A review of the evidence for a disengage deficit following parietal lobe damage

A review of the evidence for a disengage de®cit followingparietal lobe damage

Bruno J.W. Losiera, Raymond M. Kleinb,*

aDepartment of Psychology, Cape Breton Regional Hospital, Sydney, Nova Scotia, B1P 1P3, CanadabDepartment of Psychology, Dalhousie University, Halifax, Nova Scotia, B3H 4J1, Canada

Received 11 January 1999; revised 9 June 2000; accepted 10 August 2000

Abstract

We review the literature on response times to ipsilesional and contralesional targets following spatial precues in patients with damage

involving the left- and right-parietal lobes with the aim of appraising the `disengage de®cit' reported initially by Posner and colleagues

(Posner MI, Cohen A, Rafal RD. Neural systems control of spatial orienting. Proceedings of the Royal Society of London, B

1982;298:187±98). The data of individual subjects from a sub-sample of studies were submitted to analyses of variance, and data

from all studies meeting our selection criteria were submitted to meta-analytic procedures (Hunter JE, Schmidt FL. Methods of meta-

analysis: correcting error and bias in research. Newberg Park: Sagge Publications, 1990). Findings from both types of analysis

conducted on data from patients with right-hemisphere lesions indicate that: (1) the disengage de®cit phenomenon is robust following

peripheral cues, but not following central cues; (2) the disengage de®cit is large at shorter cue-target stimulus onset asynchronies

(SOAs), and decreases as SOA increases; (3) the disengage de®cit is larger in patients with a diagnosis of hemispatial neglect; and (4)

although the magnitude of the disengage de®cit appears to increase with increases in lesion size, multilobar vs unilobar involvement did

not signi®cantly alter the pattern of the disengage de®cit. We also show that responses to validly cued targets in the contralesional

hemispace were signi®cantly slower than for validly cued targets in ipsilesional hemispace. Similar, but usually smaller, effects were

observed in patients with homologous left-hemisphere damage. The implications of these results for current models of the role of the

parietal lobes in attentional orienting are discussed. q 2001 Elsevier Science Ltd. All rights reserved.

Keywords: Parietal lobe; Visual attention; Disengage de®cit; Exogenous covert orienting; Endogenous covert orienting; Meta-analysis

1. Background

A century has passed since the ®rst description of visuos-

patial neglect following posterior hemispheric damage [23],

and, although progress has been achieved in the interim, an

understanding of the underlying mechanism of neglect has

been elusive. In the last two decades, stimulated by beha-

vioral paradigms developed within cognitive psychology,

the focus of attempts to understand visuospatial neglect

has shifted from purely sensori-motor (e.g. [13]) to cogni-

tive de®cits, including those involving the representation of

space [5], the link between representations of space and

actions [51,52], and attention (e.g. [21,28,44]). Our focus

in this review is on the extinction-like reaction time (RT)

pattern often seen in variants of an attentional cuing para-

digm. This pattern has been interpreted in an attentional

framework, within which it has been attributed to a de®cit

in disengaging attention (see below). Although this pattern

might be interpreted within other [5,51,52] frameworks

(albeit with debatable differences in explanatory ef®ciency),

we will use the term `disengage de®cit' in this review.

One of the most fruitful and widely-used attention-orient-

ing protocols is the visual orienting paradigm developed by

Posner [42,45], which is the focus of this review. In a proto-

typical implementation of this paradigm, central or periph-

eral cues are presented prior to a peripheral target requiring

a simple detection response. Central cues (e.g. arrows)

usually inform the subject where the target is likely to

appear, whereas peripheral cues (e.g. luminance increase)

may or may not be informative. Following the cue, at a

variable interval, a target appears in the cued location (i.e.

valid trial) or in an uncued location (i.e. invalid trial). The

subject is instructed to press a button in response to the

detection of the target, while maintaining ®xation on a

centrally located stimulus (i.e. covert attentional orienting).

Neuroscience and Biobehavioral Reviews 25 (2001) 1±13PERGAMON

NEUROSCIENCE AND

BIOBEHAVIORAL

REVIEWS

0149-7634/01/$ - see front matter q 2001 Elsevier Science Ltd. All rights reserved.

PII: S0149-7634(00)00046-4

www.elsevier.com/locate/neubiorev

* Corresponding author. Tel.: 11-902-494-3417; fax: 11-902-494-6585.

E-mail address: [email protected] (R.M. Klein).

As illustrated in Fig. 1(a), response time (RT) to validly

cued targets is faster than RT to invalidly cued targets

[42] and RT in a neutral cue condition is often intermediate.

Posner and colleagues have proposed a framework

wherein changes in the direction of attention are broken

down into three elementary operations: disengage, move

and engage [44]. Widely, though not universally (cf. [9])

accepted, this framework will be described here and used to

organize the literature. Attention is directed toward a cued

location via these three operations as follows: First, atten-

tion is disengaged from ®xation (or from wherever it is

directed at the time of the cue); then it is moved to the

cued location; ®nally it is engaged at the cued location or

on the object residing there. When the target is presented at

the cued location, responses can be quickly initiated because

attention is already appropriately engaged to enhance its

processing and to connect the target to arbitrary (non-re¯ex-

ive) responses. In contrast, when the cue and target locations

are incongruent, then attention, being engaged at the wrong

location, must disengage from it and move to the actual

target location. These additional steps have been hypothe-

sized to delay reaction time. Support for these operations

and evidence that they are mediated by separate brain struc-

tures has been obtained from studies of brain damaged

populations (see [44,46]).

Evidence for the disengage operation stems primarily

from investigations of patients with visuospatial neglect.

Studies employing the visual orienting paradigm have

shown that these patients, like neurologically intact indivi-

duals, respond more quickly to validly cued targets, but in

addition display a dramatic interaction between cue-target

relationship and target hemispace. Although RTs to validly

cued targets presented in ipsilesional and contralesional

halves of space appear relatively comparable (but see

below), RTs to invalidly cued targets are very much slower

for targets in the contralesional (poor) half of space [see Fig.

1(b)]. The increased cost for contralesional targets follow-

ing ipsilesional cues has been referred to as a `disengage

de®cit', as if patients with neglect are impaired in disenga-

ging attention in order to orient toward objects and events in

contralesional space. In light of this ®nding, Posner wrote:

These symmetric bene®ts of valid cues can be

contrasted with the marked differences in reaction

time to ipsilesional and contralesional targets follow-

ing an invalid peripheral, a central, or neutral cue. All

three of these conditions produce a markedly greater

reaction time on the contralesional side, particularly at

short intervals¼. The main difference appears to be

that target detection in the invalid and neutral trials

®rst requires that attention be disengaged from a loca-

tion other than the target. ([43], p. 1874)

Several years have passed since the original reports by

Posner and colleagues in 1984. In a chapter from a book

dedicated to the advances in visuospatial neglect research,

Robertson and Eglin wrote in 1993:

¼Patients with parietal lobe damage detect the aster-

isk nearly as well in the contralesional and ipsilesional

sides of space when it occurs in the cued location

(nearly equal ability to move and engage attention

to cued locations). However, the delay in responding

to the asterisk is increased substantially when it occurs

in the neglected ®eld. Patients with parietal lobe

damage show an abnormal contralesional delay,

when attention must be disengaged from a location

on the intact side¼ ([53], p. 171)

Thus, the disengage de®cit is inferred from an abnormally

long response time to invalidly cued targets in the contrale-

sional half of space. To our knowledge there has been no

systematic review of this phenomenon. We provide one

here.

