Space and the parietal cortexMasud Husain1,2 and Parashkev Nachev2

1 Institute of Cognitive Neuroscience, University College, London, 17 Queen Square, London WC1N 3AR, UK2 Imperial College London, Charing Cross Hospital Campus, London W6 8RF, UK

Review TRENDS in Cognitive Sciences Vol.11 No.1

Current views of the parietal cortex have difficultyaccommodating the human inferior parietal lobe (IPL)within a simple dorsal versus ventral stream dichotomy.In humans, lesions of the right IPL often lead to syn-dromes such as hemispatial neglect that are seeminglyin accord with the proposal that this region has a crucialrole in spatial processing. However, recent imaging andlesion studies have revealed that inferior parietalregions have non-spatial functions, such as in sustain-ing attention, detecting salient events embedded in asequence of events and controlling attention over time.Here, we review these findings and show that spatialprocesses and the visual guidance of action are onlypart of the repertoire of parietal functions. Althoughsub-regions in the human superior parietal lobe andintraparietal sulcus contribute to vision-for-actionand spatial functions, more inferior parietal regionshave distinctly non-spatial attributes that are neitherconventionally ‘dorsal’ nor conventionally ‘ventral’ innature.

IntroductionStudies in monkeys originally led to the hypothesis thatthe dorsal visual stream of cortical pathways, extendingfrom the primary visual cortex to the posterior parietalcortex (PPC), has a special role in spatial perception,whereas the ventral stream to the temporal cortex has akey role in object perception [1]. Later, that view waschallenged and revised to the proposal that the dorsalstream and PPC have a crucial role in directing visuallyguided actions [2]. However, it is becoming increasinglyapparent that both these models have difficulty in captur-ing some aspects of human parietal function. In particular,recent findings have begun to question a role for the humaninferior parietal lobe (IPL) solely in spatial processes or inthe visual guidance of action – ‘vision-for-action’.

Here, we review emerging trends in this field andsuggest that a reconsideration of human parietal functionis necessary. Close inspection of data from functionalimaging and lesion studies reveals that parts of the humanIPL are involved in functions that do not involve visuallyguided action, shifts of spatial attention or spatial memory.Instead, sub-regions within the IPL seem to be involved inthe detection of salient new items embedded in a sequenceof events and in maintaining or controlling attention overtime. We start by considering the current unease thatexists over human IPL function.

Corresponding author: Husain, M. (m.husain@ion.ucl.ac.uk).Available online 28 November 2006.

www.sciencedirect.com 1364-6613/$ – see front matter � 2006 Elsevier Ltd. All rights reserve

Current models of inferior parietal lobe functionIn Goodale and Milner’s view, the dorsal ‘vision-for-action’system operates in real time to compute the absolutemetrics of the target and its position in the egocentricco-ordinates of the effector (eye or limb) [3]. Thus, accord-ing to this scheme, the dorsal stream delivers informationdirect to the motor system for immediate use for reaching,grasping or eye movements. By contrast, the ventralstream is dedicated to ‘vision-for-perception’, but mighthave a role in movement planning based on memory of theobject and its relationship to other items.

Such a distinction between dorsal and ventral systemsis supported particularly clearly by the results of lesions ofthe human superior parietal lobe (SPL; Figure 1), whichoften lead to optic ataxia or misreaching to visual targets[2,4]. The regions of the PPC that have proven far moredifficult to fit into any dorsal–ventral dichotomy are theIPL and nearby temporoparietal junction (TPJ). Milnerand Goodale acknowledged this from the outset; theyspeculated that these regions might be a high-level repre-sentational system fed largely by the ventral stream andsubserving perceptual awareness [2,4]. Their proposalwould be consistent with some aspects of hemispatialneglect, a syndrome that often follows lesions of the IPLor TPJ, particularly in the right hemisphere [5,6]. Indivi-duals with neglect often fail to be aware of contralesionalobjects (to the left for individuals with right parietaldamage), even when given unlimited time to explore theworld around them.

A different perspective on the IPL has been offered bythe scheme proposed by Rizzolatti and Matelli, who sug-gest that it might be better to consider the superior andinferior parts of the PPC as belonging to two differentstreams [7]. According to this model, the SPL is part ofa distinct ‘dorso-dorsal’ system dedicated to the onlinecontrol of action, whereas the IPL is part of the ‘ventro-dorsal’ stream that is necessary for action understandingand spatial perception. This model originated from struc-tural and functional considerations of the macaque brainbut it has also been applied to the human PPC. In fact, it ispossible that in the human brain, the ventro-dorsal systemis different in the two hemispheres because deficits ofaction control (in the form of ideomotor apraxia) are moreprominent after left-hemisphere lesions, whereas deficitssuch as hemispatial neglect are more frequent and severeafter right parietal damage.

