Ann. N.Y. Acad. Sci.

ISSN 0077-8923

A N N A L S O F T H E N E W Y O R K A C A D E M Y O F SC I E N C E S
Issue: The Year in Cognitive Neuroscience

Mapping the functional neuroanatomy of spatial

neglect and human parietal lobe functions: progress
and challenges
Patrik Vuilleumier
Laboratory for Behavioral Neurology and Imaging of Cognition, Department of Neuroscience, Medical School, and
Department of Neurology, University Hospital of Geneva, University of Geneva, Geneva, Switzerland

Address for correspondence: Patrik Vuilleumier, LABNIC/NEUFO, University Medical Center, University of Geneva,
Michel-Servet 1, 1211 Geneva, Switzerland. patrik.vuilleumier@unige.ch

Spatial neglect is generally defined by various deficits in processing information from one (e.g., left) side of space
contralateral to focal (e.g., right) hemisphere damage. Although classically associated with parietal lobe functions,
there is now compelling evidence that neglect can follow lesions in many different cortical and subcortical sites,
suggesting a dysfunction in distributed brain networks. In addition, neglect is likely to result from a combination of
distinct deficits that co-occur due to concomitant damage affecting juxtaposed brain areas and their connections, but
the exact nature of core deficits and their neural substrates still remains unclear. The present review describes recent
progress in identifying functional components of the neglect syndrome and relating them to distinct subregions of
parietal cortex. A comprehensive understanding of spatial neglect will require a more precise definition of cognitive
processes implicated in different behavioral manifestations, as well as meticulous mapping of these processes onto
specific brain circuits, while taking into account functional changes in activity that may arise in structurally intact
areas subsequent to damage in distant portions of the relevant networks.

Keywords: spatial neglect; attention; lesion mapping; parietal cortex; network; connectivity

the exact nature of the functions subserved by these

Introduction
Hemispatial neglect is a frequent and fascinating,
but still poorly understood, neuropsychological dis-
order. Although it has hitherto defied a comprehen-
sive theoretical account, research on neglect in the
past three decades has yielded a vast and rich body
of knowledge concerning various domains of per-
ception, attention, and spatial cognition. Moreover,
this research has laid a fertile ground for integrating
clinical neuropsychology with basic neuroscience by
linking particular behavioral phenomena and high-
level mental functions, such as awareness and atten-
tion, with specific neuronal properties measured at
the single-cell level. More recent progress in neu-
roimaging techniques in humans, and parallel neu-
rophysiology approaches in nonhuman primates,
has further encouraged a meticulous mapping of the
neural circuits whose damage may lead to neglect.
However, many questions remain open concerning
50
circuits and their link with specific neglect symp-
toms. This review will provide a selective overview
of current approaches and challenges to defining the
functional neuroanatomy of spatial neglect, with a
particular focus on parietal lobe functions, which
have classically been associated with this disorder.1,2
Hemispatial neglect is frequently observed after
unilateral hemispheric brain damage in humans,
most often due to stroke.3,4 It is clinically defined
as a failure to perceive, report, and orient to sen-
sory stimuli on the side of space opposite the brain
lesion. Most often, such lesions affect the right hemi-
sphere and neglect concerns the left space. For ex-
ample, patients with this syndrome may not see peo-
ple or objects located on their left side, fail to hear
voices or sounds coming from that side, miss words
on the left half of a page or even the left half of
words when reading, or eat only from the right side
of their plate (Fig. 1). These symptoms cannot be
doi: 10.1111/nyas.12161
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Vuilleumier Spatial neglect and the parietal lobe

Figure 1. Examples of tests used to assess spatial neglect. (A) Line bisection requires marking the midpoint of lines of various
lengths, presented one or many at a time. Neglect patients typically deviate rightward away from the true midpoint, especially when
the line is long. They may also omit lines on the left side of the page. (B) Cancellation requires searching and marking a target
among distractors, for example, letters or shapes like the bells illustrated here. Neglect patients typically fail to explore and detect
targets on the left side of the display. (C) The Ota cancellation task requires encircling all rings without a gap and crossing out
all those with a gap (on the circles left or right side). This may reveal misses of targets on the left side of the sheet (space-based
or egocentric neglect) as well as misses of targets with a left gap (object-based or allocentric neglect). Object-based neglect is also
observed in other tasks, for example, when patients omit (or transform) only the left part of compound words (e.g., house instead of
doghouse). (D) Copy of line drawing of a multi-item scene. This task may also reveal both omissions in the left space and omissions
of the left side of items, as illustrated here by the performance of two distinct patients (top vs. bottom sample). Drawings also often
show an apparent compression of space with items clumped together on the right side, but underuse of the left side of the sheet.
(E) Perceptual extinction is elicited by comparing the detection of two stimuli presented simultaneously on either side of space,
relative to the detection of the same stimuli presented alone. Patients without hemianopia (or sensory loss) often fail to perceive
the contralesional (left) stimulus in bilateral but not unilateral stimulation. Such extinction can be observed in different sensory
modalities.