B.J.W. Losier, R.M. Klein / Neuroscience and Biobehavioral Reviews 25 (2001) 1±132

Fig. 1. Idealized pattern of performance in a spatial cuing paradigm (A). Typical pattern of performance from which a disengage de®cit has been inferred in

patients suffering from neglect, and the pattern of results from our analysis of 36 RH-lesioned patients subjected to the peripheral cuing protocol reported in the

literature.

2. Literature

Attention, as used here, is the ability to orient covertly

(that is without shifts in gaze direction) to objects/locations

in space [42]. Covert orienting can be accomplished in

either a re¯exive or controlled manner; that is, attention

may be re¯exively drawn to an abrupt change in the envir-

onment or we can voluntarily deploy our attention toward

one location or one object in the visual ®eld, in response to

instructions or probabilities. Following Posner [42] and

Klein et al. [31] we will use the terms exogenous and endo-

genous, respectively, to refer to these different modes of

control over covert orienting. It has typically been assumed

that there is one spatial attentional resource and that differ-

ences (e.g. [25]) between endogenous and exogenous covert

orienting are merely in the method of its transportation, with

exogenous being faster and more re¯exive than endogenous

control. This view is challenged, however, by studies show-

ing that there are different effects upon target processing

depending on whether attention had been directed endogen-

ously or exogenously [6,7,29,35]. On the basis of a concep-

tual `double dissociation' in normal human performance

Klein [31,32] has suggested that there may be a fundamental

difference in the attentional resources allocated in response

to exogenous and endogenous cues. In this review we do not

necessarily endorse this proposal. However, we allude to it

because it points to the importance of distinguishing

between studies that used different methods of eliciting

shifts of attention.

The majority of studies (see Table 1) which have inves-

tigated covert orienting in patients with parietal damage

used peripheral cues that were informative about the target

location [3,11,16,33,38,41,44,47,48,56]. Because the cue in

these studies was an abrupt change in the periphery signal-

ing that the probability of the target occurring at the cued

location is greater than chance, this orienting protocol

combines the attributes of exogenous and endogenous

orienting (which we will therefore refer to as exo 1 endo).

Few studies of covert orienting following parietal damage

have employed pure forms of exogenous or endogenous

orienting. To date, Danziger et al. [12], Farah et al. [17],

LaÁdavas et al. [33] and Friedrich et al. [18] are the only

published studies to have used uninformative peripheral

cues (purely exogenous orienting). Although unique in

that none of their brain damaged patients presented with

neglect, Friedrich et al.'s study is particularly useful as

each patient was tested using both purely exogenous and

exogenous 1 endogenous protocols. Only three studies

have used central cues (purely endogenous orienting):

Nagel-Lieby et al. [39], LaÁdavas et al. [33], and, in a subset

of three patients (C.W., R.S., and L.M.), Posner et al. [47].

The disengage de®cit has usually been measured when

the patient has to shift attention from an invalidly cued

location in the good ®eld to a target in the bad ®eld. Looking

at de®cits in shifting attention between the good and bad

halves of space, however, provides only partial information

about the disengage de®cit. That is, if this de®cit represents

an inability to disengage from the current focus of attention

to one in the poor ®eld, then the disengage de®cit should be

present when the patient must disengage from a cued loca-

tion in the poor ®eld to a target presented elsewhere in the

poor ®eld. Although Baynes [3] obtained a small disengage

de®cit within the poor ®eld (i.e. poor ®eld RT: valid� 467

ms, invalid� 673 ms, as compared with good ®eld RT:

valid� 494 ms, invalid� 566 ms), she failed to collect

any data between ®elds (that is, with attention crossing

the vertical midline). Therefore, it is impossible to compare

the magnitude of this within poor ®eld disengage de®cit

with the more typical between-®eld disengage de®cit in

the same subjects. Although Losier [34] and Danziger et

al. [12] conducted studies that permit a comparison of

within and between ®eld cuing effects, their ®ndings were

different from one another.1 Further study of this relatively

neglected issue will be necessary to determine whether there

is a disengage de®cit within the poor ®eld.

In most studies (e.g. [3,11,17,38,44,47]), neurological

condition (e.g. extinction or neglect), lesion size, and loca-

tion varied considerably. From an examination of the corre-

lation between degree of involvement of different

anatomical regions and the disengage de®cit, Posner et al.

concluded that superior parietal lobe damage was necessary

to produce this phenomenon [47]. It has been proposed,

however, by Friedrich et al. [18] that it is the inferior parietal

area (including the superior temporal gyrus) that is critical

for the manifestation of the disengage de®cit. Of note, after

collapsing anatomical data from a large sample of patients

with neglect, Vallar and Perani [55] have identi®ed the

parieto-temporal junction as particularly important for

showing neglect on the line cancellation task. As such, the

disengage de®cit may not be solely a concomitant of super-

ior parietal damage, as originally proposed, but may depend

on more widespread parietal damage.

The relation between visuospatial neglect and the disen-

gage de®cit remains unclear (e.g. [38,47]). Additionally,

hemispheric asymmetries have been reported in the severity

of neglect [40], with right-hemisphere lesions leading to

more frequent and chronic de®cits than left-hemisphere

lesions. In an attempt to further delineate the role of the

parietal lobes in the disengage de®cit, Petersen et al. [41]

examined the orienting of patients following left- and right-

parietal, frontal and temporal lesions. Petersen`s samples,

B.J.W. Losier, R.M. Klein / Neuroscience and Biobehavioral Reviews 25 (2001) 1±13 3

1 Using informative peripheral cues that remained present while the

target was added to the display, Losier found a substantial between ®eld

disengage de®cit and no cuing effect, and hence no disengage de®cit, within

the poor ®eld in a group of seven patients with varying degrees of neglect.

Using uninformative peripheral cues that were presented brie¯y, Danziger

et al. [12] found a disengage de®cit within the poor ®eld (contra cue and

target: valid� 582, invalid� 740) that was greater than the cuing effect in

the good ®eld (ipsi cue and target: valid� 370, invalid� 461) though not

as great as the between ®eld disengage de®cit (cue ipsi, target contra� 916;

compare to 740) in one of their two subjects, but not in the other.

however, were very small and variable, thus limiting the

generalisability of the ®ndings.

