Perceptual Disorders

Perceptual Disorders
Oxford Handbooks Online

Josef Zihl
The Oxford Handbook of Cognitive Neuroscience, Volume 1: Core Topics
Edited by Kevin N. Ochsner and Stephen Kosslyn
Print Publication Date: Dec 2013 Subject: Psychology, Cognitive Neuroscience

Online Publication Date: Dec 2013 DOI: 10.1093/oxfordhb/9780199988693.013.0010
Abstract and Keywords
Perceptual processes provide the basis for mental representation of the visual, auditory,
olfactory, gustatory, somatosensory, and social “worlds” as well as for guiding and
controlling cognitive, social, and motor activities. All perceptual systems, i.e. vision,
audition, somatosensory perception, smell and taste, and social perception are
segregated functional networks and show a parallel-hierarchical type of organization of
information processing and encoding. In pathological conditions such as acquired brain
injury, perceptual functions and abilities can be variably affected, ranging from the loss of
stimulus detection to impaired recognition. Despite the functional specialization of
perceptual systems, association of perceptual deficits within sensory modalities is the
rule, and disorders of a single perceptual function or ability are rare. This chapter
describes cerebral visual, auditory, somatosensory, olfactory, and gustatory perceptual
disorders within a neuropsychological framework. Disorders in social perception are also
considered because they represent a genuine category of perceptual impairments.
Keywords: vision, audition, somatosensory perception, smell, taste, social perception, cerebral perceptual
disorders
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Introduction
Perception “is the process or result of becoming aware of objects, relationships, and
events by means of the senses,” which includes activities such as detecting,
discriminating, identifying, and recognizing. “These activities enable organisms to
organize and interpret the stimuli received into meaningful knowledge” (APA, 2007).
Perception is constructed in the brain and involves lower and higher level processes that
serve simpler and more complex perceptual abilities such as detection, identification, and
recognition (Mather, 2006). The behavioral significance of perception lies not only in the
processing of stimuli as a basis for mental representation of the visual, auditory, olfactory,
gustatory, somatosensory, and social “worlds” but also in the guidance and control of
activities. Thus there exists a reciprocal interaction between perception, cognition, and
action. For perceptual activities, attention, memory, and executive functions are crucial
prerequisites. They form the bases for focusing on stimuli and maintaining attention
during stimulus acquisition and processing, storing percepts as experience and concepts,
and controlling input and output activities that allow for an optimal, flexible adaptation to
extrinsic and intrinsic challenges.
The aim of this chapter is to describe the effect of pathological conditions, particularly
acquired brain injury, on the various abilities in the domains of vision, audition,
somatosensory perception, smell and taste, and social perception as well as the
behavioral consequences and the significance of these disorders for the understanding of
brain organization. Perceptual disorders can result from injury to the afferent sensory
pathways and/or to their subcortical and cortical processing and coding (p. 194) stages.
Peripheral injury usually causes “lower level” dysfunctions (e.g., threshold elevation or
difficulties with stimulus localization and sensory discrimination), whereas central
injuries cause “higher level” perceptual dysfunctions (e.g., in the domains of
identification and recognition). However, peripheral sensory deficits may also be
associated with higher perceptual disorders because the affected sensory functions and
their interactions represent a crucial prerequisite for more complex perceptual abilities
(i.e., detection and discrimination of stimuli build the basis for identification and
recognition).
Vision
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Visual perception comprises lower level visual abilities (i.e., the visual field, visual acuity,
contrast sensitivity, color and form vision, and stereopsis) and higher level visual abilities,
in particular visual identification and recognition. Visual perceptual abilities also form the
basis for visually guided behavior, such as oculomotor activities, hand and finger
movements, and spatial navigation. From its very beginning, visual neuroscience has
been concerned with the analysis of the various visual perceptual deficits and the
identification of the location of the underlying brain injury. Early clinical reports on
patients have already demonstrated the selective loss of visual abilities after acquired
brain injury. These observations have suggested a functional specialization of the visual
cortex, a concept verified many years later by combined anatomical, electrophysiological,
and behavioral evidence (Desimone & Ungerleider, 1989; Grill-Spector & Malach, 2004;
Orban, 2008; Zeki, 1993). The primary visual cortical area (striate cortex, Brodmann area
17, visual area 1, or V1) receives its input from the retina via the lateral geniculate body
(LGN) and possesses a highly accurate, topographically organized representation of the
retina and thus of the visual field. The central visual field occupies a large proportion of
the striate cortex; about half of the cortical surface is devoted to the central 10 degrees
of the visual field, which is only 1 percent of the visual field (Tootell, Hadjikhani,
Mendola, Marrett, & Dale, 1998). In addition, V1 distributes specific visual signals to the
other visual areas that are located in the surrounding cortex (for a review, see Bullier,
2003). This anatomical and functional organization enables the visual brain to deal with
the processing of global and local features of visual objects and scenes. The result of
processing at distinct levels of complexity at each stage can be flexibly and dynamically
integrated into coherent perception (Bartels & Zeki, 1998; Tootell et al., 1998; Zeki, 1993;
Zeki & Bartels, 1998). Because of the inhomogeneity of spatial resolution and acuity in
the visual field (Anstis, 1974), the field size for processing visual details (e.g., form vision)
is much smaller, comprising the inner 9 degrees of the binocular visual field (i.e., macular
region; Henderson, 2003). Occipital-parietal, posterior parietal, and prefrontal
mechanisms guarantee rapid global context extraction as well as visual spatial working
memory (Bar, 2004; Henderson, 2003; Hochstein & Ahissar, 2002).
Ungerleider and Mishkin (1982) have characterized the functional specialization of the
visual brain as consisting of two processing streams: The “where” pathway or dorsal
route, comprising occipital-parietal visual areas and connections, is specialized in space
processing; and the “what” pathway or ventral route, comprising occipital-temporal visual
areas and connections, is specialized in object processing. According to Milner and
Goodale (2008), information processed in the dorsal pathway is used for the implicit
visual guidance of actions, whereas explicit perception is associated with processing in
the ventral stream. Because visual perception usually involves both space- and object-
based information processing, cooperation and interaction between the two visual
streams are required (Goodale & Westwood, 2004). In addition, both routes interact
either directly or indirectly via attention involving the inferior parietal cortex (Singh-
Curry & Husain, 2009) and working memory involving the prefrontal cortex (Goodale &
Westwood, 2004; Oliveri et al., 2001). Eye movements play a crucial role in visual
processing and thus in visual perception (for a comprehensive review, see Martinez-
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Conde, Macknik, & Hubel, 2004). The posterior thalamus and its reciprocal connections
with cortical regions in the occipital, parietal, and frontal lobes and with the limbic
neocortex form a cortical-subcortical network subserving intentionally guided and
externally triggered attention as well as saccadic eye movements that are involved in
visual information processing (e.g., Andersson et al., 2007; Dean, Crowley & Platt 2004;
Himmelbach, Erb, & Karnath, 2006; Nobre, 2001; Olson et al., 2000; Schiller & Tehovnik,
2001, 2005). Complex visual stimuli (e.g., objects and faces) are coded as specific