A third recent view of the PPC also makes a distinctionbetween the SPL and more ventral regions in the PPC,specifically the TPJ, but this hypothesis concerns a dichot-omy that incorporates visual-attention functions more

d. doi:10.1016/j.tics.2006.10.011

Figure 1. Posterior parietal cortex of macaque monkey (left) and human (right). The human posterior parietal cortex (PPC) is divided by the intraparietal sulcus (IPS) into

two parts: the superior parietal lobe (SPL) and the inferior parietal lobe (IPL). The IPL consists of the angular gyrus (Ang) and supramarginal gyrus (Smg) and borders the

superior temporal gyrus (purple) at a region that is often referred to as the temporoparietal junction (TPJ). In macaques, the PPC also consists of an SPL (area 5) and an IPL

(areas 7a and 7b) but, according to Brodmann [71], the homologues of these macaque regions are all confined to the human SPL (yellow), so the IPL in humans consists of

novel cortical areas. Subsequent anatomists such as Bailey and von Bonin [72] disagreed with this scheme, considering the IPL to be similar across both species. It remains

to be established whether there are new functional sub-regions within the human IPL.

Figure 2. Functional imaging studies. (a) Meta-analysis of activations associated

with spatial shifts of attention in healthy individuals demonstrate activations in the

superior parietal lobe (SPL) and intraparietal sulcus (IPS), plus dorsolateral frontal

regions (different colours correspond to findings from different studies). Similar

regions are also activated when participants perform spatial working memory

tasks. Adapted, with permission, from Ref. [8], � (2002) MacMillan Publishers Ltd.

(b) By contrast, regions in the inferior parietal lobe (IPL) and IPS, together with

more ventral frontal regions, are activated by salient events (cyan), sustained

attention (red) and non-spatial selective attention protocols (yellow) such as the

attentional-blink paradigm. Adapted from Ref. [18].

Review TRENDS in Cognitive Sciences Vol.11 No.1 31

directly. Corbetta and Shulman [8] argue that the SPL andparts of the intraparietal sulcus (IPS) have a role indirecting visual attention ‘top-down’ to locations or objectsin the scene and in selecting responses of effectors (eye orlimb). By contrast, the right TPJ acts ‘as a circuit breaker’,for example, by reorienting spatial attention when it hasbeen deployed incorrectly [8]. All these models provideimportant syntheses of a large body of data that hasemerged from studies of monkey and human PPC, butthere are other findings, which we consider later, thatare still not easily incorporated into these frameworks.

Functional imaging reveals non-spatial functionsNeuroimaging investigations in humans have consistentlydemonstrated that parts of the SPL or IPS are activated bytasks such as shifting spatial attention, engaging spatialworking memory, making saccadic eye movements orreaching to a visual target [8–13] (Figure 2a). In addition,more recent reports have demonstrated evidence in SPLand IPS for topographical representations of contralateralspace for saccades to remembered locations [14,15] or inremapping spatial locations across saccades [16,17]. Notethat the SPL and IPS activations are often associated withsimultaneous activity in the dorsolateral frontal lobe(Figure 2a), in accord with the view that the SPL is partof a dorsal frontoparietal system for directing spatialattention or action. Thus these neuroimaging findingsregarding the SPL and parts of the IPSwould be consistentwith many aspects of current models of PPC function.

However, the results of several other functional imagingstudies relating to the IPL and TPJ are very different. Theydemonstrate that these areas – and more ventral frontalregions – are consistently activated when healthy indivi-duals perform non-spatial tasks [18] (Figure 2b). They havebeen identified to be active when subjects maintain vigilantattention [9,19–22] orwhen they are presented infrequentlywithunusual, salient stimuli ina repetitive stream,as in the‘oddball’ paradigm [23–26], even when no spatial shifts of

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32 Review TRENDS in Cognitive Sciences Vol.11 No.1

attention, eye or limb movements are required. Moreover,these effects occur in visual, auditory or somatosensorytasks and are therefore not modality specific. Some parietalareas in or near to the IPS, togetherwith frontal regions, arealso activated when healthy subjects perform non-spatial,selective attention tasks [27–30] such as the attentional-blink protocol, a paradigm that allows measurement of thedynamic capacity of visual attention when stimuli are pre-sented sequentially at one spatial location. Thus regions inthe IPL, TPJ and parts of the IPS form a ventral frontopar-ietal circuit that seems very different from the dorsal onethat isactive in spatial perceptual, attentional,mnemonic oraction tasks (Figure 2b).

