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A review on eye movement studies in childhood and adolescent psychiatry

Nanda N.J.Rommelse a,b,*,Stefan Van der Stigchel c ,Joseph A.Sergeant b

Department of Psychiatry,Radboud University Medical Center,Reinier Postlaan 12,6525GC Nijmegen,The Netherlands b

Department of Clinical Neuropsychology,VU University-Amsterdam,Amsterdam,The Netherlands c

Department of Experimental Psychology,Utrecht University,Utrecht,The Netherlands

a r t i c l e i n f o Article history:

Accepted 26August 2008

Available online 2October 2008Keywords:Child

Adolescent Psychiatry

Eye movement Saccade

a b s t r a c t

The neural substrates of eye movement measures are largely known.Therefore,measurement of eye movements in psychiatric disorders may provide insight into the underlying neuropathology of these dis-orders.Visually guided saccades,antisaccades,memory guided saccades,and smooth pursuit eye move-ments will be reviewed in various childhood psychiatric disorders.The four aims of this review are (1)to give a thorough overview of eye movement studies in a wide array of psychiatric disorders occurring dur-ing childhood and adolescence (attention-de?cit/hyperactivity disorder,oppositional deviant disorder and conduct disorder,autism spectrum disorders,reading disorder,childhood-onset schizophrenia,Tourette’s syndrome,obsessive compulsive disorder,and anxiety and depression),(2)to discuss the spec-i?city and overlap of eye movement ?ndings across disorders and paradigms,(3)to discuss the develop-mental aspects of eye movement abnormalities in childhood and adolescence psychiatric disorders,and (4)to present suggestions for future research.In order to make this review of interest to a broad audience,attention will be given to the clinical manifestation of the disorders and the theoretical background of the eye movement paradigms.

1.Aims and structure of this review 1.1.Aims

Eye movements are perhaps the most thoroughly studied do-main in the ?eld of cognitive neuroscience.Numerous ingenious paradigms have been developed to unravel their underlying neuro-logical and cognitive substrates.Current knowledge of these pro-cesses has been obtained by measuring eye movements in monkeys and healthy adults.These studies have provided detailed knowledge of the basic characteristics of eye movements.This,in turn,has prompted researchers to assess eye movements in vari-ous psychiatric disorders and has facilitated the understanding of the complex underlying neuropathophysiology of these disorders.Most of these studies have focused on eye movements in adult pa-tients.These ?ndings may not necessarily be extrapolated to child and adolescent patients,since the clinical manifestation and aetiol-ogy of psychiatric disorders may differ between childhood-onset and adult-onset (Carlson,Bromet,&Sievers,2000;Jaffee et al.,2002;Matsumoto et al.,2001).Moreover,eye movements them-selves may differ substantially between children and adults (Karatekin,2007;Mezzalira,Coelho Neves,Queiroz Maudonnet,o

Bilécki,&Gobbi de ávila,2005).It seems important,therefore,to review separately eye movement studies in childhood and adoles-cent psychiatric disorders to determine which eye movement dys-functions are present in these patients.

Several reviews are available on eye movement studies in adult patients (often focused on a particular disorder or eye movement paradigm;Hutton &Ettinger,2006;Lee &Williams,2000;Reuter &Kathmann,2004;Trillenberg,Lencer,&Heide,2004),whereas only two reviews are available on child and adolescent patients (Karatekin,2007;Sweeney,Takarae,Macmillan,Luna,&Minshew,2004).Both reviews were instructive in reviewing the literature on attention-de?cit/hyperactivity disorder (ADHD)and autism spec-trum disorders (ASD)American Psychiatric Association [APA](1994),but eye movement literature on Tourette’s syndrome (TS)and childhood-onset schizophrenia was reviewed in only one of these papers,and neither review focused on childhood-onset obsessive compulsive disorder (OCD),reading disorder (RD),anxi-ety and depression,or oppositional deviant disorder (ODD)and conduct disorder (CD).Therefore,the main aims of the current re-view are (1)to give a thorough overview of eye movement studies in a wide array of psychiatric disorders occurring during childhood and adolescence,(2)to discuss the speci?city and overlap of eye movement ?ndings across disorders,(3)to discuss the develop-mental aspects of eye movement abnormalities in childhood and adolescence psychiatric disorders,and (4)to present suggestions for future research.

*Corresponding author.Address:Department of Psychiatry,Radboud University Medical Center,Reinier Postlaan 12,6525GC Nijmegen,The Netherlands.Fax:+31243512211.

E-mail address:https://www.doczj.com/doc/d48071190.html,mbregts-rommelse@psy.umcn.nl (N.N.J.Rommelse).Brain and Cognition 68(2008)

391–414

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1.2.Structure

Eye movements in psychiatric disorders are of interest to vari-ous professions:cognitive neuroscientists,psychologists,and psy-chiatrists.In order to perform this review and make it of interest to a broad audience,we will brie?y discuss both the background of eye movement paradigms as well as the clinical manifestation of each disorder.For a more thorough discussion of eye movement paradigms,readers are referred to Barnes,this issue(for SPEM) and Hutton,this issue(for saccades).Furthermore,we will try to summarize the most important neurological and cognitive de?cits associated with each disorder,since these?ndings have often guided eye movement studies to focus on a particular topic/direc-tion.This review will focus on antisaccades(AS;see glossary),visu-ally guided saccades(VGS;see glossary),memory guided saccades (MGS;see glossary),and smooth pursuit eye movements(SPEM; see glossary),in order to increase comparability with other articles appearing in this issue.Therefore,eye movement studies on visual search(Theeuwes,Kramer,Hahn,&Irwin,1998;Williams, Reingold,Moscovitch,&Behrmann,1997),picture scanning (Peters,Iyer,Itti,&Koch,2005;Torralba,Oliva,Castelhano,&Hen-derson,2006),and eye movements during reading(Laubrock, Kliegl,&Engbert,2006;Rayner,1998),are not reviewed here.Only those studies are reviewed here that have included children and adolescents(participants of18years and younger).In some stud-ies,the age range included both adolescents and adults.Those studies were only included,if the medium age of the participants was18years or younger.With regard to adult psychiatric popula-tions,saccadic abnormalities are reviewed by Gooding and Basso in this special issue,and SPEM distortions by O’Driscoll.

2.Utility of eye movement recordings in psychiatric disorders

As will become evident in this review,there is a growing body of the literature investigating eye movements in children with psy-chiatric disorders.Recording eye movement paradigms provide various bene?ts over standard procedures.First,relative to reac-tion time data,eye movements provide a much richer data set which allows better understanding of the underlying neurophysio-logical mechanisms.Eye movements,while performing a task,not only provide information regarding the process measured by the task,but also regarding the metrics and dynamics of oculomotor control,such as velocity,duration and trajectories of saccades (see,e.g.,Van der Stigchel,Meeter,&Theeuwes,2006;Smyrnis, this issue).

Second,eye movement tasks are designed to have simple visu-omotor baseline(or control)conditions,e.g.,prosaccades(see glos-sary)for antisaccades.This is important from an a priori experimental point of view and has an important(empirical) advantage over non-eye movement tasks in that certain patient populations(e.g.,schizophrenia)have robust slowing of basic, re?exive manual reaction times but no(or inconsistent)de?cits in re?exive saccadic reaction times.

Third,because the execution of an eye movement is the result of a complex interaction between various cognitive processes,oculo-motor behavior tells us something about these processes and def-icits in these processes.Making an eye movement is an important way of exploring our environment.Therefore,eye movements give some indications on how children experience their daily environ-ment and can increase our knowledge about the various complex behavioral processes underlying psychiatric disorders in children.

Fourth,recent technological advances have made it increasingly easier to record eye movements with a high spatial and temporal resolution.Non-invasive techniques enable eye movement sys-tems to be relatively easily accessible while the precision of mea-surement of modern eye trackers is high.In line with this, remote eye tracking systems are also becoming more accurate. These systems have the advantage that the participant does not have to carry a head-mounted system,which can be heavy for chil-dren,especially if they are also restricted in their head movements.

Fifth,as will be revealed in the next section,eye movement tasks are generally very simple and not dif?cult to perform by chil-dren with psychiatric disabilities.The paradigms discussed in the current review require no advanced cognitive skills such as lan-guage,reading,or complex motor responding.This makes the par-adigms relatively straightforward and easy to explain to participants even at an early age.

Box1.Utility of eye movement recordings in childhood and adolescence psychiatric disorders

Bene?ts of eye movement paradigms over non-eye movement paradigms:

1.Relative to reaction time data,eye movements provide a

much richer data set which allows better understanding

of the underlying neurophysiological mechanisms.

2.Eye movement tasks are designed to have simple visuomo-

tor baseline(or control)conditions,e.g.,prosaccades for

antisaccades,which is important from an a priori experi-

mental point of view and has an important(empirical)

advantage over non-eye movement tasks in that certain

patient populations(e.g.,schizophrenia)have robust slow-

ing of basic,re?exive manual reaction times but no(or

inconsistent)de?cits in re?exive saccadic reaction times.

3.Eye movements give some indications on how participants

experience their daily environment and can increase our

knowledge about the various complex behavioral processes

underlying psychiatric disorders.

4.Recent technological advances have made it increasingly

easier to record eye movements.Techniques are becoming

increasingly accurate and non-invasive,making them

increasingly suitable for recording of eye movements in

children.

5.Eye movement tasks are generally very simple and not dif-

?cult to perform by children(with psychiatric disabilities)

and often require no advanced cognitive skills such as lan-

guage,reading,or complex motor responding.

Conditions under which eye movement paradigms would fur-ther bene?t over non-eye movement paradigms:

1.The underlying brain mechanisms of eye movement para-

digms are well documented in adults.However,much less

is known about the underlying brain mechanisms in chil-

dren and adolescents;increasing knowledge in this area

would allow for affected oculomotor behavior to more reli-

ably pinpoint to speci?c neurological problems in children

and adolescents compared to non-eye movement

paradigms.

2.The normal developmental trajectories in oculomotor

behavior have largely been studied using ad hoc samples

and only few studies have modeled the developmental tra-

jectories appropriately.Well-designed longitudinal studies

would allow for a better understanding of the developmen-

tal trajectories of eye movements.This knowledge would

allow for a more reliable investigation of continuation

and discontinuation in neurobiological parameters of psy-

chiatric disorders,which hypothetically may prove to be

more stable traits than non-eye movement parameters.

392N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

There are two conditions under which eye movement para-digms would further bene?t over non-eye movement paradigms. First,the underlying brain mechanisms of eye movement para-digms are well documented in adults(Hall&Moschovakis,2003; Leigh&Kennard,2004;Munoz,2002;Schall,1991).However, much less is known about the underlying brain mechanisms in children and adolescents.Increasing knowledge in this area would allow for affected oculomotor behavior to more reliably pinpoint to speci?c neurological problems in children and adolescents com-pared to non-eye movement paradigms and may even be used as a diagnostic tool.

Second,the normal developmental trajectories in oculomotor behavior have largely been studied using ad hoc samples and only few studies have modeled the developmental trajectories appropriately.Well-designed longitudinal studies would allow for a better understanding of the developmental trajectories of eye movements.This knowledge would allow for a more reliable investigation of continuation and discontinuation in neurobio-logical parameters of psychiatric disorders,which hypothetically may prove to be more stable traits than non-eye movement parameters.

3.Eye movement paradigms:Measurement and proposed neu-rophysiological underpinnings

Various paradigms have been used to investigate eye move-ments in children with psychiatric disorders.As mentioned ear-lier,the present review discusses four types of saccadic paradigms,namely,AS,VGS,MGS,and SPEM.These paradigms are designed to assess basic oculomotor beha-vior or to measure executive functions,such as inhibition(see glos-sary)and working memory.For a detailed review on the neuro-physiology and neuroanatomy of these paradigms,please see the papers in this special issue(SPEM,Ilg&Thier;Lencer&Trillen-berger;Sharpe;Saccades,Johnston&Everling;McDowell and col-leagues;Mueri&Nyffeler).

3.1.Antisaccades(AS)

In AS a visual onset is presented and observers are required to make an eye movement away from the onset location to its mirror position(Everling&Fischer,1998;Hallet,1978;Munoz&Everling, 2004).AS have longer latencies than saccades towards the onset and observers frequently make erroneous saccades towards the onset location.Successful performance on AS requires two pro-cesses:the top-down inhibition of a re?exive saccade(see glos-sary)to the onset location,and the execution of a voluntary eye movement to the mirror location of the onset.Typical measures in AS are the number of directional errors(re?ecting inhibitory problems:a failure to suppress an inappropriate response due to problems with top-down regulation)and saccade latency.

Neuropsychological research has revealed an important role for frontal areas in this task.For instance,imaging studies have iden-ti?ed various frontal areas that are more active during AS than dur-ing VGS,like the frontal eye?elds(see glossary),dorsolateral prefrontal cortex(DLPFC;see glossary),and the supplementary eye?elds(Everling&Munoz,2000;Funahashi,Chafee,&Gold-man-Rakic,1993).Directional errors are,therefore,generally linked to frontal dysfunctions.

3.2.Visually guided saccades(VGS)

In VGS,participants are instructed to make an eye movement to a visual stimulus presented in the periphery.This task is generally included to investigate the basic dynamics of an eye movement and is in most cases included as a baseline condition in AS or MGS.Typical measures are saccade latency,variability in latency, amplitude,under-versus overshoot,peak velocity,and duration.

Deviations in these measures of saccade metrics can pinpoint to de?cits in the neurological substrate of eye movements,such as the cerebellum(see glossary)or the frontal eye?elds(Leigh& Zee,1999).Saccade latency is,for instance,regarded as a measure of the speed of visual processing,whereas variability in latency in-dexes the regulating processes of saccade initiation.

3.3.Memory guided saccades(MGS)

In MGS,participants are instructed to look at a central?xation (see glossary)point.During this?xation,a target appears at a loca-tion in the peripheral visual?eld.The participant is not allowed to make a saccade towards the target but has to remember the loca-tion of the target.When the?xation point disappears,the partici-pant is required to make a saccade towards the memorized location.The time between the disappearance of the target and the moment the participant is allowed to make a saccade(delay period)can be varied in order to vary the visuo-spatial working memory(see glossary)load.Typical measures in MGS are accuracy (re?ecting how well the participant has remembered the location of the target),the number of anticipatory errors(re?ecting inhibi-tory problems),and saccade latency.

The neurological substrates underlying performance on the memory guided saccade task are well established:in addition to the brain areas active in basic oculomotor control,memory guided saccades activate the DLPFC,anterior cingulate(see glossary),and supplementary eye?eld(see glossary;Ettinger et al.,2005; Sawaguchi&Iba,2001;Sweeney et al.,1996).Based on these?nd-ings,de?cits in the MGS are related to frontal functioning.

3.4.Smooth pursuit eye movements(SPEM)

SPEM involve the smooth oculomotor tracking of a small object in motion with a constant(slow)speed.In order to execute correctly the task,the velocity of this non-ballistic movement has to be con-tinuously adapted to the velocity of the object.The most widely measured variable in SPEM is gain(see glossary),calculated as the ratio of eye velocity to target velocity,which can indicate dif?culties in matching gaze to target velocity.Other measures exist,such as root mean square error(the difference between target and gaze po-sition)and the number of compensatory and intrusive saccades.If the eyes do not reproduce the target motion,the saccadic system has to compensate for this error which can be indexed by the num-ber of saccades necessary to catch-up with the moving object.