categories in extrastriate regions in the ventral visual pathway (Grill-Spector, 2003;
Sigala, 2004; Wierenga et al., 2009). Top-down processes involving the prefrontal cortex
facilitate visual object recognition (Bar, 2003), and hippocampal-dependent memory
builds the basis for experience-dependent visual scanning (Smith & Squire, 2008).
(p. 195) Yet, it is still unclear how the brain eventually codes complex visual stimuli for
accurate identification and recognition; it appears, however, that complex visual stimuli
are simultaneously represented in two parallel and hierarchically organized processing
systems in the ventral and dorsal visual pathways (Konen & Kastner, 2008).
About 30 percent of patients with acquired brain injury suffer from visual disorders
(Clarke, 2005; Rowe et al., 2009; Suchoff et al., 2008). Lower level visual functions and
abilities (e.g., visual detection and localization, visual acuity, contrast sensitivity, and
color discrimination) may be understood as perceptual architecture, whereas higher
level, visual-cognitive capacities (e.g., text processing and recognition) also involve
learning and memory processes as well as executive functions. Selective visual disorders
after brain injury are the exception rather than the rule because small “strategic” lesions
are very rare and visual cortical areas are intensely interconnected. Injury to the visual
brain, that is, to visual cortical areas and fiber connections, therefore commonly causes
an association of visual disorders.
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Visual Field
A homonymous visual field defect is defined as a restriction of the normal visual field
caused by injury to the afferent postchiasmatic visual pathway, that is, an interruption in
the flow of visual information between the optic chiasm and the striate cortex.
Homonymous visual field disorders are characterized by partial or total blindness in
corresponding visual field regions of each eye. In the case of unilateral postchiasmatic
brain injury, vision may be lost in the left or right hemifield (homonymous left- or right-
sided hemianopia), the left or right upper or lower quadrants (homonymous upper or
lower quadranopia in the left or right hemifield), or a restricted portion in the parafoveal
visual field (paracentral scotoma). The most common type of homonymous visual field
disorders is hemianopia (loss of vision in one hemifield), followed by quadranopia (loss of
vision in one quadrant) and paracentral scotoma (island of blindness in the parafoveal
field region). Visual field defects are either absolute (complete loss of vision, anopia) or
relative (depressed vision, amblyopia, hemiachromatopsia). Homonymous amblyopia
typically affects the entire hemifield (hemiamblyopia), and homonymous achromatopsia
(i.e., the selective loss of color vision) typically affects one hemifield (hemiachromatopsia)
or the upper quadrant. Visual field defects differ with respect to visual field sparing.
Foveal sparing refers to sparing of the foveal region (1 degree), macular sparing refers to
the preservation of the macular region (5 degrees), and macular splitting refers to a
sparing of less than 5 degrees (for review, see Harrington & Drake, 1990). In the majority
of patients (71.5 percent of 876 cases), field sparing does not exceed 5 degrees. As a rule,
patients with small visual field sparing are more disabled, especially with regard to
reading. Stroke represents the most common etiology, but other etiologies such as
traumatic brain injury, tumors, multiple sclerosis, and cortical posterior atrophy may also
cause homonymous visual field disorders (see Zihl, 2011).
About 80 percent of patients (n = 157) with unilateral homonymous visual field loss suffer
from functional impairments in reading (hemianopic dyslexia) and/or in global perception
and overview (Zihl, 2011). Homonymous visual field loss causes a restriction of the field
of view, which prevents the rapid extraction of the entire spatial configuration of the
visual environment. It therefore impairs the top-down and bottom-up interactions that are
required for efficient guidance of spatial attention and oculomotor activities during scene
perception and visual search. Patients with additional injury to the posterior thalamus,
the occipital white matter route (i.e., fiber pathways to the dorsal visual route and
pathways connecting occipital, parietal, temporal, and frontal cortical areas) show
disorganized oculomotor scanning behavior (Zihl & Hebel, 1997; Mort & Kennard, 2003).
The impairments in global perception and visual scanning shown by these patients are
more severe than those resulting from visual field loss alone (Zihl, 1995a). Interestingly,
about 20 percent show spontaneous substitution of visual field loss by oculomotor
compensation and thus enlargement of the field of view; the percentage is even higher in
familiar surroundings because patients can make use of their spatial knowledge of the
surroundings (Zihl, 2011). In normal subjects, global visual perception is based on the
visual field within which they can simultaneously detect and process visual stimuli. The
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visual field can be enlarged by eye shifts, which is typically 50 degrees in all directions
(Leigh & Zee, 2006). The resulting field of view is thus defined by the extent of the visual
field when moving the eyes in global visual perception (see also Pambakian, Mannan,
Hodgson, & Kennard, 2004).
Reading is impaired in patients with unilateral homonymous field loss and visual field
sparing of less than 5 degrees to the left and less than 8 degrees to the right of the fovea.
In reading, the visual brain (p. 196) relies on a gestalt-type visual word-form processing,
the “reading span.” It is asymmetrical (larger to the right in left-to right-orthographies)
and is essential for the guidance of eye movements during text processing (Rayner, 1998).
However, insufficient visual field sparing does not appear to be the only factor causing
persistent “hemianopic” dyslexia. The extent of brain injury affecting in particular the
occipital white matter seems to be crucial in this regard (Schuett, Heywood, Kentridge, &
Zihl, 2008a; Zihl 1995b). That reading is impaired at the pre-semantic visual sensory level
is supported by the outcome of treatment procedures involving practice with nontext
material, which have been found to be as effective as word material in reestablishing eye
movement reading patterns and improving reading performance (Schuett, Heywood,
Kentridge, & Zihl, 2008b).
In the case of bilateral postchiasmatic brain injury, both visual hemifields are affected,
resulting in bilateral homonymous hemianopia (“tunnel vision”), bilateral upper or lower
hemianopia, bilateral paracentral scotoma, or central scotoma. Patients with bilateral
visual field disorders suffer from similar, but typically more debilitating, visual
impairments in global visual perception and reading. A central scotoma is a very dramatic
form of homonymous visual field loss because foveal vision is either totally lost or
depressed (central amblyopia). The reduction or loss of vision in the central part of the
visual field is typically associated with a corresponding loss of visual spatial contrast
sensitivity, visual acuity, and form, object, and face perception. The loss of foveal vision
also causes a loss of the central reference for optimal fixation and of the straight-ahead
direction as well as an impairment of the visual-spatial guidance of saccades and hand-
motor responses. As a consequence, patients cannot accurately fixate a visual stimulus
and shift their gaze from one stimulus to another, scan a scene or a face, and guide their
eye movements during scanning and reading. Patients therefore show severe
impairments in locating objects, recognizing objects and faces, finding their way in rooms
or places, and reading, and often get lost when scanning a word or a scene (Zihl, 2011).
Visual Acuity, Spatial Contrast Sensitivity, and Visual Adaptation
After unilateral postchiasmatic brain injury, visual acuity is usually not significantly
reduced, except for cases in which the optic tract is involved (Frisén, 1980). After
bilateral postchiasmatic injury, visual acuity can either be normal, gradually diminished,
or totally lost (i.e., form vision is no longer possible) (Symonds & MacKenzie, 1957). This
reduction in visual acuity cannot be improved by optical correction.
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When spatial contrast sensitivity is reduced, patients usually complain of “blurred” or