Recently, in an attempt to further improve our under-

standing of the relative participation of the endogenous vs

exogenous orienting mechanisms in the disengage de®cit,

LaÁdavas et al. [33] compared the performance of neglect

patients using both cuing protocols. A quadrant display

(with cues and targets at the corners of an imaginary square

centered on ®xation) was used, in contrast to the more

frequently employed horizontal display (with cues and

targets to the left and right of ®xation). Their ®ndings indir-

ectly suggest that patients with neglect display a disengage

de®cit under exogenous cuing conditions but not under

endogenous conditions. However, methodological differ-

ences between this study and most others in the literature

make comparisons dif®cult. First, unlike most studies which

have explored the disengage de®cit using RT, this study

focuses instead upon accuracy as the key dependent vari-

able. Second, the SOAs used (800 and 1500 ms) were too

long to observe the early facilitation typical of exogenous

orienting. Indeed, LaÁdavas et al. inferred successful exogen-

ous orienting from inhibition of return (IOR) (see [30] for a

review), which is not only indirect but risky, given that the

generation of IOR is linked to oculomotor programming (cf.

[49,54]). Even though it is dif®cult to compare this study to

the rest of the literature, our analysis of that literature will

nevertheless support LaÁdavas's suggestion that the disen-

gage de®cit is associated with exogenous but not endogen-

ous orienting.

The present review will shed light on the aforementioned

issues by constructing appropriate comparisons from the set

of single subjects whose data have been individually

reported. This process was guided by the following ®ve

questions. (1) How is the disengage de®cit affected by

cuing protocol (endogenous vs exogenous orienting)?

Because the answer to this question appears to be that the

disengage de®cit is robust in the exogenous but not the

endogenous protocol, and because (perhaps consequently)

most of the literature has used peripheral cues, the remain-

ing questions will be answered with reference to studies that

used peripheral cues. (2) How is the magnitude of the disen-

gage de®cit affected by left- vs right-parietal damage? (3)

What is the time course of the disengage de®cit following

RH and LH damage? (4) How does the disengage de®cit

vary with anatomical and diagnostic parameter? (5) Is there

a contralesional RT de®cit for targets that are validly cued?

3. General approach

Peer-reviewed papers reporting on the disengage de®cit

published in the last 16 years were reviewed. Fourteen

papers were retrieved from the PSYCLIT and MEDLINE

databases. Ten papers were selected on the basis of informa-

tion about patient performance and orienting paradigm

provided in the article. Two papers that were not included


Tab

le1

Met

hodolo

gic

alpar

amet

ers

of

studie

sre

vie

wed

.(?

?,In

form

atio

nnot

avai

lable

or

not

able

toin

fer

from

info

rmat

ion

pro

vid

ed)

Ref

eren

ceD

ista

nce

(cm

)V

isual

ang

leS

tim

ulu

san

gle

Tar

get

Tar

get

angle

Fix

atio

nS

OA

(ms)

Cue

Tar

get

(ms)

Ori

enti

ng

mode

No.

tria

ls

[47

]??

80

.52

Ast

eris

k??

Box

50

±1000

Box

300

ms

5000

Exo

1en

do

and

endo

200

[3]

50

6b

y1

21

by

1.8

Dig

it`1

'1

by

0.2

Fix

atio

npoin

t375

±1575

x75

ms

2000

Exo

1en

do

300

[38

]8

07

32

Cro

ss??

Box

50

±1000

Box

300

ms

5000

Exo

1en

do

368

[41

]7

62

00

.5L

ight

0.5

Lig

ht

150

±1050

Hex

agon

??E

xo

1en

do

280

[17

]5

61

04

Cro

ss4

Cro

ss50

±1000

Box

4000

Exo

384

[33

]5

07

by

11

??X

1by

1C

ross

800

±1500

Arr

ow

3000

Exo

and

endo

400

[11

]3

52

6b

y7

1.9

2b

y1

.30

Ast

eris

k1.3

by

0.9

Cro

ss167

Ell

ipse

5000

Exo

1en

do

96

[16

]6

19

.6b

y1

1.4

1.7

by

11

.4S

quar

e1.7

2C

ross

300

End

of

rect

angle

2000

Exo

1en

do

768

[39

]5

71

0??

Lig

ht

0.5

Lig

ht

200

Arr

ow

50

ms

2000

Endo

142

[18

]6

18

1.5

Ast

eris

k0.1

Box

50

±700

Box

3000

Exo

and

exo

1en

do

640?

[36

]5

7??

2.5

Colo

red

dis

k1.2

Cro

ss300

Colo

red

ring

2000

Exo

1en

do

596

in the review reported on the disengage phenomenon using

paradigms other than visual orienting (e.g. cancellation

tasks [15]), or reported on patients with bilateral parietal

damage (e.g. [56]).2 One paper is discussed in the review

where appropriate [36], but not included in the quantitative

analyses because data from a majority of the patients used

were individually reported in an included study [18]. Most

of the studies selected for this review (which are described

in Tables 1 and 2) investigated the effects of left- and right-

hemisphere damage on the disengage de®cit; consequently

we included data from both right and left-hemisphere

damage in our review.

Two types of analysis were performed on the data

provided in selected papers. Because several papers

[17,18,38,39,41,47] reported performance for each patient

tested, analyses of variance could be conducted using all the

individual patients' reaction times in each condition. A

quantitative meta-analytic approach, which allowed us to

include two further studies [11,16], was applied to the litera-

ture which used peripheral cues.

Despite a rigorous review process, an evaluation like this

one cannot guard against uncontrolled variables, methodo-

logical and sample heterogeneity, and the possibility of bias

in the published corpus of data. For instance, the patient

samples were diverse in anatomical composition, as well

as diagnostic classi®cation. Although most patients had

CT scan (or MRI) investigations supporting the anatomical

®ndings, the possibility of rater bias cannot be ruled out or

assessed. The diagnostic criteria for the assignment of

neglect were idiosyncratic and based on a wide range of

measures (e.g. from line cancellation to full batteries for

assessing neglect). The time since lesion, and lesion extent,

also varied from subject to subject. Yet, for some purposes,

the wide range of methods and sample characteristics used

across this literature provides a bene®t rather than a cost.

