© 2010 Federation of European Psychophysiology Societies

G. G. Celesia:
Journal Visual Perception
of Psychophysiology 2010; and 24(2):62–67
Hogrefe
Vol. Awareness
Publishing

Article

Visual Perception and Awareness

A Modular System
Gastone G. Celesia
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.

Chicago Council on Science and Technology, Loyola University of Chicago, IL, USA
This document is copyrighted by the American Psychological Association or one of its allied publishers.

Abstract. The study of visual processing and abnormalities due to lesions of cortical structures sheds light on visual awareness/con-
sciousness and may help us to better understand consciousness. We report on clinical observations and psychophysical testing of achro-
matopsia/prosopagnosia, visual agnosia, and blindsight. Achromatopsia and prosopagnosia reveal that visual cortices have functionally
specialized processing systems for color, face perception, and their awareness, and that furthermore these systems operate independently.
Dysfunction is limited to some aspects of visual perception; someone with achromatopsia, although not conscious of color, is aware of
the objects’ form, motion, and their relationship with sound and other sensory percepts. Perceptual awareness is modular, with neuronal
correlates represented by multiple separate specialized structures or modules. Visual agnosia shows that awareness of a complete visual
percept is absent, though the subject is aware of single visual features such as edges, motion, etc., an indication that visual agnosia is a
disruption of the binding process that unifies all information into a whole percept. Blindsight is characterized by the subject’s ability to
localize a visual target while denying actually seeing the target. Blindsight is mediated by residual islands of the visual cortex, which
suggests that sensory modules responsible for awareness can function only when structurally intact. We conclude (1) that perceptual
awareness (consciousness?) is modular, and (2) that perceptual integration is also modular, which suggests that integration among distinct
cortical regions is a parallel process with multiple communication pathways. Any hypothesis about consciousness must include these
observations about the presence of multiple parallel, but spatially and temporally different, mechanisms.

Keywords: consciousness, awareness, visual agnosia, cerebral achromatopsia, modular processing, blindsight, prosopagnosia

Introduction falsehood.” With these admonitions in mind, I emphasize

The definition of consciousness is a difficult and controver-
sial task. Most neuroscientists still agree with Huxley, who
in 1866 wrote: “What consciousness is, we know not”; and
with Crick and Koch (1990), who said consciousness is
“the most mysterious aspect of the mind-body problem.”
Avanzini (1999) suggests that “we can define conscious-
ness as the awareness of self and of internal and external
environments organized in space and time categories.” In
1994, Nobel Prize winner Francis Crick stated: “Now is the
time to think scientifically about consciousness (and its re-
lationship, if any, to the hypothetical immortal soul) and,
most important of all, the time to start the experimental
study of consciousness in a serious and deliberate way.” It
is now possible to study “the nature and function of our
subjective experience” (Güzeldere, Flanagan, & Gray
Hardcastle, 2000) that we call consciousness.
I limit this report to conscious and unconscious visual
perception as a method of promoting the understanding of
consciousness, thereby trying to sort out reliable informa-
tion from pure speculation. Eccles (1970) suggested that
any hypothesis must conform to “all existing knowledge”;
similarly Popper (1962) stated: “Coherence cannot estab-
lish truth, but incoherence and inconsistency do establish
the existing knowledge based on clinical observations.
Methods
I limit my observations to the visual system, specifically to
human data on conscious and unconscious visual percep-
tion. The data reported here stem from my personal clinical
case studies gathered over the last 40 years. Institutional
approval for experiment on humans was always obtained,
and each subject gave informed consent. The Helsinki dec-
laration on human experimentation was adhered to in the
gathering of data. Patients underwent a full neuro-ophthal-
mological examination, including visual acuity, and visual
field testing with V4e and I4e targets using Goldmann dy-
namic perimetry. They were asked to draw a clock and a
daisy on an 8½ × 11-inch sheet of paper. Color testing was
evaluated with psychophysical techniques including Ishi-
hara pseudoisochromatic plates and L’Anthony’s desatu-
rated panel D-15. Facial recognition was tested with five
US presidents’ portraits (Washington, Lincoln, Kennedy,
Nixon, and Reagan) and photographic pictures of family
members; we also tested each patient with the picture com-