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Spatial neglect and the parietal lobe
explained by elementary losses such as visual field
cuts (hemianopia), deafness, or paralysisalthough
the latter deficits can influence or exacerbate some
manifestations of neglect. Neglect for contralesional
space may affect all sensory modalities (e.g., vision,
audition, touch) to various degrees, but may also
arise in mental imagery (e.g., when describing fa-
miliar places from memory as seen from a given
standpoint5 ), in estimation of magnitude along a
mental number line,6,7 and even in mental represen-
tation of time (e.g., when attributing events to past
or future along a time line8 ). Neglect may also be ob-
served in motor behavior in the absence of any exter-
nal stimuli: for example, when searching for a poten-
tial target in complete darkness or blindfolded,9,10
patients move their eyes or hands into the ipsile-
sional (right) half of space but fail to explore the
contralesional (left) side. Patients may neglect parts
of their own body and fail to use their contrale-
sional arm or leg, even though it is not paralyzed.
Perceptual extinction is another frequent symptom
whereby a stimulus in contralesional space (in any
sensory modality) is not detected when presented si-
multaneously with another stimulus in ipsilesional
space (in the same or different modality), while an
identical contralesional stimulus is detected when
presented alone.11,12 Strikingly, neglect patients typ-
ically do not realize that they miss information or
ignore one portion of space, suggesting that anosog-
nosia for neglect is an intrinsic feature of the dis-
order which can dissociate from other forms of
anosognosia.13 Because these patients have no direct
experience of their abnormal spatial biases, they fail
to spontaneously compensate for such impairment
(even when they can verbally report having been
told about it by, for example, doctors or therapists).
Not only does spatial neglect entail puzzling
deficits in patients and raise fascinating questions
on the neural bases of consciousness and space rep-
resentation, but it also has important clinical im-
plications for the management of brain-damaged
patients and their rehabilitation. First, the presence
of neglect predicts worse recovery of concomitant
neurological deficits (e.g., paralysis), reduced inde-
pendence in everyday life, and hence heavier bur-
den for caregivers and relatives. Second, therapies
are still limited and lead to partial improvements,
often restricted to the training situation without
generalizing to everyday life. Fortunately, the sever-
ity of neglect and associated symptoms tend to show
52 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
some degree of progressive spontaneous recovery in
the months following the acute brain insult, even
though some symptoms may persist for many years.
Understanding neural dysfunctions that underlie
neglect symptoms and their recovery is therefore
an important step to envision more efficient inter-
ventions and improve rehabilitation approaches.
In recent years, neuroscience research on neglect
has begun to yield several new mechanistic insights
that will hopefully open new opportunities for ther-
apeutic interventions. Although there is no unified
theoretical framework to explain neglect, and con-
troversies still exist concerning its exact neural un-
derpinnings (as will be discussed below), there is
now general agreement that a core deficit of neglect
involves brain mechanisms controlling the orienta-
tion of attention in space.14,15 A profound impair-
ment in directing attention to the contralesional
side of space, objects, or ones own body might ac-
count for the striking loss in perception and ac-
tion toward that side, as well as the modulation
of such deficits by various procedures enhancing
attention toward that side. In the healthy brain,
attention encompasses a number of distinct pro-
cesses that play critical roles in selecting sensory
information and motor plans for conscious aware-
ness and goal-oriented behavior.16,17 Abundant re-
search has shown that normal people may also fail
to perceive and respond to stimuli when attention
is not directed to them, just like neglect patients
ignore information in their contralesional space.16
Neuroscience work has substantially broadened our
knowledge of these attentional mechanisms and be-
gun to dissect their anatomical and physiological
components. This research has contributed to a bet-
ter understanding of neglect symptoms and their
specific neural substrates,3,17,18 while neuropsycho-
logical studies of neglect have enriched and moti-
vated research on normal attentional mechanisms,
using neuroimaging in humans15 and neurophysio-
logical methods in nonhuman primates.19
However, attentional accounts alone are not suf-
ficient to explain all neglect manifestations, particu-
larly dissociations between different sectors of space
(e.g., near vs. far,20 front vs. back21 ) or the exis-
tence of nonspatial/nonlateralized deficits.22 Much
therefore remains to be determined about the ex-
act nature of the attentional deficits underlying ne-
glect and its diverse symptoms, their functional
relationship to various representations of space in
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Vuilleumier
the brain, as well as the specific role of different brain
regions or circuits in each of these processes. In-
creasing evidence indicates that spatial neglect may
involve a combination of impairments in different
component processes, and that behavioral deficits
emerge as a result of dysfunction within large-scale
brain networks whose activity is disrupted beyond
local areas of structural damage. Yet, these func-
tional components and the corresponding networks
are still largely unresolved. The present review pro-
vides a selective overview of current knowledge and
highlights some outstanding questions. It is argued
that describing neglect symptoms in terms of more
specific cognitive processes and relating them to pre-
cise neurophysiological substrates constitute an im-
portant challenge for future neglect research. This
is essential to better characterize the behavioral im-
pairment of individual patients and design appro-
priate remediation strategies. This is also crucial
to foster translation from animal research, where
a complete model of spatial neglect has not been
successfully developed and more selective manipu-
lations of brain function can be tested.
This selective overview will specifically focus
on the functional neuroanatomy of putative com-
ponents of neglect and recent work mapping its
anatomy in the parietal lobe and interconnected
brain regions. A particular emphasis will be placed
on data highlighting the role of distributed brain
networks and functional interactions across distant
regions. These data illustrate the limitations of a
strict localizationist approach of neuropsycholog-
ical deficits and underscore the value of combining
functional neurophysiological measures with more
classic structural analyses of brain injury.
Clinical and anatomical variability of
spatial neglect
The clinical presentation of neglect is heterogeneous
and variable across patients. Accordingly, in neu-
ropsychology practice, the presence of neglect is
typically assessed using several different tests rather
than with a single measure. Standardized batter-
ies have been designed to probe neglect symptoms
across a range of behaviors and tasks and are rou-
tinely used for diagnosis (e.g., BIT23 or GEREN;24
Fig. 1), often providing a global score of neglect
severity based on the sum of deficits across several
tests. However, it is common that the degree of ne-
glect differs between tests within the same patient,
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Spatial neglect and the parietal lobe
even though the overall severity of deficits tends to
correlate between different tests across patients, per-
haps simply due to lesion extent.25 Moreover, dis-
sociations between different types of neglect symp-
toms are frequent and have often been taken to make
important theoretical inferences on the architecture
of particular cognitive systems (e.g., related to spa-
tial representations or attention).
These clinical observations have led to a number
of dichotomies in the characterization of different
manifestations of spatial neglect. For example, dis-
sociations were observed between perceived versus
imagined space, perceptual versus motor space, ego-
centric (trunk-, head-, or eye-centered) versus allo-
centric space (scene- or object-based), personal ver-
sus peri- and extra-personal space (including near
vs. far), and global versus local space.18 This diver-
sity suggests that different symptoms or tests might
reflect at least partly distinct cognitive processes,
which can be affected to varying degrees in differ-
ent patients. Yet the nature of these processes and
their neural substrates still remain far from being
elucidated. It is also possible, in principle, that a
single core neglect deficit might produce different
effects on different spatial domains, due to particu-
larities or additional dysfunctions in some of these
domains.
In keeping with the diversity of behavioral man-
ifestations, neuropsychological studies have also
highlighted a diversity of brain lesions causing ne-
glect symptoms, particularly of the inferior pari-
etal lobe,26,27 but also lateral prefrontal areas,28,29
posterior thalamus (pulvinar),30,31 basal ganglia
(putamen and caudate),28,31 and even the superior
lateral32 and medial temporal lobe.33,34 Other stud-
ies have emphasized subcortical damage in paraven-
tricular white matter.35,36 This anatomical variabil-
ity has long led to the view that neglect may reflect
damage to a distributed network implicated in at-
tention and space awareness, within which different
nodes may play partly distinct roles.14 For exam-
ple, on the basis of insightful analysis of anatom-
ical connectivity as well as clinical dissociations,37
Mesulam proposed a predominant role for parietal
areas in perceptual components of spatial attention
and a role for prefrontal areas in motor exploratory
components.14
This heterogeneity in both the clinical and
anatomical presentation of neglect makes it hard
to map spatial awareness onto specific neural
53
Spatial neglect and the parietal lobe
networks in the brain, and is likely to cause some
of the discrepancies between studies attempting to
determine the neural substrates of spatial neglect
in unselected groups of patients (e.g., see Refs. 27,
32, 34, and 36). Such discrepancies might be ag-
gravated by several factors. First, different investi-
gators use different tests to establish the presence
of neglect, including, for example, line bisection27
or not,32 or excluding hemianopia32 or not.27 Fur-
ther, different studies use different kinds of line bi-
section or cancellation tasks, and/or apply differ-
ent cutoff scores for diagnosing neglect, potentially
selecting patients with different patterns of brain
damage. Second, in most studies, neglect diagnosis
is based on a composite score, typically retaining
patients with deficits on at least two tests among
a battery of several tests. This selection procedure
could lead to pooling patients with different deficits
and different patterns of brain lesion in the same
group (e.g., some patients being impaired on tests
A and B, others on tests C and D), hence unre-
liable anatomical overlap. Third, traditional lesion
mapping methods based on regional overlap or le-
sion frequency may not be appropriate to delineate
the substrates of functions subtended by multiple
equipotent sites or relying on long-range connec-
tions within distributed networks.38 For instance,
similar motor paralysis can occur after damage at
various points along the cortico-spinal tract. Like-
wise, if similar neglect symptoms arise after anterior
or posterior brain lesions, the most frequent over-
lap could potentially be found in an intermediate
but irrelevant location damaged in both popula-
tions, simply due to the variable extent of vascu-
lar territories affected by stroke. The latter problem
may be avoided by more recent lesion mapping
approaches based on a correlation of behavioral
deficits with a voxel-by-voxel analysis of brain tissue
damage (as used for image contrast change in func-
tional neuroimaging), which allow one to examine
lesionsymptom relationships at a more graded and
distributed whole-brain level.34,39,40
Thus, past research on the neural mechanisms of
neglect is somewhat characterized by a striking para-
dox. On the one hand, a rich collection of behavioral
dissociations has been carefully documented and
studied; while on the other hand, a quest for a critical
neuroanatomical substrate with unique impact on
spatial awareness has relentlessly been pursued and
debated. However, it is now increasingly recognized
54 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
that these divergences might be partly overcome by
an approach focusing on the neural mechanisms of
more specific components of neglect, characterized
in terms of more basic cognitive processes rather
than broad clinical categories only. Further, it is also
increasingly considered that the neural substrates
for such components should be characterized at the
level of functional networks of interconnected re-
gions, rather than in relation to particular regions of
interest. Nevertheless, besides a well-established re-
lation to attentional processes,15,17 the exact cogni-
tive constituents underlying various neglect symp-
toms still remain poorly specified, hence limiting the
efficacy of anatomical lesion mapping endeavors.
Attention and functional segregation in
superior parietal cortex
One of the best known cognitive functions associ-
ated with neglect and parietal lobe function is spatial
attention, for which abundant research exists at both
the behavioral and neurobiological levels. However,
attention itself is not a unitary process. For instance,
a classic dichotomy has been established between
exogenous versus endogenous mechanisms of at-
tention orienting in space.41 Exogenous orienting
occurs when attention is drawn to one location or
stimulus due to its sudden appearance or intrinsic
saliency, through automatic/reflexive mechanisms.
Endogenous orienting corresponds to more volun-
tary/controlled processes that orient attention on
the basis of task goals or instructions. Behavioral
neuropsychology studies have suggested that exoge-
nous orienting of spatial attention toward the con-
tralesional side might be most consistently impaired
in patients with spatial neglect, whereas endoge-
nous orienting might be relatively spared and does
not correlate with main neglect symptoms.42,43 Fur-
thermore, both behavioral and electrophysiological
evidence suggests that exogenous (more than en-
dogenous) attention is particularly critical to mod-
ulate the access of sensory information to conscious
awareness.44
This distinction in attention has therefore also
been applied to dissect neglect anatomy. In line with
classic lesion studies showing a predominant im-
pact of inferior parietal damage on contralesional
exogenous orienting,42 recent work with functional
magnetic resonance imaging (fMRI) points to a
key role of the temporo-parietal junction (TPJ) in
the detection of unexpected but relevant events,
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Vuilleumier Spatial neglect and the parietal lobe

Figure 2. Fronto-parietal networks controlling spatial attention. (A) Parietal and frontal areas involved in spatial attention are
linked by three distinct white-matter tracts in the superior longitudinal fasciculus (SLF). (B) Their projection sites in both the
parietal and frontal cortex correspond to the division into a dorsal attention network (DAN) typically associated with endogenous
and spatial components of orienting, and a ventral attention network (VAN) associated with more reflexive, stimulus-driven, and
nonspatial components. The SLF II might contribute to integrate activity between the VAN and the DAN by connecting inferior
parietal with superior frontal areas. (C) Depiction of SLF in relation to another major white tract connecting posterior with anterior
brain regions: inferior longitudinal fasciculus (ILF) and inferior fronto-occipital fasciculus (IFOF; unpublished data). A and B
adapted, with permission, from Ref. 159.