Such variation permits us to test hypotheses which arise in

the course of this review, and to determine the generality

and boundary conditions of the disengage de®cit. Moreover,

one of the weakest aspects of this literature is the relatively

small sample sizes that characterize most studies. As we

shall see, our review reveals the statistical signi®cance of

several trends that appear to be present across studies, but

which were not signi®cant in any or most of them. It must

also be noted that we are treating each study as one of a class

of studies that can be used to address the relation between

parietal damage and the disengage de®cit. Yet, each study

we included may have had a much more speci®c goal. Meth-

odological parameters and patient selection would have

varied depending on the nature of the speci®c question

that each study sought to answer. For the most part, our

review is focussed on the limited set of empirical questions


Tab

le2

Pat

ien

td

emo

gra

phic

s

Ref

eren

ceA

ge/

ND

xC

Tre

port

N(1

)st

atus

Day

spost

-les

ion

Rig

ht-

hem

isp

her

eg

rou

p

[43

,47

]6

8.5

/6C

VA�

67

%;

tum

or�

33%

Par

ieta

l�

17%

;par

ieta

l1�

67%

;oth

er�

16%

Posi

tive�

83%

;neg

ativ

e�

17%

Mea

n�

1264;

range�

60

±3660

[3]

48

/6C

VA�

10

0%

Par

ieta

l�

33%

;par

ieta

l1�

67%

Exti

nct

ion

Mea

n�

74;

range�

32

±110

[38

]6

1/1

2C

VA�

92

%;

tum

or�

8%

Par

ieta

l�

50%

;par

ieta

l1�

25%

;oth

er�

25%

Posi

tive�

92%

;neg

ativ

e�

8%

Mea

n�

116;

range�

31

±420

[41

]4

8/2

Tu

mo

r�

10

0%

Par

ieta

l�

50%

;par

ieta

l1�

50%

Exti

nct

ion

Info

rmat

ion

not

avai

lable

[17

]5

7/8

CV

A�

10

0%

Par

ieta

l�

13%

;par

ieta

l1�

76%

;oth

er�

13%

Posi

tive�

100%

Mea

n�

78;

range�

35

±182

[33

]6

9.5

/11

N/A

Par

ieta

l�

20%

;par

ieta

l1�

80%

Posi

tive�

100%

Mea

n�

381;

range�

90

±1037

[11

]6

3.9

/10

CV

A�

10

0%

Par

ieta

l�

10%

;par

ieta

l1�

60%

;oth

er�

30%

Posi

tive�

100%

Mea

n�

180;

range�

7±

732

[16

]5

5.1

/8C

VA�

62

.5%

Par

ieta

l1�

100%

Posi

tive�

0%

Mea

n�

2400;

range�

180

±7200

[39

]2

7/7

CV

A�

57

%;

tum

or�

28%

;

oth

er�

15

%

Par

ieta

l�

15%

;par

ieta

l1�

85%

Posi

tive�

0%

Mea

n�

636;

range�

150

±2196

[18

]5

8.2

/8C

VA�

87

.5;

tum

or�

12.5

Par

ieta

l�

25%

;par

ieta

l1�

75%

Posi

tive�

0%

Mea

n�

2895;

range�

120

±14600

[36

]6

5.2

/7C

VA�

86

%;

tum

our�

14%

Par

ieta

l1�

100%

Posi

tive�

14%

;neg

ativ

e�

86%

Mea

n�

3240;

range�

1440

±8280

Lef

t-h

emis

ph

ere

gro

up

[43

,47

]5

4.1

/7C

VA�

71

%;

tum

or�

29%

Par

ieta

l�

28%

lpar

ieta

l1�

72%

Posi

tive�

43%

;neg

ativ

e�

57%

Mea

n�

384;

range�

14

±255

[38

]5

4.6

/10

CV

A�

10

0%

Par

ieta

l�

50%

;par

ieta

l1�

30%

;oth

er�

20%

Posi

tive�

50%

;neg

ativ

e�

50%

Mea

n�

50;

range�

28

±65

[18

]5

6.9

/7C

VA�

86

%;

oth

er�

14%

Par

ieta

l�

43%

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2 Although we tried to obtain the RT data from LaÁdavas et al. [33] (whose

published paper only reported accuracy) and from Egly et al. [16] (who

reported their RT data in a manner suitable to their, but not our, purposes)

by writing to the authors repeatedly, we were unsuccessful.

listed at the end of Section 2, and therefore we do not

attempt to evaluate each study with regard to how convin-

cingly its questions were answered. Finally, by necessity,

only data from published reports were utilized. The possi-

bility that the literature itself may be biased must be consid-

ered and cannot be dismissed. Of course, this limitation

quali®es all such reviews.

4. Results

4.1. How is the disengage de®cit affected by cuing protocol

(endogenous vs exogenous orienting)?

We classi®ed each subject`s data according to whether

they were exposed to a purely endogenous, purely exogen-

ous, or hybrid (exogenous cues with meaning) orienting

paradigm. The data from patients with RH lesions, collapsed

across the SOAs used in each study, are shown in Fig. 2.3

There were too few patients with left-hemisphere lesions

who had been tested in the endogenous cuing protocol to

conduct a parallel analysis of patients with left-hemisphere

lesions. Inspection of Fig. 2 shows that subjects receiving a

peripheral cueÐwhether or not it was informativeÐ

behaved similarly. To verify this, a mixed ANOVA was

conducted with the exogenous and exogenous 1endogenous protocols as a between-groups factor and with

cue condition and target hemispace as within subject

factors. The effects of cue condition and target hemispace

were highly signi®cant, as was their interaction, which

re¯ects the disengage de®cit. However, there were no

signi®cant effects or interactions involving protocol (all Fs

involving protocol were less than 1). A slight re®nement of

this description is made possible by Friedrich et al.'s direct

comparison of these protocols in the same 15 subjects (eight

with right-sided lesions; seven with left-) [18]. We

conducted an across-experiment ANOVA on their valid

and invalid RTs (with lesion side as a between-groups

factor) which revealed, as might be expected from studies

of normal subjects (e.g. [24]), that the effect of cuing was

greater for informative peripheral cues (50 ms) than for

uninformative cues (18 ms). Importantly, the disengage

de®cit (cue X location interaction) was signi®cant,

F(1,13)� 11.4, P , 0.01, but did not interact with protocol,

F(1,13)� 1.9, P . 0.15. When this analysis was con®ned to

those subjects with right-hemisphere damage neither the

disengage de®cit, F(1,7)� 1.5, P . 0.25, nor its interaction

with protocol, F , 1, were signi®cant.

In striking contrast to the pattern with peripheral cues,

subjects receiving a central cue seemed to show a much

smaller disengage de®cit. To verify this statistically we

combined the two peripheral cuing protocols and conducted

a mixed ANOVA with protocol (peripheral vs central cuing)

as a between-subjects factor and cue condition (V, I) and

target hemispace (ipsi, contra) as within-subjects factors. In

this analysis there were signi®cant effects of target hemi-

space, F(1,25)� 8.379, P , 0.01, and cue condition,

F(1,35)� 21.0, P , 0.0001, and there was a signi®cant

interaction between these variables (viz., the disengage de®-

cit, F(1,35)� 9.1, P , 0.005). Importantly, cuing protocol

interacted signi®cantly with cue condition, F(1,35)� 8.9,

P , 0.005, and marginally with the disengage de®cit

(group by space by cue, F(1,35)� 3.89, P� 0.056).

Because of the importance of this interaction, we conducted

separate ANOVAs on the data from subjects receiving

central and peripheral cues. With central cuing the interac-

tion between space and cue condition (the disengage de®cit)

was not signi®cant, F(1,8)� 1.8, ns, whereas it was signi®-

cant with peripheral cues, F(1,27)� 20.7, P , 0.0001.