SPEM have a strong emphasis on basic oculomotor control and less on cognitive processes.The neurophysiological correlates of the pursuit system overlap with that of saccadic movements and both systems work in an integrative way(Fukushima,2003).If def-icits in SPEM are observed,it is dif?cult to pinpoint speci?c brain areas that are causing the effect,because a widespread network is responsible for correct SPEM performance.Therefore,problems in SPEM are generally not linked to speci?c neurological and/or cognitive de?cits but to fundamental de?ciencies in the function-ing of the pursuit system.

4.Overview of eye movement studies in childhood and adolescent psychiatric disorders

A summary of all the reviewed studies concerning patient char-acteristics(diagnosis,age,and gender),eye movement paradigm, analyzed dependent measures,and results is provided in Table1. All clinical descriptions are according to APA(1994),unless speci-?ed otherwise.

N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414393

4.1.Attention-de?cit/hyperactivity disorder(ADHD)

4.1.1.Clinical manifestation of ADHD

ADHD is one of the most common psychiatric conditions of childhood,characterized by symptoms of inattention,hyperac-tivity,and impulsivity(APA,1994).Inattention may manifest it-self as failing to give close attention to details,making careless mistakes in(school)work,dif?culty persisting in tasks that re-quire sustained attention,and not listening to what is being said.Hyperactivity is often characterized by?dgetiness,unable-ness to remain seated when expected to do so,excessive talking, and appearing as‘driven by a motor’.Impulsivity is often ex-pressed as lack of patience,dif?culty awaiting turn,and fre-quently interrupting others(APA,1994).Most individuals have symptoms in all three domains(combined type),although a pre-dominantly inattentive and a predominantly hyperactive-impul-sive subtypes also exist.In most cases,the severity of the symptoms become less conspicuous with age,especially signs of excessive gross motor activity(APA,1994),although the core symptoms of ADHD are believed to persist into adulthood for some of the patients(Tannock,1998).ADHD is estimated to af-fect around5%of children with an overrepresentation of boys by approximately5:1–9:1(APA,1994).Genetic factors strongly contribute to the disorder,but adverse environmental factors have also been identi?ed.The disorder is frequently accompa-nied by developmental problems,including dyslexia,speci?c and general learning dif?culties and causes signi?cant impair-ments in social relationships and school performance.Many patients also suffer from comorbid conditions such as antisocial, mood,anxiety,and substance use disorders(Biederman and Faraone,2005).

4.1.2.Neurological and cognitive problems in ADHD

Because problems with impulsivity and inattention suggest def-icits in the voluntary control of behavior,the de?cits observed in ADHD have generally been related to the neurological dysfunctions in the fronto-striatal circuitry(Castellanos,2001;Mattes,1980; Tannock,1998).Indeed,anatomical neuroimaging studies have re-vealed altered architecture of this circuitry(Castellanos et al., 1996;Yeo et al.,2003)and reduced activity in frontal and cingulate regions in subjects with ADHD compared to controls(Aman& Carmichael,1997;Rubia et al.,1999;Zametkin et al.,1990).More-over,the dopaminergic system plays an important role in the pathology of ADHD(Levy,1991;Levy&Swanson,2001)which may also account for the problems in executive functioning.With respect to the cognitive dysfunctions,children with ADHD are known to have problems in a variety of tasks related to executive control.Overall,children with ADHD perform worse than controls on inhibition tasks(Hervey,Epstein,&Curry,2004;Lijf?jt, Kenemans,Verbaten,&Van Engeland,2005;Nigg,1999;Oos-terlaan,Logan,&Sergeant,1998),working memory tasks(Karate-kin&Asarnow,1998b;Kempton et al.,1999;Martinussen, Hayden,Hogg-Johnson,&Tannock,2005;Oie,Sunde,&Rund, 1999)and show an overall lower speed of responding(Hooks, Milich,&Lorch,1994;Karatekin&Asarnow,1998a;Mason, Humphreys,&Kent,2003;Schachar,Tannock,Marriot,&Logan, 1995;Van der Meere&Sergeant,1988;Van der Stigchel et al., 2007).Current cognitive theories of ADHD have focused on re-sponse inhibition as forming the primary de?cit,although these models differ in the formulation of the fundamental impairment (for an overview see Tannock,1998).Importantly,one of the most robust?ndings in the ADHD literature is an increased variability of responding in ADHD patients compared to controls(Kuntsi, McLoughin,and Asherson,2006;Leth-Steensen,Elbaz,&Douglas, 2000),which may be related to a defective effort control mecha-nism(Leth-Steensen et al.,2000).4.1.3.Eye movement studies in ADHD

The hypothesis that children with ADHD have problems with response inhibition is partly revealed through research using AS, MGS,and intrusive saccades.These measures have in common that inappropriate/irrelevant motor responses need to be inhibited and are therefore suitable tests to investigate whether motor inhibition is indeed affected in ADHD.

4.1.4.Antisaccades

The results on antisaccade performance in ADHD are somewhat inconsistent,although the studies that found an elevated number of antisaccade errors are in the majority.In seven of10studies, more directional errors on antisaccade tasks were found in chil-dren with ADHD(Habeych,Folan,Luna,&Tarter,2006;Karatekin, 2006;Klein,Raschke,&Brandenbusch,2003;Mostofsky,Lasker, Cutting,Denckla,&Zee,2001a;Mostofsky,Lasker,Singer,Denckla, &Zee,2001b;Munoz,Armstrong,Hampton,&Moore,2003; O’Driscoll et al.,2005).No effects on directional errors were ob-served in the other three studies(Aman,Roberts,&Pennington, 1998;Hanisch,Radach,Holtkamp,Herpertz-Dahlmann,&Konrad, 2006;Rothlind,Posner,&Schaughency,1991).However,the lack of effect on antisaccade errors observed in these three studies could be explained in terms of a possible lack of statistical power and task differences.For instance,one study reported a statistical trend of p=0.16towards more directional errors(Hanisch et al., 2006).In the antisaccade task conducted by Rothlind and col-leagues(1991),each participant performed only10trials in each condition,possibly causing low statistical power.In the third study that did not report an elevated number of antisaccade errors,a dif-ferent version of the antisaccade task was used in which an addi-tional visual event occurred on the antisaccade location and a detection task was associated with the presentation of the target (Aman et al.,1998).This could account for the lack of effect, although it must be noted that patients still committed10%more direction errors than controls in that study.It thus appears that the majority of studies reporting on antisaccade performance in chil-dren with ADHD?nd an elevated number of directional errors, indicating that children with ADHD are less able than controls to suppress inappropriate responses.

There are a number of variables that in?uence antisaccade per-formance in ADHD,namely developmental effects,subtype of ADHD,cognitive manipulations,and medication.Children with ADHD did not show the normal age-related decrease in latency for correct antisaccade responses(Klein et al.,2003),suggesting an abnormal pattern of development of antisaccade performance in affected children.Another factor that seems to play a role is the speci?c subtype of ADHD.Recently,ADHD-combined subtype was compared with ADHD-inattentive subtype on antisaccade per-formance(O’Driscoll et al.,2005).Results showed that participants with ADHD-combined subtype were signi?cantly more impaired than participants with ADHD-inattentive subtype,who did not show any impairments,indicating that the de?cits in inhibiting eye movements might be mediated by brain structures implicated speci?cally in the hyperactive/impulsive symptoms of ADHD (O’Driscoll et al.,2005).Karatekin(2006)showed that reducing working memory demands or training of working memory im-proved the accuracy of adolescents with ADHD up to the level of controls on their?rst administration of the antisaccade task,which shows that cognitive manipulations can help to overcome some of the inhibitory de?cits in children with ADHD.Further,it has been investigated whether performance on the antisaccade task im-proves with administration of the stimulant methylphenidate. One of the possible effects of methylphenidate is an increase in inhibitory control through its effect on fronto-subcortical path-ways(Faraone&Biederman,1998).A repeated measures experi-ment was conducted by Klein and colleagues(Klein,Fischer,

394N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

Table1

Overview of eye movement studies in childhood and adolescence psychiatric disorders

Authors N Gender Age(years)Eye movement

tasks

Dependent variables Results

Attention-de?cit/hyperactivity disorder(ADHD)

Aman et al.(1998)22ADHD22m/0f10–14AS N Errors ns 22NC22m/0f10–14

Castellanos et al.(2000)32ADHD0m/32f6–13SPEM Gain,root mean square error,N

saccades,catch-up saccades and

anticipatory saccades

20NC0m/20f6–13MGS(delay1.2s)N Anticipatory saccades,

latency,accuracy N Anticipatory saccades: ADHD>NC(p<.001).Other DVs ns

Habeych et al.(2006)13High risk for

alcohol use

disorder+ADHD Unknown10–12AS N Errors,latency,peak velocity,

gain

N Errors:ADHD>NC(p=.02).

Other DVs ns

Hanisch et al.(2006)22ADHD15m/7f10–14VGS Latency ns 22NC14m/8f10–14AS N Errors ns

Jacobsen et al.(1996)18ADHD17m/1f9–15SPEM Gain,root mean square error,%

time tracking Root mean square error: ADHD>NC(p<.001).

22NC16m/6f9–18N catch-up,anticipatory and

back-up saccades,N square

wave jerks,amplitude catch-up,

anticipatory and back-up

saccades

Other DVs ns

Karatekin and Asarnow

(1998a)

28ADHD19m/9f M=13.9VGS Latency ns

38NC18m/20f M=14.1

Karatekin(2006)10ADHD8m/2f12.4–18.5VGS Latency ns

15NC9m/6f11.5–19.0AS N Errors,latency N Errors:ADHD>NC(p<.001).

Latency:ADHD>NC(p<.001) Klein et al.(2002)27ADHD27m/0f10–15VGS Latency ADHD unmedicated>ADHD

medicated

AS N Errors,latency N Error:ADHD

unmedicated>ADHD medicated

Latency:ADHD

unmedicated>ADHD medicated Klein et al.(2003)46ADHD41m/5f7–15VGS Latency ADHD>NC(p<.05).

46NC38m/8f7–15AS N Errors,latency N errors:ADHD>NC(p<.0001).

Latency:ADHD>NC(p<.05) Mostofsky et al.(2001a)19ADHD11m/8f7.1–16.1VGS Latency,coef?cient of variation Latency:ns

25NC13m/12f7.2–17.9Coef?cient of variation:

ADHD>NC(p<.05)

AS N errors ADHD>NC(p<.001)

MGS(delay4.5–5s)N Anticipatory saccades,

latency,accuracy

N Anticipatory saccades:

ADHD>NC(p<.01)

Coef?cient of variation Latency:ADHD>NC(p<.01).

Other DVs ns

Mostofsky et al.(2001b)14ADHD+TS14m/0f7.8–14.3VGS Latency,coef?cient of variation Latency:ADHD+TS>NC(p<.01).

Coef?cient of variation:

ADHD+TS>NC(p<.001) 10NC10m/0f8.1–12.6AS N Errors N Errors:ADHD+TS>TS

(p=.07)

MGS(delay4.5–5 s)N Anticipatory saccades,

accuracy

N anticipatory saccades:

ADHD+TS>TS(p<.05).Other

DVs ns

Munoz et al.(2003)76ADHD61m/15f6–16VGS Latency,coef?cient of variation,

amplitude,duration,peak

velocity,gap effect Latency:ADHD>NC(p<.05). Coef?cient of variation: ADHD>NC(p<.001).Duration: ADHD>NC(p<.001).Peak velocity:ADHD

75NC40m/35f6–16AS Latency,coef?cient of variation,

N errors Latency:ADHD>NC(p<.01). Coef?cient of variation: ADHD>NC(p<.001).N errors: ADHD>NC(p<.001)

O’Driscoll et al.200510ADHD-C10m/0f11–14VGS Latency,amplitude,peak

velocity

12ADHD12m/0f11–14AS N errors,latency N errors:ADHD–C>NC(p<.05).

Latency:ns

10NC10m/0f11–14

(continued on next page)

N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414395

Table1(continued)

Authors N Gender Age(years)Eye movement

tasks

Dependent variables Results

Rommelse et al.(2008)14ADHD14m/0f7–14MGS(delay3and

7s)Accuracy,latency,N

anticipatory saccades,N

intrusive saccades,peak

velocity,under/overshoot,

duration,coef?cient of variation

Accuracy:ADHD

anticipatory saccades:

ADHD>NC(p<.05).N intrusive

saccades:ADHD>NC(p<.05).

Overshoot:ADHD>NC(p<.001).

Duration:ADHD>NC p<.05).

Coef?cient of variation:

ADHD>NC(p<.01).Other DVs ns

15NC15m/0f7–14

Ross et al.(1994)13ADHD13m/0f9–12MGS(delay0.8s)N Anticipatory saccades,

latency,accuracy N Anticipatory saccades: ADHD>NC(p=.04)

10NC5m/5f9–12Other DVs ns

Rothlind et al.199120ADHD20m/0f 6.9–13.9AS N Anticipatory saccades,latency ns

21NC21m/0f 6.8–14.4

Autism spectrum disorders(ASD)

Goldberg et al.(2002)11Autism8m/3f12–18VGS(overlap and

gap)Latency,gap effect Latency:autism>NC(p<.05).

Gap effect:ns

11NC8m/3f12–18AS N Errors,latency,velocity,

accuracy N Errors:autism>NC(p<.001). Other DVs ns

MGS(1.5–3.0s)N Anticipatory saccades,

latency,velocity,accuracy N Anticipatory saccades: autism>NC(p<.01) Latency:autism>NC(p<.01). Other DVs ns

Kemner et al.(2004)16PDD Unknown M=10.9SPEM Position gain,N saccade

intrusions

ns 18NC Unknown M=10.0

Landry and Bryson(2004)15Autism Unknown 3.8–7.6VGS(disengage

and shift)Latency Latency on shift:PDD>NC

(p<.01)

13NC Unknown 2.1–6.2Latency on disengage:ns

Luna et al.(2007)61Autism Unknown8–33VGS Latency,accuracy,duration,

peak velocity Accuracy:autism

61NC Unknown8–33AS N Errors,latency N Errors:autism>NC(p<.05).

Latency:autism

MGS(delays1.0–8.0s)Accuracy,latency Accuracy:autism

Latency:ns

Rosenhall et al.(1988)11Autism6m/5f9–16VGS Latency ns

26NC Unknown7–13SPEM Autism:unable to?nish

experiment

Scharre and Creedon(1992)34Autism32m/2f2–11SPEM Autism:85%unable to?nish

experiment

Van der Geest et al.(2001)16Autism16m/0f M=10.9VGS(overlap and

gap)Accuracy,latency,gap effect Gap effect:autism

Other DVs ns

15NC15m/0f M=10.3 Reading disorder(RD)

Adler-Grinberg and Stark (1978)25RD20m/5f8.0–12.3VGS Latency,peak velocity,

amplitude

19NC15m/4f7.1–12.3SPEM Smoothness,accuracy,

maximum velocity

RD poorer SPEM(more saccades)

than NC

Bednarek et al.(2006)16RD9m/10f9.2–10.5VGS with and

without cues Latency RD

No group differences with cue

25NC13m/12f9.2–10.5

Biscaldi et al.(1994)12RD Unknown9–11VGS standard

(overlap and gap)

and sequential

(overlap,gap,and

simultaneous)Fixation quality,velocity,

position,corrective time,N

express,fast and slow regular

saccades

Standard:RD poorer?xation

quality,dif?culty hitting the

target at once,smaller primary

sac-cades,shorter RT to the left

than NC.Sequential:RD made

fewer and larger saccades and

had shorter?xations than NC

12NC Unknown9–11

Biscaldi et al.(2000)506RD Unknown7–17VGS Latency RD>NC(p=.01)

114NC62m/52f7–17AS N(corrected)errors,N misses,

latency N errors:RD>NC(p<.001).N corrections:NC>RD(p<.001).N misses:RD>NC(p<.001). Latency:ns

Biscaldi et al.(1998)93RD76m/17f8–25VGS(single and

sequential target)Single:(SD)latency,N express,

fast,slow,(too)late,

anticipatory saccades,N

corrective saccades in the same

and opposite direction.

sequential:N target saccades,N

and amplitude regression

saccades

SD latency,N fast,too late

anticipatory saccades:RD>NC

(p<.05–<.01).N slow saccades:

92NC51m/41f8–25

396N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

Table1(continued)

Authors N Gender Age(years)Eye movement

tasks

Dependent variables Results

Black et al.(1984a)28RD27m/1f7.8–16.9VGS Latency,accuracy,velocity,

acceleration,D latency abduct

and adduct movements

ns 31NC Unknown 6.0–12.2

Black et al.(1984b)26RD22m/4f8–13SPEM N(big)saccades,angle covered

by saccades M angle per

saccade,peak velocity N big saccades:RD>NC(p=.02). Angle covered by saccades and M angle:RD>NC(p=.05).Peak velocity ns

34NC19m/15f8–13

Black et al.(1984c)35RD30m/5f8–13VGS N(big)saccades,progressions,

and regressions by saccades,M

angle per saccade,peak velocity

35NC20m/15f8–13

Bogacz et al.(1974)40RD Unknown6–23VGS Step-like intrusions Normal VGS in RD.

