PLEASE SCROLL DOWN FOR ARTICLE

This article was downloaded by: [Osp Pediatrico Bambino Ges]On: 28 February 2011Access details: Access Details: [subscription number 932331918]Publisher Psychology PressInforma Ltd Registered in England and Wales Registered Number: 1072954 Registered office: Mortimer House, 37-41 Mortimer Street, London W1T 3JH, UK

Developmental NeuropsychologyPublication details, including instructions for authors and subscription information:http://www.informaworld.com/smpp/title~content=t775653638

Working Memory Impairment in Children With Developmental Dyslexia:Is it Just a Phonological Deficity?Deny Menghinia; Alessandra Finzia; Giovanni Augusto Carlesimobc; Stefano Vicaria

a Children's Hospital Bambino Gesù, Rome, Italy b S. Lucia Foundation, Rome, Italy c NeurologicalClinic, Tor Vergata University, Rome, Italy

Online publication date: 23 February 2011

To cite this Article Menghini, Deny , Finzi, Alessandra , Carlesimo, Giovanni Augusto and Vicari, Stefano(2011) 'WorkingMemory Impairment in Children With Developmental Dyslexia: Is it Just a Phonological Deficity?', DevelopmentalNeuropsychology, 36: 2, 199 — 213To link to this Article: DOI: 10.1080/87565641.2010.549868URL: http://dx.doi.org/10.1080/87565641.2010.549868

Full terms and conditions of use: http://www.informaworld.com/terms-and-conditions-of-access.pdf

This article may be used for research, teaching and private study purposes. Any substantial orsystematic reproduction, re-distribution, re-selling, loan or sub-licensing, systematic supply ordistribution in any form to anyone is expressly forbidden.

The publisher does not give any warranty express or implied or make any representation that the contentswill be complete or accurate or up to date. The accuracy of any instructions, formulae and drug dosesshould be independently verified with primary sources. The publisher shall not be liable for any loss,actions, claims, proceedings, demand or costs or damages whatsoever or howsoever caused arising directlyor indirectly in connection with or arising out of the use of this material.

DEVELOPMENTAL NEUROPSYCHOLOGY, 36(2), 199–213Copyright © 2011 Taylor & Francis Group, LLCISSN: 8756-5641 print / 1532-6942 onlineDOI: 10.1080/87565641.2010.549868

Working Memory Impairment in Children WithDevelopmental Dyslexia: Is it Just a Phonological Deficity?

Deny Menghini

Children’s Hospital Bambino Gesù, Rome, Italy

Alessandra FinziChildren’s Hospital Bambino Gesù, Rome, Italy

Giovanni Augusto CarlesimoS. Lucia Foundation, Rome, Italy

Neurological Clinic, Tor Vergata University, Rome, Italy

Stefano VicariChildren’s Hospital Bambino Gesù, Rome, Italy

Although reduced verbal span is well documented in individuals with developmental dyslexia, theexisting data on visual-spatial span are inconclusive. The aim of the present study was to ascertainwhether the working memory deficit in developmental dyslexia is confined to verbal material orwhether it also involves visual-object and visual-spatial information. Results document deficits onspan tasks tapping verbal, visual-spatial, and visual-object working memory in dyslexic children andindicate that the working memory deficit in developmental dyslexia is not limited to dysfunction ofphonological components but also involves visual-object and visual-spatial information.

Developmental dyslexia (DD) is a very prevalent disorder that affects approximately 5% ofthe population in Western countries. It is defined as a specific and persistent reduced capac-ity to decode written language despite conventional instruction, adequate intelligence, andsociocultural opportunities (Shaywitz, 1998).

Epidemiological, anatomical, and neurofunctional data (Galaburda, Sherman, Rosen, Aboitiz,& Geschwind, 1985; Lindgren, De Renzi, & Richman, 1985; Paulesu et al., 2001) supportthe position that DD is a neurobiological disorder. There is, however, controversy regardingthe cognitive deficits underlying DD. The notion that the disorder is related to a more gen-eral phonological impairment, that is, the so-called “phonological core deficit hypothesis,” hasreceived several confirmations (White et al., 2006). Nevertheless, alternative theories have beenformulated to interpret the cognitive base(s) of DD. For example, Wolf and Bowers (Bowers

Correspondence should be addressed to Stefano Vicari, M.D., Head Child Neuropsychiatry Unit, Department ofNeuroscience, I.R.C.C.S. Children’s Hospital Bambino Gesù, Piazza Sant’Onofrio 4, I-00165, Rome, Italy. E-mail:stefano.vicari@opbg.net

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

200 MENGHINI, FINZI, CARLESIMO, VICARI

& Wolf, 1993; Wolf & Bowers, 1999) proposed that naming-speed deficits, which are fre-quently present in dyslexic individuals, are a second core deficit and are largely independentof phonology. The double-deficit hypothesis proposes that phonological deficits and naming-speed problems can occur separately or can co-occur, thus causing the most impaired reading(Wolf, Bowers, & Biddle, 2000). An automatization deficit hypothesis has also been proposedto account for DD (Nicolson & Fawcett, 1990; Nicolson, Fawcett, & Dean, 2001). Accordingto this hypothesis, reading depends largely on automatization of sub-skills and can be con-sidered a fluent process only when maximum reading speed with minimum cognitive load isobserved. Indeed, deficits in automatizing skills, such as reduced implicit learning of visual-spatial sequences (Vicari, Marotta, Menghini, Molinari, & Petrosini, 2003; Vicari et al., 2005) ordeficient balancing (Fawcett & Nicolson, 1992), have been documented in dyslexic children andmay be related to dysfunction of cerebellar circuits (Menghini, Hagberg, Caltagirone, Petrosini,& Vicari, 2006; Nicolson et al., 1999).