These neuroimaging findings suggest both spatial andnon-spatial functions are represented in the human PPC,butwith a gradient extending fromSPL through IPS to IPLof spatial to non-spatial functions [18] and some intermedi-ate regions in the IPS showing activation on both spatialand non-spatial tasks [28]. Corbetta and Shulman’s modelproposes a slightly different dichotomy between superiorand inferior parietal structures, with the TPJ involved indirecting attention to salient events, for example, whenobservers have to redeploy attention to an unexpectedperipheral stimulus [8,31]. However, in our view, theIPL and TPJ also play a more general, non-spatial rolein sustaining attention over time [18] that is not capturedby the Corbetta and Shulman model. New data fromtranscranial magnetic stimulation also support the viewthat this region might have a role in non-spatial encodingof salient stimuli [32], as do a range of findings from lesionsof the human PPC, which we discuss next.

Hemispatial, spatial and non-spatial deficitsIt has often been suggested that some components ofneglect syndrome, the characteristic clinical disorder fol-lowing right IPL damage, might best be understood using aspatial conceptual framework; for example, a lack of spaceexploration to one side of the body midline, to one side ofthe head axis or to one side of the direction of gaze. In fact,there is evidence for all three egocentric spatial referenceframes modulating the extent of neglect [33]. But thedisorder need not be strictly hemispatial – that is,neglected and non-neglected space might not be demar-cated by an abrupt plane that transects space in anyegocentric coordinate frame.

Kinsbourne suggested instead that each hemisphereorients attention towards the opposite side of space, witha stronger ‘vector’ exerted by left-hemisphere systems [34].Hence a strong rightward directional bias would beexpected after unilateral right parietal damage (becauseof unopposed left-hemisphere activity). The model predictsa gradient, rather than a sharp cut-off, in the distributionof visual attention from right to left – a proposal supportedby findings of a gradient of response times to stimulipresented at different spatial locations in neglect patients[35]. This model also shows that the unilateral nature ofneglect might emerge from a directional bias in just onecomponent of the syndrome; other components thatcontribute to neglect need not be directionally lateralized.

The key feature of Kinsbourne’s directional theory is thatit predicts hyperattention (i.e. better performance) to the

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right. By contrast, the hypothesis advanced by Heilmanet al. is slightly different, suggesting that there might besome deficits on the right (‘good’) in addition to the left(neglected) side of space [36]. The authors proposed that,although the right PPC might normally direct attention toboth sides of space, the left PPC directs attention only to theright hemispace. One implication of this model is that rightPPC damage might be associated with not only a severedeficit for itemsto the left, butalsoamilderdeficit for stimulito the right [37]. Recent studies show that there are indeeddeficits on the right side of space, but they are not necessa-rily milder than on the left.

Firstly, Duncan et al. have demonstrated reducedvisual processing and short-termmemory capacity, whichcan be equivalent in severity in left and right hemifields, inIPL patients who have varying degrees of neglect [38].Importantly, a subsequent study of non-neglect patientsrevealed that IPL- and TPJ-lesioned individuals weremore severely affected than those with SPL involvement[39]. Secondly, processing of visual information from theright visual field – but not the left – might be unselective,with information that is irrelevant to the task beinginappropriately prioritized in neglect patients [40].Thirdly, attention to transient onsets and offsets of visualstimuli is disrupted bilaterally in right IPL patients [41].Fourthly, detection of briefly presented stimuli isimpaired in both visual hemifields, but worse to the left[42]. Finally, spatial functions such as keeping track ofobject locations over intervening saccades or awareness ofchanges in their locationmight all be severely disrupted inpatients with right-IPL damage, even on the right side ofspace [43–46]. All these studies show that damage to theright IPLmight lead to deficits that are not confined to onehemispace.