“foggy” vision despite normal visual acuity, accommodation, and convergence (Walsh,
1985). Impairments of contrast sensitivity have been reported in cerebrovascular
diseases (Bulens, Meerwaldt, van der Wildt, & Keemink, 1989; Hess, Zihl, Pointer, &
Schmid, 1990); after closed head trauma, encephalitis, and hypoxia (Hess et al., 1990); in
Parkinson’s disease (Bulens, Meerwaldt, van der Wildt & Keemink, 1986; Uc et al., 2005);
multiple sclerosis (Gal, 2008); and dementia of the Alzheimer type (Jackson & Owsley,
2003). Bulens et al. (1989) have suggested that impairments of contrast sensitivity for
high spatial frequencies mainly occur after occipital injury, whereas impairments of
sensitivity for lower spatial frequencies occur after temporal or parietal injury. Depending
on the severity of the sensitivity loss, patients have difficulties with depth perception, text
processing, face perception, and visual recognition. Because reduction in spatial contrast
sensitivity is not necessarily associated with reduced visual acuity, assessing visual acuity
alone is not sufficient for detecting impaired spatial contrast sensitivity.
Color Vision
Color vision may be lost in the contralateral hemifield (homonymous hemiachromatopsia)

or in the upper quadrant after unilateral occipital-temporal brain injury. Because light
sensitivity and form vision are not impaired in the affected hemifield, the loss of color
vision is selective (e.g., Short & Graff-Radford, 2001). Patients are usually aware of this
disorder and report that the corresponding part of the visual environment appears “pale,”
in “black and white,” or “like in an old movie.” In the case of cerebral dyschromatopsia,
foveal color vision is affected with and without the concomitant loss of color vision in the
peripheral visual field (Koh et al., 2008; Rizzo, Smith, Pokorny, & Damasio, 1993).
Patients with cerebral dyschromatopsia find it difficult to discriminate fine color hues.
Bilateral occipital-temporal injury causes moderate or severe loss of color vision in the
entire visual field, which is called cerebral achromatopsia (Bouvier & Engel, 2006;
Heywood & Kentridge, 2003; Meadows 1974); yet, discrimination of grays (p. 197)
(Heywood, Wilson, & Cowey, 1987) and even processing of wavelength differences
(Heywood & Kentridge, 2003) may be spared. Consequently, discriminating and sorting of
colors and associating color stimuli with their names and with particular objects (e.g.,
yellow and banana; green and grass) are affected. Patients may report that objects and
pictures appear “drained of color,” as “dirty brownish” or “reddish,” or as “black and
white.” Cerebral hemiachromatopsia is a rather rare condition. Among 1,020 patients
with unilateral homonymous visual field disorders after acquired posterior brain injury,
we found thirty cases (3.9 percent) with unilateral hemiachromatopsia and impaired
foveal color discrimination; among 130 cases with bilateral occipital injury, sixteen cases
(12.3 percent) showed complete cerebral achromatopsia. Partial cerebral achromatopsia
may also occur and may be associated with impaired color constancy (Kennard, Lawden,
Morland, & Ruddock, 1995). The ventral occipital-temporal cortex is the critical lesion
location of color vision deficits (Bouvier & Engel, 2006; Heywood & Kentridge, 2003).
Color vision may also be impaired in (mild) hypoxia (Connolly, Barbur, Hosking, &
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Moorhead, 2008), multiple sclerosis (Moura et al., 2008), Parkinson’s disease (Müller,
Woitalla, Peters, Kohla, & Przuntek, 2002), and dementia of the Alzheimer type (Jackson
& Owsley, 2003). Furthermore, color hue discrimination accuracy can be considerably
reduced in older age (Jackson & Owsley, 2003).
Spatial Vision
Disorders in visual space perception comprise deficits in visual localization, depth

perception, and perception of visual spatial axes. Brain injury can differentially affect
retinotopic, spatiotopic, egocentric, and allocentric frames of reference. Visual-spatial
disorders typically occur after occipital-parietal and posterior parietal injury; a right-
hemisphere injury more frequently causes visual spatial impairments (for comprehensive
reviews, see Farah, 2003; Karnath & Zihl, 2003; Landis 2000).
After unilateral brain injury, moderate defective visual spatial localization is typically
found in the contralateral hemifield, but may also be present in the foveal visual field
(Postma, Sterken, de Vries, & de Haan, 2000), which is associated with less accurate
saccadic localization accuracy. Patients with bilateral posterior brain injury, in contrast,
show moderate to severe localization inaccuracy in the entire visual field, which typically
affects all visually guided activities, including accurately fixating objects, reaching for
objects, and reading and writing (Zihl, 2011). Interestingly, patients with parietal lobe
injury can show dissociation between spatial perception deficits and pointing errors
(Darling, Bartelt, Pizzimenti, & Rizzo, 2008), indicating that inaccurate pointing cannot
always be explained in terms of defective localization but may represent a genuine
disorder (optic ataxia; see Caminiti et al., 2010).
Impaired monocular and binocular depth perception (astereopsis) has been observed in
patients with unilateral and bilateral posterior brain injury, with bilateral injury causing
more severe deficits. Defective depth perception may cause difficulties in pictorial depth
perception, walking (downstairs), and reaching for objects or handles (Koh et al., 2008;
Miller et al., 1999; Turnbull, Driver, & McCarthy, 2004). Impaired distance perception, in
particular in the peripersonal space, has mainly been observed after bilateral occipital-
parietal injury (Berryhill, Fendrich, & Olson, 2009).
Shifts in the vertical and horizontal axes have been reported particularly in patients with
right occipital-parietal injury (Barton, Behrmann, & Black, 1998; Bonan, Leman,
Legargasson, Guichard, & Yelnik, 2006). Right-sided posterior parietal injury can also
cause ipsilateral and contralateral shifts in the visually perceived trunk median plane
(Darling, Pizzimenti, & Rizzo, 2003). Occipital injury more frequently causes contralateral
shifts in spatial axes, whereas posterior parietal injury also causes ipsilateral shifts.
Barton and Black (1998) suggested that the contralateral midline shift of hemianopic
patients is “a consequence of the strategic adaptation of attention into contralateral
hemispace after hemianopia” (p. 660), that is, that a change in attentional distribution
might cause an abnormal bias in line bisection. In a study of 129 patients with
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homonymous visual field loss, we found the contralateral midline shift in more than 90
percent of cases. However, the line bisection bias was not associated with efficient
oculomotor compensation for the homonymous visual loss. In addition, visual field sparing
also did not modulate the degree of midline shift. Therefore, the subjective straight-ahead
deviation may be explained as a consequence of a systematic, contralesional shift of the
egocentric visual midline and may therefore represent a genuine visual-spatial perceptual
disorder (Zihl, Sämann, Schenk, Schuett, & Dauner, 2009). This idea is supported by
Darling et al. (2003), who reported difficulties in visual perception of the trunk-fixed
anterior-posterior axis in patients with left- or (p. 198) right-sided unilateral posterior
parietal lesions without visual field defects.
Visual Motion Perception
Processing of direction and speed of visual motion stimuli is a genuine visual ability.
However, in order to know how objects move in the world, we must take into account the
rotation of our eyes as well as of our head (Bradley, 2004; Snowden & Freeman, 2004).
Motion perception also enables recognition of biological movements (Giese & Poggio,
2003) and supports face perception (Roark, Barrett, Spence, Abdi, & O’Toole, 2003).
Visual area V5 activity is the most critical basis for generating motion perception
(Moutoussis & Zeki, 2008), whereas superior temporal and premotor areas subserve
biological motion perception (Saygin, 2007).
The first well-documented case of loss of visual motion perception (cerebral akinetopsia)
is L.M. After bilateral temporal-occipital cerebrovascular injury, she completely lost
movement vision in all three dimensions, except for detection and direction
discrimination of single targets moving at low speed with elevated thresholds. In
contrast, all other visual abilities, including the visual field, visual acuity, color vision,
stereopsis, and visual recognition, were spared, as was motion perception in the auditory
and tactile modalities. Her striking visual-perceptual impairment could not be explained
by spatial or temporal processing deficits, impaired contrast sensitivity (Hess, Baker, &
Zihl, 1989), or generalized cognitive slowing (Zihl, von Cramon, & Mai, 1983; Zihl, von
Cramon, Mai, & Schmid, 1991). L.M. was also unable to search for a moving target
among stationary distractor stimuli in a visual display (McLeod, Heywood, Driver, & Zihl,
1989) and could not see biological motion stimuli (McLeod, Dittrich, Driver, Perrett, &
Zihl, 1996), including facial movements in speech reading (Campbell, Zihl, Massaro,
Munhall, & Cohen, 1997). She could not extract shape from motion and lost apparent
motion perception (Rizzo, Nawrot, & Zihl, 1995). Because of her akinetopsia, L.M. was
severely handicapped in all activities involving visual motion perception, whereby
perception and action were similarly affected (Schenk, Mai, Ditterich, & Zihl, 2000).
Selective impairment of movement vision in terms of threshold elevation for speed and
direction has also been reported in the hemifield contralateral to unilateral posterior
brain injury for motion types of different complexity, combined and in separation (Billino,
Braun, Bohm, Bremmer, & Gegenfurtner, 2009; Blanke, Landis, Mermoud, Spinelli, &
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Safran, 2003; Braun, Petersen, Schoenle, & Fahle, 1998; Plant, Laxer, Barbaro, Schiffman,
& Nakayama, 1993; Vaina, Makris, Kennedy, & Cowey, 1998).
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Visual Identification and Visual Recognition
Visual agnosia is the inability to identify, recognize, interpret, or comprehend the