Verbal working memory (WM), which is a limited capacity system for the temporary stor-age of information from a variety of sources for further manipulation, is consistently impairedin dyslexic individuals. According to the influential model developed by Baddeley and Hitch(1974), in humans WM is subserved by the cooperation of two major systems. The first con-sists of a number of peripheral “slave” systems devoted to the temporary storage and rehearsalof information belonging to a single modality. The articulatory loop is a two-component slavesystem specialized for the temporary storage of verbal material. One component, the phono-logical store, is devoted to the passive maintenance of verbal information in a phonologicalcode. The second component, articulatory rehearsal, prevents the decay of material stored inthe phonological store by refreshing the memory trace. It is also involved in the re-coding ofvisually presented verbal material into a phonological format. The visual-spatial sketchpad is aperipheral slave system specialized for the temporary storage of visual material. Although thefunctioning of this system has been far less investigated than that of the articulatory loop, a two-component internal fractionation has been hypothesized. In fact, neuropsychological evidencein brain-lesioned individuals and neurofunctional data in healthy humans support the hypothe-sis that the temporary memory of visual-object information (such as colors and shapes) and thespatial location of objects are processed by functionally independent subsystems (Smith et al.,1995; Vicari, Bellucci &, Carlesimo, 2006). More recently, Baddeley (2000, 2001) introduced anew slave system in the WM model, that is, the episodic buffer, which synergistically combinesinformation from various subsystems into a form of temporary representation. The second majorsystem in Baddeley’s WM model, that is, the central executive system, temporarily stores andprocesses information from many modalities. It is central to many cognitive domains includinglearning, planning, and problem solving, as well as language acquisition, comprehension, andproduction.

Many studies investigating verbal WM in DD have documented reduced verbal span indyslexic children compared to age-matched normal readers (for a review see Snowling, 2000).Different hypotheses have been advanced to account for the association between poor readingand reduced verbal span in dyslexic individuals. Some authors have proposed that an impair-ment of subvocal rehearsal mechanisms might be associated with reading retardation (Baddeley,1978). Indeed, according to Jorm (1983), to the extent that retarded readers do not utilize thearticulatory loop adequately, they tend to have a reduced memory span, poor short-term memoryfor serial order, proneness to phonological confusion and less use of rehearsal. Nevertheless,

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 201

other research provides evidence that a reduced speech rate in dyslexic individuals may bethe source of both impaired subvocal rehearsal and reading deficits (McDougall, Hulme, Ellis,& Monk, 1994). Finally, others have found rehearsal intact and have suggested that impair-ment of the phonological store is at the base of the deficits in DD (Kibby, Marks, Morgan, &Long, 2004).

Involvement of other components of the WM system in dyslexics’ impaired reading is con-troversial. Indeed, existing data on the visual-spatial sketchpad in DD are inconclusive. In fact,some recent studies have documented normal visual-spatial WM in dyslexic individuals (Jeffries& Everatt, 2004; Kibby et al., 2004), whereas others have reported deficits in this domain (Olson& Datta, 2002; Smith-Spark & Fisk, 2007). Controversial results have also been reported for cen-tral executive system functioning in DD. Indeed, while some studies have documented reducedefficiency of this system in dyslexics (Smith-Spark, Fisk, Fawcett & Nicolson, 2003) others havenot (Roodenrys, Koloski, & Grainger, 2001). Smith-Spark and co-workers (Smith-Spark et al.,2003) suggested a possible link between deficits in visual-spatial span and reduced efficiency ofthe central executive in DD. These authors provided evidence that reduced visual-spatial spanin dyslexic individuals is related to task complexity and is evident only when the experimentalprocedure requires a high memory-updating load.

Among other possible explanations of the contradictory findings reported in the literature,discrepancies among studies regarding the inclusion criteria adopted and the kind of memorytasks used to assess WM should be considered. Concerning the first issue, different demographiccharacteristics (such as chronological age) and general intellectual functioning, as well as thepresence of co-morbidities in the recruited samples of dyslexics, are relevant points of contrastamong studies. For example, some studies explored WM functioning in children (i.e., Jeffries &Everatt, 2004) and some in adults (i.e., Smith-Spark & Fisk, 2007); other studies included chil-dren with attention deficit hyperactivity disorder (ADHD) (Kibby et al., 2004), whereas othersconsidered only children with attention/behavioral disorders (i.e., Swanson, 1991); some stud-ies reported only the performance of individuals with average intelligence (i.e., Howes, Bigler,Lawson, & Burlingame, 1999), whereas others also included the performance of individuals withless than normal intelligence (Gathercole, Alloway, Willis, & Adams, 2006). As for the kind ofmemory tasks used, some studies relied on traditional measures of verbal and spatial spans (i.e.,Jeffries & Everatt, 2004), whereas others adopted more complex tasks to separately assess thecontribution of the slave systems and the central executive to performance (i.e., Cohen-Mimran& Sapir, 2007; Smith-Spark & Fisk, 2007).

The aim of the present study was to clarify the nature of the short-term memory deficit in DD.For this purpose we tested verbal, visual-object, and visual-spatial memory span in a sampleof dyslexic children and in a group of age-matched normally reading children. Our predictionswere the following: first, because of the vast amount of research supporting a deficit of verbalWM in individuals with DD, reduced verbal span would be found in the dyslexic children; sec-ond, if, as predicted by the “phonological core deficit hypothesis,” WM deficits in children withDD are related only to reduced phonological resources and/or to a dysfunctional ArticulatoryLoop, no difference would be found in visual-object and visual-spatial WM in dyslexic childrenand normal readers. On the contrary, evidence that these individuals also suffer from a reducedvisual-object and/or visual-spatial span would extend the deficit to other components of the WMsystem, thus challenging the view that DD is a pure phonological deficit. To avoid any con-founds from the literature, we enrolled only individuals with isolated reading disability in the

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

202 MENGHINI, FINZI, CARLESIMO, VICARI

dyslexic group, that is, with normal intelligence and without concomitant ADHD deficits, andused memory tasks conceived to be easily performed by children and to be minimally demandingon attentional and executive resources.

METHOD

Participants

Performance of two groups of Italian children was evaluated. The first group was comprised of54 dyslexic children (age range 8.4–13.8) and the second group of 46 normal readers (age range8.1–14.3). To take into account developmental changes in the short-term memory domain, wesplit each of the two groups of participants into two subgroups including, respectively, childrenin primary school (from third to fifth grade) and in middle school (from fifth to eighth grade).The primary school subgroups were comprised of 28 dyslexic children (F/M = 14/14; M age= 9.8 ± 0.7) and 22 normal readers (F/M = 10/12; M age = 10.1 ± 1.0). The middle schoolsubgroups were comprised of 26 dyslexic children (F/M = 8/18; M age = 12.4 ± 0.9) and 24normal readers (F/M = 10/14; M age = 12.6 ± 0.9).