Other investigations have revealed that parietaldamage can lead to deficits on non-spatial tasks even whenstimuli are presented at only one spatial location. Theattentional-blink protocol, which we discussed previouslyin the context of functional imaging studies, has also beenemployed in patients to index the dynamic control of visualattention when stimuli are presented sequentially at fixa-tion [47,48]. These investigations have demonstrated thatindividuals with IPL lesions – including those with spatialneglect – are dramatically impaired in visual-processingability, even when attention does not have to be shiftedacross space. By contrast, lesions of the SPL do not lead toattentional-blink deficits [48]. A second series of studieshas focused on tests of the ability to maintain vigilantattention. Resection of the right IPL leads to impairment inthe ability to sustain visual attention over prolonged inter-vals [49]. In addition, right-hemisphere neglect patientswho have parietal involvement are also impaired at main-taining vigilant attention on non-spatial tasks, regardlessof whether the stimuli are auditory or visual [50,51].

This wide range of findingsmakes it difficult to sustain asimple ‘spatial’ or indeed ‘hemispatial’ account for neglect.Instead, these results reveal that deficits occur on bothsides of space in the syndrome; some of them might bespatial in nature, but evidently others are not. The datasuggest that a combination of spatial and non-spatialimpairments exists in neglect [18], and this might explain

Review TRENDS in Cognitive Sciences Vol.11 No.1 33

why it has been difficult to frame the syndrome in terms ofany dorsal–ventral dichotomy (discussed in Ref. [4]).

Human and monkey parietal cortex might not be thesameOur review of the lesion and imaging data in humanssuggests the SPLmight have a key role in spatial functionsand vision-for-action. We consider this part of the humanparietal cortex to have strong similarities to the monkeyPPC. By contrast, some regions within the human IPLhave non-spatial functions that do not map easily to the‘dorsal’ stream (see also Refs [2,4]). In fact,monkey parietalcortex might not be a complete model for the human PPC.In our opinion and that of Milner [52], there is no goodevidence for a long-lasting and severe neglect syndrome inmonkeys such as that seen in humans [53]. Althoughparietal-cortex or white-matter damage in macaque mon-keys leads to various impairments in contralateral space,there is no description of their everyday behaviour, in ourview, that equals the profound deficits observed in humansby clinicians. Crucially, there is also no evidence for hemi-spheric differences for neglect-like symptoms in any mon-key model, whereas in humans neglect is far more commonand prominent after right-sided damage.

Second, although functional imaging, electrophysio-logical and tractography studies now point to severalhomologous regions across species [10,13,54,55], thereare, in addition, regions of human PPC that seem not tohave clear homologues in macaques [55,56]. Comparativeanatomy considerations suggest that the IPL hasexpanded greatly in humans compared with monkeys[57], particularly its posterior aspects – the angulargyrus and TPJ [55]. Comparison of the relative differencein location between functionally homologous regions (e.g.the motion sensitive area V5/MT and primary auditorycortex) reveal a large expansion of the cortex between theseareas in humans (Figure 3). The crucial question is

Figure 3. Expansion of posterior brain regions. Human posterior brain regions in the pa

positions in macaque (left) and human (right) brains of landmark regions such as prima

has shifted posteriorly and inferiorly in humans compared with its location in the dept

regions in monkey and human brains is to compare connectivity of regions. The recen

cortex from the superior colliculus (connected to area LIP within the IPS of macaque), ve

region (connected to area 7a in macaque). But there is a region within the human IPL (m

regions and might be a candidate zone for a novel cortical region within the IPL. Pane

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whether this expansion is due to the evolution of new areasor simply duplication or enlargement of old ones [57,58].

To answer this question definitively will requireconverging evidence using several techniques, includingperhaps comparative functional imaging. Two otherapproaches also show considerable promise. First, diffu-sion-weighted MRI tractography potentially allows homo-logies to be identified between parietal areas in human andmonkey brain that show similar patterns of connectivity.Intriguingly, one recent innovative tractography studydemonstrated that a portion of the IPL in humans mightnot have a clear homology to parts of the PPC in macaquemonkeys [59], raising the possibility that this region mightbe a ‘new’ cortical zone in the human brain (Figure 3). Thesecond method involves combining post-mortem structuralimaging with the painstaking process of detailed cytoarch-itectonicmapping. This technique has been used to identifya zone in the human posterior IPL that again seems not tohave a direct homologue in the macaque brain [60].