including orienting and disengaging from current
focus of attention in exogenous attention condi-
tions. By contrast, more superior regions in the
intraparietal sulcus (IPS) have been linked with
voluntary shifting and/or maintaining attention to
relevant locations or objects.45 This anatomical dis-
tinction has therefore led to an influential model of
spatial attention (Fig. 2) comprising both a dorsal
fronto-parietal network linking the IPS with supe-
rior frontal cortex (frontal eye fields, FEF), and a
ventral network linking the TPJ with the inferior
frontal gyrus (operculum/insula). According to this
model, damage to the ventral system would not only
impair contralesional exogenous orienting but also
induce subsequent dysfunction in the dorsal system
and hence additional endogenous orienting biases
toward the ipsilesional side, leading to full-blown
spatial neglect.15 Moreover, damage to the TPJ re-
liably correlates with the presence of extinction on
bilateral visual stimulation,46,47 consistent with the
notion that this phenomenon may reflect exogenous
capture by ipsilesional distractors and impaired re-
orienting to the contralesional side.42
However, recent work suggests that this
functionalanatomical dichotomy in attention
between dorsal and ventral attention areas

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Spatial neglect and the parietal lobe Vuilleumier

Figure 3. Multiple areas within the human parietal cortex. Both the superior parietal lobe (SPL) and inferior parietal lobe (IPL)
or temporo-parietal junction (TPJ) can be divided in different cortical regions on the basis of their cytoarchitectonic characteristics
and functional response profile during attention or other cognitive tasks. In particular, the intraparietal sulcus (IPS) contain
distinct subareas, showing either increased activation during bilateral relative to unilateral visual stimulation when attention is
directed to the contralateral side (middle segment), or decreased activation during bilateral relative to unilateral visual stimulation
when attention is directed to another stimulus at fixation (posterior segment near the transverse occipital sulcus, TOS). In the
TPJ, the supramarginal gyrus (SMG) is activated during spatial reorienting and other task-resetting conditions but unaffected by
completion between the two hemifields, whereas activity in the angular gyrus (AG) is not only modulated by attentional reorienting
and spatial working memory tasks, but also decreased by bilateral relative to unilateral contralateral stimulation. Other areas in
the TPJ include the parietal operculum (POp) and the posterior superior temporal gyrus (STG), which are involved in vestibular
information processing.

(Fig. 2) may not be as simple as it was initially
thought. Dysfunction in the IPS induced by tran-
scranial magnetic stimulation (TMS) may also pro-
duce deficits in exogenous attention,48 and lesions
in the IPS correlate with extinction-like deficits for
contralesional visual stimuli when these are pre-
sented with a simultaneous ipsilesional distractor
(particularly in symmetrical position).49,50 The lat-
ter extinction-like deficits were found in a visual
discrimination task, rather than detection, while at-
tention was endogenously directed to the contrale-
sional side in the presence of a competing stimulus
on the ipsilesional side. This may not necessarily re-
flect the same loss in awareness as observed for clin-
ical extinction, where attention must be directed to
two targets simultaneously.11,51 Moreover, whereas
patients with contralesional extinction and neglect
most often have right-hemisphere lesions,52 compe-
tition costs in the discrimination of contralesional
stimuli during bilateral stimulation can occur after
focal lesion restricted to the IPS in either hemi-
sphere without other signs of neglect.50 In keep-
ing with these neuropsychological findings, fMRI in
healthy participants show selective activation in the
IPS (particularly in its middle horizontal segment;
see Fig. 3) when attending to a contralateral visual
stimulus in the presence of ipsilateral distractors,
relative to the same stimulus presented alone.49 No
such increase in the IPS is seen for bilateral versus
unilateral visual stimulation when these are irrele-
vant and attention is maintained at fixation.53 The
middle IPS might therefore play an important role in
controlling selective attention to contralateral loca-
tions in the presence of competing inputs, perhaps
by contributing to the computation of a saliency
map,54 which may integrate both topdown goal-
driven mechanisms and bottomup sensory signals.
Damage to this region may thus be an important
component of attentional deficit in neglect and con-
tribute to perceptual extinction in some patients.
On the other hand, a more posterior region
of the IPS (near the transverse parieto-occipital

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Vuilleumier Spatial neglect and the parietal lobe

Figure 4. Dissociable effects of bilateral visual competition in superior and inferior parietal cortex in healthy volunteers. (A) Visual
stimulation paradigm with either unilateral right, unilateral left, bilateral, or no stimulation in the peripheral visual field, while
attention is maintained on central targets at fixation to perform either a demanding (high load) or easy (low load) discrimination
task. (B) Bilateral areas in the posterior IPS show decreased response to bilateral versus unilateral peripheral stimulation, with
stronger suppression during higher attentional demands at fixation. Symmetrical effects occur in the right (plotted in bar graphs)
and left posterior IPS. (C) Bilateral areas in the IPL (overlapping with angular gyrus) also show decreased response to bilateral
versus unilateral peripheral stimulation but irrespective of attentional demands at fixation. In addition, only the right IPL responds
to unilateral ipsilateral stimulation (right panel), whereas the left IPL responds to contralateral stimulation only (right panel).
Adapted, with permission, from Ref. 55.

sulcus, TPOS; see Fig. 3) has been found to ex-
hibit a suppressive effect (rather than enhancement)
due to competition between the two visual hemi-
fields when peripheral stimuli are task irrelevant.55
In healthy subjects, this more posterior region shows
reduced fMRI activation to bilateral relative to uni-
lateral peripheral stimulation, but this suppressive
effect arises only when attentional demands at fix-
ation are high (difficult detection task), presum-
ably reflecting a reduction in the representation of
surrounding visual space when attention is focused
(Fig. 4A and B). This competition effect indicates
suppressive interactions between bilateral sensory
inputs, rather than active filtering or disengaging
from distractors, unlike the competition enhance-
ment seen in the middle IPS when attended stimuli
are presented with distractors. The posterior IPS
might thus mediate a capacity-limited representa-
tion of salient visual locations based on bottom
up inputs, rather than behavioral goals. Note that,
by contrast, sensory competition across the two vi-
sual hemifields does not seem to modulate stimulus-
driven responses of earlier retinotopic visual areas
in striate and extrastriate occipital cortex.55 Such
competition in low-level visual areas may, how-
ever, occur when peripheral stimuli are attended,56