The clinical diagnosis of dyslexia was made on the basis of the Diagnostic and StatisticalManual of Mental Disorders, 4th ed. (DSM-IV) recommendations (American PsychiatricAssociation, 1994). The dyslexic group included only children whose reading speed or accu-racy level was at least 2 standard deviations (SD) below the mean of their chronological ageon the word or non-word reading subtests of the Battery for the Diagnosis of Dyslexia (Sartori,Job, & Tressoldi, 1995). A substantial proportion of the dyslexic children (29/54; 53.7%) scoredlower than 2 SD below the mean of their chronological age in both reading speed and accuracy.However, 11/54 (20.4%) of the dyslexic children scored in this range only for reading speed and14/54 (25.9%) only for reading accuracy.

Other inclusion criteria for the dyslexic group included the following: normal general intel-ligence, as documented by a Wechsler Intelligence Scale for Children–Revised (WISC–R) IQof no less than 90 (Wechsler, 1993); performance above the 10th percentile on the ColouredProgressive Matrices (Raven, 1994); normal or corrected to normal visual acuity; no significantco-morbidities, such as ADHD, as documented by a score within the normal range (90th per-centile) on the Italian version of the ADHD rating scale for parents (Cornoldi, Gardinale, Masi,& Pettenò, 1996) and less than five inattentive/hyperactive symptoms based on the DSM-IVcriteria.

The control group was matched to the dyslexic children for chronological age, non-verbalintelligence (as measured by Raven’s Coloured Progressive Matrices) and socioeconomic level.The criteria for inclusion in the control sample were the same as those for the dyslexic group(including the absence of ADHD). The only obvious difference was that these children hadto perform within the normal range on the word and non-word subtests of the Battery for theDiagnosis of Dyslexia (Sartori et al., 1995).

The dyslexic children were tested at the Children’s Hospital Bambino Gesù in Santa Marinella(Rome, Italy) and the normally reading children were tested at their schools. Observations werecarried out only after the parents had given their informed consent. The study was approved bythe local ethics committee.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 203

Measures

Verbal, visual-spatial, and visual-object span tasks. Vicari’s (2007) battery of tasks wasused to assess verbal, visual-spatial, and visual-object span.

The material for the verbal span task consists of a list of eight, two-syllable low frequencywords. In the first block, the examiner reads aloud two words at a rate of one item per second. Theparticipants are required to repeat the two words in the same order. Then, four additional stringsof two words are presented. If the child is successful in at least three of the five sequences, asequence one word longer is presented. If the child fails (less than three correct answers in ablock), the task is discontinued. The same procedure is used for sequences of increasing length(up to a maximum of seven words).

In the visual-spatial span task, the material consists of a non-verbalizable geometric shapedepicted in high contrast colors (green–red) that appears for two seconds in one of seven pos-sible positions on the computer screen (Figure 1). After one second (ISI), the same geometricshape appears in a second position and then disappears after two seconds. After 500 msec (delayinterval), two empty cells (a 2 × 3 cm) are presented in the same spatial positions as before andthe child has to indicate the order in which the stimuli appeared. If the child is successful in atleast three of five, two-position sequences, a sequence one block longer is presented. Also in thiscase, the same testing procedure is used for sequences of increasing length (up to a maximum ofseven spatial positions).

A similar procedure is used for the visual-object span task (Figure 1). In this case, the exper-imental material consists of seven complex geometric figures depicted in high contrast colors(green–red). To ensure that the children do not use a verbal strategy to encode the stimuli, a pilotstudy was conducted prior to standardization of the battery of WM tasks (Vicari, 2007). Resultsdocumented that typically developing children do not rely on a verbal strategy to encode stimuliin the visual-object span. At the onset of the task, two figures are presented, one at time, for twoseconds at the center of the computer screen with a 1-sec ISI; 500 msec after the disappearanceof the second figure, the two stimulus figures are presented aligned in the center of the screen ina random position (left vs. right) and the participant is asked to indicate the order in which theyappeared. Also in this case, if the child is successful in at least three of the five trials, a sequenceone figure longer is presented and the task continues until a maximum of seven figures have beenpresented.

The score for all span tasks is computed by assigning 0.5 to each sequence of items correctlyreproduced by the participant (maximum score = 17.5).

Attention and visual-perceptual tasks. Difficulties in visual-perceptual processing mayaffect performance on visual WM tasks. Moreover, a deficit of focused or sustained attentionmay interfere with performance on WM tasks, irrespective of the material to be processed.To control for these sources of variability, both the dyslexic children and the normal read-ers were also administered tasks assessing visual and auditory attention and visual-perceptualprocessing.

In Map Mission (Manly et al., 2002), a subtest of the Test of Everyday Attention for Children,participants are presented with a color-printed, A3-laminated city map. Eighty targets represent-ing restaurants (i.e., small knife and fork symbols) are randomly distributed across the map.Distracting symbols of the same size, such as supermarket trolleys, cups or cars, are also present.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

204 MENGHINI, FINZI, CARLESIMO, VICARI

Visual-spatial Span Task

(c)

Visual-object Span Task

(c)

(a)

(a)

(b)

(b)

FIGURE 1 Examples of the stimuli used for the Visual-Spatial SpanTask and for the Visual-Object Span Task. For the Visual-Spatial SpanTask, Panel a shows the first figure, which appears for 2 sec in one ofseven possible positions on the computer screen. Panel b shows the samefigure, which appears after 1 sec in another position and then disappearsafter 2 sec. Panel c shows the two empty cells, which, after 500 msec, arepresented in the same spatial positions as before. For the Visual-ObjectSpan Task, Panel a shows the first figure, which appears for 2 sec at thecenter of the computer screen. Panel b shows the second figure, whichappears after 1 sec in the center of the computer screen and then disap-pears after 2 sec. Panel c shows the two figures, which, after 500 msec,are presented simultaneously aligned in the center of the screen.

Participants use a pen to circle as many targets as possible in one minute. The performance scoreis the number of target symbols correctly marked by the participant (maximum score = 80).

In Code Transmission (Manly et al., 2002), another subtest of the Test of Everyday Attentionfor Children, participants are asked to monitor a stream of auditory information (digits),presented at a rate of one digit every 2 sec, for the occurrence of a rare target. Participants have to

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 205

report the digit that appears immediately before a particular target sequence (e.g., 5, 5). The num-ber of targets correctly detected is recorded as a measure of performance accuracy (maximumscore = 40).