Neither dorsal nor ventral: the human IPLThe findings discussed here raise several important issues.Both the imaging and lesion data suggest that the humanSPL, together with parts of the adjoining IPS, have closehomologies to the macaque parietal cortex. Thus theseareas might be the equivalent of the target of a dorsalstream inmonkeys. However, parts of the human IPL seemto be neither ‘dorsal’ nor ‘ventral’. They have non-spatialfunctions that are not related to object processing, as foundin ‘ventral’ stream temporal cortical areas. Instead, theyseem to have a role in detecting salient new itemsembedded in a sequence of events (as indexed by the‘oddball task’) [23–26] and maintaining or controllingattention over time (as measured by vigilance andnon-spatial attentional paradigms) [9,19–22,27–30].

This perspective of human parietal cortex also hasimportant implications for understanding the neglect

rietotemporal regions have expanded considerably. (a) Comparison of the relative

ry auditory cortex (A1) and the motion-sensitive area V5/MT reveals how the latter

hs of the superior temporal sulcus in macaque. (b) One way to map homologous

t study by Rushworth et al. [59] demonstrates connections in the human parietal

ntral premotor cortex (connected to area 7b in macaque) and the parahippocampal

arked within the white circle) that seems not to have connections to any of these

l b adapted from Ref. [59], with permission from Oxford University Press.

Box 1. Anatomy of neglect

The anatomical locus of neglect has recently become the subject of

controversy. The debate has centred on evidence derived from

patients with focal brain lesions, usually caused by stroke in the

territory of the middle cerebral artery (MCA). The region most

consistently implicated is the right IPL [5,6]. Recently, an alternative

crucial locus has been proposed in the superior temporal gyrus (STG)

[65,66]. The disparity between this new proposal and the results of

other studies has attracted considerable debate and has been

attributed to differences in clinical selection criteria, quality of

imaging and the methods of ensuring comparisons between homo-

logous structures across subjects. However, the size of the difference

between studies is too large to be accounted for by these factors

alone.

It is probable that a single locus for neglect is implausible. The

syndrome is functionally heterogeneous, incorporating several com-

ponent deficits [18,33,51] that are likely to result from disruption of

circuits distributed beyond the parietal lobe. Indeed, neglect might

occur following damage to lateral frontal regions, consistent with the

known frontoparietal circuits revealed by functional imaging in

healthy individuals (Figure 2). The syndrome also follows lesions to

subcortical structures and even in patients with strokes in the

distribution of the posterior cerebral artery (PCA) who do not have

direct involvement of lateral parietal or frontal regions [6].

A contributory factor in such cases might be the interruption in

functional connectivity between regions: such diaschetic effects are

suggested by the correlation between neglect and focal cortical

hypoperfusion following subcortical lesions [67]. More directly,

damage to frontoparietal fibres has also been shown to be associated

with neglect [62,68] whereas lesions affecting the splenium or

connections from the parahippocampal region to the parietal cortex

have been shown to be predictive of neglect following PCA stroke

[6,69,70]. Patients who have chronic neglect are more likely to have

involvement of multiple cortical areas, which reinforces this view.

The anatomy of neglect revealed by these studies suggests a

complexity that is hard to capture adequately by current lesion-

mapping techniques. Most methods rely on performing a statistical

test independently at each inter-subject aligned voxel, without any

attempt to capture correlations across different brain regions.

Because the structure of the vascular tree introduces a marked

inhomogeneity in the shape and distribution of stroke lesions, this

approach is inherently insecure. Indeed, the only global feature of the

lesion commonly modelled – overall lesion size – will inevitably

distort any spatial inference because of the strong inhomogeneity in

lesion volume across the brain (Figure I). Further progress in this field

will have to await the introduction of novel multivariate methods.

However, the investigation of functions that might have no

counterpart in non-human primates presents a special challenge. In

the absence of detailed neurophysiology and experimental lesion

studies, there is little to constrain speculation based on the abundant –

yet purely correlational – data generated by functional imaging. It is,

therefore, imperative that lesion-mapping methods are developed that

match the ease and flexibility of functional imaging and can be widely

used to test the predictions generated from it. Only by considering

the results of studies on healthy brains in combination with the effects

of lesions in patients is it possible to make strong inferences about

the functional specialization of regions within the human parietal

cortex.

Figure I. Spatial inhomogeneity of mean lesion volume. Voxel-wise map of the

rank correlation between total lesion volume and probability of damage, given a

clinical and radiological diagnosis of stroke, derived from a sample of 456

patients. Only voxels affected in eight or more patients are shown. Note the

strong centrifugal gradient of mean lesion size, with more peripheral (cortical)

voxels being involved in larger lesions. Scale gives value of Spearman’s rho.