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Spatial neglect and the parietal lobe
suggesting that the latter effects result from changes
in topdown attentional factors rather than in a
purely sensory-driven manner.
Taken together, these findings converge with
other results indicating that several subregions exist
in and around the IPS, each with a distinct func-
tional profile of activity during attentional tasks.53,57
Moreover, in addition to the above, a more supe-
rior and medial parietal region appears critically in-
volved in attention shifts across different domains,
including spatial shifts between locations, stimuli, or
tasks,58 while it is not influenced by sensory compe-
tition between concurrent stimuli. Other more ante-
rior regions in and around the IPS are also involved
in coding spatial locations for eye and limb move-
ments, integrating not only visual inputs but also
other sensory modalities.57 Accordingly, in nonhu-
man primates, many different subareas have been
identified in posterior parietal cortex along the IPS,
implicated in attention control and sensorimotor
transformation across different sensory and motor
domains (such as lateral (LIP) and ventral (VIP)
areas of the IPS). It is likely that large brain lesions
(as typically observed after stroke) will affect more
than one of these parietal areas, and hence the clini-
cal manifestations of neglect will likely result from a
combination of deficits in different kinds of parietal
computations. Furthermore, variations in the extent
of damage will destroy or disconnect different subre-
gions in different patients, and thus presumably lead
to corresponding variations in performance across
different clinical tasks. For example, one might spec-
ulate that a loss of contralesional visual informa-
tion in the posterior IPS/TPOS, in the presence of
intact inputs from the ipsilesional field, may con-
tribute to the apparent compression of space or line
length typically observed in neglect patients,59 with-
out disrupting the ability to voluntarily direct at-
tention to the contralesional extremity of such lines
(and even extend them toward the neglected side60 )
when more anterior or inferior regions in parietal
cortex are preserved. In contrast, a combination of
damage extending from the posterior to middle or
anterior IPS might cause additional deficits in cod-
ing for contralesional locations (and hence orient
attention there) when attention is captured by con-
current information on the ipsilesional side (e.g.,
in multi-item scenes). Conversely, sparing of the
IPS may account for intact endogenous orienting of
attention in neglect patients43,61 when their lesion
58 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
involves other areas. Increased knowledge on the
functional parceling of superior parietal cortex will
certainly enhance our understanding of deficits in
attention, spatial competition, and sensorymotor
transformations that potentially contribute to spa-
tial neglect.
Functional segregation in the inferior
parietal cortex
Like damage to the IPS, lesions in the inferior pari-
etal lobe (IPL) can also produce behavioral deficits
in processing a contralesional target that is simulta-
neously presented with ipsilesional distractors,42,50
as exemplified by the common presence of percep-
tual extinction in these patients.46,62 However, this
impairment may have a different cause than the
competition effects caused by IPS lesions. Indeed,
fMRI data in healthy participants suggest that activ-
ity in the TPJ for contralateral visual stimuli is not
modified by the presence of contralateral stimuli
per se.53,63 Rather, the TPJ activates whenever atten-
tion is (exogenously or endogenously) drawn to one
side and must be reoriented toward task-relevant
information in the opposite side (invalid vs. valid
attention),15 even in the absence of a competing
stimulus.49,64 Interestingly, these reorienting effects
appear more strongly associated with the right than
left TPJ,65 in contrast to attentional effects observed
in superior parietal areas that are most often sym-
metrical in both hemispheres.
However, here again, the TPJ is likely to be frac-
tionated into several distinct functional subareas
(Fig. 3). More anterior regions in the right supra-
marginal gyrus are selectively recruited by reorient-
ing attention to unattended or unexpected targets,
with no effects of sensory competition between mul-
tiple stimuli.53 The same regions are also activated
in other nonspatial conditions involving breaches
in expectations and adaptive changes in current
task contingencies.66 It has therefore been suggested
that these regions may function as a circuit breaker
that interrupts and resets ongoing activity in brain
networks to respond to novel and unexpected in-
formation. In contrast, a more posterior area in
the right angular gyrus (Fig. 3) shows a combi-
nation of effects due to attention reorienting and
stimulus competition,53 but with responses signif-
icantly reduced by the presence of bilateral relative
to unilateral stimuli when these are unattended and
presented with a central target.55 These responses
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Vuilleumier
in the IPL are also asymmetrical between the two
visual hemifields: the left parietal cortex activates
to unilateral right distractors, whereas the right IPL
activates to either left or right unilateral distractors,
more than to bilateral stimuli in both hemispheres
(Fig. 4A and C). This asymmetry in contralateral
responses accords with the longstanding view that
the right parietal lobe may represent both sides of
space, while the left represents only the contralateral
right side.14,26,67 In such patients, the intact left IPL
may still allow (or favor) responses to right stimuli;
whereas in left parietal patients, intact regions in the
right hemisphere can monitor stimuli from either
left or right hemifield.
Nonetheless, the mechanisms for a suppression
of IPL response to bilateral peripheral distractors
(compared to unilateral distractors) remain un-
clear. Other findings also indicate greater responses
in right IPL to a single target presented alone as
compared to multiple targets or a single target pre-
sented with distractors.63 Speculatively, the pattern
of effects in the angular gyrus might reflect a com-
plex role of these cortical areas for the individuation
of behaviorally relevant or salient objects, perhaps
contributing to the formation of token represen-
tations that bind together different spatiotemporal
attributes into a unique and distinctive event. No
such individuation may occur when bilateral and
symmetric stimuli are presented simultaneously at
unattended locations, as they may appear as part of
the background rather than outstanding elements in
a scene. Token representations are conceptualized as
a temporary episodic registration of the current in-
stantiation of a particular object or event, in terms
of what was where and when, allowing the mainte-
nance of perceptual unity and continuity of objects
when they move or change in the scene, but also
linking different images of the same object across
body or eye movements.68,69 Capacity limitation in
token representation is thought to explain percep-
tion failures in situations where similar sensory in-
formation must be bound to different items in ei-
ther space or time, such as repetition blindness.70
Thus, when two instances of a particular object
are seen in rapid succession or close proximity, the
brain often forms only a single token and people
perceive only one of the two objects. In vision,
the formation of token representation might re-
quire the integration of inputs from both the dorsal
(occipito-parietal) and ventral (occipito-temporal)
Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
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Spatial neglect and the parietal lobe
streams, processing information about object loca-
tion and identity, respectively, which would be con-
sistent with neuropsychological accounts proposing
a key role for the IPL in binding both streams.71 A
deficit in token formation and event individuation
might contribute to the phenomenon of contrale-
sional perceptual extinction typically seen in pa-
tients with IPL damage, possibly due to disruption
in such dorsalventral integration.51,72 This phe-
nomenon might be exacerbated when combined
with an extension of the TPJ lesions to supra-
marginal cortex, causing additional impairment in
reorienting or resetting mechanisms after capture of
attention by ipsilesional distractors (i.e., impaired
attentional disengagement).15,42,43 Deficient token
formation may explain the exacerbation of percep-
tual extinction or neglect symptoms when bilateral
stimuli are perceptually similar11,51 and appear si-
multaneously in time at symmetrical locations.72,73
These effects can extend beyond vision to other sen-
sory modalities, as suggested by auditory and tactile
extinction,74 consistent with a supramodal or cross-
modal function of the angular gyrus.75,76 Even with-
out a concomitant impairment in reorienting, defi-
cient tokenization processes after IPL damage might
also account for nonspatial disturbances commonly
observed in these patients, with or without clinical
neglect. For instance, neglect patients show abnor-
mal temporal dynamics of attention, with difficul-
ties in distinguishing between two targets appearing
in rapid succession at a central location,77 judging
the relative onset and offset of visual events,78,79
and integrating discontinuous stimuli in a coher-
ent percept of apparent motion.80 Interestingly, the
latter deficits are not spatially lateralized but ob-
served in both hemifields, even though they might
exacerbate contralesional spatial biases when com-
bined with other lateralized (e.g., reorienting) im-
pairments. Interestingly, deficits in temporal dis-
crimination abilities for two concurrent targets were
found to correlate with damage in right angular
gyrus, unlike spatial biases in the same temporal
order judgment tasks that correlate with more an-
terior damage in the TPJ (supramarginal gyrus), in
addition to other differences in white matter and
cerebellum.79
Similar or nearby regions in right angular gyrus
might subserve other cognitive functions crucial for
attention and spatial cognition, including working
memory maintenance and updating. Accordingly,
59
Spatial neglect and the parietal lobe
nonlateralized deficits in spatial working memory
are commonly observed in neglect patients and
may contribute to their behavioral deficits in var-
ious tasks, particularly search (cancellation) tasks
in which patients often tend to recursively explore
the same location and revisit previously marked
targets.81 Such deficits in spatial short-term mem-
ory after IPL lesion have been observed in both
sides of space81,82 but may predominate on the con-
tralesional side.83 Thus, in a visual search task, ne-
glect patients showed no difference in target detec-
tion latencies when targets changed locations within
the left hemifield during search, relative to when
they remained at the same locations, while loca-
tion changes within the right hemifield disrupted
performance, suggesting a lack of stable represen-
tation for explored location in contralesional but
not ipsilesional space.83 Such impairment in spatial
memory might partly be secondary to impaired spa-
tial remapping processes that allow maintaining and
updating the representation of a stimulus location
when its perceived position (e.g., on retina) is mod-
ified by changes in body (e.g., eye) position.84,85 For
example, a visual location (even in the intact right
hemifield) may vanish from memory when neglect
patients make a single saccade to a more rightward
location, whereas locations in either hemifield can
be remembered across similar time delays without
intervening movement.84 This pattern has been in-
terpreted as an inability of spatial memory to main-
tain or transfer contralesional visual information in
gaze-centered coordinates. Moreover, spatial mem-
ory deficits correlate with neglect severity and lesion
extension in IPL and subcortical white matter.81,82,84
Nonlateralized deficits in sustained attention and
alertness have also been linked with IPL lesions and
neglect.86,87
Finally, other areas in the TPJ may correspond to
cortical projections sites for the vestibular system,
integrating information critical for the coding of
body position in space, with a well-established right-
hemisphere dominance.88 Recent evidence from
brain imaging in healthy participants suggests that
several subareas in the TPJ may process vestibular
inputs, including the parietal operculum in partic-
ular (Fig. 3), but also the posterior insula and su-
perior temporal gyrus.89,90 Damage to these regions
might therefore also contribute to some of the well-
known anomalies in spatial representations in ne-
glect patients, including deviation in the subjective
60 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
perception of straight-ahead orientation and trunk
midline position.91,92
Even if it remains nonexhaustive, this overview
indicates that not only the superior parietal cortex
around the IPS, but also the inferior parietal lobe
and the TPJ contain a number of distinct subre-
gions that make different contributions to attention
and spatial cognition. While conjoint damage to this
collection of cortical regions and their connections
is likely to account for many typical aspects of ne-
glect, variations in the exact impact of lesion across
patients may help explain some dissociations in clin-
ical presentation, although the precise understand-
ing and mapping of these different functions within
parietal cortex still remain far from resolved. Fur-
thermore, parietal areas do not function in isolation
but are connected to several prefrontal and subcor-
tical areas to form distributed networks whose co-
ordinated functioning can also be impaired by focal
damage in parietal cortex, as further discussed in
subsequent sections.
Behavioral dissociations and
neuroanatomy of neglect components
Even though deficits in spatial attention and damage
to its neural substrates in parietal cortex constitute a
major component of the neglect syndrome, it is clear
that purely attentional disturbances (even those af-
fecting exogenous mechanisms43 ) are not sufficient
to account for all neglect phenomena. For exam-
ple, neglect of contralesional space during manual
or ocular exploration in complete darkness9 cannot
be explained by a capture of exogenous attention
by ipsilesional stimuli (at least in a straightforward
manner). Likewise, dissociations affecting a selec-
tive domain (such as far vs. near space, front vs.
back space, extrapersonal vs. personal space, and
locations within vs. between objects) all imply addi-
tional brain systems supporting stimulus awareness
in a more elaborate format than just based on asym-
metry in the control of exogenous attention orient-
ing. These behavioral observations have been taken
to indicate the role of higher order representations of
space, which might integrate sensory (multimodal)
inputs with motor planning for different effectors
(e.g., eyes, limbs) or different action sectors, such as
reaching or avoiding (near space), and looking or
walking (far space).20,21,57,93
Several studies have investigated the neu-
roanatomical substrates underlying some of these
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Vuilleumier
differences in the spatial distribution of neglect
deficits. A frequent approach is to compare lesions
in patients with and without deficits in particu-
lar clinical tests. For example, neglect on line bi-
section has been reported to be more common
after posterior (parietal) damage, whereas neglect
on cancellation tasks is more severe after ante-
rior (frontal) or subcortical lesions.94,95 Likewise,
omissions of targets in left space during cancella-
tion tasks (space-based or egocentric neglect) have
been linked with damage (or hypoperfusion) in in-
ferior parietal lobe, whereas omissions of the left-
sided features of targets irrespective of their loca-
tion in space during cancellation (stimulus-based
or allocentric neglect) were associated with dys-
function in lateral and inferior temporal lobe.96,97
The latter findings were interpreted in terms of dis-
tinct neural systems for controlling attention be-
tween and within objects in the dorsal-parietal and
ventral-temporal visual stream, respectively. How-
ever, other lesion studies used different clinical tests
to define neglect in egocentric (viewer-centered)
or allocentric (either stimulus- or scene-centered)
coordinates and found different neuroanatomical
correlates,98,99 or instead implicated partly overlap-
ping brain regions.62,99,100 In keeping with this, func-
tional neuroimaging work in healthy volunteers also
suggests a differential recruitment of fronto-parietal
versus occipito-temporal regions in egocentric ver-
sus allocentric spatial tasks, as well as shared pro-
cessing in posterior parietal cortex.101103 A similar
distinction between a dorsal action-related stream
and a ventral perception-related stream of visual
processing has been made to account for dissociable
forms of neglect in near and far space,20,103,104 but no
systematic lesion study has been performed in a large
patient group yet. Taken together, these anatomical
data converge with the idea that different represen-
tations of visual space might be distinguished in
terms of their use for action or perception, even
though the exact computations and neural systems
supporting these representations, and their inter-
action with attention and awareness, still need to
be more precisely determined. Moreover, egocen-
tric neglect deficits can be further subdivided with
respect to different reference frames centered on the
eye, head, trunk, or even limb,105 suggesting distinct
contributions of representations controlling and/or
monitoring the position or movement of specific
body parts.
Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
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Spatial neglect and the parietal lobe
Other dissociations between extrapersonal
(space-centered) and personal (body-centered) ne-
glect have been investigated using voxelwise lesion
mapping.106,107 In one study,106 each spatial domain
was assessed using a battery of different tasks (in-
cluding cancellation and reading, but not line bi-
section, for extrapersonal space), and impairment
was diagnosed when patients performed below a
given cut-off score on at least two tasks in the same
domain. Personal neglect was found to correlate
with lesions in the postcentral somatosensory cor-
tex, adjacent white matter, and inferior parietal lob-
ule. This pattern differed from extrapersonal neglect
whose severity correlated with lesions mainly affect-
ing the inferior frontal cortex and superior tempo-
ral regions, partly overlapping with areas previously
associated with exogenous attention and vestibular
processing.
Motivated by the heterogeneity of anatomical
findings and symptoms examined across past stud-
ies, a few meta-analyses were recently performed
using an activation likelihood estimation (ALE)
procedure originally developed for functional neu-
roimaging studies. By combining results from more
than 20 lesion mapping studies published in the
past decade, these meta-analyses have generally con-
firmed the notion that different manifestations of
spatial neglect can be linked to both distinct and
common neural substrates.47,108 The most consis-
tent findings were found for extinction (in the
TPJ), line bisection (in posterior parietal cortex),
and to a lesser degree, cancellation tasks (in pre-
frontal more often than parietal cortex), whereas
other neglect symptoms (such as allocentric or
personal neglect) showed greater dispersion across
brain sites (Fig. 5). In addition, all studies converged
to show a critical involvement of hemispheric white-
matter structures, whose damage is not only fre-
quent but often shared between different neglect
deficits, particularly for the superior longitudinal
fasciculus (SLF), inferior fronto-occipital fasciculus
(IFOF), and thalamic radiations (see also below and
Fig. 2C). Such meta-analyses are extremely useful
and promising, as they provide a data-driven sta-
tistical tool to assess consistency across studies. Yet,
they remain limited due to the fact that the clinical
tests and diagnostic criteria may vary substantially
between studies, even when considering a specific
task (e.g., cancellation) or a specific spatial domain
(e.g., allocentric). While this variability might help
61
Spatial neglect and the parietal lobe Vuilleumier