Before concluding that this difference is due to procedural

differences between the protocols or to more fundamental

differences between endogenous and exogenous orienting, it

is important to rule out alternative explanations based on

differences in patient performance. As a group those

subjects who experienced the endogenous cuing protocol

showed a smaller cuing effect in the good ®eld and a smaller

contralesional RT de®cit on valid trials than those subjects

who experienced peripheral cues. Perhaps the disengage

de®cit is smaller when the cuing effect is smaller (because

attention is less intensely engaged); or perhaps the disen-

gage de®cit is smaller when the contralesional RT de®cit is

smaller. If either of these possibilities were con®rmed, then

it would not be necessary to conclude that the difference is

due to the use of endogenous vs exogenous orienting.

Because data for a reasonably large number of individual

subjects are available from the peripheral cue condition, it is

possible to determine whether the disengage de®cit is

somehow tied to either of these differences (see Fig. 3) by


Fig. 2. Data from the cuing literature with parietal patients organized by

cuing protocol (see text for explanation).

3 Friedrich et al. [18] provides a direct comparison of the exogenous vs

exogenous 1 endogenous protocols and will be discussed shortly. Their

data were not included in this analysis because their 15 patients were tested

in both protocols, and it would be illegitimate to include the same subjects

in two groups of what is otherwise a between-subjects comparison. Frie-

drich et al.'s patients, with their data collapsed across the two peripheral

cuing protocols, will be included in the analyses for questions 2, 4 and 5.

selecting subjects (from those who experienced the periph-

eral cuing protocol) in order to match the ipsilesional cuing

effect or contralesional RT de®cit that was observed in the

group of nine subjects who experienced central cues. First,

we selected a sub-group of subjects in the peripheral cuing

condition who showed as small a cuing effect in the good

®eld as did the subjects experiencing the endogenous proto-

col. The performance of patients receiving peripheral cues

selected to match the small cuing effect seen in subjects

exposed to the pure endogenous protocol showed a signi®-

cant disengage de®cit, F(1,12)� 12.2, P , 0.01. Second,

we selected a subgroup of subjects receiving peripheral

cues whose contralesional RT de®cit on valid trials was

equated with that seen in the endogenous group. Visual

inspection of the data from this subgroup also reveals that

the disengage de®cit was still present, F(1,12)� 7.2,

P� 0.02. Together these ad hoc comparisons suggest that

the absence of a disengage de®cit with endogenous cuing is

not due to either the smaller cuing effect or the smaller

contralesional RT de®cit seen in the subjects who experi-

enced central cues. Although we tentatively attribute the

absence of a disengage de®cit with central cuing to the

nature of endogenous orienting, an alternative will be eval-

uated in the general discussion.

4.2. How is the magnitude of the disengage de®cit with

peripheral cues affected by left- vs right-parietal damage?

The peripheral cuing data from individuals with both

right (n� 36) and left- (n� 24) hemisphere damage were

subjected to a mixed analysis of variance with side of

damage as a between subject variable, and target hemispace

(ipsilesional/contralesional) and cue condition as within

subject variables. All the main effects and interactions

were signi®cant. Importantly, there was a signi®cant 3-

way interaction among side of damage, target hemispace

(good vs poor) and cue, F(1,58)� 6.07, P� 0.0167, re¯ect-

ing the fact that the disengage de®cit is much smaller

following lesions to the left-hemisphere (see Fig. 4). Sepa-

rate ANOVAs conducted on the left and right-hemisphere

patients revealed that the interaction between these vari-

ables (the disengage de®cit) was signi®cant for both groups,

F(1,23)� 10.263, P� 0.0039, and F(1,35)� 18.639,

P� 0.0001, for left and right-hemisphere patients, respec-

tively).

A meta-analytic approach was employed to explore the

consistency of the disengage de®cit in right-lesioned

patients, using a larger sample of studies. Cuing effects

from each right-hemisphere study were calculated by

subtracting valid RT from invalid RT in both ipsilesional

and contralesional halves of space. Next, the average disen-

gage de®cit was calculated by subtracting the ipsilesional

difference score from the contralesional difference score.

This score was divided by the standard deviation of the

difference score for each study included in the analysis, to

obtain an effect size (see Table 3). A total of seven studies

were analyzed with effect sizes ranging from 0.93 [41] to

0.41[16].

4.3. What is the timecourse of the disengage de®cit with

peripheral cues following RH and LH damage?

To determine the timecourse of the disengage de®cit, we

examined the data from a set of studies with the following in

common: (a) use of peripheral cues; (b) individual patient

data was reported; and (c) SOAs of 50, 150, 500/550, and

1000 ms were used. Having already established that the

disengage de®cit is much larger following right than left-

hemisphere damage, here we analyzed these two groups

separately with SOA as a factor. In these analyses, costs

plus bene®ts, also referred to as the cuing effect (invalid


Fig. 3. Middle panel shows data from the literature using central cues (from

right panel, Fig. 2). Left panel shows data from studies with peripheral cues

from which speci®c subjects have been selected to match the ipsilesional

cuing effect found with central cues. The right panel shows a similar match

based on the size of the ®eld de®cit on valid trials.

Fig. 4. Performance following peripheral cues by patients with left- and

right-hemisphere lesions involving the parietal lobes.

minus valid) is the dependent variable, hence a disengage

de®cit would be re¯ected in a main effect of hemispace.

In the analysis of patients with right-hemisphere lesions

we found a signi®cant effect of hemispace [F(1,25)� 19.1,

P� 0.0002], SOA [F(3,75)� 3.195, P� 0.0283], and a

signi®cant interaction between SOA and hemispace

[F(3,75)� 3.964, P� 0.011]. Inspection of the right-hemi-

sphere data (Fig. 5) suggests that there is a disengage de®cit

at every interval, and that it is maximal at the shortest inter-

val and decreases with increasing SOA. Although this

pattern was remarked upon by Posner et al. and can be

seen in the individual studies, it was not signi®cant in any

of them individually [17,38,47]. In the parallel analysis of

patients with left-hemisphere damage we found only a

signi®cant effect of hemispace, F(1,16)� 7.03,

P� 0.0174 (Fig. 5). As is clear from Fig. 5, the disengage

de®cit following right-hemisphere damage declines precipi-

tously with SOA reaching the relatively constant and rela-

tively small disengage de®cit seen following left-

hemisphere damage.4

4.4. How does the disengage de®cit with peripheral cues

vary with anatomical and diagnostic parameters?

Two groups were formed using available anatomical data

on patients from the current sample. The ®rst group included

patients whose lesions were con®ned to the parietal lobes,

and the second group was comprised of patients for whom

lesions included, but were not restricted to, the parietal area.

A mixed-factorial analysis with cue condition (valid vs

invalid) and target hemispace (good vs poor) as within

subject factors, and side of lesion (left/right) and extra-

parietal involvement (parietal/parietal 1 ) as between

subject factors, revealed highly signi®cant effects of side

of lesion (subjects with right-hemisphere lesions were

slower), cue and hemispace. The interaction between cue

and hemispace was signi®cant, F(1,56)� 19.001,

P , 0.0001, re¯ecting the disengage de®cit. Lesion side

interacted with cue and hemispace and with the disengage

de®cit (all as expected from the analyses described in the

previous section). Importantly, neither the main effect of

extra-parietal involvement nor its interaction with any

other factors were signi®cant (F , 1 for the interaction

between extra-parietal involvement and the disengage de®-

cit). Two caveats constrain the implications of this ®nding.