34 Review TRENDS in Cognitive Sciences Vol.11 No.1

syndrome [18]. Recent studies of the anatomy of neglecthave been controversial (Box 1). Although the argumenthas often focussed on the contribution of single brainregions it is evident that most patients have large lesionsthat extend over several crucial areas. Moreover, the syn-drome is heterogeneous, with different patients havingdifferent combinations of cognitive deficit [51]. Many indi-viduals with neglect have brain damage that spans thecortex of the SPL, IPS and IPL [6,51,61] and the underlyingwhite matter [62]. Given what we know of the functions ofthese parietal regions, one would expect such damage tolead to a combination of spatial and non-spatial deficits inneglect patients [18], and this is exactly what has beenfound with careful testing using a battery of spatial andnon-spatial tasks [51].

New experimental approaches to the neglect syndrome,using a combination of high-resolution anatomy and beha-vioural tests designed to assess spatial or non-spatialfunctions, have begun to show how the heterogeneity inthe syndromemight be explained in this way. For example,

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those neglect patients who have posterior damage and adeficit in keeping track of spatial locations across saccadeshave lesions that include a small zone in the IPS [43]. Bycontrast, neglect patients in which the posterior cortex islesioned but this small area of the IPS is spared do notshow this deficit. Similarly, lesions of the right TPJ – butnot the SPL – lead to impairments in responding to rare,salient events such as when a target is presented at anunexpected location [63], whereas damage near the IPS isassociated with interference from right-sided irrelevantdistractors [61]. The interaction of spatial and non-spatialfactors, and the precise combination of these, might becrucial in determining the manifestations of neglect acrossdifferent patients [18].

Concluding remarksCurrent models of the parietal cortex have difficulties incapturing elements of human IPL function. Our reviewpoints to the conclusion that parts of the human IPL do notfit a role in spatial processing or vision-for-action, as might

Box 2. Questions for future research

� Just as novel parietal regions might have emerged in humans,

might there also be specializations in monkey parietal regions that

are not present in man (e.g. related to the special visuomotor

abilities that might be required for an arboreal existence)?

� What are the differences in underlying cognitive deficits between

neglect following left- and right-hemisphere lesions? For exam-

ple, the data reviewed here would suggest that major deficits in

sustained attention would not be expected following left-IPL

lesions. Better characterisation of neglect following left-hemi-

sphere lesions would be an important step forward.

� Although several dissociable behavioural components of neglect

have now been clearly identified, their corresponding anatomical

loci have proved challenging to establish. Component deficits

might be masked or confounded by interactions between different

components. Similarly, a faithful analysis of the underlying

anatomy might require lesion-mapping methods that capture

correlations between different anatomical areas. Can such richly

multivariate analyses be successfully performed with the neces-

sarily constrained datasets used in human lesion-mapping

research?

� The fine functional parcellation of the cortex achieved with fMRI is

yet to be matched by a correspondingly detailed map of the

connections between remote areas. Therefore, the behavioural

effects of white-matter lesions are hard to relate to the underlying

functional architecture. Would the development of a detailed

standardized map of white-matter tracts improve our under-

standing of the consequences of damage that involves parietal

grey- and white-matter regions?

Review TRENDS in Cognitive Sciences Vol.11 No.1 35

be assumed from considerations of the monkey PPC.Rather, some regions in the human IPL seem to participatein the detection of salient new items embedded in a rapidsequence of events and inmaintaining or controlling atten-tion over time. This view of parietal cortex can also accom-modate findings that demonstrate both homologous andnon-homologous sub-regions of parietal cortex in macaquemonkeys and humans (Figure 3). Monkeys with parietallesions might not demonstrate the full-blown neglect syn-drome observed in humans because they do not have thecomplement of spatial and non-spatial deficits that arecommon following human lesions [18].

In addition, hemispheric differences between left andright IPL are an important feature of the human parietalcortex. Whereas right IPL and TPJ lesions commonly leadto neglect, damage to the homologous region in the lefthemisphere in humans often leads to the syndrome ofapraxia [64]. However, some left IPL patients might alsoshow evidence of right-sided neglect. Clearly, the precisedistinctions in function between left and right IPL remainto be fully established (see Box 2 for Questions for futureresearch). But it is evident that such substantial differ-ences in function across the hemispheres has not beenobserved in monkeys, demonstrating the need to be cau-tious when making extrapolations from monkey studies tohuman parietal cortex.

AcknowledgementsOur research is funded by The Wellcome Trust.

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