24NC Unknown7–15SPEM Uni-and bi-directional

saccades,saccadic jerks More abnormal saccades in RD than NC

Brown et al.(1983a)34RD34m/0f10–12VGS N(non-)predictive saccades Overall no differences between

NC and RD,

33NC33m/0f10–12some indication total N saccades

NC>RD

Brown et al.(1983b)34RD34m/0f10–12VGS(saccadic,

predictive and

unpredictive ramp

tracking)Latency,N and amplitude saccades,gain,velocity,N saccades,regressions

35NC35m/0f10–12

De Luca et al.(1999)10RD8m/2f10.1–17.1VGS Amplitude,N forward and

backward corrective saccades

ns 11NC Unknown M=11.8

Dossetor and Papaioannou (1975)10RD Unknown6–15VGS Latency RD>NC(p<.01),RD children

faster when saccades are

directed to the left,opposite

pattern for control children 10NC Unknown6–15

Eden et al.(1994)26RD Unknown10.9–12.2VGS Accuracy RD

39NC Unknown10.2–12.1SPEM Qualitative assessment of

smoothness RD poorer performance than NC (p<.002)

Fischer and Hartnegg

(2000a)

262RD Unknown7–17VGS N intrusive saccades RD>NC

99NC Unknown7–17AS N intrusive saccades RD>NC

Fischer and Hartnegg (2000b)85RD60m/25f8–15VGS Latency RD better after training,

comparable to NC

AS N(uncorrected)errors,latency

antisaccades,correction times,

N misses

RD better after training on all

DVs,comparable to NC

Fischer and Weber(1990)20RD Unknown9–17VGS N express saccades,N fast

regular saccades N express saccades:RD>NC.N fast regular:RD

17NC Unknown9–17

Jerˇa?bek and Krejcˇová(1991)52RD46m/6f M=10.5VGS Dysmetric saccades,

sponteneous nystagmus,gaze

direction nystagmus 61%of RD abnormal.Dysmetric saccades in29%of RD. Sponteneous nystagmus in11%. Gaze direction nystagmus in12%

41NC Unknown M=10SPEM Irregularity RD more irregular than NC

Leisman et al.(1978)20RD19m/1f7–11VGS Latency ns

20NC16m/4f7–11

Leisman and Schwartz (1978)20RD19m/1f7–11VGS Amplitude,duration,mean

angular velocity

ns 20NC16m/4f7–11SPEM Amplitude,duration,mean

angular velocity

Olson et al.(1983)34RD27m/7f8.3–13.8VGS N small and large regressive and ns 36NC31m/5f8.3–13.8progressive saccades

Pavlidis(1985)13RD12m/1f8–13VGS N total,regressive and

progressive saccades N total and regressive saccades: RD>NC(p<.001)N progressive saccades:NC>RD

10NC6m/4f7–10

Pavlidis(1981)12RD Unknown10–16VGS N total,regressive and

progressive saccades

All DVs:RD>NC(p<.001)

12NC Unknown10–16

(continued on next page)

N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414397

Table1(continued)

Authors N Gender Age(years)Eye movement

tasks

Dependent variables Results

Petri and Anderson(1980)16RD13m/3f6–11VGS Saccade duration-amplitude

relationship

18NC12m/6f6–11

Raymond et al.(1988)6RD4m/2f8.8–13.3VGS N and amplitude undershoot,

latency

6NC0m/6f9.9–10.1

Stanley et al.(1983)15RD12m/3f11–13VGS N regressions and corrections ns 15NC9m/6f11–13

Ygge et al.(1993)86RD68m/16f9VGS Dysmetria,latency,velocity ns 86NC68m/16f9SPEM Tracking ability,N saccadic

intrusions

ns Childhood-onset schizophrenia

Friedman et al.(1993)6psychosis Unknown Adolescents SPEM Gain,N corrective catch-up

saccades,%time tracking,

corrective catch-up saccade

amplitude Corrective catch-up saccade amplitude:psychosis>NC (p=.02).Other DVs ns

11NC Unknown Adolescents

Gordon et al.(1994)10Schizophrenia Unknown10–18SPEM Gain,covered distance of total,

catch-up,and intrusive

saccades,N intrusive saccades Gain:schizophrenia

(p<.01).Covered distance: schizophrenia>NC(p<.01).N intrusive saccades: schizophrenia>NC

12NC Unknown10–18

Jacobsen et al.(1996)17Schizophrenia10m/7f10–18SPEM Gain,root mean square error,%

time tracking,N catch-up,

anticipatory and back-up

saccades,N square wave jerks,

amplitude catch-up,

anticipatory and back-up

saccades Gain and%time tracking: schizophreniaNC(p<.01)

22NC16m/6f9–18

Karatekin and Asarnow

(1998a)

13schizophrenia7m/6f M=14.4VGS Latency ns

38NC18m/20f M=14.1

Kumra et al.(2001)29Schizophrenia16m/13f6–18SPEM Qualitative impairment score,

gain,root mean square error,N

total,catch-up,anticipatory and

large anticipatory saccades Qualitative impairment score and gain:schizophrenia and psychosis>NC(p=.001)Root mean square error: schizophrenia and

psychosis>NC(p=.003).N total and catch-up saccades: schizophrenia>NC(p=.03). Other DVs ns

26Psychosis22m/4f6–18 38NC24m/14f6–18

Mather(1985)9at-risk Unknown12–19VGS Latency,amplitude,accuracy,N

double-jump saccades N double-jump saccades:at-risk>NC(p=.03).Other DVsns

8NC Unknown15–20SPEM Latency,N and amplitude of

intrusive saccades N intrusive saccades:at-

risk>NC(p=.03).Other DVs ns

Pollack and Krieger(1958)15Schizophrenia Unknown7–9SPEM Abnormality No differences between

schizophrenic and NC 9NC Unknown3–10

Ross(2003)49Schizophrenia35m/14f6–15SPEM Gain,N catch-up,leading and

large anticipatory saccades Gain:schizophreniaNC.N leading saccades:at-risk>NC.N catch-up saccades:ns

60at-risk29m/31f6–15 80NC38m/42f6–15

Ross et al.(2005)45Schizophrenia33m/12f 5.8–16.0MGS(delay1–3s)N anticipatory saccades,

latency,accuracy N anticipatory saccades: schizophrenia>NC(p<.001). Accuracy:schizophrenia

64at-risk35m/29f 5.8–16.0

84NC39m/45f 5.8–16.0Latency:ns

Ross et al.(1996)13at-risk5m/8f6–15SPEM Gain,root mean square error,N

and amplitude Gain:at-risk

19NC9m/10f6–15Catch-up and

anticipatory

saccades Error:at-risk>NC(p=.04).N anticipatory saccades:at-risk>NC(p=.002).Other DVs ns

Ross et al.(1999)10Schizophrenia7m/3f7–15SPEM%of total eye movement due to

anticipatory saccades Anticipatory saccades: schizophrenia>NC(p<.001), at-risk>NC(p=.003)

13at-risk5m/8f6–15

19NC9m/10f6–15

398N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

Table1(continued)

Authors N Gender Age(years)Eye movement

tasks

Dependent variables Results

Schiffman et al.200690at-risk Unknown11–13Visual pursuit

movements(fast,

smooth,accurate,

and Jerky movements,?xation

losses,inaccurate speed (combined as normal versus abnormal)parallel motion)

82NC Unknown11–13

Schreiber et al.(1997)21at-risk10m/11f10–18VGS N hypometric and hypermetric

saccades,N non-?xations,N

omissions N hypometric saccades:at-risk>NC(p<.05)

21NC10m/11f10–18Other DVs ns.

Tourette’s syndrome(TS)

Bollen et al.(1988)28TS21m/7f8–15VGS towards

stationary and

newly appearing

targets

Latency,peak velocity ns

norm values Fixation during

distraction

N errors,square wave jerks ns

SPEM Gain ns

Jackson et al.(2007)7TS5m/2f11–17VGS and AS

(mixed)with and

without cues N errors,latency ns main effects of group,but TS

had less dif?culty switching

between tasks

12NC Unknown11–17

Mostofsky et al.(2001b)14TS14m/0f8.4–14.6VGS Latency,coef?cient of variation

of latency Latency:TS P NC(p=.07).Other DV ns

10NC10m/0f8.1–12.6AS N errors ns

MGS(delay4.5–5s)N anticipatory saccades,

accuracy(gain)

Mueller et al.(2006)9TS8m/1f9–16VGS and AS

(mixed)with cues N errors,latency N errors and latency:TS=NC on

nonswitch trials,but TS perform

better(p<.05)on switch trials

for N errors and latency

19NC Unknown9–16

Narita et al.(1997)1TS1m13VGS Gain Saccades were hypometric

AS N errors10of10trials erroneous

saccades.

SPEM Gain,N intrusive saccades Gain was normal,frequent

intrusive saccades

Nomura et al.(2003)79TS79m/0f6–12VGS Latency,amplitude,peak

velocity

19NC19m/0f6–12MGS(delay

unknown)Latency,amplitude,peak

velocity N distracted saccades

TS made less distracted saccades

than NC(p<.05),but TS were

further removed from target

(p<.05).Other DVs ns

Childhood-onset-obsessive compulsive disorder(OCD)

Rosenberg et al.(1997a)18OCD9m/9f8.8–16.9VGS Accuracy,latency,peak velocity ns

18NC9m/9f8.7–16.8AS N errors,latency,accuracy N errors:OCD>NC(p=.003).

Oher DVs ns

MGS(delay1–8s)N anticipatory saccades,

accuracy,latency N anticipatory errors:OCD P NC (p=.07).Other DVs ns

Predictive saccadic

task

accuracy,latency ns Anxiety and depression

Hardin et al.(2007)16Anxiety9m/7f9–17AS under reward,

punishment,and

neutral conditions

with low to high

saliences N errors,latency N errors:depression>NC

(p=.005),anxiety in between

depression and NC,not

in?uenced by condition.

Latency:no main effect,but

anxious less improvement under

reward and punish-ment than

NC with depression in between

11Depression5m/6f9–17 30NC15m/15f9–17

Jazbec et al.(2005)11Anxiety8m/3f9–17AS under reward,

punishment,and

neutral conditions N errors,latency,peak velocity N errors:https://www.doczj.com/doc/d48071190.html,tency:NC

improved with reward or

punishment(p=.05),no effect of

condition on depression

(p=.52),anxiety worsened with

punishment(p=.03).Peak

velocity:NC improve with

reward or punishment(p=.01),

but anxious and depression do

not(p=.84and.89)

12Depression4m/8f9–17

28NC13m/15f9–17

Note.NC,normal controls;N,number;ADHD,attention-de?cit/hyperactivity disorder;OCD,obsessive compulsive disorder;DVs,dependent variables;ns,not signi?cant;AS, antisaccades;VGS,visually guided saccades;MGS,memory guided saccades;SPEM,smooth pursuit eye movement.

N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414399

Fischer,&Hartnegg,2002)who tested boys with ADHD on medica-tion?rst,then later without medication,or the reverse.Partici-pants showed bene?cial effects of methylphenidate on response inhibition,which was later con?rmed for both subtypes of ADHD (O’Driscoll et al.,2005).This indicates that the mechanisms responsible for the de?cits in antisaccade performance are related to the areas in?uenced by methylphenidate.

4.1.

5.Visually guided saccades

Based on the prosaccade/visually guided saccade data col-lected during antisaccade experiments,it is clear that VGS laten-cies are consistently more variable in ADHD compared to controls (Mostofsky et al.,2001a,2001b;Munoz et al.,2003).The study with the largest sample of ADHD patients(N=76)found longer and more variable latencies,reduced peak velocity and increased durations of VGS compared to controls(Munoz et al.,2003).With respect to augmented prosaccade latencies,this was found to be non-signi?cant in studies with a smaller sample(Hanisch et al., 2006;Karatekin&Asarnow,1998a;Mostofsky et al.,2001a; O’Driscoll et al.,2005),but signi?cant in another study(Klein et al.,2003).Taken together,latency of VGS is more variable and possibly slower in children with ADHD,presumably indicat-ing that children with ADHD have dif?culty in regulating pro-cesses of saccade initiation.

4.1.

5.1.Memory guided saccades.MGS in ADHD have been reported in?ve studies(Castellanos et al.,2000;Mostofsky et al.,2001a, 2001b;Rommelse et al.,2008;Ross,Hommer,Breiger,Varley,& Radant,1994).These studies have revealed inconsistent results with respect to the accuracy of saccades towards the memorized target.Normal accuracy was observed in three studies(Mostofsky et al.,2001a,2001b;Ross et al.,1994),while de?cits in accuracy were reported in two studies(Castellanos et al.,2000;Rommelse et al.,2008).A possible explanation for these inconsistent?ndings might be differences in the paradigms used,mainly the large range in delay periods used in various studies,which varied between0.8 and7s.Consistently,however,all?ve studies reported more antic-ipatory saccades in patients with ADHD compared to controls(Cas-tellanos et al.,2000;Mostofsky et al.,2001a,2001b;Rommelse et al.,2008;Ross et al.,1994),indicating problems with inhibitory control in children with ADHD in https://www.doczj.com/doc/d48071190.html,tencies of MGS were re-ported in four studies,and were found to be normal in ADHD in three of four studies(Castellanos et al.,2000;Rommelse et al., 2008;Ross et al.,1994),suggesting response initiation to be nor-mal.Only one study reported saccade metrics during MGS,in which boys with ADHD tended to overshoot their saccades relative to controls(Rommelse et al.,2008).This was hypothesized to be caused by dysfunctions of the cerebellum and/or related to changes in the dopaminergic transmission in ADHD.Further re-search is needed to establish the prevalence of eye movement deviancies on the memory guided saccade paradigm in ADHD. 4.1.5.2.Smooth pursuit eye movements.There have been only two studies investigating SPEM in children with ADHD.Therefore,there seems to be no general agreement whether children with ADHD have fundamental problems in SPEM tasks.Although earlier stud-ies have described dif?culties in suppressing intrusive saccades during SPEM(Bala et al.,1981;Bylsma&Pivik,1989;Shapira, Jones,&Sherman,1980),these studies adopted inclusion criteria that predated the publication of the DSM-IV.In a more recent study,it was found that children with ADHD were affected in a glo-bal measure of SPEM,the root mean square error(Jacobsen et al., 1996).This measure is an index of the extent to which the eyes do not reproduce target motion.The effect on the global measure was not observed in a SPEM experiment investigating only girls with ADHD,although observed was a non-signi?cant tendency to-ward a greater root mean square error in ADHD girls compared to control girls(Castellanos et al.,2000).

