, and match any visually presented object. This ‘apperceptive
agnosia’ can be found in the presence of normal visual acuity, colour and
motion vision (Benson and Greenberg, 1969), indicating that phenomena are
prior to object vision. The next stage of conscious vision is disturbed in
‘associative agnosia’, a syndrome in which objects are seen—can be drawn,
copied, matched, described—but are not recognized: their use, meaning, and
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232 Mind & Language
individuality are (consciously) inaccessible to the patient (Lissauer, 1889;
Rubens and Benson, 1971). The reverse disorder has never been reported:
one can suffer from agnosia despite possessing the full repertoire of phenom-
enal vision, but one cannot suffer a loss of phenomenal vision and retain
conscious object recognition (see Stoerig, 1996).
This sequence of processing stages has a correlate in the lesions causing
the syndromes. The phenomenal stage is lost following lesions to primary
visual cortex. Individual qualia are selectively lost following lesions to early
extrastriate visual cortical areas (see Cowey, 1994, for review): cerebral ach-
romatopsia (colour-blindness) for instance results from lesions to the occipi-
totemporal gyrus (e.g. Meadows, 1974), and cerebral akinetopsia (motion-
blindness) from lesions to a highly myelinated area in the occipito-temporo-
parietal region (see Zeki, 1991, for review). Early visual cortical areas there-
fore seem to be necessary for phenomenal vision. Object vision is lost follow-
ing poorly defined extensive extrastriate cortical lesions, which could indi-
cate that the binding of phenomena into objects requires a different kind of
processing to act on the same set of areas involved in generating the
phenomenal representations (Singer, 1990). Object recognition finally
requires the visual cortical areas to connect to memory, and can be lost when
fibre bundles travelling to the temporal lobes and hippocampal structures
are destroyed (Albert et al., 1979).
Phenomenal vision thus appears prior to object vision and recognition,
and a destruction of the primary visual cortex causes its loss.

3.2 Images Generated in Cortical Blindness Are Apperceived

It has been known for a century that even patients with complete cortical
blindness caused by bilateral occipital damage can for a limited period of
time experience visual hallucinations (Seguin, 1886). The hallucinated images
are assumed to be caused by pathological hyper-excitation in temporal lobe
structures (Gloning et al., 1967; Kölmel, 1985). The patients consciously
apperceive these images, and they report them, at least if they don’t worry
that the asking party will judge them to be out of their mind. It follows
that if a phenomenal image is generated in a cortically blind field, it can be
apperceived, indicating that the disturbance is not at the level of appercep-
tion.