meaning of visual stimuli even though basic visual functions (i.e., the visual field, visual
acuity, spatial contrast sensitivity, color vision, and form discrimination) are intact or at
least sufficiently preserved. Visual agnosia either results from defective visual perception
(e.g., synthesis of features; apperceptive visual agnosia) or from the loss of the “bridge”
between the visual stimulus and its semantic associations (e.g., label, use, history;
associative or semantic visual agnosia). However, objects can be recognized in the
auditory and tactile modalities, and the disorder cannot be explained by supramodal
cognitive or aphasic deficits (modified after APA, 2007). Lissauer (1890) interpreted
apperceptive visual agnosia as “mistaken identity” because incorrectly identified objects
share global (e.g., size and shape) and/or local properties (e.g., color, texture, form
details) with other objects, which causes visual misidentification. Cases with pure visual
agnosia seem to be the exception rather than the rule (Riddoch, Johnston, Bracewell,
Boutsen, & Humphreys, 2008). Therefore, a valid and equivocal differentiation between a
“genuine” visual agnosia and secondary impairments in visual identification and
recognition resulting from other visual deficits is often difficult, in particular concerning
the integration of global and local information (Delvenne, Seron, Coyette, & Rossion,
2004; Thomas & Forde, 2006). In a group of 1,216 patients with acquired injury to the
visual brain we have found only seventeen patients (about 2.4 percent) with genuine
visual agnosia. Visual agnosia is typically caused by bilateral occipital-temporal injury
(Barton, 2008a) but may also occur after left- (Barton, 2008b) or right-sided posterior
brain injury (Landis, Regard, Bliestle, & Kleihues, 1988). There also exist progressive
forms of visual agnosia in posterior cortical atrophy and in early stages of dementia
(Nakachi et al., 2007; Rainville et al., 2006).
Farah (2000) has proposed a useful classification of visual agnosia according to the type
of visual material patients find difficult to identify and recognize. Patients with visual
object and form agnosia are unable to visually recognize complex objects or pictures.
(p. 199) There exist category-specific types of object agnosia, such as for living and
nonliving things (Thomas & Forde, 2006), animals or artifacts (Takarae & Levin, 2001). A
particular type of visual object agnosia is visual form agnosia. The most elaborated case
with visual form agnosia is D.F. (Milner et al., 1991). After extensive damage to the
ventral processing stream due to carbon monoxide poisoning, this patient showed a more
or less complete loss of form perception, including form discrimination, despite having a
visual resolution capacity of 1.7 minute of arc. Visually guided activities such as pointing
to or grasping for an object, however, were spared (Carey, Dijkerman, Murphy, Goodale,
& Milner, 2006; James, Culham, Humphrey, Milner, & Goodale, 2003; McIntosh,
Dijkerman, Mon-Williams, & Milner, 2004). D.F. also showed profound inability to visually
recognize objects, places, and faces, indicating a more global rather than selective visual
agnosia. Furthermore, D.F.’s visual disorder may also be explained in terms of an
allocentric spatial deficit rather than as perceptual deficit (Schenk, 2006). As Goodale
and Westwood (2004) have pointed out, the proposed ventral-dorsal division in visual
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information processing may not be as exclusive as assumed, and both routes interact at
various stages. However, automatic obstacle avoidance was intact in D.F. while correct
grasping was possible for simple objects only (McIntosh et al., 2004), suggesting that the
“what” pathway plays no essential role in detecting and localizing objects or in the spatial
guidance of walking (Rice et al., 2006). Further cases of visual form agnosia after carbon
monoxide poisoning have been reported by Heider (2000). Despite preserved visual acuity
and only minor visual field defects, patients were severely impaired in shape and form
discrimination, whereas the perception of color, motion, and stereoscopic depth was
relatively unimpaired. Heider (2000) identified a failure in figure–ground segregation and
grouping single elements of a composite visual scene into a “gestalt” as the main
underlying deficit. Global as well as local processing can be affected after right- and left-
sided occipital-temporal injury (Rentschler, Treutwein, & Landis, 1994); yet, typically
patients find it more difficult to process global features and integrate them into a whole
percept (integrative or simultaneous agnosia; Behrmann & Williams, 2007; Saumier,
Arguin, Lefebvre, & Lassonde, 2002; Thomas & Forde, 2006). Consequently, patients are
unable to report more than one attribute of a single object (Coslett & Lie, 2008).
Encoding the spatial arrangements of parts of an object requires a mechanism that is
different from that required for encoding the shape of individual parts, with the former
selectively compromised in integrative agnosia (Behrmann, Peterson, Moscovitch, &
Suzuki, 2006). Integration of multiple object stimuli into a holistic interpretation seems to
depend on the spatial distance of local features and elements (Huberle & Karnath, 2006).
Yet, shifting fixation and thus also attention to all elements of an object in a regular
manner seems not sufficient to “bind” together the different elements of spatially
distributed stimuli (Clavagnier et al., 2006). The integration of multiple visual elements
resulting in a conscious perception of their gestalt seems to rely on bilateral structures in
the human lateral and medial inferior parietal cortex (Himmelbach, Erb, Klockgether,
Moskau, & Karnath, 2009). An alternative explanation for the impairment in global visual
perception is shrinkage of the field of attention and thus perception (Michel & Henaff,
2004), which might be elicited by attentional capture (“radical visual capture”) to single,
local elements (Takaiwa, Yoshimura, Abe, & Terai, 2003; Dalrymple, Kingstone, & Barton,
2007). The pathological restriction and rigidity of attention impair the integration of
multiple visual elements to a gestalt, but the type of capture depends on the competitive
balance between global and local salience. The impaired disengaging of attention causes
inability to “unlock” attention from the first object or object element to other objects or
elements of objects (Pavese, Coslett, Saffran, & Buxbaum, 2002). Interestingly, facial
expressions of emotion are less affected in simultanagnosia, indicating that facial stimuli
constitute a specific category of stimuli that attract attention more effectively and are
possibly processed before attentional engagement (Pegna, Caldara-Schnetzer, & Khateb,
2008). It has been proposed that differences in local relative to more global visual
processing can be explained by different processing modes in the dorsal and medial
ventral visual pathways at an extrastriate level; these characteristics can also explain
category-specific deficits in visual perception (Riddoch et al., 2008). The dual-route
organization of visual information has also been applied to local–global perception.
Difficulties with processing of multiple stimulus elements or features (within-object
Page 12 of 40