Journal of Psychophysiology 2010; Vol. 24(2):62–67 Hogrefe Publishing

DOI: 10.1027/0269-8803/a000014
 G. G. Celesia: Visual Perception and Awareness 63

pletion from the WAIS. Visual evoked potentials (VEPs) to

alternating checks of 15 and 31 minutes of arc were record-
ed in most of the patients. Patient with blindsight had sac-
cade monitoring during the presentation of targets to the
blind and to the spared field. For details of the experimental
procedures we refer to prior publications (Celesia & Bri-
gell, 2005; Celesia, Bushnell, Toleikis, & Brigell, 1991).
Every patient underwent multiple MRI and CT as appro-
priate to determine the extent of cerebral lesions.

Results
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The data presented here can be subdivided into three topics:

(1) specific disorders of visual perception such as cerebral
achromatopsia; (2) deficit of visual integration such as vis-
ual agnosia; (3) blindsight.

Specific Disorders of Visual Gnosis Limited

to One Specific Aspect of Perception
These disorders (Celesia, 2005, 2007) include cerebral ach-
romatopsia, prosopagnosia, topographic agnosia, visual
language disturbances, and pure alexia. For brevity I limit
my presentation here to cerebral achromatopsia and pro-
sopagnosia. Cerebral achromatopsia is the failure to recog-
nize colors due to a lesion of the central nervous system.
The subjects are aware of their deficit and complain that
they see everything in black and white or in shades of gray.
Prosopagnosia is “a failure to recognize people known to
the patient on the basis of visual perception of their faces”
(Hecaen & Angelergues,1962). We report three cases of ce-
rebral achromatopsia (CA) due to cerebral ischemic in-
farcts. The subjects were tested repeatedly over 1 to 5 years
after the initial stroke. All patients had at least a superior
altitudinal visual field defect (Table 1), prosopagnosia, and
alexia without agraphia. The patients complained that they
could not see colors, but saw all images only in shades of
gray. As shown in Table 1, they all failed L’Anthony and
Ishihara’s color plates testing. They were able to imagine
objects in color, and two of them even claimed dreaming in
color. None of the subjects had any deficit in somatosensory
perception, audition, comprehension, or memory. MRIs of
the brain revealed a bilateral lesion involving the lingual,
fusiform gyri and part of the parahippocampal gyri (see
Figure 1).

Deficit of Visual Integration

The subject is a female aged 26 who developed severe head-
aches and had difficulty seeing. According to her mother, her
blindness had started on February 20, 2003. The patient could
not see her family members although she could see changes

Hogrefe Publishing Journal of Psychophysiology 2010; Vol. 24(2):62–67

 64 G. G. Celesia: Visual Perception and Awareness
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Figure 3. MRI of the lesions observed in the subject with

This document is copyrighted by the American Psychological Association or one of its allied publishers.