Figure 5. Meta-analysis of 20 lesion-mapping studies of neglect symptoms. The likelihood of lesion peaks is illustrated on an
inflated brain template for six different neglect measures, including (A) line bisection (purple spheres); (B) cancellation tasks (red
spheres); (C) global scores from a combination of tasks (green spheres); (D) allocentric object-centered tests (blue spheres); (E)
personal body-centered tests (black spheres); and (F) perceptual extinction on double stimulation (orange spheres). Adapted, with
permission, from Ref. 47.

to highlight common processes implicated in a given
neglect component, differences in sensitivity or ad-
ditional demand characteristics across clinical tests
might blur the role of more specific processes. Dif-
ferences in the delay since lesion onset and the inter-
val between radiological and behavioral assessment
may further complicate the comparison between
studies.40,109
A more general limitation of many studies at-
tempting to delineate lesions associated with differ-
ent types of neglect symptoms is that these symp-
toms are defined according to broad and clinically
defined dichotomies (e.g., personal vs. extraper-
sonal or egocentric vs. allocentric space), rather
than more specific cognitive processes. However,
it is plausible (and even likely) that some of these
spatial abilities rely on more than one unitary cog-
nitive function. For example, allocentric judgment
tasks may involve object shape recognition, sym-
metry detection, and disengagement from compet-
ing information, each underpinned by distinct neu-
ral substrates (just like perceptual extinction may
reflect both spatial and temporal deficits in atten-
tion subserved by different areas in parietal cortex).
Furthermore, neglect symptoms are most often
measured with a single test, adapted from clinical
practice. However, these clinical tests have been de-
veloped to be sensitive to the presence of deficits,
rather than specific symptoms, and hence tend to
tap into different abilities.
One approach to identifying specific functional
components (or building blocks) contributing to

62 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences.
Vuilleumier Spatial neglect and the parietal lobe

Figure 6. Lesion mapping of neglect factors. Factorial analysis of performance across various tests identified three separate
functional components that accounted for neglect in different domains and were associated with different lesion sites. Factor 1
correlated with the lesion in posterior parietal cortex (and to a lesser degree in superior frontal cortex) and predicted neglect in line
bisection, text reading, and drawing. Factor 2 correlated with the lesion in inferior frontal cortex (and to a lesser degree in parietal
cortex) and predicted neglect in cancellation tasks and drawing. Factor 3 correlated with the lesion in the temporal lobe (with a
peak in the deep medial region and extension toward the inferior later cortex) and predicted neglect in single-word reading and
object-based tasks (allocentric neglect). Adapted, with permission, from Ref. 34.

one or many neglect symptoms has been to ap-
ply factorial analyses or clustering statistics on the
performance of patients across a large range of dif-
ferent tasks.24,34,110,111 This approach exploits con-
comitant variations among a collection of corre-
lated variables to reduce these variables to a lower
number of potentially underlying, but unobserved,
factors. For example, it is possible that variations
of neglect severity across a battery of clinical tests
might reflect deficits in, say, two distinct cognitive
factors (e.g., exogenous and endogenous attention),
each associated with a particular neural system (e.g.,
ventral and dorsal parieto-frontal networks). Using
a range of standard tests in large groups of brain-
damaged patients (n = 40200), factorial analysis
studies have indeed pointed to the role of at least two
or three separate factors explaining neglect behav-
ior across different kinds of tests. These factors ap-
pear remarkably consistent across studies,24,34,110,111
and cluster along the following dimensions: (1) ex-
ploratory functions involving overt motor behav-
ior and distractor interference (search component),
particularly associated with performance on can-
cellation tasks, drawing, and writing; (2) percep-
tual functions recruited for encoding, maintaining,
and/or shifting across multiple locations in space
(deploy component), and associated with perfor-
mance on line bisection, text reading, and figure-
ground segregation; (3) allocentric representations
(object-based component) associated with perfor-
mance on single-word reading and omissions of
contralesional features within objects. Of course,
neglect is likely to involve more than these three fac-
tors, which altogether explained only between 50%
and 85% of the variance in tests across the different
studies. Hence, other factors must explain the resid-
ual variance. Nevertheless, these data demonstrate
that different neglect deficits may implicate at least
partly distinct cognitive processes, while the same
cognitive process may contribute to different deficits
in different tasks. For example, in one study,34 ne-
glect on drawing from copy was found to be pre-
dicted by a combination of deficits in two different
components (search and deploy).
Furthermore, this data-driven approach may also
allow delineating the neuroanatomical substrates
associated with higher level factors explaining be-
havior across different tasks (with or without clini-
cally overt neglect), rather than mapping the cor-
relates of neglect in a single test that may be
underpinned by multiple cognitive processes. For
example, in the study mentioned above,34 the ex-
ploratory search factor was predominantly associ-
ated with damage to the inferior and posterior mid-
dle prefrontal gyri; whereas the perceptual deploy
factor was associated with damage to both inferior
and superior parietal lobe, and to a lesser degree,
to posterior frontal areas (Fig. 6). These data ac-
cord with recent meta-analyses suggesting differ-
ential contribution of frontal and parietal lesions
to cancellation and line bisection tasks, respectively
(see Refs. 47 and 108), but also show that simi-
lar cognitive processes may be implicated in other
behavioral manifestations. Frontal lobe damage
may contribute to greater distractor interference29
and perseveration112 during cancellation tasks. In

Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences. 63
Spatial neglect and the parietal lobe
addition, the same study34 revealed that a third
object-based factor correlated with damage to
both medial (parahippocampal) and lateral (infe-
rior sulcus) temporal lobe areas, again converg-
ing with other findings from studies on allocen-
tric neglect.9698 Interestingly, Verdon et al.34 found
that patients with more severe and pervasive ne-
glect, involving more than one of the three factors
identified above, had more common extension of
their lesion to subcortical regions in paraventric-
ular white matter,34 suggesting that disconnection
of white-matter tracts might influence multiple do-
mains of spatial cognition simultaneously (see also
below).
Additional research is needed to refine these fac-
tors and understand the exact cognitive processes
underlying them. Even though the heterogeneity of
neglect symptoms might be compatible with the ex-
istence of a core syndrome, with optional satellite
deficits in other domains,113 the nature of this core
disorder still remain unclear beyond purely descrip-
tive clinical features. Moreover, this core syndrome
itself might encompass a combination of more ele-
mentary deficits that do not lead to clinical neglect
when damaged in isolation. To better dissect and de-
fine the specific cognitive components contributing
to neglect behavior, and to understand their role in
different deficits, future research should use a large
variety of tests tapping onto distinct domains and
large group of patients, both with and without a
clinical diagnosis of neglect.
Distributed networks and connections
In keeping with the view that spatial awareness and
its disturbances in neglect result from a combination
of interactive processes, recent research has high-
lighted the role of distributed brain networks in the
control of attention,14,15 as well as the widespread
impact of damage to subcortical connections in ne-
glect patients.34,36,114,115 It has long been known that
damage to deep white-matter regions may lead to
long-lasting and severe forms of neglect, but it is
only during the past few years that advances in
neuroimaging techniques (such as diffusion tensor
imaging, DTI) have fostered more systematic in-
vestigations concerning the precise anatomical con-
nectivity of brain networks implicated in neglect.
Converging evidence from several lesion mapping
studies34,114,116,117 and meta-analyses47,108 points to
a greater frequency of lesions along intrahemi-
64 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
spheric tracts in right brain-damaged patients with
neglect relative to those without, in particular in the
SLF (Fig. 2A) and inferior fronto-occipital fasciculus
(IFOF; Fig. 2C), reciprocally connecting posterior
and anterior brain regions. In addition, the thala-
mic radiations projecting to fronto-parietal cortex
are also frequently involved. These white-matter le-
sions appear to be shared across a range of different
deficits (e.g., egocentric or allocentric neglect) and
are more frequent when patients show neglect across
many different tests,34,99,108 suggesting that subcor-
tical disconnections may influence several cognitive
subcomponents simultaneously and thus produce a
common pattern of deficits across different spatial
domains.
Moreover, precise white-matter tract-based
statistics in patient groups, as well as single-case
dissection analysis, suggest that specific portions of
the SLF might differentially be implicated.36,117 SLF
has been proposed to be segregated into three dis-
tinct bundles: SLF1 connects superior parietal cor-
tex with more superior frontal areas (overlapping
with the dorsal endogenous attention network),
whereas SLF3 connects the inferior parietal cortex
with more inferior frontal areas (overlapping with
the ventral exogenous attention network), and SLF2
connects inferior parietal with superior frontal re-
gions (possibly implicated in cross-talks between
networks; see Fig. 2). Damage to SLF2 (or nearby
superior occipito-frontal fibers, SOF) appears as the
best predictor among white-matter tracts for the
presence and/or severity of spatial neglect, regard-
less of test.116,117 Nevertheless, voxelwise regression
analysis suggests that line bisection deficits tend to
correlate more with lesions in superior paraventric-
ular and deep parietal lobe white matter, whereas
visual cancellation deficits correlate with more ante-
rior lesions under the precentral and middle frontal
gyri, near the FEF,117 in agreement with previous
lesion data suggesting distinct roles for frontal and
parietal cortical areas in neglect symptoms.34,94,95
In addition, transient neglect on line bisection can
also be induced by electrical stimulation of white-
matter fibers in the depth of the inferior parietal
lobe, corresponding to SLF2 or SOF.118 These find-
ings are consistent with diffusion tensor imaging
work in healthy volunteers supporting a crucial in-
volvement of these fronto-parietal tracts in normal
visuospatial attention. Indeed, some portions of SLF
show strong hemispheric asymmetry, with a right
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Vuilleumier
preponderance that is the most pronounced for
SLF3.119 In addition, the degree of asymmetry in
SLF2 volume between right and left hemispheres
in individual participants correlates with asymme-
tries in their performance on visual attention tasks,
including the magnitude of right-side pseudo ne-
glect on line bisection and a left hemifield advan-
tage in the Posner cueing paradigm.
Taken together, these data suggest that disrupted
communication between frontal and parietal areas
may play a major role in the occurrence of ne-
glect, perhaps due to abnormal integration of dorsal
and ventral attention systems within and between
hemispheres.15,115 Even though it remains debated
whether the white-matter lesions alone can lead to
persistent neglect after stroke and whether cortical
damage is more critical,116 the extension of lesions
to specific white-matter tracts clearly appear to con-
tribute to the severity of neglect and to the range of
clinical manifestations, perhaps by impacting mul-
tiple functional systems simultaneously.
It is also possible that particular symptoms may
involve distinct white-matter tracts. For example, a
single-case study suggested that additional damage
to interhemispheric fibers in the posterior corpus
callosum (splenium) might be responsible for rep-
resentational neglect in mental imagery.120 Interest-
ingly, abnormal white matter in posterior corpus
callosum has been found to predict the severity of
neglect on clinical tests (BIT) in stroke patients,121
as well as the degree of spatial biases in temporal
order judgments.79 This differs from other studies
reporting no association between callosal lesion and
neglect,116,117 but the latter studies used different
tests to diagnose neglect (mainly cancellation and
line bisection). Of note, the total BIT score shown to
correlate with anomalies in posterior corpus callo-
sum included representational drawing tests as well
as behavioral measures from everyday life,121 but
unfortunately this study did not examine correla-
tions for specific subtests. A role for callosal dam-
age would be consistent with one of the rare lesion
models of neglect in monkey,122 in which neglect
was observed when combining optic tract section
with commissurotomy, or after deep leucotomy dis-
connecting the parietal cortex from both ipsilateral
and contralateral visual inputs, but not after other
lesions including parietal cortical ablation alone or
combined with frontal eyefield ablation. Likewise,
Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
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Spatial neglect and the parietal lobe
simultaneous interruption of both inter- and in-
trahemispheric communication might result from
deep brain lesions extending to both paraventric-
ular and paracallosal fibers. This may interrupt or
weaken the access of contralesional sensory infor-
mation to attentional networks in the right hemi-
sphere, while at the same time disrupting fronto-
parietal interactions that control attention orienting
in space and the selection of behaviorally relevant
events for conscious awareness.
In sum, recent connectivity approaches to ne-
glect anatomy support the view that parietal and
frontal areas dynamically interact within large-scale
networks whose activity is crucial to subserve spa-
tial attention and awareness.14,15,114 One may specu-
late that reciprocal fronto-parietal communication
might implement winner-take-all threshold mech-
anisms that allow the modulation and selection
of high-order spatial representations (e.g., saliency
maps) and/or sensory event representations (e.g.,
tokens) computed in posterior parietal areas.123125
Interruption of white-matter fibers in SLF (and pos-
sibly other tracts) might contribute to the abnormal
spatial biases arising in the selection of these repre-
sentations for conscious awareness.12 Furthermore,
besides fronto-parietal and callosal disconnections,
subcortical brain lesions may disrupt other white-
matter fibers that are also likely to play an important
role in space representation and attention. These in-
clude connections between parietal cortex and early
visual areas (or other sensory areas),126 as well as
connections with subcortical nuclei, such as the pul-
vinar, or with superior colliculus, both of which
have direct interactions with parietal cortex.127 For
example, a functional imbalance within subcorti-
cal circuits is suggested by the classic Sprague effect
in cats, whereby an apparent contralesional neglect
(i.e., blindness or deafness) after unilateral parieto-
occipital lesion can be nullified by additional de-
struction or deactivation of the superior colliculus
on the other side128 an effect suggesting that im-
paired spatial orienting may be primarily caused by
losses of descending signals on structurally intact
collicular circuits (see also Ref. 129). Future studies
using advanced diffusion imaging in patients and
animal models should help clarify the functional
role of these different cortical-subcortical path-
ways in spatial cognition and their role in neglect
disorders.
65
Spatial neglect and the parietal lobe Vuilleumier