representation) are often referred to as “ventral” simultanagnosia, and impaired

processing of multiple spatial stimuli (between-object representation) as “dorsal”
simultanagnosia (Karnath, Ferber, Rorden, & Driver, 2000). Dorsal simultanagnosia is one
component of the Bálint-Holmes syndrome, which consists of (p. 200) spatial (and
possibly temporal) restriction of the field of visual attention and thus visual processing
and perception, impaired visual spatial localization and orientation, and defective depth
perception (Moreaud, 2003; Rizzo & Vecera, 2002). In addition, patients with severe
Balint’s syndrome find it extremely difficult to shift their gaze voluntarily or on command
(oculomotor apraxia or psychic paralysis of gaze) and are unable to direct movement of
an extremity in space under visual guidance (optic or visuomotor ataxia). As a
consequence, visually guided oculomotor and hand motor activities, visual-constructive
abilities, visual orientation, recognition, and reading are severely impaired (Ghika, Ghika-
Schmid, & Bogousslavsky, 1998).
In face agnosia (prosopagnosia), recognition of familiar faces, including one’s own face, is
impaired or lost. The difficulties prosopagnosic patients have with visual face recognition
also manifest in their oculomotor scan path during inspection of a face; global features
such as hair or the forehead, for example, are scanned in much more detail than genuine
facial features such as the eye or nose (Stephan & Caine, 2009). Other prosopagnosic
subjects may show partial processing of facial features, such as the mouth region
(Bukach, Le Grand, Kaiser, Bub, & Tanaka, 2008). Topographical (topographagnosia) or
environmentalagnosia refers to defective recognition of familiar environments, in reality
and on maps and pictures; however, patients may have fewer difficulties in familiar
surroundings and with scenes with clear landmarks, and may benefit from semantic
information such as street names (Mendez & Cherrier, 2003). Agnosia for letters (pure
alexia) is a form of acquired dyslexia with defective visual recognition of letters and
words while auditory recognition of letters and words and writing are intact. The
underlying disorder may have a pre-lexical, visual-perceptual basis because patients can
also exhibit difficulties with nonlinguistic stimuli (Mycroft, Behrmann, & Kay, 2009).
Audition
Auditory perception comprises detection, discrimination, identification, and recognition
of sounds, voice, music, and speech. The ability to detect and discriminate attributes of
sounds improves with practice (Wright & Zhang, 2009) and thus depends on auditory
experience. This might explain interindividual differences in auditory performance, in
particular recognition expertise and domain specificity concerning, for example, sounds,
voices, and music (Chartrand, Peretz, & Belin, 2008). Another factor that crucially
modulates auditory perceptual efficiency is selective attention (Shinn-Cunningham &
Best, 2008).
Page 13 of 40

The auditory brain possesses tonotopic maps that show rapid task-related changes to
subserve distinct functional roles in auditory information processing, such as pitch versus
phonetic analysis (Ozaki & Hashimoto, 2007). This task specificity can be viewed as a
form of plasticity that is embedded in a context- and cognition-related frame of reference,
whereby attention, learning and memory, and mental imagery can modulate processing
(Dahmen & King, 2007; Fritz, Elhilali, & Shamma, 2005; Weinberger, 2007; Zatorre,
2007). The auditory cortex forms internal representations of temporal characteristic
structures, which may build the further basis for sound segmentation, complex auditory
objects processing, and also multisensory integration (Wang, Lu, Bendor, & Bertlett,
2008). In the discrimination of speech and nonspeech stimuli, which is based on subtle
temporal acoustic features, the middle temporal gyrus, the superior temporal sulcus, the
posterior part of the inferior frontal gyrus, and the parietal operculum of the left
hemisphere are involved (Zaehle, Geiser, Alter, Jancke, & Meyer, 2008). Environmental
sounds are mainly processed in the middle temporal gyri in both hemispheres (Lewis et
al., 2004), whereas vocal communication sounds are preferentially coded in the insular
region (Bamiou, Musiek, & Luxon, 2003). Music perception is understood as a form of
communication in which formal codes (i.e., acoustic patterns) and their auditory
representations are employed to elicit a variety of perceptual and emotional experiences
(Bharucha, Curtis, & Paroo, 2006). Musical stimuli have also been found to activate
specific pathways in several brain areas, which are associated with emotional behavior,
such as insular and cingulate cortices, amygdala, and prefrontal cortex (Boso, Politi,
Barale, & Enzo, 2006). For the representation of auditory scenes and categories within
past and actual experiences and contexts, the medial and ventrolateral prefrontal cortex
appears to play a particular role (Janata, 2005; Russ, Lee, & Cohen, 2007).
The auditory system also possesses a “where” and a “what” subdivision for processing
spatial and nonspatial aspects of acoustic stimuli, which allows detection, localization,
discrimination, identification, and recognition of auditory information, including vocal
communication sounds (speech perception) and music (Kraus & Nicol, 2005; Wang, Wu, &
Li, 2008).
(p. 201) Auditory Perceptual Disorders
Unilateral and bilateral injury to left- or right-sided temporal brain structures can affect
processing of spatial and temporal auditory processing capacities (Griffiths et al., 1997;
Polster & Rose, 1998) and the perception of environmental sounds (Tanaka, Nakano, &
Obayashi, 2002), sound movement (Lewald, Peters, Corballis, & Hausmann, 2009), tunes,
prosody, and voice (Peretz et al., 1994), and words (pure word deafness) (Shivashankar,
Shashikala, Nagaraja, Jayakumar, & Ratnavalli, 2001). Functional dissociation of auditory
perceptual deficits, such as preservation of speech perception and environmental sounds
but impairment of melody perception (Peretz et al., 1994), impaired speech perception
but intact environmental sound perception (Kaga, Shindo, & Tanaka, 1997), and impaired
perception of verbal but spared perception of nonverbal stimuli (Shivashankar et al.,
Page 14 of 40