First, this analysis is nonspeci®c in the sense that the

parietal 1 group could have damage to any area outside

the parietal lobe. On the basis of a speci®c test, Friedrich

et al. [18], whose data were included in this analysis, argued

that damage to the superior temporal gyrus at the junction

between the parietal and temporal lobes is more important in

generating the disengage de®cit than is damage to the more

superior regions of the parietal lobe. We will return to this

possibility in Section 5. Second, it should not be concluded

on the basis of this negative outcome that lesion size is

immaterial for the size of the disengage de®cit. In two

studies which reported [47], or permit calculation of [18],

the correlations between lesion size and the disengage de®-

cit (measured at the 50 ms SOA), the correlations

(r10� 0.45 for Posner et al. and r13� 0.5 for Friedrich et

al.) were positive, consistent and, considered together,

highly signi®cant (P , 0.01, one tailed).

Next, patients were partitioned along a diagnostic

criterion; that is, by whether they showed signs of neglect

and/or extinction (classi®ed as Neglect), or showed neither

of these (Non-Neglect). This parcellation of the sample into


Table 3

Mean cuing effects (invalid minus valid RT) for ipsilesional (Ipsi-X) and

contralesional targets (contra-X), the disengage de®cit (MeanD), standard

deviations (SD) and unbiased effect sizes (ES) for the disengage de®cit in

patients with right-hemisphere lesions (n� number of patients included

from each study)

Study n Ipsi-X Contra-X MeanD SD ES

[11] (Exp 1) 10 88.5 334.5 246.0 272.3a 0.90

[38] 12 53.2 273.0 219.8 332.9 0.66

[41] 2 29.0 122.5 103.5 110.8 0.93

[17] 8 136.0 358.6 234.0 305.3 0.77

[47] 6 90.0 409.5 311.5 495.3 0.63

[16] 13 60 87 27.0 b 0.41

[18] 8 24.8 38.4 13.6 31.4 0.43

a Lacking an SD of the difference score or inferential statistics from

which to estimate it, we averaged the SDs of the four conditions contribut-

ing to the two difference scores.b We used inferential statistics to generate the ES.

Fig. 5. Timecourse of the disengage de®cit (invalid minus valid RT for

ipsilesional targets subtracted from invalid minus valid RT for contrale-

sional targets) in patients with left- and right-parietal lesions.

4 Friedrich et al. [18] used different SOAs, and so could not be included in

the preceding analysis. This pattern was, nevertheless, con®rmed via

across-experiment ANOVAs we conducted on Friedrich et al.'s patients

with left- and right-hemisphere damage. In patients with left-hemisphere

damage the disengage de®cit did not interact with SOA (F , 1), whereas in

patients with right-hemisphere damage the interaction was marginally

signi®cant [F(1,21)� 2.47, P , 0.09), with the disengage de®cit (which

was not signi®cant in this group) declining with increasing SOA.

diagnostic categories conforms to Morrow and Ratcliff's

conjecture that the disengage de®cit improves with the reso-

lution of neglect ([38], p. 265). Analysis of variance

revealed signi®cant main effects of diagnosis, target hemi-

space, cue condition and a hemispace by cue interaction

(disengage de®cit). Several higher order interactions invol-

ving diagnosis were signi®cant; importantly, diagnosis

interacted with the disengage de®cit (diagnosis £ cue £hemispace, F(1,56)� 7.802, P� 0.0071. As can be seen

in Fig. 6, following damage to either the left or right-hemi-

sphere, individuals with signs of neglect showed a larger

disengage de®cit than those without signs of neglect.

4.5. Is there a contralesional RT de®cit for targets that are

peripherally and validly cued?

Patients with posterior, right-hemisphere damage

responded signi®cantly more slowly to validly cued targets

in the contralesional (RT� 585 ms) than ipsilesional

(RT� 485 ms) hemispace, t(35)� 2.936, P� 0.0058.

Although this pattern is present in each of the ®ve studies

contributing to this analysis, in no case did the authors indi-

cate whether the trend was signi®cant (though Posner et al.

[47] noted that it was present in 11 out of 13 patients with

lesions to either the left or right-hemisphere, which is signif-

icant at P , 0.05, by sign test). When a similar analysis was

conducted on the sample of left-hemisphere patients a smal-

ler, but highly signi®cant difference was again obtained; that

is, validly cued targets were responded to signi®cantly more

slowly in the contralesional (RT� 472 ms) than ipsilesional

(RT� 432 ms) hemispace (t(23)� 4.532, P� 0.0001). The

manner in which the disengage de®cit has been described in

the literature would lead many readers to infer that, when

validly cued, targets are detected with similar speed in the

good and poor ®elds (see, for example, the quote from

Robertson and Eglin [53], reprinted in Section 1 of this

paper). However, even when preceded by valid cues there

is a de®cit responding to targets presented to the damaged

hemisphere, as noted in preceding analyses.

The meta-analytic strategy permitted us to include one

additional study on this question (i.e. [11]). Table 4 lists

the means, pooled standard deviations (SDs), and effect

sizes for the right-hemisphere group. A total of six studies

were entered in the analysis with ES values ranging from

0.44 [38] to 1.10 [18]. Note that, whereas Friedrich et al.`s

patients (none of whom presented with neglect or extinc-

tion) showed the smallest effect in milliseconds, it was

nevertheless highly reliable.

5. General discussion

The data currently available on the disengage de®cit

following parietal damage are more de®nitive in their

outcomes when combined than when examined on a

study-by-study basis. The disengage de®cit is robustly

observed when attention is drawn to a cue in the periphery

(whether or not the cue is informative). However, when

attention is manipulated by purely endogenous means, the

disengage de®cit is often not apparent. Following a periph-

eral cue the disengage de®cit is large at short intervals, and

while it declines with time since the cue, it is still present

when the SOA is as long as 1 s. It is larger following right

than following left-hemisphere damage; and larger for

patients who show clinical signs of neglect. Although the

magnitude of the disengage de®cit increases with increases

in lesion size, nonspeci®c damage to regions outside the

parietal lobes does not seem to play a special role in the

magnitude of this de®cit. Finally, response times to validly

cued targets presented to the poor ®eld are signi®cantly

slower than those to the good ®eld. In the next section, we

discuss the implications of some these ®ndings.


Fig. 6. Disengage de®cit (as in Fig. 5) for patients showing signs of neglect

or extinction (Neglect) or showing neither of these signs (NonNeglect).

Patients with left- and right-hemisphere lesions are shown separately.

Numbers at the bottom of each histogram represent the total number of

patients contributing to the corresponding data.