Distant functional effects of focal lesions was altered during the acute stage after stroke only,
and then fully recovered in parallel to full-blown ne-
Disconnection between areas, either due to white-
glect symptoms.133 These data have therefore been
matter lesions or destruction of one cortical or
interpreted as evidence that widespread dysfunction
subcortical gray-matter structure, can produce a
in the ventral fronto-parietal attention network may
dysfunction in structurally intact portions of the
cause left spatial neglect by inducing secondary dis-
corresponding brain network, by interrupting or
turbances in the structurally intact dorsal attention
distorting the flow of communication between dis-
network. However, increased activity in left pari-
tant regions. Such dysfunction may correspond to
etal cortex does not always correlate with contrale-
the phenomenon of diaschisis, a transient suppres-
sional deficits but might also reflect compensatory
sion of neuronal activity and cerebral blood flow
processes.134 Neglect deficits in the acute stage after
in anatomically preserved circuits following dam-
subcortical or inferior parietal lesions are also asso-
age in a separate but functionally related neuronal
ciated with more diffuse and bilateral hypo-activity
region, which is often observed in the acute stage
in areas of the dorsal attention network, including
after stroke and tends to progressively recede dur-
the IPS and FEF.135,136 Conversely, focal damage in
ing subsequent recovery. Diaschisis in cortical areas
the IPS can produce spatial biases in selective visual
has sometimes been proposed to account for neglect
attention without concomitant changes in activity
symptoms arising after subcortical lesions in white
for intact areas in the TPJ or frontal lobe.50
matter or deep gray nuclei, and can be assessed with
Distant functional effects of parietal lesions also
perfusion imaging measures.130 Diaschisis in dis-
arise in intact sensory regions during specific task
tinct cortical territories may also account for differ-
demands. For instance, fMRI in patients with right
ences in the clinical manifestations of neglect (e.g.,
parietal damage shows a reduced activation to left
egocentric or allocentric deficits).97
visual stimuli in intact retinotopic visual cortex of
Distant dysfunction following focal damage can
the damaged hemisphere (Fig. 7), but only when
also influence the functional dynamics of well-
attention is actively engaged by a demanding task at
defined networks during particular task demands
fixation (detection of prespecified targets), whereas
as well as during resting state conditions.115,131,132
retinotopic responses are normal and symmet-
In particular, functional MRI in stroke patients
ric under passive visual stimulation (with fixation
has shown that acute damage in the right TPJ is
maintained at screen center without a concurrent
associated with reduced activity in intact regions
detection task).137 This reduction in retinotopic ar-
of the ipsilateral IPS, which might in turn cause
eas also correlates with reduced ability of patients to
an interhemispheric imbalance with a relative in-
report left-sided stimuli during the central attention
crease of activity in the opposite left IPS, possibly
task. These data suggest that although visual inputs
accounting for the typical rightward spatial biases
are preserved for both hemifields, a functional im-
in attention orienting in neglect patients.131 More-
balance between hemispheres with reduced percep-
over, such interhemispheric asymmetry in the IPS
tual processing in the damaged side occurs as soon
was reported to correlate with spatial asymmetry in
as attention resources are allocated to competing in-
attention performance on the Posner orienting task,
formation (even when the latter is presented at a cen-
and to abate with neglect recovery in more chronic
tral location in space). Furthermore, such attention-
stages. In addition, disrupted functional connectiv-
dependent reduction in stimulus-evoked responses
ity between right inferior parietal and frontal ar-
appeared to be progressively exacerbated from ear-
eas was also found to predict left neglect severity,
lier to later retinotopic areas along the visual stream
and these functional changes in connectivity were
(i.e., with small effects in V1 but much larger effects
more frequent in patients with damage to SLF,115 in
in V4, where visual responses to contralateral stim-
keeping with the view that the latter white-matter
uli were actually abolished during higher attention
tract may play a crucial role in coordinating fronto-
demand at fixation). Reduced activity in intact right
parietal areas (see above). However, these anomalies
occipital cortex is also observed during attentional
in the functional connectivity of the TPJ persisted af-
tasks in right brain-damaged patients with left ne-
ter recovery in the chronic stage, whereas intra- and
glect relative to those without.134 Similar decreases
interhemispheric functional connectivity of the IPS

66 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences.
Vuilleumier Spatial neglect and the parietal lobe

Figure 7. Attention-dependent changes in visual cortex activity after right posterior parietal damage. Responses to visual stimula-
tion in the contralesional left (LVF) and ipsilesional right (RVF) hemifields were compared either (A, B) during a passive condition
while fixation was maintained at screen center without any task, or (C) during an active attentional task requiring the detection
of infrequent red target at fixation. In two patients (JC, upper row; AH, lower row) with damage restricted to the right posterior
parietal lobe, visual responses in structurally intact right occipital cortex were preserved during the passive condition, but markedly
reduced during the central attention tasks. Retinotopic mapping analysis showed that this suppression arose in all visual areas but
with increasing effects from V1 to V4. No differential effect was observed in these retinotopic areas for bilateral versus unilateral
visual stimulation. Adapted, with permission, from Ref. 137.

in occipital activity may even occur at baseline, with-
out any visual stimuli in peripheral hemifields, but
arising when a central fixation cross is presented
during catch trials while the patient is expecting a
possible target on one or the other side.138 These
findings demonstrate that structurally intact visual
areas fail to activate normally after parietal lesion,
presumably due to the loss of topdown or reentrant
modulatory signals, but the exact source of these sig-
nals remains unresolved. One possible source might
arise in superior parietal regions computing saliency
maps of space that can then be used to bias sensory
processing in lower visual areas through direct or
indirect feedback connections.
A modulation of intact sensory areas in neglect
patients has also been observed during manipula-
tions of egocentric spatial coordinates while sensory
stimulation was actually kept constant. Thus, con-
tralateral occipital activation and visual detection
performance for left visual stimuli were found to
be reduced in a right parietal patient when his gaze
was directed straight ahead or leftward, but restored
when gaze was directed rightward such that stimuli
in the left retinal hemifield now fell in right ego-
centric space (unpublished observations). Likewise,
tactile detection on the right hand and contralateral
activation of left somatosensory cortex were reduced
in a right parietal patient with neglect when his in-
tact right hand was placed in the left (contralesional)
egocentric space.139 These modulations of sensory
cortical areas accord with modulations of visual and
tactile extinction by posture reported in previous
behavioral studies.105,140 The presence of visual and
tactile extinction after stroke has also been found
to correlate with changes in resting perfusion val-
ues in occipital and inferior parietal cortical areas,
respectively.141
These findings indicate that disturbances in spa-
tial attention and spatial representation due to focal
parietal damage may have a profound impact on the
functioning of structurally intact sensory areas at
lower stages of perceptual processing. Furthermore,
these changes have direct consequences for percep-
tual awareness and thus provide a proximate neural
substrate for at least some of the clinical manifes-
tations associated with neglect. These phenomena
blur a strict functional distinction between primary
sensory losses (e.g., hemianopia after occipital dam-
age) and secondary attention-dependent or space-
related suppression of sensory processing (e.g.,

Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences. 67
Spatial neglect and the parietal lobe Vuilleumier

Figure 8. False positive in anatomical lesion mapping. Lesion maps show a voxelwise contrast between structural brain damage in
patients with hemianopia and those without hemianopia, as clinically assessed by confrontation and noted in neurological clinical
records (n = 30 unselected patients with a focal right hemisphere ischemic stroke). Lesion peaks (blue to cyan) can be observed
in occipital and ventral temporal areas, as expected, but also in posterior parietal areas, suggesting that damage in the latter may
induce pseudo-hemianopia due to attentional disturbances rather than true visual field cut (unpublished data).

extinction after parietal damage). On the one hand,
this further highlights the role of distributed and
interactive networks in subserving spatial aware-
ness. On the other hand, this also calls for caution
when interpreting the results of anatomical le-
sion mapping studies in neglect patients, since fo-
cal lesion in a given cortical or subcortical site
may cause symptoms through distant influences on
another distant, but connected site. A striking il-
lustration is provided by voxelwise lesion-symptom
mapping (VLSM) analysis of visual field deficits
(hemianopia) as assessed by confrontation tests dur-
ing clinical examination, which may reveal lesions
in the occipital lobe (as expected) but also in pari-
etal cortex (see Fig. 8). The latter false-positive re-
sult suggests that visual dysfunction caused by pari-
etal damage might occasionally result in a pseudo-
hemianopia that is mistakenly diagnosed as true
hemianopia.105,142,143 More precise anatomical and
DTI analysis might be necessary to verify that such
findings are not caused by interruption of optic ra-
diations in the depth of the parietal lobe, although
this seems unlikely given the frequent subsequent
recovery of pseudo-hemianopia and its modulation
by postural changes.105 Moreover, similar functional
effects might explain that (apparent) sensorimotor
disorders are more frequently reported after right
than left hemisphere lesions.144
However, impaired awareness in extinction (and
other neglect-related phenomena) cannot exclu-
sively be accounted for by attenuated neuronal re-
sponses in sensory pathways. Several fMRI stud-
ies of extinction on double stimulation in parietal
patients have compared brain responses to iden-
tical contralesional stimuli when these are con-
sciously perceived or extinguished (relative to an ab-
sence of stimulation), and these studies consistently
found preserved activation in early visual145,146 or
somatosensory147,148 areas despite a lack of stimulus
awareness on extinction events. Critically, awareness
of the same sensory events (relative to extinction)
correlated with enhanced activation at higher stages
along sensory pathways coupled with concomitant
activation of intact parietal and frontal areas in the
intact left hemisphere145147 (see also Ref. 134). Neu-
roimaging studies of perceptual awareness in healthy
people have reported a similar pattern of isolated
activation in sensory areas during unconscious pro-
cessing, but more widespread recruitment of fronto-
parietal areas during conscious processing.149 Thus,
findings in neglect patients converge with other data
to support the notion that awareness is dependent
on distributed neural mechanisms in fronto-parietal
networks that allow the broadcasting of stimulus in-
formation in large-scale brain networks associated
with attention, working memory, and goal-directed
behavior.12,14
More generally, these findings demonstrate that
neglect and related disorders (such as extinction)
do not reflect the destruction of a single module
specialized for spatial awareness, and that their neu-
ral substrates extend beyond the site of structural
brain damage. Instead, several aspects of neglect
may arise from a complex interplay between de-
fective processes due to the lesion and abnormal
residual activity in anatomically preserved regions,
as observed for the IPS during spatial orienting131
or early visual cortex during extinction.137 Simi-
lar functional changes leading to imbalanced activ-
ity between or within hemispheres might under-
lie other neglect components, such as egocentric
spatial biases, deviation of subjective body mid-
line, and common postural anomalies.113,150 How-
ever, the exact nature of the modulatory or inter-
active signals exerted between areas is still poorly
understood.