4.1.

5.3.Variability in ADHD.As noted earlier,an increased variabil-ity of responding in ADHD patients compared to controls is one of the most robust?ndings in the ADHD literature(Kuntsi et al., 2006;Leth-Steensen et al.,2000).Results on variability measures have been included in four of the discussed studies in three differ-ent paradigms.All four of these studies have found an increased variability in children with ADHD compared to controls.Increased variability has been observed in antisaccades(Munoz et al.,2003), visually guided saccades(Mostofsky et al.,2001a,2001b;Munoz et al.,2003),and memory guided saccades(Rommelse et al.,2008).

4.1.

5.4.Conclusions on ADHD.Overall,there are several studies that have investigated eye movements in children with ADHD. They have primarily focused on testing executive functions to verify the hypothesis that intentional motor systems as mediated by the prefrontal areas are affected in ADHD.Indeed,a failure of top-down regulation has been found in AS,in which elevated numbers of directional errors are observed and in MGS,in which more anticipatory errors are observed.Furthermore,a wide vari-ety of paradigms have found more intrusive saccades in ADHD. Intrusive saccades are de?ned as inappropriate eye movements and may also be regarded as tapping response inhibition, although it is not a failure to inhibit a response to an external stimulus,but rather a primary failure of visual?xation.More intrusive saccades are reported in a variety of tasks,such as the go-nogo tasks(Castellanos et al.,2000),an ocular?xation task (Gould,Bastain,Israel,Hommer,&Castellanos,2001),a visual search task(Van der Stigchel et al.,2007),memory saccade tasks (Rommelse et al.,2008),a task requiring prolonged?xation (Munoz et al.,2003)and during pro-and antisaccade tasks (Klein et al.,2003).In line with results from other modalities, an increased variability is consistently observed in children with ADHD.These results indicate a consistent reduction in ability to suppress unwanted saccades and to control voluntary behavior in ADHD.These?ndings lend support for the presence of inhibi-tion de?cits in children with ADHD and suggest functioning of frontal areas like the DLPFC is impaired in ADHD.Since basic eye movement control may also be deviant,dysfunctions of the frontal eye?elds and cerebellum may be implicated.

4.2.Oppositional deviant disorder and conduct disorder(ODD and CD) 4.2.1.Clinical manifestation of ODD and CD

ODD is characterized by a recurrent pattern of negativistic,de?-ant,disobedient,and hostile behaviors toward authority?gures per-sisting for at least six months.A proportion of children with ODD later develop CD(Loeber,Burke,Lahey,Winters,&Zera,2000),character-ized by a repetitive and persistent pattern of behaviors in which the basic rights of others and major age-appropriate societal norms or rules are violated(APA,1994;Loeber et al.,2000).ODD and CD fre-quently co-occur with ADHD(Loeber et al.,2000).

4.2.2.Neurological and cognitive problems in ODD and CD

Frontal lobe dysfunctioning and damage have been frequently associated with violence and aggressive behavior,especially when located in the orbitofrontal cortex(Burke,Loeber,&Birmaher, 2002).Furthermore,impairments in the functioning of the amyg-dala have been associated with diminished interpretation of social cues(like facial expressions).Abnormalities in the connections be-tween the amygdala and prefrontal lobes may be associated with a negative affective style in children with disruptive behavior disor-ders(Burke et al.,2002).Cognitively,impairments in inhibition ap-pear important in disruptive behavior disorders(Burke et al.,

400N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

2002),although impairments in working memory have also been found independent of possible confounding ADHD in one study (Séguin,Boulerice,Harden,Tremblay,&Pihl,1999),but not in an-other study(Oosterlaan,Scheres,and Sergeant,2005).

4.2.3.Eye movement studies in ODD and CD

We were unable to locate any eye movement studies speci?-cally targeting children with disruptive behavior disorders.It is highly likely,however,that a(substantial)proportion of the chil-dren with ADHD participating in eye movement studies had a comorbid disruptive behavior disorder which may have contrib-uted to the?ndings of eye movement de?cits found in these stud-ies.Given that disruptive behavior disorders and ADHD frequently co-occur,common underlying pathology(such as frontal lobe dys-functions,inhibitory problems,and/or generalized executive func-tioning problems)may be expected.In line with this,it is reasonable to hypothesize that eye movement studies in children with disruptive behavior disorders will show de?cits similar to those found in ADHD(i.e.,more directional errors on antisaccade tasks,slower and more variable latencies on VGS tasks,more antic-ipatory saccades on memory guided saccade tasks,and more intru-sive saccades in general).Clearly,work needs to be done in this area of child and adolescent pathology.

4.3.Autism spectrum disorders(ASD)

4.3.1.Clinical manifestation of ASD

ASD entails a spectrum of disorders,namely autism,Asperger’s disorder,and pervasive developmental disorder-not otherwise speci?ed(PDD-NOS),characterized by signi?cant social de?cits, repetitive behaviors,and restricted interests(Akshoomoff,2005; DiCicco-Bloom et al.,2006).Social de?cits include a marked impairment in the use of non-verbal behaviors(eye contact and facial expressions),a failure to develop age-appropriate peer rela-tionships,a lack of spontaneous enjoyment and interest sharing with other people,and a lack of social or emotional reciprocity (APA,1994).Repetitive behaviors and restricted interests may in-clude a preoccupation with one or more stereotyped and re-stricted patterns of interests that is abnormal in intensity or focus,in?exible and non-functional routines,stereotyped and repetitive motor mannerisms(like hand?apping),and persistent preoccupation with parts of objects(APA,1994).Onset of ASD is by de?nition before the age of three(APA,1994).Unlike Asperger’s syndrome,autism is also characterized by qualitative impairments in verbal communication,re?ected by delay in(or total lack of)the development of spoken language,inability to ini-tiate or sustain a conversation with others,stereotyped or repet-itive use of language,and lack of social imitative or make-believe play appropriate for developmental level(APA,1994;DiCicco-Bloom et al.,2006).PDD-NOS is often diagnosed,when a child does not meet the full criteria for autism or displays subthreshold symptomatology(APA,1994).Once considered as a rare disorder affecting only0.05%of children(APA,1994),current estimates indicate a prevalence around0.5–0.6%(DiCicco-Bloom et al., 2006;Rutter,2005).ASD is more common in boys than girls (APA,1994)and is strongly genetically determined.In most cases of autism,mental retardation is present,as well as a range of behavioral symptoms like hyperactivity,a short attention span, impulsivity,and aggressiveness(APA,1994).

4.3.2.Neurological and cognitive problems in ASD

ASD is associated with an abnormal enlargement of brain volume, mainly during early childhood(DiCicco-Bloom et al.,2006).Growth abnormalities have been reported for the cerebellum,cerebrum, amygdala,and possibly hippocampus(Akshoomoff,2005;DiCicco-Bloom et al.,2006).Brain enlargement re?ects both cerebral and cerebellar,and both white and gray matter (DiCicco-Bloom et al.,2006).The most prominent cognitive problems in ASD are impairments in social skills and language,but impair-ments in speci?c aspects of executive functioning,such as abstracting rules,shifting attention,learning from feedback,and maintaining fo-cus on multiple aspects of information processing during decision making,have also been reported(Akshoomhoff,2005).

4.3.3.Eye movement studies

Given that the major impairments of autistic children lie in so-cial skills and communication,the majority of eye movement stud-ies in autism have focused on scan patterns of social scenes and facial expressions.Only seven studies have investigated the para-digms discussed in the present review,aiming to assess basic ocu-lomotor behavior and frontal circuitry in children with autism.

4.3.3.1.Antisaccades.Two studies have focused on antisaccade per-formance in children with autism(Goldberg et al.,2002;Luna,Doll, Hegedus,Minshew,&Sweeney,2007).Both studies observed more directional errors in autistic participants compared to controls. Furthermore,this basic de?cit in response inhibition was present throughout development(Luna et al.,2007).The results were inconsistent as to whether children with autism are slower to exe-cute a correct antisaccade:one study failed to?nd an effect (Goldberg et al.,2002),whereas the other study found that young autistic participants were even faster to initiate a correct antisac-cade than controls(Luna et al.,2007).

4.3.3.2.Visually guided saccades.Children with autism do not seem to respond slower than age-matched controls on simple VGS.Three of four studies did not?nd an effect of latency on VGS(Luna et al., 2007;Rosenhall,Johansson,&Gillberg,1988;Van der Geest,Kem-ner,Camfferman,Verbaten,&Van Engeland,2001),although one study did observe children with autism to be slower than normals (Goldberg et al.,2002).Therefore,it seems that the dynamics of saccades are normal,although more studies are needed to con?rm this.Whether children with autism have dif?culties with atten-tional engagement is unclear.By computing the gap effect,the dis-engagement of attention and?xation can be measured.Two studies reported this and have found con?icting results:one study found a signi?cant gap effect(Van der Geest et al.,2001)and one study did not(Goldberg et al.,2002).A third study found latency differences in a group of young children with autism on shift trials in which the?xation point remained on screen,but no latency dif-ferences on disengage trials,when the?xation point was removed before the peripheral target was presented(Landry&Bryson, 2004),suggesting dif?culties disengaging attention from the?xa-tion point.It should be noted that in this study there was no expli-cit task instruction to look at the peripheral stimulus.Overall,VGS appear normal in autism and there is insuf?cient evidence to claim dif?culties with attentional engagement within the oculomotor domain for children with autism.

4.3.3.3.Memory guided saccades.The two studies that focused on AS are the only ones that investigated MGS in children with aut-ism(Goldberg et al.,2002;Luna et al.,2007).The results of these studies are inconsistent,however.On the one hand,Luna and colleagues(2007)found de?cits in accuracy and no effect of sac-cade latency in the young group(8–17years)of their clinical population.On the other hand,Goldberg and colleagues(2002) found no effect of accuracy of MGS but slower saccade latency compared to controls.They also reported more response sup-pression saccades,a variable not reported by Luna and col-leagues.These?ndings suggest that impairments in MGS may be present in children with autism,although the speci?city of de?cits is unclear.

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4.3.3.4.Smooth pursuit eye movements.One study reported SPEM in children with PDD and observed no de?cits(Kemner,Van der Geest,Verbaten,&Van Engeland,2004).Only two relatively dated studies have focused on SPEM in children with autism(Rosenhall et al.,1988;Scharre&Creedon,1992).Both studies reported impairments in SPEM in autism,since the vast majority of autistic children were unable to perform the experiment,making saccadic instead of smooth movements.Fundamental problems with pur-suit tasks were later con?rmed in a study that included partici-pants with autism of different age groups(Takarae,Minshew, Luna,Krisky,&Sweeney,2004).The authors analyzed which de?-cits in SPEM occurred in the group younger than16years old.They found lower gain and less accurate initial catch-up saccades(see glossary;saccades to catch-up with the moving target when gain was too low),but only for targets moving into the right visual?eld. De?cits in the closed-loop were speci?c to adults with autism. More studies on SPEM are necessary in order to draw?rm conclu-sions on SPEM performance in children with autism,although it seems that some impairments are present.

4.3.3.

5.Conclusions for ASD.It is dif?cult to draw?rm conclusions based on the above eye movement studies in ASD,because a large body of the?ndings is inconsistent.However,an elevated number of antisaccade errors has been consistently reported.Because suc-cessful performance on the antisaccade task relies heavily on fron-tal structures,one possible interpretation is that the social dif?culties in autism result primarily from disturbances in the frontal cortical areas.Since smooth pursuit also appears abnormal, various non-cortical areas may also be involved in the neuropa-thology of ASD.

4.4.Reading disorder(RD)

4.4.1.Clinical manifestation of RD

RD,also know as dyslexia,manifest itself as a level of reading achievement(i.e.,accuracy,speed,and/or comprehension)that falls signi?cantly below that expected given the child’s age,intelli-gence,and education(APA,1994).Symptoms of RD include an inability to distinguish among common letters and to associate common phonemes with letter symbols.RD is seldom diagnosed before the end of kindergarten because formal reading instruction usually does not begin until this point(APA,1994).RD is heteroge-neous and various attempts have been made to identify more homogeneous subtypes of RD(Bakker,1979;Stanovich,Siegel,& Gottardo,1997).Often the division between phonological and sur-face RD is made,with the?rst representing a true developmental deviancy and the latter representing a form of developmental de-lay(Stanovich et al.,1997).Phonological RD is a persistent,chronic condition(Shaywitz&Shaywitz,2005).Nevertheless,adolescents and adults with RD may learn to read words accurately,although not?uently or automatically(Shaywitz&Shaywitz,2005).Preva-lence rates of RD vary between4%(APA,1994)up to17%(Shaywitz &Shaywitz,2005),depending on the criteria applied.RD is more common in boys than in girls(60–80%of patients is male)and runs in families(APA,1994).Children with RD often have associated de?cits in related domains,such as problems in oral language, writing,and https://www.doczj.com/doc/d48071190.html,orbid ADHD and motor coordina-tion problems are also frequently observed(Habib,2000).

4.4.2.Neurological and cognitive problems in RD

Functional brain imaging studies have shown that the poster-ior brain systems in the left hemisphere fail to function properly during reading and non-reading tasks requiring visual processing (Shaywitz&Shaywitz,2005).This results in the development of compensatory brain mechanisms,such as an increased activity in anterior sites(like the inferior frontal gyrus)and in analog pos-terior sites in the right hemisphere(Shaywitz&Shaywitz, 2005).Naturally,research in the cognitive?eld has focused on language processes.The phonological theory is most widely sup-ported.This theory entails that speech is natural and inherent, but reading is acquired and must be taught(Shaywitz& Shaywitz,2005).Children have to develop the insight that spo-ken words can be dissected into phonemes and that letters in a written word represent these sounds.Apparently,such aware-ness is largely missing in children with RD(Shaywitz&Shaywitz, 2005).Consequently,the child has dif?culty decoding the word and then identifying it.Higher order cognitive and linguistic functions are generally intact(Shaywitz&Shaywitz,2005).How-ever,some evidence exists regarding problems in executive functions,such as verbal working memory and inhibition,in children with RD(Brambati et al.,2006;Van der Schoot,Licht, Horsley,Sergeant,2000;Willcutt,Pennington,Olson,Chhabildas, Hulslander,2005).

4.4.3.Eye movement studies in RD

Since RD is by de?nition a selective impairment of reading re-lated processes in the absence of de?cits in non-reading higher order cognitive processes(Shaywitz&Shaywitz,2005),the vast majority of eye movement studies in RD has focused on examin-ing and manipulating eye movements during reading tasks.These studies lie outside the scope of this review and will not be de-scribed here.Furthermore,many studies have focused on measur-ing ophthalmological problems in children with RD.Overall up to 75%of children with RD have some sort of ophthalmological problem,such as problems with tracking or motion perception, causing disturbed binocular vision(Habib,2000).Elementary per-ceptual abnormalities have been reported in RD children,such as a reduced processing speed of visual information(longer visual persistence at low spatial frequency and a slower?icker fusion rate)and an altered contrast sensitivity(Habib,2000).Seen in this context,it brings no surprise that the studies relevant to this review have almost all focused on measuring VGS or SPEM.Only two studies measured AS and to our knowledge no studies have used MGS.