2001), suggests a modular architecture similar to that in the visual cortex (Polster &
Rose, 1998).
Auditory Agnosia
Auditory agnosia is defined as the impairment or loss of recognition of auditory stimuli in

the absence of defective auditory functions and language and cognitive disorders that can
(sufficiently) explain the recognition disorder. As in visual agnosia, it may be difficult to
validly distinguish between genuine and secondary auditory agnosia. It is impossible to
clearly differentiate sensory-perceptual from perceptual-cognitive abilities because both
domains are required for auditory recognition. For example, patients with intact
processing of steady-state patterns but impaired processing of dynamic acoustic patterns
may exhibit verbal auditory agnosia (Wang, Peach, Xu, Schneck, & Manry, 2000) or have
(additional) difficulties with auditory spatial localization and auditory motion perception
(Clarke, Bellmann, Meuli, Assal, & Steck, 2000). Auditory agnosia for environmental
sounds may be associated with impaired processing of meaningful verbal information
(Saygin, Dick, Wilson, Dronkers, & Bates, 2003) and impaired recognition of music (Kaga,
Shindo, Tanaka, & Haebara, 2000); yet, perception of environmental sound (Shivashankar
et al., 2001) and music may also be spared even in the case of generalized auditory
agnosia (Mendez, 2001). However, there exist examples of pure agnosia for recognizing
particular categories of auditory material, such as environmental sounds (Taniwaki,
Tagawa, Sato, & Iino, 2000), speech (pure word deafness) (Engelien et al., 1995; Polster
& Rose, 1998), and music perception. Musical timber perception can be affected after
left- or right temporal lobe injury (Samson, Zatorre, & Ramsay, 2002). Agnosia for music
(music agnosia, amusia) and agnosia for other auditory categories are frequently
associated but can also dissociate; they typically occur after right unilateral and bilateral
temporal lobe injury (Vignolo, 2003). Amusia may affect discrimination and recognition of
familiar melodies (Ayotte, Peretz, Rousseau, Bard, & Bojanowski, 2000; Sato et al., 2005).
However, there is evidence for a less strong hemispheric specificity for music perception
because cross-hemisphere and fragmented neural substrates underlie local and global
musical information processing at least in the melodic and temporal dimensions
(Schuppert, Munte, Wieringa, & Altenmüller, 2000).
Somatosensory Perception
The somatosensory system provides information about object surfaces that are in direct
contact with the skin (touch) and about the position and movements of body parts
(proprioception and kinesthesis). Somatosensory perception thus includes detection and
discrimination of (fine) differences in touch stimulation and haptic perception, that is, the
perception of shape, size, and identity (recognition) of objects on the basis of touch and
kinesthesis. Shape is an important cue for recognizing objects by touch; edges, curvature,
Page 15 of 40

and surface areas are associated with three-dimensional shape (Plaisier, Tiest, & Kappers,
2009). Exploratory motor procedures are directly linked to the extraction of specific
shape properties (Valenza et al., 2001). Somatosensory information is processed in
anterior, lateral, and posterior parietal cortex, but also in frontal, cingulate, temporal,
and insular cortical regions (Porro, Lui, Facchin, Maieron, & Baraldi, 2005).
Somatosensory Perceptual Disorders
Impaired haptic perception of (micro) geometrical properties, which may be associated

with a failure to recognize objects, has been reported after injury to the postcentral
gyrus, including somatosensory areas SI and SII, and the posterior parietal cortex
(Bohlhalter, Fretz, & Weder, 2002; Estanol, Baizabal-Carvallo, & Senties-Madrid, 2008).
Difficulties to identify objects using hand manipulation only have been reported after
parietal injury (Tomberg & Desmedt, 1999). Impairment of the perception of stimulus
shape (morphagnosia) may result from defective processing of spatial orientation in two-
and three-dimensional space (Saetti, De Renzi, & Comper, 1999). (p. 202) Tactile object
recognition can be impaired without associated disorders in tactile discrimination and
manual shape exploration, indicating the existence of “pure” tactile agnosia (Reed,
Caselli, & Farah, 1996).
Body Perception Disorders
Disorders in body perception may affect body form and body actions selectively or in
combination (Moro et al., 2008). Patients with injury to the premotor cortex may show
agnosia for their body (asomatognosia); that is, they describe parts of their body to be
missing or disappeared from body awareness (Arzy, Overney, Landis, & Blanke, 2006).
Macro and, less frequently, micro somatognosia have been reported as transient and
reversible modifications of body representation during migraine aura (Robinson & Podoll,
2000). Asomatognosia either may involve the body as a whole (Beis, Paysant, Bret, Le
Chapelain, & Andre, 2007) or may be restricted to finger recognition (“finger agnosia”;
Anema et al., 2008). Body misperception may also result in body illusion, a deranged
representation of the body concerning its ownership labeled “somatoparaphrenia” (Vallar
& Ronchi, 2009). Distorted body perception may also occur in chronic pain (Lotze &
Moseley, 2007).
Olfactory and Gustatory Perception
Page 16 of 40

The significance of the sense of smell is still somehow neglected. This is surprising given
that olfactory processing monitors the intake of airborne agents into the human
respiratory system and warns of spoiled food, leaking natural gas, polluted air, and
smoke. In addition, it determines to a large degree the flavor and palatability of foods and
beverages, enhances life quality, and mediates basic elements of human social
relationships and communication, such as in mother–child interactions (Doty, 2009).
Olfactory perception implies detection, discrimination, identification, and recognition of
olfactory stimuli. Olfactory perception shows selective adaptation; the perceived intensity
of a smell drops by 50 percent or more after continuous exposure of about 10 minutes,
and recovers again after removal of the smell stimulus (Eckman, Berglund, Berglund, &
Lindvall, 1967). Continuous exposition to a particular smell, such as cigarette smoke,
causes persistent adaptation to that smell on the person and in the environment.
Smell perception involves the caudal orbitofrontal and medial temporal cortices.
Olfactory stimuli are processed in primary olfactory (piriform) cortex and also activate
the amygdala bilaterally, regardless of valence. In posterior orbitofrontal cortex,
processing of pleasant and unpleasant odors is segregated within medial and lateral
segments, respectively, indicating functional heterogeneity. Olfactory stimuli also show
that brain regions mediating emotional processing are differentially activated by odor
valence and provide evidence for a close anatomical coupling between olfactory and
emotional processes (Gottfried, Deichmann, Winston, & Dolan, 2002).
Gustation is vital for establishing whether a specific substance is edible and nutritious or
poisonous, and for developing preferences for specific foods. According to the well-known
taste tetrahedron, four basic taste qualities can be distinguished: sweet, salt, sour, and
bitter. A fifth taste quality is umami, a Japanese word for “good taste.” Perceptual taste
qualities are based on the pattern of activity across different classes of sensory fibers
(i.e., cross-fiber theory; Mather, 2006, pp. 44) and distributed cortical processing (Simon,
de Araujo, Gutierrez, & Nicolelis, 2006). Taste information is conveyed through the
central gustatory pathways to the gustatory cortical area, but is also sent to the reward
system and feeding center via the prefrontal cortex, insular cortex, and amygdala (Simon
et al., 2006; Yamamoto, 2006). The sensation of eating, or flavor, involves smell and taste
as well as interactions between these and other perceptual systems, including
temperature, touch, and sight. However, flavor is not a simple summation of different
sensations; smell and taste seem to dominate flavor.
Olfactory Perceptual Disorders
Olfactory perception can be impaired in the domains of detection, discrimination, and

identification/recognition of smell stimuli. Typically, patients experience hyposmia or
dysgeusia (decrease) or anosmia (loss of sense of smell) (Haxel, Grant, & Mackay-Sim,
2008). However, distinct patterns of olfactory dysfunctions have been reported, indicating
differential breakdown in olfactory perception analogous to visual and auditory modalities
Page 17 of 40