3.3 Stored Visual Information Is Accessible in Cortically Blind Patients

Stored visual information about the shape, the colour, and the particular
movement of objects can be accessed by patients who have suffered a lesion
that caused a cortical blindness. Phenomenal imagery appears to be lost
along with phenomenal vision; at least that is the conclusion rendered prob-
able by Farah et al.’s (1992) finding that following an occipital lobe resection
the patient’s ‘internal screen’ shrank in tandem with her visual field. In con-
trast, such cortically blind patients are still able to describe the shape of an
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 Phenomenal Vision and Apperception 233
animal’s eyes and ears (Goldenberg and Artner, 1991) and respond to a var-
iety of questions requiring recall of detailed visual information (Chatterjee
and Southwood, 1995)—always provided they have accumulated the infor-
mation before the lesion. This indicates again that it is not the conscious
access to visual information that is lost in blindsight. If the visual information
has passed through the phenomenal stage before the lesion occurred, it
remains consciously accessible; if it has not passed through that stage
because it was only presented after the lesion, it cannot be apperceived.
For Nelkin to be right, for blindsight to be a loss of apperception in the
presence of visual phenomena, the results I listed above have to be explained
in a different manner. This may be possible in some instances. One could
argue that while the cortically blind patient loses apperception of the
phenomenal representation of the external visual world, previously stored
visual information remains apperceivable, as do endogenously generated
images (hallucinations). Blindsight would then be an extraordinary discon-
nexion syndrome with the patient losing the many different ways in which
we consciously access phenomenal visual information. The patient loses the
connection between vision and language areas because he cannot report that
he sees, let alone what he sees, although it is phenomenally represented; the
patient loses the connections between vision and motor areas because he
cannot deliberately sign that or what he sees; the patient loses the connec-
tions between vision and memory areas because he cannot consciously recall
anything he has phenomenally seen after his lesion; and the patient loses
the connections between vision and planning areas because he cannot use
the phenomenally represented information for any explicit future plan or
action. For this, his visual cortex would have to be disconnected effectively
from all the rest of the cortex. Such a situation could result from a lesion
that leaves striate and early extrastriate cortical areas intact while destroying
the surrounding tissue in a way that disrupts all connections to parietal,
temporal and frontal lobe areas (see Nakamura and Mishkin, 1986, for an
experimental study). At the same time though, not only visual memories
but also in addition a particular kind of phenomenal image, namely the
hallucinated one, could be apperceived.
Although this scenario is not impossible, I do not find it a plausible scen-
ario for cortical blindness and blindsight. I do however agree that phenom-
enal representations can exist without apperception. I also agree that visual
information can be consciously accessed when it is not phenomenally rep-
resented provided it has at some time passed through a phenomenal state.

4. Is Unconscious Vision Perception?

Do the neuroendocrine, reflexive and ‘blindsight’ forms of unconscious vis-

ual information processing qualify as perception? Or should the term be
reserved for conscious perception? One could argue for the latter purely on
pragmatic grounds; it is simpler to just write ‘perception’ whenever one
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234 Mind & Language
means conscious sensory perception. But there could be a more interesting
reason to reserve the term for conscious perception: if perception was essen-
tially tied to consciousness, then any form of unconscious vision could per
definitionem not qualify as perception.
If this is not a mere matter of definition, perception must involve conno-
tations that only link it to conscious states. The connotations that Nelkin
(p. 151) addresses, referring primarily to Searle’s writing (1983, 1989), are
intentionality and aspectuality.
I’ll address mostly intentionality, which I take to mean ‘aboutness’ in the
sense that intentional states are always about something. Above, I have put
forward the hypothesis that the various levels of visual information pro-
cessing are all about something. What varies is what they are about; that
grows increasingly complex. It is light levels for melatonin suppression; light
levels plus information about the light’s spatiotemporal distribution that vis-
ual reflexes are about; it is that plus wavelength, motion, and disparity that
blindsight is about. Phenomenal vision is about colour, motion, depth, and
brightness; object vision is about visual objects and perspective; and recog-
nition, in addition, is about the objects’ meaning. The information that gets
used at these different processing levels grows, with new properties being
added at each stage. It is not a question of ‘no aboutness’ turning into ‘about-
ness’ when consciousness appears.
In addition to this aboutness, unconscious vision is intentional because it
serves the organism. It serves it by helping self-preservation—by adapting
it, him or her to the day-and-night cycle (melatonin-suppression); by pre-
venting it, him or her from harm through over-exposure to high intensity
light (pupil reflex); by allowing navigation and prehension on the basis of
visual information that is not phenomenally represented (blindsight). As
unconscious vision is intentional in this sense of serving a biological pur-
pose, it is also aspectual, i.e. seen from a viewpoint, namely that of the organ-
ism that is unconsciously processing the visual information. Whether this is
an organism which is in principle incapable of conscious states in any form,
or whether it is one who through some pathology is incapable solely of
conscious vision, does not make a difference. If there is both unconscious
and conscious intentionality, then intentionality is not essentially connected
to consciousness. This view is in agreement with Nelkin, who arrives at it
via a different series of arguments (pp. 150–62). By virtue of its aboutness,
unconscious vision may qualify as perception.

Institute of Physiological Psychology II

Heinrich-Heine-University

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