4.4.4.Antisaccades

As far as the authors are aware,only two studies compared the performance of RD children to that of controls on an antisaccade task(Biscaldi,Fischer,&Hartnegg,2000;Fischer&Hartnegg, 2000a).Both studies reported an impaired performance of RD chil-dren,re?ected by an increased number of directional errors and misses,and a lower number of corrections(Biscaldi et al.,2000) and more intrusive saccades(Fischer&Hartnegg,2000a).However, Fischer and Hartnegg(2000b)also showed that the performance of RD children on an antisaccade task could be improved by training, even to the extent that performance was comparable to that of controls.Thus,some evidence exists indicating impaired inhibitory processing in RD,but these problems can be overcome by training.

4.4.

5.Visually guided saccades

Saccades are essential during reading.While reading,the eyes do not move continuously from left to right along the printed line, but proceed by successive saccades and?xations(Pavlidis,1980). Even though VGS are not similar as saccades during reading(i.e., VGS are mainly elicited by the onset of a peripheral stimulus), the majority(26of27studies)traced on eye movements on non-linguistic tasks in RD children have focused on measuring VGS. However,even though this is a widely studied topic in RD,no con-sensus has been reached as to whether or not VGS are impaired in RD.This is largely due to differences in task paradigms and meth-ods applied,which is probably related to the wide time span in

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which the studies were conducted(from1975to2006).This has also consequences for the kind of dependent variables studied, which vary considerably between studies.Nevertheless,some con-sistent variables and results are present.

Ten studies reported latency.Seven of these did not?nd any latency differences between RD children and controls(Adler-Grinberg&Stark,1978;Biscaldi,Gezeck,&Stuhr,1998;Black, Collins,De Roach,&Zubrick,1984a;Brown et al.,1983b;Leisman, Ashkenazi,Sprung,&Schwartz,1978;Raymond,Ogden,Fagan,& Kaplan,1988;Ygge,Lennerstrand,Rydberg,Wijecoon,& Pettersson,1993).Three studies did?nd differences in latency,of which two reported RD children to have slower saccade latencies than controls(Biscaldi et al.,2000;Dossetor&Papaioannou, 1975)and one study reported the reverse?nding(Bednarek,Tar-nowski,&Grabowska,2006).Enhanced variability in latency has been found in one study(Biscaldi et al.,1998).However,the overall pattern of?ndings suggests saccade latency to be normal in RD children.The same conclusion can be drawn for velocity,a variable related to latency.Six studies reported(peak)velocity.Five studies found no differences in peak velocity between RD children and controls(Adler-Grinberg&Stark,1978;Black,Collins,De Roach, &Zubrick,1984c;Black et al.,1984a;Leisman&Schwartz,1978; Ygge et al.,1993)and one study reported RD children to be faster, when directing their saccades to the left(Biscaldi,Fischer,&Aiple, 1994).The relation between duration and amplitude(which can be seen as an index of velocity)has been reported to be normal(Petri &Anderson,1980).Taken together,the?ndings indicate that the speed of VGS is normal in RD children.

Six studies that have reported amplitude of VGS,all reported this to be normal in RD(Adler-Grinberg&Stark,1978;Biscaldi et al.,1998;Brown et al.,1983b;De Luca,Di Pace,Judica,Spinelli, &Zoccolotti,1999;Leisman&Schwartz,1978;Raymond et al., 1988).It thus does not appear that RD children under-or overshoot the target stronger compared to controls,when directing their saccades.

A variety of saccades has been studied in RD.No consistent ter-minology has been used in describing the kind of saccades studied, which is probably related to the wide time span in which the studies were conducted.We will describe here the most frequently studied ones.Six studies have reported a comparable type of saccade, namely directed at the target before allowed to do so.However,this type of saccade has been variously labeled‘predictive’,‘forward’,‘anticipatory’,or‘progressive’saccade.The studies reporting on a deviant high frequency of this type of saccades in RD are in the minority(Biscaldi et al.,1998;Pavlidis,1981,1985)compared to the studies reporting on no difference between children with RD and controls(Black et al.,1984c;Brown et al.,1983a,1983b;De Luca et al.,1999;Olson,Kliegl,&Davidson,1983;Stanley,Smith,&Ho-well,1983).The frequency of a saccade directed backwards to the target when overshooting the target(variously labeled corrective, backward,or regressive saccade)was generally found to be normal in most(Biscaldi et al.,1998;Black et al.,1984c;Brown et al.,1983a, 1983b;De Luca et al.,1999;Olson et al.,1983;Stanley et al.,1983) though higher in some studies(Pavlidis,1981,1985).Higher fre-quencies of fast and slow saccades(Biscaldi et al.,1998),Express saccades(Fischer&Weber,1990),big saccades(Black,Collins,De Roach,&Zubrick,1984b),dysmetric saccades(Jerˇa?bek&Krejcˇová, 1991),and intrusive saccades(Fischer&Hartnegg,2000a)have been found in RD.However,these saccades were either only re-ported in one study or?ndings of deviancy were discon?rmed in an-other study,as is the case for big saccades(Black et al.,1984c)and intrusions(Bogacz,Mendilaharsu,&De Mendilaharsu,1974).Prob-ably due to inconsistent terminology,no conclusion can be drawn from these?ndings.It appears,however,that RD may be associated with an increased frequency of saccades in general made during VGS(Brown et al.,1983a;Pavlidis,1981,1985).4.4.6.Smooth pursuit eye movements

SPEM are not used in reading(Adler-Grinberg&Stark,1978). This would only occur if the text was moving,while in fact,the reading material must be held stationary to read ef?ciently (Adler-Grinberg&Stark,1978).Nevertheless,quite a few studies have investigated SPEM in RD.From the seven studies traced that have targeted SPEM in RD,?ve have found dysfunctions(Adler-Grinberg&Stark,1978;Black et al.,1984b;Bogacz et al.,1974; Eden,Stein,Wood,&Wood,1994;Jerˇa?bek&Krejcˇová,1991)while two have not(Leisman&Schwartz,1978;Ygge et al.,1993).Abnor-malities in RD include an increased frequency of(big)saccades (Adler-Grinberg&Stark,1978;Black et al.,1984b),more abnormal saccades(Bogacz et al.,1974),reduced smoothness(Eden et al., 1994),and increased irregularity(Jerˇa?bek&Krejcˇová,1991).Veloc-ity of pursuit,when reported,appears normal in RD(Black et al., 1984b;Leisman&Schwartz,1978;Ygge et al.,1993).Overall,SPEM in children with RD appear to be characterized by an increased fre-quency of(abnormal)saccades,resulting in a decreased smooth-ness,but velocity appears intact in RD.

4.4.7.Conclusions for RD

Literature on non-linguistic eye movement paradigms in RD is dated,resulting in considerable discrepancies between studies in applied terminology,paradigms,and technology.The majority of studies have been conducted in the seventies and eighties when the advanced eye movement technology used currently was not available.This makes drawing of?rm conclusions concerning eye movement dysfunctions in RD hazardous.Nevertheless,some re-sults appear consistent.RD appears associated with a somewhat increased number of saccades during VGS tasks and SPEM,though exactly what type of saccades is unclear.These?ndings may pin-point problems in the integration of the saccadic and pursuit net-works.Antisaccade task performance may also be slightly de?cient in RD,as evidenced by an increase number of errors and misses,reduced number of corrections,and more intrusive saccades,but these?ndings await replication,since only two stud-ies have reported these?ndings.It is safe to say that eye move-ment research in RD is in urgent need of modern studies,using the latest technology to analyze eye movement performance.Stan-dardized terminology would allow for a better comparison be-tween studies with RD children and other types of pathology. The reason why non-linguistic eye movements in RD have not been investigated in recent studies,may be because de?cits in cognitive processes that are directly related to reading are easier to translate to an etiological explanation for RD.The direct impact of de?cits in non-linguistic eye movement on reading is more complicated.

4.5.Childhood-onset schizophrenia

4.5.1.Clinical manifestation of childhood-onset schizophrenia

The essential features of schizophrenia are a mixture of positive and negative symptoms that have been present for a signi?cant portion of time during a1-month period,with some symptoms persisting for at least6months and signi?cantly interfering with social and/or occupational functioning(APA,1994).Positive symp-toms re?ect an excess or distortion of normal functions and in-clude delusions,hallucinations,disorganized thinking and/or speech,and severely disorganized or catatonic behavior(APA, 1994).Negative symptoms re?ect a diminution or loss of normal functions and include affective?attening,alogia(diminution of thoughts re?ected in decreased?uency and productivity of speech),and avolition(inability to initiate or persist in goal-direc-ted activities)(APA,1994).Schizophrenia usually has its onset in late adolescence and early adulthood and is often preceded by a variety of signs and symptoms(such as social withdrawal and loss of interest in school or work).Prevalence rates vary between0.2%

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and2%.Schizophrenia is somewhat more common in males than females and strongly related to genetic factors,although discor-dance between monozygotic twins suggest environmental factors also to play a role(APA,1994).Schizophrenia with childhood onset is rare:50times less frequent than adult-onset(Asarnow, Tompson,&McGrath,2004;Remschmidt,2002;Ross,Heinlein,& Tregellas,2006),though does exist and appears broadly similar in presentation to the adult-onset form(Asarnow et al.,2004). However,some speci?c diagnostic issues are related to child-hood-onset schizophrenia.Disorganized speech may be dif?cult to diagnose before the age of seven,since the speech of young children is frequently less logical and coherent(Asarnow et al., 2004),as well as delusions and hallucinations,which may be less elaborate in children compared to adults(APA,1994).Furthermore, a deterioration of functioning may be dif?cult to establish.Hence, comparing the child to his/her non-affected siblings may aid in determining a failure to achieve what would have been expected for the child(APA,1994).The vast majority of children with schizo-phrenia suffer from comorbid disorders,such as ADHD,ODD, depression,and separation anxiety disorder(Ross et al.,2006). Compared to adulthood-onset,schizophrenia with childhood onset is more common among boys,more strongly associated with struc-tural brain abnormalities,and has a poorer prognosis(APA,1994).

4.5.2.Neurological and cognitive problems in childhood-onset schizophrenia

The most common structural brain abnormalities documented in schizophrenic adult patients are enlargement of the ventricular system and prominent sulci in the cortex.Other abnormalities have also been reported,such as a decreased temporal and hippo-campal size,increased size of the basal ganglia(see glossary),and decreased cerebral size(APA,1994).These abnormalities have also been found in childhood-onset schizophrenia.It appears that the reduction of total cerebral volume in children with schizophrenia is caused by a reduction of gray matter(Remschmidt,2002).A vari-ety of soft neurological signs have been associated with adult schizophrenia,such as poor motor development and coordination, and left/right confusion(APA,1994;Remschmidt,2002).A wealth of literature has been published on cognitive de?cits in schizo-phrenic adult patients.Mainly problems in changing response set,focused attention,and formulation of abstract concepts have been found.Disorientation and memory impairment may also be present(APA,1994).Studies speci?cally targeting cognitive func-tioning in children with schizophrenia have found an overall lower cognitive functioning(lower IQ),increased distractibility,and de-creased verbal comprehension and perceptual organization.Signif-icant delays in motor development and coordination have been reported in children with schizophrenia(Remschmidt,2002).

4.5.3.Eye movement studies in childhood-onset schizophrenia

Eye movement studies in childhood-onset schizophrenia have targeted two groups of subjects:children having schizophrenia themselves and children at-risk for developing schizophrenia be-cause their parent(s)and/or sibling(s)have schizophrenia.Even though this at-risk group may not portray the symptoms of schizo-phrenia,this group of children is informative,since they might de-velop schizophrenia at a later age.Eye movement dysfunctions assessed in this group might thus be informative precursors for schizophrenia.

4.5.4.Visually guided saccades

To our knowledge,only one study reported VGS in schizo-phrenic children and found no dysfunctions(Karatekin&Asarnow, 1998a).Two studies reported VGS in at-risk children.Mather (1985)analyzed the VGS of nine at-risk children,and found that at-risk children made more double-jump saccades.The latency,amplitude and accuracy of saccades appeared normal.Schreiber et al.(1997)analyzed the VGS performance of21at-risk children and reported an increased frequency of hypometric saccades in at-risks.The frequency of hypermetric saccades,non-?xations and omissions was normal.Thus,some slight deviations in VGS ap-pear to be present in at-risk children but VGS studies in childhood-onset schizophrenia are clearly lacking and future research is needed.

4.5.5.Smooth pursuit eye movements

The vast majority of eye movement studies with schizophrenic patients(both children and adults)have focused on the assessment of SPEM.SPEM has a strong emphasis on oculomotor control and less on cognitive processes and is frequently used in schizophrenia given the motor development and coordination problems associ-ated with the disorder.All eight studies that have administered a SPEM task in schizophrenic children(or those at-risk for develop-ing the disorder)have found abnormalities on various measures on the task(Friedman,Schulz,&Jesberger,1993;Gordon et al.,1994; Jacobsen et al.,1996;Kumra et al.,2001;Mather,1985;Ross,2003; Ross,Hommer,Radant,Roath,&Freedman,1996;Ross et al.,1999). Six of the eight studies reported abnormalities in visual pursuit movements;two studies did not?nd pursuit abnormalities in15 schizophrenic children(Pollack&Krieger,1958)and90at-risk children(Schiffman et al.,2006).As the authors of the latter study indicated,their eye movement measures were probably not the same as assessed in SPEM tasks.SPEM tasks appear,therefore,sen-sitive in detecting eye movement abnormalities related to child-hood-onset schizophrenia.

With respect to individual task measures,the most widely mea-sured variable in SPEM is gain(ratio of eye velocity to the target velocity).All four studies on gain in children or adolescents with schizophrenia report a reduced gain(Gordon et al.,1994;Jacobsen et al.,1996;Kumra et al.,2001;Ross,2003.Reduced gain has also been reported in one(Kumra et al.,2001)of two studies in children with psychosis(Friedman et al.,1993;Kumra et al.,2001)and in one(Ross et al.,1996)of two studies in at-risk children(Ross, 2003;Ross et al.,1996).These?ndings concur with?ndings of re-duced gain in adult-onset schizophrenia(Gordon et al.,1994;Ross et al.,2002)and suggest a reduced pursuit velocity is a character-istic sign of pathology in(childhood-onset)schizophrenia.

Another variable in SPEM is the root mean square error.Two studies reported this measure in children with schizophrenia (and psychosis)and one study reported this measure in at-risk children,all reported an increased root mean square error (Jacobsen et al.,1996;Kumra et al.,2001;Ross et al.,1996.These ?ndings are in line with reports in adult-onset schizophrenia (Gordon et al.,1994)and suggest that children with(a risk for developing)schizophrenia have dif?culty in accurately pursuing a moving target.

Other task variables include various forms of saccades,such as corrective catch-up and back-up saccades,intrusive saccades(not directed at the moving target),and anticipatory saccades(lead-ing)saccades.Studies vary in which type of saccades are re-ported.Five studies have reported the frequency of catch-up saccades(Friedman et al.,1993;Jacobsen et al.,1996;Kumra et al.,2001;Ross,2003;Ross et al.,1996).Only one of these stud-ies observed that children with schizophrenia make more catch-up saccades than controls(Kumra et al.,2001).Four studies did not?nd catch-up saccade differences between(at-risk)schizo-phrenics and controls.However,the amplitude of catch-up sac-cades appears to be larger in children with schizophrenia(or psychosis)in three of four studies(Friedman et al.,1993;Gordon et al.,1994;Jacobsen et al.,1996;Ross et al.,1996).The one study that reported back-up saccades documented an increased frequency and amplitude of these types of saccades in schizo-

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phrenic children(Jacobsen et al.,1996).With respect to intrusive saccades,two studies that reported on this measure found chil-dren with schizophrenia and children at-risk had a larger number of intrusive saccades than controls(Gordon et al.,1994;Mather, 1985).Results are clear for anticipatory(leading)saccades,with ?ve of six studies reporting an increased number and/or ampli-tude of these saccades in(at-risk)schizophrenics(Jacobsen et al.,1996;Kumra et al.,2001;Ross,2003;Ross,Heinlein,Zerbe, &Radant,2005;Ross et al.,1996,1999).Taken together,frequent abnormalities in various types of saccades during SPEM are ob-served in children with schizophrenia and at-risk children.The most consistent?nding is an increased frequency of anticipatory (leading)and intrusive saccades.Frequency of catch-up saccades appears to be normal.Insuf?cient data is available regarding the frequency of back-up saccades in childhood-onset schizophrenia.