In the Visual Perception Test (Hammill, Pearson, & Voress, 1994), subtest 2, participants arepresented with a multiple-choice display consisting of vertically arranged figures and their task isto correctly match a line drawing to one of the figures. In each of 25 items, the wrong alternativesdiffer from the target due to minor changes in orientation or spatial relations between constitutiveelements (maximum score = 25). In subtest 4 of the same test, participants are requested toidentify from 2 to 4 drawings in a confounding context or within overlapping images (maximumscore = 18).

RESULTS

Attention and Visual-Perceptual Abilities

Performance scores of the dyslexic children and the normal readers on tasks of general intelli-gence, word and non-word reading, visual and auditory attention and visual-perceptual abilitiesare reported in Table 1. In both primary- and middle-school subsamples, the two groups ofparticipants (DD and NR) performed similarly on a measure of general intelligence based onvisual data (Raven’s Coloured Progressive Matrices). However, the dyslexics scored consistentlyworse than the normal readers on tasks assessing attention and visual-perceptual abilities. Indeed,except for the Map Mission test for children in primary school and the Visual Perception Test—subtest 2 for children in middle school, differences between groups were statistically significant.

Memory Span

Performance scores of dyslexic and normally reading children on the verbal, visual-object, andvisual-spatial span tasks were analyzed by means of a 2 × 2 × 3 mixed ANOVA with Group (NRvs. DD) and School (Primary vs. Middle school) as between-subject factors and Type of Span(Verbal vs. Visual-spatial vs. Visual-object) as within-subject factor. Results showed significantmain effects of Group, F(1, 96) = 65.4, p < .001, due to overall higher scores of normal readers(M = 10.9 ± 3.7) compared to dyslexics (M = 6.9 ± 1.9), and Type of Span, F(2, 192) = 141.5,p < .001, due to the participants’ higher scores on the Visual-spatial task (M = 12.3 ± 5.3) thanon the Visual-object task (M = 7.5 ± 3.7; p < .0001) which, in turn, were higher than on theVerbal task (M = 6.8 ± 1.6; p < .05). The Group × Type of Span interaction was also significant,F(1,96) = 20.2, p < .001. Indeed, even though the normal readers obtained higher scores thanthe dyslexic children on all three span tasks (Verbal, F(1,96) = 5.9, p = .02; Visual-object,F(1,96) = 35.1, p < .001; Visual-spatial, F(1,96) = 26.4, p < .001), the group difference wassignificantly higher on the Visual-object than on the Verbal task, F(1,96) = 14.6, p < .001, andon the Visual-spatial than on the Verbal task, F(1,96) = 25.0, p< .001. The School effect, F(1,96)= 1.0, the Group × School interaction, F(1,96) = 0.1, the School × Type of Span interaction,F(2,192) = 0.4, and the Group × School × Type of Span interaction, F(2,192) = 0.2, were not

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

TAB

LE1

Neu

rops

ycho

logi

calA

sses

smen

tCom

paris

ons

ofC

hild

ren

With

Dev

elop

men

talD

ysle

xia

and

Nor

mal

Rea

ders

inP

rimar

yor

Mid

dle

Sch

ool

Gro

upG

roup

Pri

mar

ySc

hool

Mid

dle

Scho

ol

Dys

lexi

csN

orm

alR

eade

rsF

-Tes

tD

ysle

xics

Nor

mal

Rea

ders

F-T

est

Mea

sure

MSD

MSD

F-s

core

pM

SDM

SDF

-sco

rep

WIS

C–R

VIQ

a10

1.0

12.8

93.9

10.1

PIQ

a11

1.3

13.8

108.

513

.1FS

IQa

106.

212

.310

0.6

9.8

CP

Mb

27.0

4.2

27.9

3.7

0.60

ns30

.82.

630

.83.

20.

01ns

Wor

dR

eadi

ngE

rror

sc13

.28.

42.

11.

437

.0<

.001

8.9

6.6

0.7

0.7

66.4

<.0

01Sp

eedd

205.

094

.890

.722

.630

.5<

.001

145.

855

.960

.510

.018

<.0

01N

on-W

ord

Rea

ding

Err

orsc

15.1

5.5

4.4

3.0

36.7

<.0

0111

.16.

22.

51.

345

.1<

.001

Spee

dd12

4.6

52.4

74.3

3.0

54<

.001

101.

545

.145

.110

.885

.5<

.001

Att

enti

onA

sses

smen

tM

apm

issi

onb

31.3

8.3

33.6

7.6

1.0

ns40

.69.

146

.77.

96.

8<

.05

Cod

etr

ansm

issi

onb

32.5

6.0

37.6

2.1

14.5

<.0

135

.34.

138

.22.

68.

3<

.01

Vis

ual-

Per

cept

ion

Ass

essm

ent

VPT

-Sub

test

2b20

.14.

022

.43.

04.

9<

.05

22.1

3.3

23.4

1.4

3.0

nsV

PT-S

ubte

st4b

13.1

2.4

15.0

1.4

10.7

<.0

113

.12.

915

.91.

617

.6<

.01

WIS

C-R

=W

echs

ler

Inte

llige

nce

Scal

efo

rC

hild

ren–

Rev

ised

;V

IQ=

Ver

bal

Inte

llige

nce

Quo

tient

;PI

Q=

Perf

orm

ance

Inte

llige

nce

Quo

tient

;FS

IQ=

Full

Scal

eIn

telli

genc

eQ

uotie

nt;C

PM=

Col

oure

dPr

ogre

ssiv

eM

atri

ces;

VPT

=V

isua

lPer

cept

ualT

est.

Prim

ary

scho

olgr

oup

cons

iste

dof

28ch

ildre

nw

ithD

evel

opm

enta

lD

ysle

xia

and

22N

orm

alR

eade

rs.

Mid

dle

scho

olgr

oup

cons

iste

dof

26ch

ildre

nw

ithD

evel

opm

enta

lDys

lexi

aan

d24

Nor

mal

Rea

ders

.a St

anda

rdSc

ores

.bR

awSc

ores

.c Num

ber

ofer

rors

outo

f11

2w

ords

.dM

easu

rem

enti

nse

cond

s.c N

umbe

rof

erro

rsou

tof

48no

n-w

ords

.