Table 4

Means, standard deviations and unbiased ES of validly cued responses from

patients with right-hemisphere lesions

Study n Ipsi Contra MeanD SD ES

[11] (Exp 1) 10 543.0 753.0 210.0 330.0a 0.64

[38] 12 497.8 648.8 150.9 339.7 0.44

[41] 2 371.0 436.5 65.5 65.9 0.99

[17] 8 549.2 685.2 127.9 175.8 0.73

[47] 6 508.1 571.6 63.3 67.5 0.96

[18] 8 415.8 445.1 29.3 26.7 1.10

a Lacking an SD of the difference score we averaged the SDs of the two

conditions contributing to the two difference scores.

5.1. Absence of a disengage de®cit with endogenous

orienting (central cues)

To explain the absence of a disengage de®cit with endogen-

ous orienting (central cues) it might be argued that the parietal

lobes are particularly involved in exogenous control of covert

(and probably overt) orienting, whereas other brain systems

(e.g. frontal ones) have a greater responsibility for endogenous

control [33,50]. Alternatively, it has been suggested that

exogenous control is primarily a right-hemisphere function

while endogenous control is primarily a left-hemisphere func-

tion [27]. If true, this would entail impoverished exogenous,

but not endogenous, orienting following right parietal lobe

damage. Such a link, when viewed in conjunction with the

association between exogenous orienting and feature integra-

tion [6,7], converges with the suggestion that parietal cortex

and/or systems with which it interacts closely might play a

special role in the binding of features into objects that is so

important in pattern recognition [1,2,8].

Although this proposal may be intuitively appealing,

there is an important caveat to consider. Jon Driver [14]

notes that most of the data showing almost no disengage

de®cit with endogenous orienting come from a single study

[39] where the possible target locations were not marked. In

contrast, the peripheral locations in Posner et al. [47] were

marked, and the two right-hemisphere-lesioned subjects

who were administered the central cuing protocol in that

study showed a robust disengage de®cit (205 ms).5 Even

when attention is successfully allocated in response to the

endogenous cues, it might be argued that when there is

nothing to engage attention uponÐbesides empty spaceÐ

disengaging attention should not present any special dif®-

culty. This comment itself raises an interesting point. When

the possible target locations are marked, the very fact that a

patient is suffering from left neglect or extinction means that

phenomenologically the marker in the right visual ®eld is

more salient than that in the left, and therefore exogenous

control of attention in response to this salience differenceÐ

in advance of any cuesÐmay be biased toward the good ®eld.

Indeed, our demonstration that the literature on the disengage

de®cit reveals a highly signi®cant advantage for the good ®eld

even on valid trials would seem to follow from this point.

Peripheral cuing studies that did not use marked locations

could provide converging evidence for or against the propo-

sal that the presence of something in the periphery for atten-

tion to be engaged upon and disengaged from is essential to

observe a disengage de®cit.6 We are aware of three such

cases. In Experiment 1 of D'Erme et al. (which is repre-

sented in the meta-analyses of Tables 3 and 4) there were no

markers, the informative peripheral cue was a small asterisk

presented for 150 ms, and 17 ms after the cue was termi-

nated a target dot was presented in the cued or uncued hemi-

space. A large disengage de®cit was observed (an average of

246 ms across ten right-hemisphere patients) suggesting that

the presence of something to disengage from is not essential

to obtain a disengage de®cit.

In another study of peripheral cuing without markers,

Marangolo et al. [36] presented colored rings as cues for

100 ms, and 200 ms later presented colored target disks the

size of the hole in the cue rings. In 12 patients with right-

and left-parietal damage, Marangolo et al. did not ®nd a

signi®cant disengage de®cit. The difference between

D'Erme et al. [11] and Marangolo et al.'s ®ndings are

most likely due to the subject selection criteria: All of

D'Erme et al's parietal subjects were suffering from mild

or severe neglect, whereas in Marangolo et al. only one of

the 12 patients was experiencing neglect. Given the ®ndings

reported in Section 4.4 for question 4, which showed that the

disengage de®cit is much more apparent in patients with

neglect or extinction, the absence of a disengage de®cit in

Marangolo et al. need not be attributed to the absence of

peripheral markers after the cue is removed. Because six of

the patients tested by Marangolo et al. were also tested by

Friedrich et al. [18] (who used peripheral markers), it is

possible to generate a within-subject assessment of the

role of markers using these subjects. We made such a

comparison.7 Although there was a signi®cant effect of

cue condition, neither the 2-way interaction between cue

and target hemispace, nor the 3-way interaction with experi-

ment (presence of markers) was signi®cant.

Finally, in Posner et al. [47], the peripheral cuing data

reported for two right-hemisphere-lesioned subjects had

been collected following the onset rather than the bright-

ening of a 300 ms box (see p. 1865 and Fig. 1 of that study).

Therefore, for these two subjects at the two longest SOAs

used in this study, the cue would have been removed by the

time the target had appeared. Even though there was no

peripheral object to disengage from, the average disengage

de®cit of these two subjects was very large (270 ms).

These analyses of pertinent data from Posner et al. [47],

D'Erme et al. [11], Marangolo et al. [36], and Friedrich et al.

[18], suggest that the presence of markers is not critical for

the manifestation of a disengage de®cit following peripheral

cues. If this conclusion can be extended to orienting with

central cues, then the near absence of a disengage de®cit with

endogenous orienting (see Fig. 3) points in the direction of a

fundamental difference between exogenously and endogen-

ously controlled shifts of visual attention, with a special role

for parietal cortex in exogenous orienting. Nevertheless, a


5 Nevertheless, the overall pattern of performance of these two patients is

dif®cult to interpret with con®dence. Targets in the good ®eld did not show

the costs and bene®ts that typically follow central cuing. At the one interval

(150 ms) where both subjects showed positive effects of the cue, the disen-

gage de®cit was actually negative.6 We thank an anonymous reviewer for making this suggestion.

7 For these six subjects, we averaged the data from Friedrich et al.'s

second experiment (which, like Marangolo et al., used informative periph-

eral cuing) after averaging across the SOAs (150 1 450) most similar to

Marangolo et al.`s (300) then combined with the data reported in Maran-

golo et al., and conducted an ANOVA with experiment, cue condition and

target hemispace as within-S variables.

dedicated test of this interesting proposal would certainly be

useful.

5.2. Left- vs right-sided lesions

The disengage de®cit is a concomitant of both right- and

left-hemisphere parietal damage, but the magnitude of the

de®cit is much larger following right-hemisphere damage

(see Figs. 4, 5). This ®nding is not surprising considering

that visuospatial de®cits are encountered more frequently

following damage to the right-hemisphere. For instance,

visuospatial neglect (an inability to orient or respond to

contralesional objects) has been noted following both left-

and right-parietal lesions (e.g. [13]), but it is reported less

frequently and less severely following left-hemisphere

damage (see [40]).