(Luzzi et al., 2007). Interestingly, selective inability to recognize the favorite foods by
smell can also occur despite preserved detection and evaluation of food stimuli as
pleasant or familiar (Mendez & Ghajarnia, 2001).
Chronic disorders in olfactory perception and recognition have been reported after
(traumatic) brain injury mainly to ventral frontal cortical structures (Fujiwara, Schwartz,
Gaom Black, & Levine, 2008; Haxel, Grant, & Mackay-Sim, 2008; Wermer, Donswijk,
Greebe, Verweij, & Rinkel, 2007), in (p. 203) Parkinson’s disease and multiple sclerosis, in
mesial temporal epilepsy, and in neurodegenerative diseases, including dementia of the
Alzheimer type, frontal-temporal dementia, cortical-basal degeneration, and Huntington’s
disease (Barrios et al., 2007; Doty, 2009; Jacek, Stevenson, & Miller, 2007; Pardini, Huey,
Cavanagh, & Grafman, 2009). It should be mentioned, however, that hyposmia and
impaired odor identification can also be found in older age (Wilson, Arnold, Tang, &
Bennett, 2006), in particular in subjects with cognitive decline. Presbyosmia has been
found in particular after 65 years of age, with no difference between males and females,
and with a weak relationship between self-reports of olfactory function and objective
olfactory function (Mackay-Sim, Johnston, Owen, & Burne, 2006). Olfactory perceptual
changes have also been reported among subjects receiving chemotherapy (Bernhardson,
Tishelman, & Ruthqvist, 2009), in depression (Pollatos et al., 2007), and in anorexia
nervosa (Roessner, Bleich, Banashewski, & Rothenburger, 2005).
Gustatory Perceptual Disorders
Gustatory disorders in the form of quantitatively reduced (hypogeusia) or qualitatively

changed (dysgeusia) gestation have been reported after subcortical, inferior collicular
stroke (Cerrato et al., 2005), after pontine infarction (Landis, Leuchter, San Millan Ruiz,
Lacroix, & Landis, 2006), after left insular and opercular stroke (Mathy, Dupuis, Pigeolet,
& Jacquerye, 2003), in multiple sclerosis (Combarros, Miro, & Berciano, 1994), and in
diabetes mellitus (Stolbova, Hahn, Benes, Andel, & Treslova, 1999). The anteromedial
temporal lobe plays an important role in recognizing taste quality because injury to this
structure can cause gustatory agnosia (Small, Bernasconi, Sziklas, & Jones-Gutman,
2005). Gustatory perception also decreases with age (>40 years), which is more
pronounced in males than in females (Fikentscher, Roseburg, Spinar, & Bruchmuller,
1977).
Smell and taste dysfunctions, including impaired detection, discrimination, and

identification of foods, have been frequently reported in patients following (minor) stroke
in temporal brain structures (Green, McGregor, & King, 2008). Abnormalities in taste and
smell have also been reported in patients with Parkinson’s disease (Shah et al., 2009).
Social Perception
Page 18 of 40

Social perception is an individual’s perception of social stimuli (i.e., facial expression,

prosody and gestures, and smells), which allow inferring motives, attitudes, or values
from the social behavior of other individuals. Social perception and social cognition, but
also sensitivity to the social context, and social action, belong to particular functional
systems in the prefrontal brain (Adolphs, 2003; Adolphs, Tranel, & Damasio, 2003). The
amygdala is involved in recognizing facial emotional expressions; the orbitofrontal cortex
is important to reward processing; and the insula is involved in representing “affective”
states of our own body, such as empathy or pain (Adolphs, 2009). The neural substrates of
social perception are characterized by a general pattern of right-hemispheric functional
asymmetry (Brancucci, Lucci, Mazzatenta, & Tommasi, 2009). The (right) amygdala is
crucially involved in evaluating sad but not happy faces, suggesting that this brain
structure plays a specific role in processing negative emotions, such as sadness and fear
(Adolphs & Tranel, 2004).
Disorders in Social Perception
Patients with traumatic brain injury may show difficulties with recognizing affective
information from the face, voice, bodily movement, and posture (Bornhofen & McDonald,
2008), which may persistently interfere with successful negotiation of social interactions
(Ietswaart, Milders, Crawford, Currie, & Scott, 2008). Interestingly, face perception and
perception of visual social cues can be affected while the perception of prosody can be
relatively spared, indicating a dissociation between visual and auditory social-perceptual
abilities (Croker & McDonald, 2005; Green, Turner, & Thompson, 2004; Pell, 1998).
Impaired auditory recognition of fear and anger has been reported following bilateral
amygdala lesions (Scott et al., 1997). Impairments of social perception, including
inaccurate interpretation and evaluation of stimuli signifying reward or punishment in a
social context, and failures to translate emotional and social information into task- and
context-appropriate action patterns are often observed in subjects with frontal lobe
injury. Consequently, patients may demonstrate inadequate social judgments and decision
making, social inflexibility, and lack of self-monitoring, particularly in social situations
(Rankin, 2007). Difficulties with facial expression perception have also been reported in
mood disorders (Venn, Watson, Gallagher, & Young, 2006).
Conclusion and Some Final Comments

The systematic study of individuals with perceptual deficits has substantially contributed
to the (p. 204) understanding of the role of perceptual abilities and their underlying
sophisticated brain processes, as well as the neural organization of the perceptual
modalities. Combined neurobiological, neuroimaging, and neuropsychological evidence
supports the view that all perceptual systems are functionally segregated and show a
parallel-hierarchical type of organization of information processing and coding. Despite
Page 19 of 40