206

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 207

significant. Univariate analyses contrasting the performance of the two groups of participants inthe two schools separately revealed that the normal readers scored significantly higher than thedyslexics on all span tasks. In particular, in the Primary school sample the normal readers scoredsignificantly higher than the dyslexics on the Verbal task, M = 7.3 ± 1.1 vs. M = 5.7 ± 1.6,F(1,48) = 16.7, p< .001, the Visual-object task, M = 9.6 ± 3.9 vs. M = 5.2 ± 1.7, F(1,48) =27.1, p < .001, and the Visual-spatial task, M = 14.7 ± 6.2 vs. M = 9.2 ± 2.9, F(1,48) = 17.9,p < .001. In the middle-school sample, significant differences were also found on the Verbal task,F(1,48) = 9.8, p< .01, the Visual-object task, F(1,48) = 31.5, p < .001, and the Visual-spatialtask, F(1,48) = 26.2, p < .001, with the normal readers (respectively, M = 7.8 ± 1.5; M = 10.0± 4.1; M = 15.7 ± 5.5) scoring consistently higher than the dyslexic children (M = 6.5 ± 1.4;M = 5.1 ± 1.5; M = 9.7 ± 2.4).

To control for any confounding effects exerted by attentional and visual-perceptual abilities onspan task performance, in a new analysis of the span data performance scores on Map Mission,Code Transmission, and subtests 2 and 4 of the Visual Perception Test were entered as covariates.Results of the contrasts involving the Group and School factors did not substantially change:Group, F(1,94) = 42.0, p < .001, Group × Type of Span interaction, F(2,188) = 16.9, p < .001;School, F(1,94) = 0.1; Group × School, F(1,94) = 0.01.

By analyzing the standardized z-scores of individual participants on the span tasks based onthe means and standard deviations of the normally reading children, it emerged that the deficitin the dyslexic group was not limited to just a few children but affected a substantial proportionof them. Indeed, 27/54 (50%), 38/54 (70%), and 24/54 (44%) of the dyslexic children scoredlower than 1 SD below the mean of the normal readers on the verbal, visual-object, and visual-spatial span tasks, respectively. By contrast, only 6/46 (13%), 10/46 (26%), and 8/46 (17%) ofthe normal readers scored in this range.

DISCUSSION

The main result of the present study is that a group of dyslexic children (ranging in age from8 to 13 years) obtained lower scores than a group of age-matched normal readers not only ona task of verbal span but also on span tasks assessing the short-term retention of sequencesof abstract figures and spatial positions. This pattern of results did not vary as a function ofchildren’s age. Indeed, we obtained substantially the same results when the data analysis wasconfined to children in the last three years of primary school or the first three years of middleschool. These results are at variance with the theory that dyslexic children have an isolated verbalWM deficit, possibly secondary to a deficit of phonological processing or as the expression ofa dysfunctional Articulatory Loop (Jeffries & Everatt, 2004; Kibby et al., 2004). By contrast,they are in keeping with previous data showing deficits in dyslexic individuals in the temporarystorage of visual as well as verbal material (Smith-Spark et al., 2003; Smith-Spark & Fisk, 2007).

The dyslexic children performed worse than the normally reading children also on tasksassessing attentional and visual-perceptual abilities. The finding of reduced visual processingabilities in DD is not new (for a review see Stein & Walsh, 1997). Indeed, converging resultsconsistently support the hypothesis of a relationship between DD and poor performance onvisual-spatial and motion perception tasks (Felmingham & Jakobson, 1995; Talcott, Hansen,Assoku, & Stein, 2000). A reduced capacity to allocate visual and auditory attention has also

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

208 MENGHINI, FINZI, CARLESIMO, VICARI

been documented in dyslexic individuals (e.g., Facoetti, Paganoni, Turatto, Marzola, & Mascetti,2000). It should be noted, however, that in the present study the short-term memory deficit dis-closed by the dyslexic children could not be accounted for by concomitant deficits of attentionand visual-perceptual abilities. Indeed, significant group differences between dyslexic and nor-mally reading children on the three span tasks still held after controlling performance on thecognitive tasks tapping these abilities.

In light of Baddeley’s model, the reduced performance of dyslexic individuals on memoryspan tasks involving both verbal and visual data can be interpreted as resulting from the simul-taneous impairment of both the articulatory loop and the visual-spatial sketchpad components ofthe WM system or, alternatively, as an expression of deficient functioning of the central executivecomponent of the system.

Our data do not provide a strong case for the hypothesis that a deficit in the functioning of thevisual-spatial sketchpad is at the base of the reduced visual spans in dyslexic individuals. Indeed,even though the deficits of dyslexic children on visual-perceptual tasks might suggest that adeficit in encoding visual stimuli interfered with their storage in the visual-spatial sketchpad, thesignificant difference between dyslexic and normally reading children on the visual span tasksstill held after controlling performance on the visual-perceptual tasks. From a neurobiologicalperspective, the distributed cortical representations of cerebral areas devoted to the short-termretention of different materials make it unlikely that localized brain dysfunction could affect all ofthem simultaneously. Indeed, lesional and functional neuroimaging data in humans indicate thatthe neural circuits specifically dedicated to the various slave systems are basically independent.In particular, there is a striking material-dependent hemispheric specialization in the storage ofverbal data and visual material (Wager & Smith, 2003). Moreover, in the posterior regions of theright hemisphere distinct areas in the temporal and parietal lobes are involved in the temporarystorage of visual-object and visual-spatial information (Stuss & Alexander, 2007).

As our tasks do not require integrating information from different modalities (visual, spa-tial, and verbal) it cannot be assumed that a deficit in the episodic buffer is at the origin of theWM deficits found in the dyslexic children. In fact, we agree with Zimmer, Speiser, and Seidler(2003) that the episodic buffer is involved in retrieving multi-componential information about anitem, its features and its location. Differently, when a single component of information has to beprocessed in a WM task, such as ours, only peripheral slave systems are involved.