Figure 1. Diagram of the lesions observed in the three pa-
tients with cerebral achromatopsia and prosopagnosia. The
lesions were bilateral and involved both the lingual and fu-
siform gyri.
Figure 2. 26-year-old woman with visual agnosia, who
could copy alphabetic letters, numbers, and line drawings,
but was unable to identify what she was seeing or drawing.
Her drawing of a daisy was poor, and she realized “that is
not quite it.” Her performance suggests that she could cor-
rect register form perception, lines, and edges as well as
their correct position and orientation, but could not “bind”
together this information to identify the whole visual per-
cept.
visual agnosia (same subject as in Figure 2). Note the spar-
ing of the striate cortices.
in the lighting. The patient stated that her sight appeared to be
black with occasional movements and lights. On February 22
she behaved as if blind, claiming she could not see, but when
pressed she was able to cooperate and agreed she has some
vision (Table 2). She stated that she could identify family
members and friends by their voice, but she could not “see”
them. When asked to draw from memory a daisy she drew a
circle and stated “that is not quite it,” though she did not know
why. When asked to copy drawing of shapes (circle, triangle,
square, etc.) she was able to do so, but could not identify any
of the shapes (see Figure 2) When asked to match images such
as a house and a cross, she did it correctly but then did not
know what the objects were. When looking at an illustration
she could not describe it and stated “I cannot make sense of
it.” She could not identify any of the Ishihara color plates. She
showed correct registration of the constituents of form, line,
and edge elements as well as their correct position and orien-
tation. She could at times identify a line drawing, but only in
isolation, not as a part of a whole illustration. She could not
“bind together” these form elements into a whole perception.
She had in fact visual agnosia, though she had no difficulties
recognizing and interpreting perceptions from other sensory
systems (olfactory, auditory, and somatosensory). As shown
in Figure 3 she had bilateral lesions of the white matter in-
volving most of the connections from and to the visual cor-
tices. Areas 17, 18, 19, the lingual, fusiform, and parahippo-
campal gyri were intact.

Table 3. Visual performance in blindsight

Patient Age Localization Perception Pupillary Pupillary Recogni- PVEPs to PVEPs to PVEPs to VEP Map- Activation
with visual target of changes response response tion of any 15’ checks 31’ checks 60’ checks ping & am- of area 17 on
blindsight (forced in illumi- to light to Accom- visual per- plitude dis- PET/SPECT
choice) nation modation cepts tribution
Case KC 65 yes yes yes yes Absent Absent Absent Delayed nt yes
Case JB 81 yes yes yes yes Absent Absent Normal nt nt yes
Case GA 59 yes yes yes yes Absent nt Delayed nt Normal yes
Case TR 58 yes yes yes yes Absent Delayed Normal Normal Normal yes
Note: nt = not tested.