this type of functional organization, pure perceptual disorders are the exception rather
than the rule. This somehow surprising fact can be explained by three main factors: (1)
focal brain injury is only rarely restricted to the cortical area in question; (2) the rich,
typically reciprocal fiber connections between cortical areas are frequently also affected;
and (3) perception may depend on spatiotemporally distributed activity in more than just
one cortical area, as is known, for example, in body perception (Berlucchi & Aglioti,
2010). Thus, an association of deficits is more likely to occur. Furthermore, complex
perceptual disorders, such as recognition, may also be caused by impaired lower level
perceptual abilities, and it is rather difficult to clearly distinguish between lower and
higher level perceptual abilities. In addition, recognition cannot be understood without
reference to memory, and it is therefore not surprising that it has been suggested that the
brain structures underlying visual memory, in particular in the medial temporal lobe, also
possess perceptual functions and can thus be understood as an extension of the ventral
visual processing stream (Baxter, 2009; Suzuki, 2009). Consequently, rather than trying to
map perceptual functions onto more or less separate brain structures, a more
comprehensive understanding of perception would benefit from the study of cortical
representation of functions crucially involved in defined percepts (Bussey & Saksida,
2007). This also holds true for the perception–action debate, in particular in vision, which
is treated as an exploratory activity, that is, a way of acting based on sensorimotor
contingencies, as proposed by O’Regan & Noë (2001). According to this approach, the
outside visual world serves as its own representation, whereas the experience of seeing
occurs as a result of mastering the “governing laws of sensorimotor contingency” and
thereby accounts for visual experience and “visual consciousness.” If one applies this
approach to the pathology of visual perception, then the question arises as to which
visual perceptual disorders would result from the impaired representation of the
“outside” visual world, and which from the defective “mastering of the governing laws of
sensorimotor contingency.” Would visual perceptual disorders of the first type not be
experienced by patients, and thus not represent a disorder and not cause any handicap,
because there is no “internal” representation of the outside world in our brains and thus
no visual experience? Modulatory effects of producing action on perception such that
observers become selectively sensitive to similar or related actions are known from visual
imitation learning and social interactions (Schutz-Bosbach & Prinz, 2007), but in both
instances, perception of action and, perhaps, motivation to observe and attention directed
to the action in question are required. Nevertheless, a more detailed understanding of the
bidirectional relationships between perception and action and the underlying neural
networks will undoubtedly help us to understand how perception modulates action and
vice versa. Possibly, the search for associations and dissociations of perceptions and
actions in cases with acquired brain injury in the framework of common functional
representations in terms of sensorimotor contingencies represents a helpful approach to
studying the reciprocal relationships between perception and action. Accurate visually
guided hand actions in the absence of visual perception (Goodale, 2008) and impaired
eye–hand coordination and saccadic control in optic ataxia as a consequence of impaired
visual-spatial processing (Pisella et al., 2009) are examples of such dissociations and
Page 20 of 40

associations. Despite some conceptual concerns and limitations, the dual-route model of
visual processing proposed by Milner and Goodale (2008) is still of theoretical and
practical value (Clark, 2009).
An interesting issue is implicit processing of stimuli in the absence of experience or

awareness, such as detection, localization, and even discrimination of simple visual
stimuli in hemianopia (“blindsight”; Cowey, 2010; Danckert & Rosetti, 2005);
discrimination of letters in visual form agnosia (Aglioti, Bricolo, Cantagallo & Berlucchi,
1999), discrimination of forms in visual agnosia (Kentridge, Heywood, & Milner, 2004;
Yang, Wu, & Shen, 2006); and discrimination of faces in prosopagnosia (Le, Raufaste,
Roussel, Puel, & Demonet, 2003). Such results suggest sparing of function in the
particular brain structure, but they may also be explained by stimulus processing in
structures or areas that also contribute to a particular perceptual function. However,
spared processing of stimuli is not identical with perception of the same stimuli. A
paradigmatic example of implicit processing of visual stimuli in the absence of the
primary visual (p. 205) cortex, blindsight, has helped us to understand the nature of
visual processing, but it is still unknown whether it is used or useful in everyday life
activities; that is, it may not have any perceptual significance (Cowey, 2010).
Furthermore, cognition plays an important role in perception, in particular attention,

memory, and in monitoring of perceptual activities. Therefore, perceptual disorders can
also result from or at least be exaggerated by cognitive dysfunctions associated with
acquired brain injury. The parietal cortex may be one of the brain structures that serve as
a bridge between perception, cognition, and action (Gottlieb, 2007). Future research on
perceptual disorders should therefore also focus on the effect of injury to brain structures
engaged in attention, memory, and executive functions involved in perception, such as the
temporal lobe, hippocampus, (posterior) parietal cortex, and prefrontal cortex. As a
result, the framework for interpreting perceptual disorders after brain injury, as well as in
other pathological states, could be further widened substantially. The search for
fundamental requirements for visual perception and the coupling between brain functions
underlying perception and cognition may further help to define perceptual dysfunction
with sufficient validity and thus contribute to the significance of perception (Pollen,
2008). Research on functional plasticity in subjects with perceptual disorders using
experimental practice paradigms may, in addition, contribute to a more comprehensive
and integrative understanding of perception in the framework of other functional systems
in the brain, which are known to modulate perceptual learning and thus functional
plasticity in perceptual systems (Gilbert, Li & Piech, 2009; Gilbert & Sigman, 2007).
Author Note
Page 21 of 40

Preparation of this chapter has been supported in part by the German Ministry for
Education and Research (BMBF grant 01GW0762). I want to thank Susanne Schuett for
her very helpful support.
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Josef Zihl
Josef Zihl is research group leader and head of the outpatient clinic for
neuropsychology, Max Planck Institute of Psychiatry.
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Perceptual Disorders

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Print Publication Date: Dec 2013 Subject: Psychology, Cognitive Neuroscience

Abstract and Keywords

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Visual Acuity, Spatial Contrast Sensitivity, and Visual Adaptation

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When spatial contrast sensitivity is reduced, patients usually complain of “blurred” or

Color vision may be lost in the contralateral hemifield (homonymous hemiachromatopsia)

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Disorders in visual space perception comprise deficits in visual localization, depth

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Visual Motion Perception

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Visual Identification and Visual Recognition

Visual agnosia is the inability to identify, recognize, interpret, or comprehend the

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representation) are often referred to as “ventral” simultanagnosia, and impaired

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(p. 201) Auditory Perceptual Disorders

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Auditory agnosia is defined as the impairment or loss of recognition of auditory stimuli in

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Somatosensory Perceptual Disorders

Impaired haptic perception of (micro) geometrical properties, which may be associated

Body Perception Disorders

Olfactory and Gustatory Perception

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Olfactory Perceptual Disorders

Olfactory perception can be impaired in the domains of detection, discrimination, and

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Gustatory Perceptual Disorders

Gustatory disorders in the form of quantitatively reduced (hypogeusia) or qualitatively

Smell and taste dysfunctions, including impaired detection, discrimination, and

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Social perception is an individual’s perception of social stimuli (i.e., facial expression,

Disorders in Social Perception

Conclusion and Some Final Comments

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An interesting issue is implicit processing of stimuli in the absence of experience or

Furthermore, cognition plays an important role in perception, in particular attention,

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Anstis, S. M. (1974). A chart demonstrating variations in acuity with retinal position.

Bar, M. (2003). A cortical mechanism triggering top-down facilitation in visual object

Bar, M. (2004). Visual objects in context. Nature Reviews Neuroscience, 5, 617–628.

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Barton, J. J. S. (2008a). Structure and function in acquired prosopagnosia: Lessons from a

Barton, J. J. S. (2008b). Prosopagnosia associated with a left occipitotemporal lesion.

Baxter, M. G. (2009). Involvement of medial temporal structures in memory and

Behrmann, M., & Williams, P. (2007). Impairments in part-whole representations of

and size constancy following bilateral occipito-parietal damage. Experimental Brain

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perceptual deficits in associative visual (prosop)agnosia: A single case study.

Desimone, R., & Ungerleider, L. G. (1989). Neural mechanisms of visual processing in

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