A more parsimonious account of the deficit involving the temporary storage of both verbal andvisual information assumes that there is reduced availability of processing resources in the centralexecutive component of the WM system in dyslexic individuals. Indeed, in the functional archi-tecture of WM, the central executive coordinates various slave systems, integrating their storagecapacities and making available attentional resources for online processing of incoming informa-tion. Failure of the central executive to supervise the activity of both peripheral “slave” systems(i.e., the articulatory loop and the visual-spatial sketchpad) could fully account for impairmenton both verbal and visual-spatial span tasks. As previously noted, experimental data exist thatsupport the role of reduced functioning of the central executive system in the deficits of dyslexicindividuals on visual-spatial tasks. In particular, Smith-Spark and co-workers (2003) documenteda visual-spatial span deficit in dyslexic individuals only when the task called for high memoryupdating; and Swanson and Sachse-Lee (2001) reported that the performance of dyslexic individ-uals and controls on verbal and visual-spatial tasks no longer differed once executive ability wascontrolled for. Related to the claim of a deficit of processing resources in the central executiveis the hypothesis of an automatization deficit in dyslexics. Nicolson and Fawcett (1995; see also

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 209

Moores, Nicolson, & Fawcett, 2002) proposed that impairment of automatizing skills is a centraldeficit in DD. Specifically, in the case of low cognitive load these individuals compensate theirimpairments by means of conscious processes, but in experimental conditions that tax attentionalresources (e.g., in the case of high updating loads) deficits in automatization and fluency becomeevident and dyslexic children’s performance worsen. In fact, as previously noted, in this studyspan tasks were selected that do not tax the resources of the central executive. In fact, the chil-dren were simply requested to report the sequence of verbal or visual items without any furthercognitive elaboration. Moreover, as the delay interval between sequence presentation and recallwas extremely short (500 msec), it is unlikely that the central executive contributed to sequencemaintenance. Inconsistent with the hypothesis that a central executive impairment was respon-sible for the span deficit in our group of dyslexic children is the fact that they performed worseon the span tasks that were easiest for the normal readers. Indeed, the largest difference in per-formance level between the dyslexic and the normally reading children was on the visual-spatialspan that, on the other side, was the task on which our experimental sample obtained the high-est scores. Finally, the significant difference between the dyslexics and the normal readers onthe span tasks cannot be explained by their performance on the visual and auditory attentiontasks (which, instead, presumably taxed the cognitive resources of the central executive). Indeed,although the dyslexic children scored worse than the normal readers on the visual and auditoryattention tasks, there was still a significant difference between groups on all span tasks, evenwhen attention task performance were entered as covariates in the statistical analysis.

An alternative account of the pervasive impairment of the dyslexic children on our verbaland visual short-term memory tasks has to do with their difficulty on sequencing tasks. Indeed,studies on motor timing have documented sequencing behavior deficits in dyslexic individuals.In particular, the performance of these children seemed particularly impaired during the repro-duction of tasks that involved tapping complex rhythms (Tiffin-Richards, Hasselhorn, Richards,Banaschewski, & Rothenberger, 2004), and sequence learning deficits in dyslexic individualshave been demonstrated using different experimental procedures, such as visual-spatial andmotor tasks or procedural learning tasks (Menghini et al., 2006; Nicolson et al., 1999; Vicariet al., 2003, 2005). Indeed, all the short-term memory tasks used in the present study requiredencoding and successively reproducing the items in the exact temporal sequence they were pre-sented in. Memory of the temporal sequence was particularly emphasized in the visual tasks.In fact, in the verbal task participants had to recall both the item and the order of presenta-tion, whereas in the visual-object and the visual-spatial task the children had to reproduce onlythe exact sequential order of the stimuli. The emphasis of our visual span tasks on sequentialmemory is unique in the literature investigating the issue of visual span in dyslexic individuals.Indeed, in previous studies dyslexics and controls were first given a sequence of spatial loca-tions and then presented with the entire spatial grid (typically a 4 × 4 or a 5 × 5 array) andrequested to recall both the item and the sequential order of the presentation (e.g., Jeffries &Everatt, 2004; Kibby et al., 2004; Smith-Spark et al., 2003). Interestingly, in these studies thedyslexic individuals performed at the same level as the normal readers. Also in Smith-Sparkand co-workers’ study (2003), dyslexics and normal readers performed similarly on this kind oftask and a significant difference emerged only when the updating load of the memory task wasincreased, thus taxing the resources in the central executive system. To reconcile these contrast-ing results, it can be hypothesized that dyslexic individuals are not particularly impaired in theshort-term memory of spatial positions but show deficits in encoding and/or short-term retentionof temporal sequences of events. The more the task emphasizes memory of the sequential order

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

210 MENGHINI, FINZI, CARLESIMO, VICARI

(as was the case in our visual tasks) the worse these individuals perform. Instead, when lessemphasis is placed on serial order memory and the task mainly requires remembering spatial (orother item) features, then these individuals may perform at average or near average levels. Thisinterpretation of the discrepant data between the current and previous studies is obviously con-jectural, based on the indirect comparison of experimental procedures that were not conceivedto be “process pure,” that is, which did not fully separate memory of the item from memory ofthe sequential order of the stimuli. Further studies are needed in which experimental conditionsare manipulated in the same experimental sample to separately assess the ability of dyslexicindividuals to remember the visual/spatial features of the stimuli or the sequential order of theirpresentation.

Notably, the sequencing deficit of dyslexics could be related to dysfunction of cerebellar cir-cuits. Indeed, among the different theories on cerebellar functions (Bower & Parsons, 2003) ithas been proposed that the cerebellum has a role in sequencing incoming sensory patterns andoutgoing responses (Braitenberg, Heck, & Sultan, 1997). In fact, deficits in learning sequencesof events in patients with cerebellar lesions are well documented (e.g., Leggio et al., 2008).The cerebellar contribution to sequence learning might be its role in recognizing discordancesbetween input from the deviant event and sensory memory representation of the regular aspectsof sequence stimulation (Restuccia, Della, Valeriani, Leggio, & Molinari, 2007; Tesche & Karhu,2000). We realize that any attempt to identify the brain structure specifically involved in the WMdeficit displayed by dyslexic children would be entirely speculative. Nevertheless, cerebellarabnormalities in dyslexic individuals have been reported in several anatomical and functionalstudies (Laycock et al., 2008; Nicolson et al., 1999; Menghini et al., 2006). Therefore, in futurestudies it would be interesting to investigate whether the cerebellum has a role in influencing theWM abilities of dyslexic individuals. However, the cerebellum, may not be the only brain struc-ture associated with the WM deficit found in dyslexic children. In view of the frontal deficitsobserved in dyslexics (for a review see Gabrieli, 2009) and repeated confirmations of the role ofprefrontal brain areas in sequence learning (Rauch et al., 1995; Willingham, Salidis, & Gabrieli,2002), we must consider that the sequencing deficits in DD may be related to a dysfunction ofpremotor.

One limitation of the present study is that the intellectual abilities of normal readers werenot evaluated with a verbal intelligence scale. In particular, the unavailability of verbal and per-formance IQs for these children precluded controlling for these variables in the comparison ofdyslexics’ and normal readers’ performance on the span tasks. Another limitation of this study isthe lack of neuroimaging data, which made it impossible to directly evaluate neuropsychologicalperformance in light of structural and functional brain measures.