68 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences.
Vuilleumier Spatial neglect and the parietal lobe

Conclusions underlying both distinct and partly overlapping

forms of amnesia. To be comprehensive, however, a
Significant progress has been made in the past
componential model of neglect should go beyond
decade regarding the cognitive and neuroanatom-
dichotomous categories of symptoms (e.g., ego-
ical systems involved in spatial neglect, but many
centric vs. allocentric, endogenous vs. exogenous,
questions and challenges remain. There is now
local vs. global), but identify independent cogni-
growing consensus that neglect cannot be consid-
tive processes that can account for behavior across
ered as a monolithic disorder with a unique neu-
different tasks and correspond to specific neural sys-
ral substrate in the parietal lobe (or elsewhere in
tems. Converging data from factorial analyses and
the brain). Rather, it is probably best understood as
anatomical studies suggest that these basic compo-
a clinical syndrome consisting of different compo-
nent processes are likely to include spatial biases
nents, which may constitute some core features, but
in attention due to impaired resistance to exoge-
also variable manifestations depending on the site
nous interference and stimulus competition, distor-
and extent of brain damage.18,113
tions in egocentric representations, deficits in spatial
However, the suspected core features are still too
remapping, as well as nonlateralized losses in work-
often purely descriptive (e.g., referring to general
ing memory or temporal event resolution, among
contralesional spatial deficits in behavior), and need
others.
to be better defined in terms of underlying cog-
A functional fractionation of the neglect syn-
nitive processes. Different researchers tend to em-
drome into component processes also dovetails
phasize different impairments as the characteristic
with the progress made in delineating the complex
signature of spatial neglect, such as deviations in
anatomical parceling of the human parietal lobe and
egocentric coordinates, distortions in internal rep-
its interconnections with other brain areas. Stud-
resentations of space, or asymmetries in the control
ies in humans and monkeys demonstrate that the
of attention, among others. Moreover, these puta-
parietal cortex is constituted of many distinct sub-
tive core symptoms also occur in isolation without
regions with different functions contributing to at-
qualifying for full-blown neglect, including, for ex-
tention and space representation,53,57 such that pari-
ample, spatial biases in egocentric straight-ahead,151
etal lesions in humans will inevitably affect several
exogenous attention orienting,42 or bilateral stimu-
of these regions and hence cause a combination of
lus competition.50 This suggests that the definition
different component deficits even when damage is
of a core syndrome of neglect itself is likely to incor-
relatively focal and restricted to the parietal lobe,
porate a combination of elementary deficits, impli-
as succinctly reviewed above. For instance, damage
cating distinct cognitive and neural systems, whose
to neuronal populations in the mid-IPS might im-
impairment will not lead to typical neglect when
pair the ability to maintain representation of salient
present singly. In fact, this view echoes previous ac-
or task-relevant locations in contralesional space,49
counts proposing that neglect might result from the
while extension to more posterior IPS might abolish
co-occurrence of two deficits (e.g., contralesional
the representation of unattended visual locations on
spatial biases in attention combined with concomi-
the contralesional side in the presence of competing
tant local biases152 or with nonlateralized deficits
inputs,55 and damage to superior IPS may addition-
in working memory153 ), although the latter com-
ally disrupt the ability to voluntarily shift attention
ponents are probably insufficient to explain other
to previously unattended information,45,58 such that
neglect features.
a combination of these deficits due to a single lesion
An important challenge for future research is
could potentially account for a defective represen-
therefore to develop a coherent component pro-
tation of line length during bisection tasks and im-
cess model of spatial neglect, to identify the basic
paired computing of newline returns during text
ingredients of the core syndrome, if any, and clar-
reading, hence a common factor shared by these
ify whether clinically distinct entities may exist or
different tasks in posterior parietal regions.34 Con-
not (e.g., extinction vs. neglect). Similar componen-
versely, extension of damage to anterior parietal ar-
tial approaches have already provided useful theo-
eas or sensorimotor regions may disrupt space rep-
retical frameworks in other neuropsychological do-
resentations in relation to different body-centered
mains, for instance in relation to memory processes
or action-based coordinates,57,154 and hence

Ann. N.Y. Acad. Sci. 1296 (2013) 5074 

C 2013 New York Academy of Sciences. 69
Spatial neglect and the parietal lobe
contribute to modulation by body or limb
position,105 or to deficits in spatial remapping dur-
ing body or eye movements;84 whereas damage to
inferior parietal and superior temporal regions may
lead to anomalies in cortical vestibular processes
and egocentric deviations.88,90,92 Further extension
to distinct subregions in inferior parietal cortex
will add to clinical manifestations, for instance,
contributing to perceptual extinction through a
combination of deficits in reorienting or resetting
mechanisms,42,66 alertness,86,87 and spatiotemporal
tokenization of sensory events,72,78 each dependent
on distinct subregions in IPL.53 This functional
parceling of the parietal lobe clearly argues against a
single module whose damage would be responsible
for parietal neglect.
Furthermore, besides a mixture of deficits due to
damage in parietal lobe, neglect symptoms will be
further nuanced when lesions extend to other corti-
cal areas (e.g., leading to greater distractor interfer-
ence during search after frontal lesion, object-based
deficits after temporal lesion) or to subcortical nu-
clei (e.g., pulvinar, basal ganglia) and white-matter
tracts (inter- or intrahemispheric). Moreover, be-
yond structural damage to specific brain regions,
functional changes may occur in anatomically in-
tact regions, and these will also directly bear on
perceptual and behavioral symptoms (such as re-
duced sensory responses of retinotopic visual cor-
tex to contralesional stimuli when attention is en-
gaged at fixation137 or following reduced activation
of the IPS after IPL damage131 ). Altogether, these
data show that a strict lesion localization approach is
insufficient to fully account for complex neuropsy-
chological deficits, such as spatial neglect, and that
understanding the latter requires a comprehensive
model of brain function in terms of dynamically in-
teractive networks wherein damage in one area can
cause changes in one or many other interconnected
areas.
Even without being exhaustive, the current re-
view highlights that understanding the functional
neuroanatomy of neglect is a tremendously com-
plex endeavor and undoubtedly remains a major
challenge for neuroscience, despite many exciting
new insights on spatial cognition, attention, and
parietal lobe function. Future work will need to
dissect with ever increasing precision the respec-
tive contributions and interactions of many differ-
ent neuronal populations within and between large-
70 Ann. N.Y. Acad. Sci. 1296 (2013) 5074 
Vuilleumier
scale networks. However, time is ripe to address this
challenge and make new progress by exploiting the
methodological advances and complementarities of
current neuroimaging techniques, in both patients
and healthy volunteers, in combination with a care-
ful analysis of neglect components and underlying
cognitive processes. Precise lesion mapping studies
should be integrated with structural connectivity
analysis and functional measures assessing distant
consequences of focal brain destruction and/or dis-
connection, as well as high resolution imaging stud-
ies of cortical responses in well-defined conditions.
Although not covered in this review, electroen-
cephalography (EEG) and magnetoencephalogra-
phy (MEG) recordings can also provide valuable
information on intact versus altered dynamics of
neural processing within spared networks after fo-
cal brain damage,146,155158 but are too rarely used
in patients with neglect or extinction. Such electro-
physiological measures would be particularly use-
ful to interpret functional changes observed in dis-
tant areas137 or distributed networks115 after parietal
damage, and to determine whether such changes re-
flect early, late, or feedback/reentrant stages in stim-
ulus processing,158 or even baseline changes arising
before stimulus-evoked responses.138
Ultimately, better defining the intricate neural
architecture implicated in neglect will not only
provide fascinating knowledge on brain processes
mediating our representation of space, selective at-
tention, and conscious awareness, but it is also cru-
cial to better understanding the handicapping disor-
ders observed in brain-damaged patients and offer
appropriate therapeutic interventions correspond-
ing to individual deficits.
Acknowledgments
This work was partly supported by Grants from the
Swiss National Science Foundation (No. 114014)
and the Geneva Academic Society (Foremane fund).
This paper is dedicated to the memory of Jon Driver
with whom many stimulating discussions about ne-
glect were initiated and still continue today in the
authors work. Special thanks go to Arnaud Saj, Vin-
cent Verdon, and Roland Vocat, who contributed to
some of the work reviewed here and made help-
ful comments; and to Marteen Vaessen for creating
Figure 2C.
C 2013 New York Academy of Sciences.
Vuilleumier
Conflicts of interest
The author declares no conflicts of interest.
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