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 G. G. Celesia: Visual Perception and Awareness
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Blindsight
Fendrich, Wessinger, and Gazzaniga (1992) define blind-
sight as the “residual visual capacity in the absence of ac-
knowledged awareness.” We studied four subjects with
cortical blindness related to bilateral occipital infarcts.
They were able to localize visual targets although denied
having seen them. They were not aware of what “their eyes
have taken in nor what their brain have processed” (Weis-
krantz, 1993). As shown in Figure 4, positron emission
tomography (PET) showed increased cerebral blood flow
(rCBF) to visual stimulation with flashes and patterns in
the primary visual cortex of one subject. Similarly activa-
tion of the visual cortical areas was demonstrated by sin-
gle photon emission computed tomography (SPECT) in
the other three patients. VEPs to pattern stimulation were
recorded in all four cases. These patients (Table 3) had
preserved visually evoked potentials to pattern and flash
stimulation and had preserved rCBF in areas 17, 18, and
19. We concluded that visual information reached residual
islands of primary visual cortex but did not reach aware-
ness.
Discussion
As aptly stated by Crick (1994), there are many “forms of
consciousness, such as those associated with seeing,
thinking, emotion, pain and so on. Self-consciousness . . .
is probably a special case of consciousness.” The data pre-
sented here are confined to visual consciousness and based
on clinical and psychophysical observation of brain-dam-
aged individuals. As stated eloquently by Zeki and Bartels
(1999b): “Despite an increasing sophistication in the in-
struments that are able to detect and measure cortical ac-
tivity, a high and honorable place must still be reserved
for a much simpler and older technique, that of clinical
observation.” Psychophysical techniques such as visual
field perimetry, assessment of color vision, motion percep-
tion, and other visuo-perceptual testing are indispensable
to properly evaluating the visual system. The study of
Hogrefe Publishing
65
Figure 4. Regional cerebral blood
flow (rCBF) determined via positron
emission tomography (PET) in a pa-
tient with blindsight. rCBF is ex-
pressed in ml/100 g/minute. Four re-
gions of interest were selected,
roughly corresponding to the location
of areas 17, 18, and 19. The number
above each bar indicates the rCBF val-
ue. Note the increased rCBF with vis-
ual stimulation indicating neuronal ac-
tivation of the visual areas.
brain-damaged individuals provides results that cannot be
obtained in any other way. The three cases of achromatop-
sia and prosopagnosia show not only that the visual cortex
has functionally specialized processing systems for color
and face perception and awareness, but also that these sys-
tems can “act fairly autonomously” (Zeki & Bartels,
1999a). Dysfunction of these systems does not affect au-
ditory, olfactory, somatosensory, and other visual aware-
ness not related to color or facial recognition. The subject
with achromatopsia, although not conscious of color, is
aware of the objects’ form, motion, and their relationship
with sound and other sensory percepts. This indicates that
perceptual awareness is modular, with neuronal correlates
of awareness represented by multiple specialized but sep-
arate structures or modules. Furthermore, these cortical
processing areas are also perceptual sites. Zeki (2008)
suggests that each of these systems represent its own “mi-
croconsciousness.” In two of our subjects mnemonic rep-
resentations of prior experiences associated with color and
faces (imagining, dreaming) were preserved, suggesting
that these representations were stored in different regions
than the fusiform and lingual gyri, and were thus accessi-
ble to the subject via separate pathways. The multifaceted
complexity of the visual perception is clearly shown by
the patients’ restricted visual deficit while preserving oth-
er visual consciousness/awareness. If visual awareness is
modular with specialized structures or modules for color,
object, motion, and other features distributed both in space
and time, to see a complete conscious visual percept there
must be a process that unifies or binds all this “microcon-
sciousness” into a complete visual consciousness. Should
this hypothesis be correct, it follows that a disruption of
this binding process interferes with the awareness of a
complete visual percept, while preserving the awareness
of single visual features such as edges, motion, etc. This
is essentially what happened to our subject with visual ag-
nosia: She showed correct registration of the constituents
of form perception – line and edge elements at their cor-
rect position and orientation. She could at times even iden-
tify lines in a drawing, but only in isolation, not as a part
of a whole illustration. But she failed to bind these form
elements together into a whole percept. Feature extraction
Journal of Psychophysiology 2010; Vol. 24(2):62–67
 66 G. G. Celesia: Visual Perception and Awareness
was preserved, but she was unable to integrate the various
aspects of the object into a complete image. The patient
had no difficulty integrating percepts from other sensory
systems (olfactory, auditory, and somatosensory). Rather,
her binding deficit was localized to the visual system. The
MRI showed that the visual cortices were intact, the bilat-
eral lesions being localized in the white matter disrupting
the input/output connections among the various visual
modules. The function of the network necessary for bind-
ing was impaired.
Our four cases of blindsight are remarkable because
they show that visual information reached the primary