4.5.6.Memory guided saccades

One large study reported MGS in children with schizophrenia and at-risk children(Ross et al.,2005).Children with schizophrenia made more anticipatory saccades and were less accurate in their saccades than https://www.doczj.com/doc/d48071190.html,tency appeared to be normal.No MGS de?cits were found in at-risk children.

4.5.7.Conclusions for childhood-onset schizophrenia

Eye movement studies in childhood-onset schizophrenia have focused on measuring SPEM,probably to allow for comparison with adult-onset schizophrenia,since SPEM is the most frequently applied eye movement paradigm in adult patients(Ross et al., 2002).Overall,clear SPEM abnormalities are evident in gain(de-crease),anticipatory saccades(increase),root mean square error (increase),and intrusive saccades(increase)in childhood-onset schizophrenia,supporting the hypothesis that dysfunctions are present in the brain networks involved in smooth pursuit(cortical eye?elds,cerebellum,striatum,and/or brainstem).No de?cits have been reported for catch-up saccades in childhood-onset schizophrenia.Preliminary results suggest problems may be pres-ent in VGS and MGS,however,the number of studies available pre-cludes drawing conclusions.

4.6.Tourette’s syndrome(TS)

4.6.1.Clinical manifestation of TS

TS is characterized by multiple motor tics(stereotype move-ments,like eye blinking,grimacing,and jaw,neck,shoulder or limb movements)and one or more vocal tics(like clicks,grunts, and coughs)that may appear simultaneously or at different peri-ods during the illness(Albin&Mink,2006).Tics occur frequently during a day,recurrently throughout a period of more than one year without a tic-free period of more than three months(APA, 1994).Tics can vary in type and frequency over time and are often preceded by urges that are very dif?cult to resist.TS usually be-gins during childhood or early adolescence and by de?nition be-fore the age of18(APA,1994).In most cases,the severity of the disorder reaches its peak during the second decade of life and diminishes by the end of adolescence(Swain,Scahill,Lombroso, King,&Leckman,2007).The estimated prevalence rates of TS vary:once considered as a rare disorder(0.04–0.05%),recent studies using comprehensive ascertainment techniques indicate a larger incidence of TS(up to1%)(Albin&Mink,2006;APA, 1994).Males are1.5–3times more often affected than females. TS is strongly in?uenced by genetic factors,often causing multi-ple family members to portray tics(Albin&Mink,2006;APA, 1994;Swain et al.,2007),although environmental factors such as stress are known to in?uence the expression of tics(Swain et al.,2007).TS is frequently associated with OCD and it may be dif?cult to distinguish complex tics from compulsions(Albin&Mink,2006).ADHD is also a common comorbid disorder of TS( APA,1994).

4.6.2.Neurological and cognitive problems in TS

The underlying complex neural circuitry associated with TS is described in detail in Swain et al.(2007).Considerable knowledge of the underlying neural circuitry has been gathered from studying procedural learning,habit formation,and internally and externally guided motor control in TS.The most important brain structures involved in TS are the basal ganglia,of which the striatal organiza-tion and function seems to be abnormal(Albin&Mink,2006).The direct and indirect basal ganglia pathways provide a balance of excitation and inhibition that may be disrupted in TS.The frontal lobes may play an important role in the suppression of tics(Swain et al.,2007).It appears that TS patients have increased levels of dopaminergic innervation of the striatum and blockage of the dopaminergic receptors can suppress tics(Swain et al.,2007).From a cognitive point of view,inhibitory de?cits are the most fre-quently studied.TS patients appear to have de?cits in prepulse inhibition,manifested in the inability to?lter out unnecessary sen-sory information and resulting in a diminished ability to manage sensory inputs to motor programs(Swain et al.,2007).However, several executive functions(inhibition,visual working memory, planning,cognitive?exibility,and verbal?uency)have found to be normal in TS children(Verté,Geurts,Roeyers,Oosterlaan,& Sergeant,2005).

4.6.3.Eye movement studies in TS

Recently well-designed eye movement studies reviewed below investigated eye movements in pediatric TS patients.These studies have mainly focused upon targeting inhibition by measuring AS, which?ts within the theoretical framework of TS being character-ized as a disinhibitory disorder related to dysfunctions of the basal ganglia.VGS have been measured frequently and in some cases MGS and SPEM in TS.

4.6.4.Antisaccades

Three studies and one case report have measured AS in pediat-ric TS patients(Jackson,Mueller,Hambleton,&Hollis,2007; Mostofsky et al.,2001b;Mueller,Jackson,Dhalla,Datsopoulos,& Hollis,2006;Narita,Shawkat,Lask,Taylor,&Harris,1997).In all three studies,TS patients did not commit more erroneous saccades (i.e.,directional errors)than controls,suggesting that children with TS were not more prone than controls to making a directional error towards the target.Similar normal results were found in TS pa-tients,when they had to maintain their?xation during the presen-tation of distracting stimuli(Bollen et al.,1988).Moreover,two studies reported that TS patients had a paradoxically greater level of cognitive control than controls,since TS patients had less dif?-culty than controls switching between prosaccades and AS within the same task(Jackson et al.,2007;Mueller et al.,2006).The case report by Narita and colleagues(1997),however,reported a com-plete failure of AS(10errors in10trials)in their13-year-old TS pa-tient,but this may be explained by severe general oculomotor abnormalities in this patient.It appears that TS is not associated with inhibitory problems in antisaccade tasks.

4.6.

5.Visually guided saccades

Five studies have reported VGS in children and adolescents with TS and all reported normal latency in TS children(Bollen et al., 1988;Jackson et al.,2007;Mostofsky et al.,2001b;Mueller et al., 2006;Nomura,Fukuda,Terao,Hikosaka,&Segawa,2003).Peak velocity(Bollen et al.,1988;Nomura et al.,2003),variation in la-tency(Mostofsky et al.,2001b)and amplitude(Nomura et al., 2003)were normal when analyzed.These?ndings suggest VGS to be normal in pediatric TS patients.

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4.6.6.Memory guided saccades

MGS have been reported in two studies(Mostofsky et al., 2001b;Nomura et al.,2003).Mostofsky and colleagues applied de-lays of4.5–5s and found a normal accuracy of saccades towards the memorized target in TS patients compared to controls.Nomura and colleagues did not report on deviations in the number of cor-rect saccades towards the memorized target in TS children, although it appeared that TS patients had reduced amplitude of saccades towards the memorized target.In line with the?ndings of normal inhibitory performance on the antisaccade tasks,both studies found no greater degree of anticipatory saccades towards the memorized target in TS patients.These two studies suggest that visuo-spatial working memory and inhibitory control are in-tact in TS children,in a memory guided saccade paradigm,though replication of these?ndings is required.

4.6.7.Smooth pursuit eye movements

SPEM have not been studied extensively in TS children.Bollen et al.(1988)reported normal gain during pursuit in28TS children, although their performance was compared to norm values and not to gender-and age-matched control group,so no?rm conclusions can be drawn.One case report is available(Narita et al.,1997) reporting on normal pursuit in a13-year-old TS patient.

4.6.8.Conclusions for TS

Taken together,pediatric TS does not seem to be associated with dysfunctions in eye movements in the paradigms studied, suggesting the brain areas and cognitive processes involved in the various eye movement paradigms appear intact in TS.

4.7.Childhood-onset obsessive compulsive disorder(OCD)

4.7.1.Clinical manifestation of childhood-onset OCD

OCD is an impairing disorder characterized by recurrent obses-sions and compulsions that are time consuming and/or cause marked distress or signi?cant impairment.Early onset OCD might be associated with an increased genetic susceptibility for the disor-der(Chabane et al.,2005).Obsessions are persistent ideas, thoughts,impulses,or images that cause marked anxiety or https://www.doczj.com/doc/d48071190.html,pulsions are repetitive behaviors,such as checking and ordering,or mental acts,like counting or repeating words silently (APA,1994).The goal of the compulsions is to prevent or reduce the anxiety triggered by the obsessions.OCD usually begins grad-ually during adolescence or young adulthood,is(partially)deter-mined by genetic factors and is equally common in both sexes (about2.5%),although the symptoms appear somewhat earlier in males than in females(APA,1994,Chabane et al.,2005; Mataix-Cols,Concei??o do Rosario-Campos,&Leckman,2005). The disorder is heterogeneous,even to the extent that two patients with the same diagnosis can display non-overlapping symptom patterns(Mataix-Cols et al.,2005),and co-occurs frequently with TS(APA,1994).Presentation of OCD in children is generally similar to that in adults,although children may fail to realize the exces-siveness or unreasonableness of their obsessions and compulsions and generally do not request help(APA,1994).

4.7.2.Neurological and cognitive problems in childhood-onset OCD

Obsessive compulsive symptoms have mainly been linked to activation in the orbitofrontal cortex,with less consistent results for involvement of the anterior cingulate gyrus,striatum,thalamus (see glossary),lateral frontal and temporal cortices,amygdala,and insula(Mataix-Cols et al.,2005).In animal models and studies of patients with lesions in the orbitofrontal areas and its ventral stri-atal target?elds,a selective disturbance in the ability to suppress responses to irrelevant stimuli has been found(O’Hearn, Rosenberg,Dick,&Sweeney,1996).In line with this,an MRI study on pediatric patients with OCD showed these patients to have vol-umetric abnormalities in the ventral prefrontal cortical and striatal regions(Rosenberg&Keshavan,1998).Interestingly,no abnormal-ities were found in the dorsolateral prefrontal cortex,a brain area strongly involved in working memory(Blumenfeld&Ranganath, 2006),which suggests that OCD is selectively associated with inhi-bition problems but not with working memory(i.e.,forgetting whether an action has been completed and therefore checking it) or generalized executive dysfunctions,as has been previously sug-gested(Frampton,2004).

4.7.3.Eye movement studies in childhood-onset OCD

Studies using eye movement paradigms are scarce in OCD and focus almost exclusively on adult patients.Only one study has re-ported on children(Rosenberg et al.,1997a).Four tasks were administered,all hypothesized as tapping into prefrontal cortical functions:an AS task,a MGS task,a VGS task with unpredictable targets,and a predictive saccade task.Children with OCD commit-ted signi?cantly more erroneous saccades compared to age-matched controls on the AS task as well as marginally signi?cantly more anticipatory saccades on the MGS task,supporting the hypothesis that OCD is associated with inhibitory problems possi-bly related to(orbito)frontal dysfunctions.No other dysfunctions in oculomotor performance were found,suggesting working mem-ory and general oculomotor control mechanisms are intact in pedi-atric OCD patients.Thus,preliminary results suggest that a disturbance in inhibition may underlie the repetitive behavior characterizing the illness.However,no?rm conclusions can be drawn until these?ndings are replicated in other studies compris-ing larger samples.

4.8.Anxiety and depression

4.8.1.Clinical manifestation of anxiety and depression

Anxiety in children may manifest itself in several distinct syn-dromes,of which separation anxiety disorder,overanxious disor-der,and speci?c phobias are the most common(Bernstein, Borchardt,&Perwien,1996).Separation anxiety is characterized by excessive anxiety concerning separation from home or attach-ment?gures,which causes clinically signi?cant distress or impair-ment in social and/or academic functioning(APA,1994).Children suffering from this disorder often refuse to go to school,have sleeping dif?culties,and repeated nightmares.Overanxious disor-der encompasses excessive anxiety and worries,which are out of proportion to the actual likelihood of the feared event and are dif-?cult to control for the child.Children with this disorder may be overly conforming,perfectionist,and unsure of themselves and tend to redo tasks because of excessive dissatisfaction with less-than-perfect performance(APA,1994).Speci?c phobias are marked and persistent fears cued by the presence or anticipation(see glos-sary)of a speci?c object or situation(such as animals,seeing blood, receiving an injection).These fears may be expressed by crying, tantrums,or clinging in children and they may be unaware of the unreasonableness of their fears.Anxiety disorders are quite com-mon in childhood and adolescence,with estimates varying be-tween4%and15%,and tend to be familial(APA,1994;Bernstein et al.,1996).Slightly more girls than boys are affected.The most frequent comorbid disorder of an anxiety disorder is another anx-iety disorder,followed by comorbid depression(APA,1994).

It has been suggested that anxiety and depression are variants of a single mood disorder,but the more widely held view is that de-spite their considerable overlap,the two constructs are separate entities(Brady&Kendall,1992).Both disorders are characterized by negative affectivity,but depression involves low positive affect, whereas anxiety is not related to positive affect(Brady&Kendall, 1992).Nevertheless,common genetic and environmental factors

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relate to both disorders and symptoms of anxiety often precede symptoms of depression(Brady&Kendall,1992).Depression is characterized by a marked depressed mood,though it may be ex-pressed as irritableness in children,and/or the loss of interest in activities(APA,1994).It is often accompanied by a reduced appetite, sleeping problems,feelings of worthlessness or guilt,and concen-tration problems.In children,somatic complaints,irritability,and social withdrawal are particularly common.Like anxiety,depres-sion is more common in females than males and is familial.Typical age of onset is(early)adulthood,but it can occur in children(0.4–2.5%)and adolescents(0.4–8.3%)(APA,1994;Birmaher et al.,1996).

4.8.2.Neurological and cognitive problems in anxiety and depression

Anxiety disorders have been associated with an increased activity of the amygdala,as well as an increased activity of the anterior cin-gulate and decreased activity of the medial prefrontal cortex(Anand &Shekhar,2003).In depression,a decreased activation of the ante-rior cingulate cortex may lead to a dysregulation of certain limbic areas,such as the amygdala(Anand&Shekhar,2003).The dorsolat-eral prefrontal cortex appears to be under activated in depression (Anand&Shekhar,2003).Little research is available on cognitive problems in children and adolescents with anxiety and depression. It appears that anxious children have an overall lower level of cogni-tive functioning and academic achievement and problems have been found both on verbal,non-verbal,and executive(?exibility and inhi-bition)tasks(Kusché,Cook,&Greenberg,1993).Comparable prob-lems in executive functions were found in anxious-depressed boys (Emerson,Mollet,&Harrison,2005).