5.3. Timecourse of the disengage de®cit

In accordance with previous reports (e.g. [47]), the disen-

gage de®cit was greatest with short cue-target intervals and

decreased as the interval was lengthened. This decay of the

disengage de®cit appears to be a associated with dramatic

improvements in RT for invalidly cued targets in the

contralesional ®eld. This pattern provides converging

evidence for an association between the disengage de®cit

and the re¯exive orienting system (as discussed above),

because orienting in response to a peripheral cue would

initially be primarily controlled re¯exively by the stimulus

whereas endogenous control in response to a cue's meaning

begins to operate later [26].

5.4. Anatomy and diagnosis

Anatomical analysis provided additional support for the

role of parietal lobes in the manifestation of attentional

de®cit. Involvement of additional structures (e.g. temporal

or frontal cortex) did not change the nature or the pattern of

the de®cit. As noted earlier, however, this analysis was

nonspeci®c, comparing damage con®ned to the parietal

lobes with damage to the parietal lobes plus any other

brain structures. One recent study [18] carefully selected

patients with damage ªrestricted to the posterior association

cortex in one hemisphere and sparing the frontal lobesº, and

then classi®ed them on the basis of lesion location in order

to directly assess the relative contributions of damage to the

superior parietal lobe (SPL) and temporo-parietal junction

(TPJ) to the disengage de®cit. Analyses reported by Frie-

drich et al., aimed at the question, ªdoes the disengage de®-

cit vary with lesion location?º pointed in the direction of

TPJ involvement and against a special role for the SPL.

Nevertheless, reanalysis of the data reported in Friedrich

et al. suggests that further work is needed to ®rmly establish

a special role for the TPJ in the manifestation of the disen-

gage de®cit. In an analysis of variance of the valid and

invalid data from both of Friedrich et al.'s experiments

there was a signi®cant disengage de®cit [cue £ location,

F(1,13)� 9.218, P , 0.0096], but this did not interact

signi®cantly with anatomy (TPJ vs PAR, F , 1) nor did it

interact with SOA [F(3,39) , 1]. Although these ®ndings

do not support a separate analysis of the shortest SOA, we

looked at the 50 ms SOA because our review of the litera-

ture shows that the disengage de®cit is very much larger at

this interval (at least following right-hemisphere damage)

and Friedrich et al. noted that ªthis pattern of de®cit appears

to be particularly marked at the short SOAsº (p. 199). In this

analysis neither the disengage de®cit (F(1,13)� 2.454,

P . 0.1) nor its interaction with anatomy

(F(1,13)� 2.613, P . 0.1) were signi®cant. The disengage

de®cit is unusually small in this study (22 ms), when

compared with that seen in the other four studies which

have used peripheral cues and reported individual patients`

data (ranging from 93±232 ms). Thus, even if one were to

accept Friedrich et al.'s description that ªan extinction-like

response time pattern was found for the TPJ but not for the

PAR groupº (p. 193, Abstract), it would be risky to general-

ize this to the literature on the disengage de®cit. Although

Friedrich et al.'s selection of patients, which was based on

lesion location, was quite reasonable given their question

(damage to which location is more important in generating

the disengage de®cit), in retrospect it is unfortunate that

there were no patients with neglect or extinction because

our review (see Section 4.4 and next paragraph) suggests

this is important for observing a disengage de®cit and

because, as suggested by Vallar and Perani`s review [55],

the link to TPJ might have been stronger had patients with

neglect been included.

5.5. Contralesional RT de®cit

Inspection of the pooled data reveals that reaction times

to validly cued targets are slower in contralesional than

ipsilesional space. This ®nding has not been mentioned at

all in some previous studies, or has only been alluded to and

then dismissed due to lack of statistical signi®cance. Given

the increased power inherent in our method of combining

studies, we are con®dent that there is slowed responding to

contralesional targets, even following valid cues (cf. [34] for

con®rmation of this ®nding). It would appear that previous

studies separately lacked the statistical power to establish

this conclusion. Although this effect was signi®cant in both

left- and right-hemisphere parietal patients, the effect was

three times greater in right-hemisphere patients.

6. Summary

The present review provides the ®rst opportunity to eval-

uate all available data on the visual orienting of patients

with parietal damage. Our ®ndings are clear. Unilateral

damage to the parietal area affects an individual`s ability

to respond to targets presented in the contralesional side of

space. In particular, and as expected, patients with right-

parietal damage were slower to respond to invalidly cued


targets in contralesional space compared to responses in

ipsilesional space. Additionally, although patients with

left-parietal damage also display a disengage de®cit, the

magnitude of this de®cit is markedly smaller (52 ms), than

what is seen following right-parietal damage (186 ms) (See

Fig. 4). This difference is particularly salient immediately

after cue presentation (See Fig. 5). Overall, patients with

left-parietal damage responded to validly cued targets

approximately 84 ms faster than their right-parietal counter-

parts. Additionally, the response time impairment in

contralesional space following valid cues was much greater

with right (99 ms) than with left (40 ms) parietal damage.

Right-parietal damage thus appears to yield both a greater

contralesional RT de®cit and a greater disengage de®cit.

Finally, the disengage de®cit was much larger at short

cue-target intervals and decayed rapidly; it was larger in

patients suffering from neglect or extinction than those

with parietal damage without these symptoms.

Kinsbourne`s model of interhemispheric inhibition (for

review see [28]) together with current theories of visuospa-

tial neglect may provide a useful framework for understand-

ing some of the present ®ndings. Collective evidence also

suggests that visuospatial neglect is a consequence of a

disruption in the `normal` representation of the three-dimen-

sional environment (e.g. [4,5,19]). We propose that the

disengage de®cit, either across or within (cf. [3]) a hemi-

®eld, is an exemplar of a disruption in three dimensional

representation of space. Electrophysiological recording (i.e.

[20]), neuroimaging data [10], and computational modeling

[9] converge on the following assumptions.

1. Input modules channel information about the environ-

ment from the dorsal visual pathway, as proposed by

Mishkin and colleagues [37].

2. In a spatially graded fashion to attention modules resid-

ing in the left- and right-hemispheres.

3. The left-hemisphere contains one attention module repre-

senting only the right side of space, while the right-hemi-

sphere contains two, one representing each side of space

(see [10,20,57]).

4. All three modules converge onto a response module,

which may or may not be structurally (i.e. anatomically)

related to the parietal lobes.

5. As suggested by the neural network model of Cohen and

colleagues [9], as well as by Kinsbourne [28], in a resting

state the excitatory and inhibitory inputs in the system

sum to zero, resulting in no directional attentional bias.

6. However, under conditions in which an imbalance in

hemispheric activation exists, an orienting bias contral-

ateral to the activated hemisphere ensues. The imbalance

can be created by differential stimulation arising from

various spatial coordinates (i.e. left- vs right-hemispace),

or from impaired processing capacity secondary to

neuronal compromise (e.g. damage).

7. As shown by Cohen et al. [9] such an arrangement will

result in the disengage de®cit pattern following damage

to the attention modules in the right-hemisphere.

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A review of the evidence for a disengage deficit following parietal lobe damage