In conclusion, we report evidence that dyslexic children suffer from reduced memory spansnot only for verbal material, as predicted by the “core phonological deficit” hypothesis, but alsofor visual-object and visual-spatial material. The attentional and visual-perceptual difficultiespresent in our sample of dyslexic children cannot account for this deficit. Although direct involve-ment of the visual-spatial sketchpad or the central executive components of the WM systemcould be at the base of the pervasive deficit of short-term memory in these individuals, our datado not provide a direct confirmation. The role of a more basic impairment in temporal sequenc-ing, which might interfere with performance on tasks requiring the ordered recall of sequencesof stimuli, is a possibility that must be explored directly by contrasting performance on tasksrequiring and on tasks not requiring memory of the sequence order.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 211

REFERENCES

American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington,DC: Author.

Baddeley, A. D. (1978). The trouble with levels: A reexamination of Craik and Lockhart’s framework for memoryresearch. Psychological Review, 85, 139–152.

Baddeley, A. D. (2000). The episodic buffer: A new component of WM? Trends in Cognitive Science, 4, 417–423.Baddeley, A. D. (2001). Is working memory still working? American Psychologist, 56, 851–864.Baddeley, A. D., & Hitch, G. (1974).Working memory. In G. H. Bower (ed.), The psychology of learning and motivation:

Advances in research and theory (vol. 8, pp. 47–89). New York: Academic Press.Bower, J. M., & Parsons, L. M. (2003). Rethinking the “lesser brain.” Scientific American, 289, 50–57.Bowers, P. G., & Wolf, M. (1993). Theoretical links among naming speed, precise timing mechanisms and orthographic

skill in dyslexia. Reading and Writing, 51, 69–85.Braitenberg, V., Heck, D., & Sultan, F. (1997). The detection and generation of sequences as a key to cerebellar function:

Experiments and theory. Behavioral and Brain Sciences, 20, 229–277.Cohen-Mimran, R., & Sapir, S. (2007). Deficits in working memory in young adults with reading disabilities. Journal of

Communication Disorders, 40, 168–183.Cornoldi, C., Gardinale, M., Masi, A., & Pettenò, T. (1996). L’ Impulsività e autocontrollo. Impulsività ed autocontrollo,

Interventi e tecniche metacognitive. Trento: Erickson.Facoetti, A., Paganoni, P., Turatto, M., Marzola, V., & Mascetti, G. G. (2000). Visual-spatial attention in developmental

dyslexia. Cortex, 36, 109–123.Fawcett, A. J., & Nicolson, R. I. (1992). Automatisation deficits in balance for dyslexic children. Perceptual and Motor

Skills, 75, 507–529.Felmingham, K. L., & Jakobson, L. S. (1995). Visual and visuomotor performance in dyslexic children. Experimental

Brain Research, 106, 467–474.Gabrieli, J. D. (2009). Dyslexia: A new synergy between education and cognitive neuroscience. Science, 325, 280–283.Galaburda, A. M., Sherman, G. F., Rosen, G. D., Aboitiz F., & Geschwind, N. (1985). Developmental dyslexia: Four

consecutive patients with cortical anomalies. Annals of Neurology, 18, 222–233.Gathercole, S. E., Alloway, T. P., Willis, C., & Adams, A. M. (2006). Working memory in children with reading

disabilities. Journal of Experimental Child Psychology, 93, 265–281.Hammill, D., Pearson, N., & Voress, J. (1994). TPV. Test di percezione visiva e integrazione visuo-motoria. Trento:

Erickson.Howes, N. L., Bigler, E. D., Lawson, J. S., & Burlingame, G. M. (1999). Reading disability subtypes and the Test of

Memory and Learning. Archives of Clinical Neuropsychology, 14, 317–339.Jeffries, S., & Everatt, J. (2004). Working memory: Its role in dyslexia and other specific learning difficulties. Dyslexia,

10, 196–214.Jorm, A. F. (1983). Specific reading retardation and working memory: A review. British Journal of Psychology, 74,

311–342.Kibby, M. Y., Marks, W., Morgan, S., & Long, C. J. (2004). Specific impairment in developmental reading disabilities:

A working memory approach. Journal of Learning Disability, 37, 349–363.Laycock, S. K., Wilkinson, I. D., Wallis, L. I., Darwent, G., Wonders, S. H., Fawcett, A. J., et al. (2008). Cerebellar

volume and cerebellar metabolic characteristics in adults with dyslexia. Annals of the New York Academy of Sciences,1145, 222–236.

Leggio, M. G., Tedesco, A. M., Chiricozzi, F. R., Clausi, S., Orsini, A., & Molinari M. (2008). Cognitive sequencingimpairment in patients with focal or atrophic cerebellar damage. Brain, 131, 1332–1343.

Lindgren, D. S., De Renzi, E., & Richman, L. C. (1985). Cross-national comparison of developmental dyslexia in Italyand the United States. Child Developmental, 56, 1404–1417.

Manly, T., Nimmo-Smith, I., Watson, P., Anderson, V., Turner, A., & Robertson, I. H. (2002). The differential assess-ment of children’s attention: The Test of Everyday Attention for Children (TEA-Ch), normative sample and ADHDperformance. Journal of Child Psychology and Psychiatry, 42, 1065–1081.

McDougall, S., Hulme, C., Ellis, A., & Monk, A. (1994). Learning to read: The role of short-term memory andphonological skills. Journal of Experimental Child Psychology, 58, 112–133.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

212 MENGHINI, FINZI, CARLESIMO, VICARI

Menghini, D., Hagberg, G. E., Caltagirone, C., Petrosini, L., & Vicari, S. (2006). Implicit learning deficits in dyslexicadults: An fMRI study. Neuroimage, 33, 1218–1226.

Moores, E., Nicolson, R. I., & Fawcett, A. J. (2002). Attention deficits in dyslexia: Evidence for an automatisation deficit?European Journal of Cognitive Psychology, 15, 321–348.