4.8.3.Eye movement studies in anxiety and depression

To the best of our knowledge,only two studies are available documenting on eye movements in children with anxiety disorders and depression.Jazbec,McClure,Hardin,Pine,and Ernst(2005) administered an AS task under neutral,reward and punishment conditions to anxious and depressed adolescents.No group differ-ences were found regarding accuracy and no group by condition interaction was found thus indicating that anxiety and depression in adolescents were not associated with an increased number of erroneous https://www.doczj.com/doc/d48071190.html,tency and peak velocity differed between the groups and group differences were modulated by condition. Normal adolescents showed an improvement in latency and peak velocity,when rewarded or punished for their performance.This was not found in anxious and depressed adolescents.Indeed,the opposite effect was found in anxious adolescents for latency(i.e. an increase),particularly when punished.These?ndings suggest that performance on the AS task can be in?uenced by motivation in normally developing adolescents,but a motivation manipula-tion has no effect or a deteriorating effect in anxious and depressed adolescents.The AS task was used two years later by Hardin, Schroth,Pine,and Ernst(2007),who manipulated the frequency of reward and punishment,although this did not appear to in?u-ence results.In contrast to the previous study,group differences were present for accuracy:depressed adolescents made more er-rors than healthy adolescents;anxious adolescents performed intermediately between both groups.These group differences were not in?uenced by condition.In agreement with the previous study, groups were differently affected by condition with respect to la-tency.Again,the latency of healthy adolescents improved more strongly when rewarded or punished than the latency of anxious or depressed adolescents.Taken together the results of both stud-ies suggest that there is preliminary evidence for deviations in the performance of anxious and depressed adolescents on an AS task. Mainly the insensitivity of the latency of saccades for reward or punishment appears to be a sensitive indicator of pathology relat-ing to negative affectivity,possibly re?ecting de?cits in the speed of inhibiting a response(Jazbec et al.,2005).5.Overlap and speci?city of?ndings across eye movement paradigms and across psychiatric disorders

Table2provides an overall summary of?ndings of(ab)normal-ity of eye movements in psychiatric disorders.AS have been inves-tigated in the majority of disorders reviewed here.An elevated number of directional errors appears present in ADHD,ASD,RD, OCD,and anxiety and depression.No AS have been investigated in schizophrenia or ODD/CD.Only TS does not appear to be associ-ated with an increased frequency of directional errors.These?nd-ings suggest that AS are sensitive in detecting abnormal psychological functioning in general,but cannot be used for iden-tifying speci?c types of pathology.Rather,most psychiatric disor-ders in childhood and adolescence appear related to dysfunctional inhibitory control,as indicated by the inability to suppress re?exive saccades towards the target(prosaccades),sug-gesting impaired frontal functioning is common in most childhood psychiatric disorders.

VGS have also been frequently investigated,but appear less sen-sitive to general psychiatric deviancy than AS.ASD,schizophrenia, TD,and OCD do not appear to be associated with dysfunctional VGS.The majority of studies on VGS in RD have documented nor-mal performance,although a general elevated number of saccades appears related to RD.Only in ADHD have problems in VGS been consistently reported:children with ADHD have overall more var-iable and possibly somewhat slower saccade latencies than control children.This suggests VGS to be an interesting research tool to ex-plore the uniqueness of underlying neurological pathology of ADHD and also suggests that most childhood disorders are not characterized by de?cits in the basic neurological substrate of eye movements,such as the cerebellum and frontal eye?elds.

MGS appear de?cient in various psychiatric disorders.A de-creased accuracy of MGS has been found in ADHD,ASD,and schizo-phrenia,suggesting these disorders may share a weakness in visuo-spatial memory abilities.An elevated number of anticipatory saccades during MGS has been documented in ADHD,ASD,schizo-phrenia,and OCD,making this measure sensitive to inhibitory problems occurring in most psychiatric disorders,but insensitive in detecting speci?c pathology.Like the?ndings on AS,the?ndings on MGS suggest impaired frontal functioning is common in child-hood psychiatric disorders.

Although strongly related to schizophrenia,abnormalities in SPEM are also found in other disorders.Frequently found abnor-malities in schizophrenia,such as reduced gain,increased root mean square error,and increased saccade frequency,have been found in relation to ADHD,ASD,and RD.Only TS does not seem to be related to problems in SPEM.Since SPEM involve a complex interaction between various cortical and subcortical brain areas, it is dif?cult to interpret these?ndings with respect to speci?city and overlap of cognitive and neurological dysfunctions across the various disorders.

Overall,the AS,MGS,and SPEM paradigms were able to discrim-inate between psychologically normal and abnormal subjects, making them useful tools in experimental and clinical practice. However,they lack speci?city,making it dif?cult to distinguish be-tween eye movement dysfunctions amongst the various disorders. The reverse appears to be true for VGS,which appear generally normal in most disorders,but de?cient in ADHD.

6.Developmental aspects of eye movement abnormalities in childhood and adolescence psychiatric disorders

All eye movement tasks discussed in this review are heavily in?uenced by developmental changes in brain maturation(Luna and colleagues,this issue).Mainly AS and MGS,and to a lesser ex-

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tent VGS and SPEM,continue to develop through adolescence (Klein,Foerster,Hartnegg,&Fischer,2005).It may thus be feasible that the eye movement de?cits associated with childhood and ado-lescent psychiatric disorders described in this review,correct themselves by the end of adolescence.A brief review of adult eye movement literature may indicate whether characteristic eye movement dif?culties present in children and adolescents with a disorder are also present (or not)in adults with the disorder.Importantly,however,psychiatric disorders occurring during childhood and adolescence may not necessarily be comparable to psychiatric disorders occurring during adulthood.Other genetic and environmental factors may in?uence psychiatric functioning during childhood/adolescence and adulthood.Certain disorders typically become apparent during childhood and remit during late adolescence/adulthood (ADHD,ASD,and TS),whereas others typi-cally become apparent in late adolescence/adulthood (schizophre-nia,OCD,and depression).Adults having a disorder that usually improves during late adolescence/adulthood and children having

a disorder that usually does not become apparent until late adoles-cence/adulthood,may be atypical groups.Thus,even though reviewing adult eye movement literature may shed light on the developmental continuity of eye movement de?cits reported in children and adolescents with psychiatric disorders,comparing re-sults is somewhat hazardous.

6.1.Attention-de?cit/hyperactivity disorder

As described earlier and in Table 2,ADHD in childhood and ado-lescence is characterized by an increase of AS errors,an increase in VGS latency,and also with more anticipatory saccades and de-creased accuracy on MGS,and with some SPEM abnormalities.One study assessed eye movements in both children and adults with ADHD and found similar de?cits in VGS and AS in both groups (Munoz et al.,2003),which was in line with ?ndings from another study on abnormalities during VGS and AS in adults with ADHD (Feifel,Farber,Clementz,Perry,&Anllo-Vento,2004).In addition,

Table 2

General conclusions regarding ?ndings of (ab)normal eye movements across various paradigms in psychiatric disorders in childhood and adolescence Disorders

Eye movement paradigms AS

VGS

MGS

SPEM

Conclusion

ADHD

------ADHD characterized by inhibitory problems across paradigms,possibly re?ecting

dysfunctions in frontal areas like DLPFC.Basic eye movement control may also be impaired,re?ecting frontal eye ?eld and cerebellar deviations

"errors

"SD latency,

possibly "latency

"anticipatory saccades,;accuracy

"root mean square error,"saccades

ODD/CD ????

ODD and CD may be associated with similar eye movement ?ndings as ADHD given the high degree of comorbidity between ADHD and ODD/CD

ASD

--ASD associated with inhibitory problems,

possibly re?ecting frontal cortex dysfunctions.Saccadic control appears normal,but smooth pursuit not,which may suggest various non-cortical areas may be involved in ASD

"errors

"anticipatory saccades,"saccades,;gain

;accuracy,"latency

--?

--RD appears related to an increased number of saccades across paradigms studied and with decreased smooth persuit,possibly re?ecting problems in the integration of the saccadic and pursuit networks

"errors,"misses "saccades

"saccades,;smoothness

Schizophrenia ?+

----Schizophrenia characterized by abnormal

smooth pursuit,re?ecting abnormal functioning of cortical eye ?elds,cerebellum,striatum,and brainstem.Frontal functioning may also be abnormal.

"anticipatory saccades,"root mean square error,

;accuracy ;gain,"saccades TS +++

TS appears not associated with eye movement abnormalities,inhi bitory or working memory problems,suggesting most cortical and non-cortical areas involved in eye movements function normally

OCD

OCD may be associated with inhibitory de?cits related to problems in the (orbito)frontal areas.Basic saccadic control appears normal

"errors

"anticipatory saccades AD/

depression -??

AD and depression associated with insensitivity of saccade latency for reward or punishment,possibly re?ecting abnormalities in inhibition related to frontal areas

"errors,"latency

Conclusion

AS sensitive in detecting general abnormal

functioning,but not in discriminating between disorders

VGS not sensitive in

detecting general abnormal functioning,but appears discriminative for ADHD

MGS sensitive in detecting general abnormal

functioning,but not in discriminating between disorders SPEM sensitive in detecting general abnormal

functioning,but not in discrim

Note.+,(probably)normal;-,possibly abnormal;--,probably abnormal;---,abnormal;?,not investigated.

AS,antisaccades;VGS,visually guided saccades;MGS,memory guided saccades;SPEM,smooth pursuit eye movements;ADHD,attention de?cit hyperactivity disorder;ASD,autism spectrum disorders;RD,reading disorder;TS,Tourette’s syndrome;OCD,obsessive-compulsive disorder;AD,Anxiety disorder;ODD,oppositional deviant disorder;CD,conduct disorder.

408N.N.J.Rommelse et al./Brain and Cognition 68(2008)391–414

a further study reported an increase in the percentage of prema-ture saccades during MGS in young adults with ADHD(Ross, Harris,Olincy,&Radant,2000),which has also been reported in children and adolescents with ADHD.However,accuracy of MGS appeared normal in ADHD adults in this study and no SPEM impairment were present in a group of adults with ADHD(Ross, Olincy,Harris,Sullivan,&Radant,2000).Overall,eye movement de?cits on paradigms most strongly associated with ADHD in childhood and adolescence(AS and VGS)appear also present in adults with ADHD,with some mixed/negative results found for eye movement de?cits on paradigms less robustly associated with ADHD(MGS and SPEM).

6.2.Oppositional deviant disorder and conduct disorder

We were not able to locate any studies documenting eye move-ments in adults with conduct disorder or criminal behavior,as was the case in children with ODD or CD.

6.3.Autism spectrum disorder

With respect to ASD,several studies have documented on AS, VGS,en MGS in autistic adults.Mixed?ndings have been reported for VGS,although most studies reported no abnormalities (Minshew,Luna,&Sweeney,1999;Takarae,Minshew,Luna,& Sweeney,2007),but some found some evidence for abnormal accuracy during VGS(Luna et al.,2007).However,a functional magnetic resonance imaging(fMRI(see glossary))study and an ERP(event-related potential)study found atypical brain activation (Takarae et al.,2007)and ERP potentials(Kawakubo et al.,2007) during VGS in adults with ASD even when behavioral data for VGS was normal(Takarae et al.,2007),suggesting the underlying neural substrate for VGS may be abnormal in ASD in adults.Normal behavioral data on VGS are in line with?ndings in children and adolescents with ASD.An increased number of errors during AS and MGS in adults with ASD has been documented in two studies (Luna et al.,2007;Minshew et al.,1999),and is in line with?nd-ings for children and adolescents with ASD.Furthermore,abnor-malities in SPEM have been found in adults with ASD,as well as children and adolescents(Takarae et al.,2004).It thus seems that most?ndings on abnormalities in eye movements documented in children and adolescents with ASD appear also to be present in adults with ASD.

6.4.Reading disorder

In adults with RD,increases in frequency of saccades during dif-ferent VGS paradigms have been documented(Biscaldi et al.,1998; Fischer,Biscaldi,&Otto,1993),with additional evidence for abnor-mal saccade latencies(Biscaldi et al.,1998;Fischer et al.,1993; Ram-Tsur,Faust,Caspi,Gordon,&Zivotofsky,2006).The?ndings for an increase in saccades during VGS are in line with the?ndings reported in children and adolescents,although abnormal latencies have not been reported consistently in childhood and adolescent literature.

6.5.Schizophrenia

The number of studies on eye movements in adults with schizo-phrenia is far greater than the number of studies on eye move-ments in children and adolescents with schizophrenia,since schizophrenia in the former group is more common than schizo-phrenia in the latter group.Abnormalities in SPEM performance (reduced gain and an increased number of saccades)and reduced brain activation during SPEM have been consistently found in adults with schizophrenia(Boudet et al.,2005;Keedy,Ebens,Keshavan,&Sweeney,2006;Smyrnis et al.,2007;Zanelli et al., 2005),and is in line with?ndings of children and adolescents with the disorder(Ross et al.,2002).In addition,abnormal AS,VGS,and MGS performance and abnormal brain activation during these types of saccades have also been found in adults with schizophre-nia(Boudet et al.,2005;Keedy et al.,2006;Zanelli et al.,2005), suggesting abnormal eye movements in adult schizophrenia are generalized across paradigms and even correlated across para-digms(Zanelli et al.,2005).Findings for AS,VGS,and MGS perfor-mance in children and adolescents with schizophrenia are scarce, but suggest some abnormalities may be present in MGS.No abnor-malities have been reported for VGS in children and adolescents with schizophrenia and no studies have investigated AS in this group.All in all,SPEM abnormalities are evident in both children, adolescents and adults with schizophrenia,but?ndings are not yet conclusive regarding eye movement abnormalities in other paradigms.

6.6.Tourette’s syndrome

Pediatric TS does not seem to be associated with dysfunctions in eye movements in the paradigms studied,suggesting the brain areas and cognitive processes involved in the various eye move-ment paradigms appear intact in TS.This is remarkable,given that studies on adult TS generally report on longer latencies,more anticipatory and intrusive saccades,and abnormal amplitudes in adult TS patients(Dursun,Burke,&Reveley,2000;Farber,Swerd-low,&Clementz,1999;LeVasseur,Flanagan,Riopelle,&Munoz, 2001;Munoz,LeVasseur,&Flanagan,2002;Straube,Mennicken, Riedel,Eggert,&Müller,1997).The abnormal eye movement?nd-ings in adults with TS might be explained by the fact that individ-uals with tics persisting into adulthood may be an atypical group (Albin&Mink,2006),since the symptoms of TS diminish substan-tially during adolescence and only20%or fewer of children with TS continue to experience a moderate level of impairment by the age of20(Swain et al.,2007).

6.7.Obsessive compulsive disorder

In contrast to childhood and adolescents literature,studies on eye movement in OCD in adults are numerous.As performance appears normal in adults with OCD,except for a somewhat long-er latency(Maruff,Purcell,Tyler,Pantelis,&Currie,1999; Rosenberg,Dick,O’Hearn,&Sweeney,1997b;Van der Wee et al.,2006).This contrasts with the one study in childhood-on-set OCD,where an increase of the number of errors was found (Rosenberg et al.,1997a),although an increase in errors has also been reported in adults with OCD when the peripheral visual targets were presented close to central?xation(Rosenberg,Dick, O’Hearn,&Sweeney,1997b).Some abnormalities have been re-ported in VGS in adults with OCD,such as reduced peak velocity (Rosenberg,Dick,O’Hearn,&Sweeney,1997b),decreased accu-racy(Gambini,Abbruzzese,&Scarone,1993)and an increased number of predictive and corrective saccades(Spengler et al., 2006).This contrasts with normal VGS in the one OCD child study(Rosenberg et al.,1997a).However,normal VGS has also been reported in adults with OCD(Maruff et al.,1999;Nickoloff, Radant,Reichler,&Hommer,1991;Van der Wee et al.,2006),as was normal latency and accuracy(Gambini et al.,1993; Rosenberg,Dick,O’Hearn,&Sweeney,1997b).It thus remains inconclusive as to whether or not OCD in childhood and/or adulthood is associated with impairments in VGS.MGS,though not heavily investigated in adults or children/adolescents with OCD,appeared normal in one study on adults(Rosenberg,Dick, O’Hearn,&Sweeney,1997b),but characterized by an increased number of anticipatory saccades in children(Rosenberg et al.,

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1997a).Clearly,more studies are needed to draw?rm conclu-sions for MGS in OCD.SPEM has been examined only in adults with OCD,but not children or adolescents,and?ndings are inconsistent.Normal SPEM has been reported(Nickoloff et al., 1991;Spengler et al.,2006),slightly abnormal SPEM has been reported(normal pursuit except for smaller catch-up saccades) (Clementz,Farber,Lam,&Swerdlow,1996),as well as abnormal SPEM(reduced gain and/or increased number of anticipatory saccades or square wave jerk intrusions)(Gambini et al.,1993; Pallanti et al.,1996;Sweeney,Palumbo,Halper,&Shear,1992). These inconsistent?ndings may be related to differences in velocity of the targets in the different studies,because it has been suggested that patients with OCD may have only a modest SPEM de?cit that is elicited only while following faster velocity targets(Clementz et al.,1996).In conclusion,?ndings for eye movement impairments in adult OCD are evident,partly overlap with?ndings of the one study in children and adolescents with OCD,and suggest more studies are needed that examine eye movements in childhood-onset OCD.