visual cortex as demonstrated by the presence of VEPs
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
and the increased rCBF in the striate and extrastriate ar-
eas during visual stimulation with flashes or patterns. Yet
the subject denied seeing any visual stimulus, although
able to localize the target. In our cases, blindsight was
mediated by residual islands of visual cortex; yet the cor-
tical modules were sufficiently damaged to prevent con-
scious perception. These cases suggest that the sensory
modules responsible for microconsciousness can func-
tion only when structurally intact. Additionally, the dis-
sociation between cerebral activation and perception cau-
tions us about interpreting images of cerebral activation
as indicative of conscious perception.
But are these phenomena limited to the visual system?
We need to address the issue of whether modularity is
restricted to the visual system or is a general phenome-
non. If the observations reported above exist in another
sensory system, we could assume that modularity is a uni-
versal event. Clinical observations in the auditory system
provide the answer: Amusia and auditory agnosia are dys-
functions reported in the auditory system comparable to
the type of visual deficits just described. Amusia is the
loss of musical talent (Hou, 2003) usually related to dam-
age to the temporal lobe. McFarland and Fortin (1982)
describe an accomplished organist who suddenly lost his
ability to play familiar melodies as the result of an infarc-
tion of the right superior temporal and supramarginal
gyri. Schuppert, Munte, Wieringa, and Altenmuller
(2000) investigated perceptual musical functions in pa-
tients suffering from unilateral cerebrovascular cortical
lesions and found deficits in melodic and temporal musi-
cal appreciation in left temporal lobe-damaged patients
and overall impairment of music perception in right tem-
poral lobe-damaged patients. They concluded that recep-
tive amusia indicate “autonomous, yet partially integrated
neural subsystems underlying the processing of melodic
and temporal stimuli.” DiPietro, Laganaro, Leemann, and
Schnider (2004) reported amusia after a left temporal-pa-
rietal stroke in a professional musician. They described
“preserved metric judgment and normal performance in
all aspects of melodic processing,” while “he lost the
ability to discriminate or reproduce rhythms.” They con-
cluded that the temporal lobe does the “modality-specific
encoding of musical temporal information.” Thus percep-
Journal of Psychophysiology 2010; Vol. 24(2):62–67
tual awareness of music is modular and separate from
other auditory sensory perceptions.
Auditory agnosia is less well defined, but it usually
refers to impaired ability to recognize sound while having
a normal hearing. Clarke, Bellmann, Meuli, Assal, and
Steck (2000) described a subject deficient in recognizing
environmental sounds but with normal auditory localiza-
tion and auditory motion perception. Ulrich (1977) de-
scribed a case of auditory agnosia characterized by im-
pairment of acoustic discrimination and amusia. Vignolo
(2003) reported that right hemisphere lesions tended ei-
ther to disrupt the apperception of environmental sounds,
sparing music entirely, or to disrupt environmental
sounds and melody, sparing rhythm, whereas left hemi-
sphere lesions tended to spare melody and to disrupt
rhythm, either selectively or in association with the se-
mantic identification of environmental sounds. Ulrich
(1977) suggests that there is an analogy between auditory
agnosia and the syndrome of “perceptive visual agnosia.”
These cases confirm that sensory awareness (microcon-
sciousness) is processed by different modules, working
separately but in parallel.
How the various modules are bound together remains
to be discovered. Neuroscience has shown that the pro-
cess of sensory integration is a complex one that involves
many other cortical areas with continuous feedback and
feedforward. Communication among different areas may
be conducted by gamma frequency oscillations. Synchro-
nization at gamma and beta frequencies has been ob-
served in monkeys across several brain structures (Gre-
goriou, Gotts, Zhou, & Desimone, 2009). Enhanced os-
cillatory coupling (or synchronization) observed between
prefrontal and visual cortex during attention had a shift
in time of 8 to 13 ms allowing for spikes “initiated in one
area to affect cells at a peak depolarization phase in the
coupled area” (Gregoriou et al., 2009). Interactions be-
tween widespread neural regions in the brain is very fast
and “underlie fluid, organized behavior” (Knight, 2007).
In conclusion, neuroscience has shown from both clinical
and laboratory studies in humans and primates that
1. perceptual consciousness/awareness is modular,
2. perceptual integration (binding) is modular,
3. integration among distinct cortical regions is a fast, fluid
multipath process with communication pathways tuned
to different frequencies.
As Peissig and Tarr (2007) stated: “Despite this pro-
gress, the field is still faced with the challenge of devel-
oping a comprehensive theory that integrates this ever-
increasing body of results and explains how we perceive,
recognize” and be conscious of objects, their surround-
ing, and our relationship to them. Any hypothesis con-
cerning consciousness must include this knowledge
about multiple parallel but spatially and temporally dif-
ferent mechanisms.
Hogrefe Publishing
 G. G. Celesia: Visual Perception and Awareness
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Gastone G. Celesia
3016 Heritage Oak Lane
Oak Brook, IL 60523
USA
Tel. +1 630 968-2199
E-mail g.celesia@comcast.net
Journal of Psychophysiology 2010; Vol. 24(2):62–67