Nicolson, R. I., & Fawcett, A. J. (1990). Automaticity: A new framework for dyslexia research? Cognition, 35, 159–182.Nicolson, R. I., & Fawcett, A. J. (1995). Dyslexia is more than a phonological disability. Dyslexia: An International

Journal of Research and Practice, 1, 19–37.Nicolson, R. I., Fawcett, A. J., Berry, E. L., Jenkins, I. H., Dean, P., & Brooks, D. J. (1999). Association of abnormal

cerebellar activation with motor learning difficulties in dyslexic adults. Lancet, 353, 1662–1667.Nicolson, R. I., Fawcett, A. J., & Dean, P. (2001). Developmental dyslexia: The cerebellar deficit hypothesis. Trends in

Neurosciences, 24, 508–511.Olson, R., & Datta, H. (2002). Visual-temporal processing in reading-disabled and normal twins. Reading and Writing,

15, 127–149.Paulesu, E., Demonet, J. F., Fazio, F., McCrory, E., Chanoine, V., Brunswick, N., et al. (2001). Dyslexia: Cultural

diversity and biological unity. Science, 291, 2165–2167.Rauch, S. L., Savage, C. R., Brown, H. D., Curran, T., Alpert, N. M., Kendrick, A., et al. (1995). A PET investigation of

implicit and explicit sequence learning. Human Brain Mapping, 3, 271–286.Raven, J. C. (1994). CPM, Coloured Progressive Matrices, series A, AB, B. Firenze: Giunti O.S. Organizzazioni Speciali.Restuccia, D., Della, M. G., Valeriani, M., Leggio, M. G., & Molinari, M. (2007). Cerebellar damage impairs detection

of somatosensory input changes. A somatosensory mismatch-negativity study. Brain, 130, 276–287.Roodenrys, S., Koloski, N., & Grainger, J. (2001). Working memory function in attention deficit hyperactivity disordered

and reading disabled children. British Journal of Developmental Psychology, 19, 325–337.Sartori, G., Job, R., & Tressoldi, P. E. (1995). Batteria per la valutazione della dislessia e della disortografia evolutiva.

Firenze: Giunti O.S. Organizzazioni Speciali.Shaywitz, S. E. (1998). Dyslexia. The New England Journal of Medicine, 29, 307–312.Smith, E. E., Jonides, J., Koeppe, R. A., Awh, E., Schumacher, E. H., & Minoshima, S. (1995). Spatial versus object

working memory: PET investigations. Journal of Cognitive Neuroscience, 7, 337–356.Smith-Spark, J. H., & Fisk, J. F. (2007). Working memory functioning in developmental dyslexia. Memory, 15, 34–56.Smith-Spark, J. H., Fisk, J. E., Fawcett, A. J., & Nicolson, R. I. (2003). Investigating the central executive in adult dyslex-

ics: Evidence from phonological and visuospatial working memory performance. European Journal of CognitivePsychology, 15, 567–587.

Snowling, M. J. (2000). Dyslexia: A cognitive-developmental perspective. Oxford: Blackwell.Stein, J., & Walsh, V. (1997). To see but not to read; the magnocellular theory of dyslexia. Trends of Neuroscience, 20,

147–152.Stuss, D. T., & Alexander, M. P. (2007). Is there a dysexecutive syndrome? Philosophical Transactions of the Royal

Society London B: Biological Sciences, 362, 901–915.Swanson, H. L. (1991). Operational definitions and learning disabilities: An overview. Learning Disability Quarterly,

14, 242–254.Swanson, H. L., & Sachse-Lee, C. (2001). A subgroup analysis of working memory in children with reading disabilities:

Domain-general or domain-specific deficiency? Journal of Learning Disability, 34, 249–263.Talcott, J. B., Hansen, P. C., Assoku, E. L., & Stein, J. F. (2000). Visual motion sensitivity in dyslexia: Evidence for

temporal and energy integration deficits. Neuropsychologia, 7, 935–943.Tesche, C. D., & Karhu, J. T. (2000). Anticipatory cerebellar responses during somatosensory omission in man. Human

Brain Mapping, 9, 119–142.Tiffin-Richards, M. C., Hasselhorn, M., Richards, M. L., Banaschewski, T., & Rothenberger, A. (2004). Time reproduc-

tion in finger tapping tasks by children with attention-deficit hyperactivity disorder and/or dyslexia. Dyslexia, 10,299–315.

Vicari, S. (2007). Promea, Prove di Memoria e Apprendimento per l’Età Evolutiva. Firenze: Giunti O.S. OrganizzazioniSpeciali.

Vicari, S., Bellucci, S., & Carlesimo, G. A. (2006). Evidence from two genetic syndromes for the independence of spatialand visual working memory. Developmental Medicine and Child Neurology, 48, 126–131.

Vicari, S., Finzi, A., Menghini, D., Marotta, L., Baldi, S., & Petrosini, L. (2005). Do children with developmental dyslexiahave an implicit learning deficit? Journal of Neurology, Neurosurgery and Psychiatry, 76, 1392–1397.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011

WORKING MEMORY DEFICITS IN DEVELOPMENTAL DYSLEXIA 213

Vicari, S., Marotta, L., Menghini, D., Molinari, M., & Petrosini, L. (2003). Implicit learning deficit in children withdevelopmental dyslexia. Neuropsychologia, 41, 108–114.

Wager, T. D., & Smith, E. E. (2003). Neuroimaging studies of working memory: A meta-analysis. Cognitive, Affective,Behavioral Neuroscience, 3, 255–274.

Wechsler, D. (1993). Wechsler Intelligence Scale for Children–Revised (WISC–R). Firenze: Giunti O.S. OrganizzazioniSpeciali.

White, S., Milne, E., Rosen, S., Hansen, P., Swettenham, J., Frith, U., et al. (2006). The role of sensorimotor impairmentsin dyslexia: A multiple case study of dyslexic children, Developmental Science, 9, 237–269.

Willingham, D. B., Salidis, J., & Gabrieli, J. D. (2002). Direct comparison of neural systems mediating conscious andunconscious skill learning. Journal of Neurophysiology, 88, 1451–1460.

Wolf, M., & Bowers, P. (1999). The “Double-Deficit Hypothesis” for the developmental dyslexias. Journal ofEducational Psychology, 91, 1–24.

Wolf, M., Bowers, P. G., & Biddle, K. (2000). Naming-speed processes, timing, and reading: A conceptual review.Journal of Learning Disabilities, 33, 387–407.

Zimmer, H. D., Speiser, H. R., & Seidler, B. (2003). Spatio-temporal working-memory and short-term object-locationtasks use different memory mechanisms. Acta Psychologica, 114, 41–65.

Downloaded By: [Osp Pediatrico Bambino Ges] At: 11:19 28 February 2011