6.8.Anxiety and depression

Studies reporting on eye movements in relation to anxiety and depression in adults are not numerous,but some consistent?nd-ings do emerge.Errors on AS have been found to be related to anx-iety,though not related to depression(Sha?q-Antonacci et al., 1999;Smyrnis et al.,2003).Depression was found to be related to poorer saccade latency(Sha?q-Antonacci et al.,1999),though not consistently(Smyrnis et al.,2003).An increase in AS errors and latency has also been documented in anxious and depressed children and adolescents.VGS and MGS have hardly been studied in adults with anxiety and depression,as was the case in the child-hood and adolescent literature.One study documented on normal peak velocity and accuracy on VGS,but slower latency in adults with depression(Mahlberg,Steinacher,Mackert,&Flechtner, 2001).SPEM is a more frequently studied task,and pursuit gain has been found abnormal in several studies in relation to depres-sion in adults(Flechtner,Steinacher,&Mackert,1997;Kathmann, Hochrein,Uwer,&Bondy,2003;Malaspina et al.,1994),though not in all studies(Smyrnis et al.,2007).Because only AS have been studied in children and adolescents with anxiety and depression, comparison between eye movement results in children/adoles-cents and adults is limited,but results for AS appear to agree be-tween children/adolescents and adults with anxiety and depression.

7.Recommendations for future research

It has become clear from reviewing the literature on eye movement studies in childhood and adolescence psychiatric dis-orders that for each disorder,a line of research has evolved rel-atively independently of the lines of research for the other disorders.This is largely driven by hypotheses regarding the nat-ure of the underlying neurological and cognitive problems of each disorder.For example,the vast majority of studies in RD has focused on VGS,since it has been hypothesized that reading problems might be partly related to saccadic dysfunctioning (Pavlidis,1980,1981,1985).Since SPEM abnormalities have been consistently found in adults with schizophrenia,the most obvious and dominant area of focus in childhood-onset schizo-phrenia has been SPEM.This is,of course,a sensible approach when comprehensively unravelling the eye movement impair-ments associated with that disorder.Different illnesses raise dif-ferent questions and,thus,different methodologies can be of value.However,increasing knowledge is gained on the shared genetic,neurobiological and neuropsychological impairments of psychiatric illnesses.Eye movement research may contribute to this line of research by standardizing methodologies and/or by including several groups of psychiatric patients and comparing those with controls in a study,instead of one group of patients comparing to controls.We do not advocate that studying eye movements in one psychiatric disorder is less sensible that studying eye movements in several psychiatric illnesses in order to compare eye movement de?cits across disorders,but rather want to emphasize that the latter approach(examining eye movements in several groups of psychiatric illnesses instead of just one)has not received enough attention in the eye move-ments literature,but should be given more consideration in light of the increasing knowledge on shared genetic,neurobiological, and neuropsychological factors across disorders.Therefore,our ?rst recommendation for future research is to use similar eye movement paradigms in various disorders in order to examine the speci?city and overlap of eye movement de?cits for these disorders.For example,ADHD frequently co-occurs with ODD/ CD and RD.It would facilitate the understanding of the nature of the individual disorders and their overlap if eye movements would be measured in children suffering from one or a combina-tion of these disorders in a so-called double dissociation design (Cantwell,1995;De Jong,Oosterlaan,&Sergeant,2006).The same is true for OCD and TS.In addition to this,it is likely that the available studies have included patients with multiple disor-ders,while reporting the effect of one disorder on eye move-ments.That is,the vast majority of children suffering from a psychiatric disorder suffer from at least one other psychiatric disorder(Caron&Rutter,1991).Failure to take these comorbid conditions into account when analyzing eye movement perfor-mance,as has been done in almost all eye movement studies, makes it dif?cult to determine the communality and speci?city of?ndings for these childhood disorders.

Some disorders have received considerable attention from eye movement researchers,whereas other disorders have not. We were unable to locate any studies investigating eye move-ments in children with behavioral problems(ODD/CD),hardly any studies in children with anxiety/depression and OCD,and only a few studies in children with TS.Clearly,more work is needed in investigating eye movements in these pediatric psy-chiatric groups.It may prove valuable to expand the focus of re-search in RD and schizophrenia outside respectively the areas of SPEM and VGS,since the few studies that have done that,have found de?cits.

A?nal recommendation for future research relates to the developmental aspect of disorders in childhood and adolescence. Many children suffering from a psychiatric disorder become psy-chiatrically impaired adults.However,this is not a100%continu-ity,since some children do not suffer from psychiatric problems, when grown up or suffer from another disorder than that diag-nosed in childhood(Hollis,2000;Mannuzza,Klein,Bessler,Mal-loy,&LaPadula,1993;Zoccolillo,Pickles,Quinton,&Rutter, 1992).Thus,there is both continuity and discontinuity in psychi-atric development.A recommendation for future research is to longitudinally study eye movement parameters in children with psychiatric disorders growing up.Like for certain neurobiological and cognitive measures,some eye movement parameters mea-sured early in life may prove to be related to psychiatric function-ing later in life.This eye movement parameter may than be used to form a more homogeneous subgroup of patients having the eye movement de?cit in common,for whom the longitudinal out-come of their disease may be more similar than for the whole group of patients with that disorder.In addition,the eye move-ment de?cit may also shed light on the involvement of brain areas/systems in causing the disorder at an early stage for this subgroup of patients.

410N.N.J.Rommelse et al./Brain and Cognition68(2008)391–414

六年级上册语文造句、四字词语、成语填空练习(答案)

六年级语文造句练习班级：姓名：类型一：词语造句一、根据“成熟”的不同意思各造一个句子。 1.指植物的果实完全长成：秋天到了，苹果成熟了，远看像一个个小灯笼。 2.发展完善的程度：时机尚未成熟，警察局逮捕犯罪嫌疑人的计划还需要再完善。二、根据“墨水”的不同意思各造一个句子。 1.墨水（墨汁）：今天我买了一瓶红色墨水，花了我5元钱。 2.墨水（学问）：鲁迅满肚子的墨水，写出的文章不计其数。三、根据“仿佛”的不同意思各造一个句子。 1.仿佛（差不多）：我和闰土仿佛年龄。 2.仿佛（好像）：中秋的月亮挂在天空，仿佛是一块大玉盘。四、根据“谎言”的不同意思各造一个句子。 1.谎言（善意的谎言）：老教授用善意的谎言，鼓励年轻人成才的美德值得学习。 2.谎言（恶意的谎言）：他常常用花言巧语，编制各种谎言骗取钱财，令人憎恶！五、根据“大方”的不同意思各造一个句子。 1.大方（不小气）：他待人很大方，从不斤斤计较，深得别人喜爱。 2.大方（不拘束）：舞蹈演员在舞台上表演，大方自然，一点儿也不紧张、拘束。六、根据“精神”的不同意思各造一个句子。 1.表现出来的活力：王老师一头短发，一身西服，整个人显得很精神。 2.活跃、有生气：你看，赛场上同学们精神抖擞，各个摩拳擦掌。 3.人的意识、思维活跃等：雷锋助人为乐的精神，要世世代代传承下去。七、根据“骄傲”的不同意思各造一个句子。 1.表示自豪的意思：我为祖国在科技上取得的巨大成就感到骄傲！ 2.表示自满的意思：一考到90分，他就骄傲了，常常在同学们面前夸耀自己。八、根据“厉害”的不同意思各造一个句子。 1.表示批评的意思：你真厉害！这么容易的题目你都会做错！ 2.表示表扬的意思：刘翔真厉害！又获得好成绩，他是我们中国人的骄傲！九、根据“毛病”的不同意思各造一个句子。 1.表示疾病的意思：一到冬天，爸爸的腿隐隐作痛，应该是老毛病又犯了。

六年级上语文期末试题

六年级上语文期末试题一、看拼音写词语。（10分） kān cè bǔ rǔ yóu yù dǐnɡ lǐ mó bài 六年级上语文期末试题 hūn yōnɡ jiān rèn fán zhípī bō zhǎn lànɡ（）（）（）（）二、选择准确的答案；六年级上语文期末试题（6分） 1.下列带点字读音错误的一项是（）。 A 耸（sǒnɡ）立 B 衣襟（jīn） C 骤（zòu）雨 D 餐（cān）馆 2. 下列词语中有错别字的一项是（）。 A 广袤无垠 B 唱念坐打 C 废墟 D 杀戮 3. 下列词语中带点字解释正确的一项是（）。 A 悲愤欲绝（断绝） B 生死攸关（所） C 节衣缩（缩小）食 D 狂风怒号（标志） 4．与“横行霸道”感情色彩一样的词语是（）。 A 艰苦卓绝 B 喜出望外 C 忠于职守 D 负隅顽抗 5. （）春节；家家户户都在忙着准备年货。 A 临近 B 邻近 C 靠近 D 挨近 6.下列哪个词语与其他词语不属于同类？（） A 余音绕梁 B 锣鼓喧天 C 一碧千里 D 惟妙惟肖三、按要求写词语或句子。（10分） 1. 下面的横线上该填什么风呢？（4分）细雨暴雨送爽知劲草2．根据“地道”的不同读音造句。（2分） dì dào： dì dɑo： 3．请将句子补充完整。（1分）

处处留心皆学问；。《古今贤文》（读书篇）4．在原句上用修改符号修改病句。（其中有3个错别字；3个病句）（3分）冬天到了；同学们纷纷穿上了绵衣和手套。下课铃声一响；大家立既整队进入操场；参加跑操活动。经过一个冬天的锻练；使同学们增强了身体。四、填空。（13分） 1.那些小丘的线条是那么；就像只用；不用墨线勾勒的中国画那样；到处；。这种境界；既；又；既愿；又想坐下低吟一首的小诗。 2. 我们爱你——桂林山水的；杭州西湖的；黄山、庐山的；长江、黄河的。我也能接着写一句：我们爱你——的…… 3. 《詹天佑》一文主要写了詹天佑在修筑铁路的过程中所发生的、、三件事；说了詹天佑是我国杰出的爱国工程师。本学期我们学过的像詹天佑这样伟大的人物还有情系家乡孩子的大作家；爱国科学家 4.后生们的胳膊、腿、全身；有力地搏击着；急速地搏击着；大起大落地搏击着。它着你；着你；着你。从所填的词语；我体会到。五、阅读短文；回答问题。（27分=6分+10分+11分）（一）船长（节选）船长哈尔威屹立在舰桥上；一个手势也没有做；一句话也没有说；随着轮船一起沉入了深渊。人们透过阴森可怖的薄雾；凝视着这尊黑色的雕像徐徐沉入大海。哈尔威船长一生都要求自己忠于职守；履行做人之道。面对死亡；他又一次运用了成为一名英雄的权利。 1．这两段话应该怎样读？请用“√”选择。（2分）语速：①急促②平缓③适中

尊重的素材

尊重的素材（为人处世）思路人与人之间只有互相尊重才能友好相处要让别人尊重自己，首先自己得尊重自己尊重能减少人与人之间的摩擦尊重需要理解和宽容尊重也应坚持原则尊重能促进社会成员之间的沟通尊重别人的劳动成果尊重能巩固友谊尊重会使合作更愉快和谐的社会需要彼此间的尊重名言施与人，但不要使对方有受施的感觉。帮助人，但给予对方最高的尊重。这是助人的艺术，也是仁爱的情操。—刘墉卑己而尊人是不好的，尊己而卑人也是不好的。———徐特立知道他自己尊严的人，他就完全不能尊重别人的尊严。———席勒真正伟大的人是不压制人也不受人压制的。———纪伯伦草木是靠着上天的雨露滋长的，但是它们也敢仰望穹苍。———莎士比亚尊重别人，才能让人尊敬。———笛卡尔谁自尊，谁就会得到尊重。———巴尔扎克人应尊敬他自己，并应自视能配得上最高尚的东西。———黑格尔对人不尊敬，首先就是对自己的不尊敬。———惠特曼

每当人们不尊重我们时，我们总被深深激怒。然而在内心深处，没有一个人十分尊重自己。———马克·吐温忍辱偷生的人，绝不会受人尊重。———高乃依敬人者，人恒敬之。———《孟子》人必自敬，然后人敬之；人必自侮，然后人侮之。———扬雄不知自爱反是自害。———郑善夫仁者必敬人。———《荀子》君子贵人而贱己，先人而后己。———《礼记》尊严是人类灵魂中不可糟蹋的东西。———古斯曼对一个人的尊重要达到他所希望的程度，那是困难的。———沃夫格纳经典素材 1元和200元（尊重劳动成果）香港大富豪李嘉诚在下车时不慎将一元钱掉入车下，随即屈身去拾，旁边一服务生看到了，上前帮他拾起了一元钱。李嘉诚收起一元钱后，给了服务生200元酬金。这里面其实包含了钱以外的价值观念。李嘉诚虽然巨富，但生活俭朴，从不挥霍浪费。他深知亿万资产，都是一元一元挣来的。钱币在他眼中已抽象为一种劳动，而劳动已成为他最重要的生存方式，他的所有财富，都是靠每天20小时以上的劳动堆积起来的。200元酬金，实际上是对劳动的尊重和报答，是不能用金钱衡量的。富兰克林借书解怨（尊重别人赢得朋友）

那一刻我感受到了幸福_初中作文

那一刻我感受到了幸福本文是关于初中作文的那一刻我感受到了幸福，感谢您的阅读！每个人民的心中都有一粒幸福的种子，当它拥有了雨水的滋润和阳光的沐浴，它就会绽放出最美丽的姿态。那一刻，我们都能够闻到幸福的芬芳，我们都能够感受到幸福的存在。在寒假期间，我偶然在授索电视频道，发现(百家讲坛)栏目中大学教授正在解密幸福，顿然引起我的好奇心，我放下了手中的遥控器，静静地坐在电视前，注视着频道上的每一个字，甚至用笔急速记在了笔记本上。我还记得，那位大学教授讲到了一个故事：一位母亲被公司升职到外国工作，这位母亲虽然十分高兴，但却又十分无奈，因为她的儿子马上要面临中考了，她不能撇下儿子迎接中考的挑战，于是她决定拒绝这了份高薪的工作，当有人问她为什么放弃这么好的机会时，她却毫无遗憾地说，纵然我能给予儿子最贵的礼物，优异的生活环境，但我却无当给予他关键时刻的那份呵护与关爱，或许以后的一切会证明我的选择是正确的。听完这样一段故事，我心中有种说不出的感觉，刹那间，我仿拂感觉那身边正在包饺子的妈妈，屋里正在睡觉的爸爸，桌前正在看小说的妹妹给我带来了一种温馨，幸福感觉。正如教授所说的那种解密幸福。就要选择一个明确的目标，确定自已追求的是什么，或许那时我还不能完全诠释幸福。当幸福悄悄向我走来时，我已慢慢明白，懂得珍惜了。那一天的那一刻对我来说太重要了，原本以为出差在外的父母早已忘了我的生日，只有妹妹整日算着日子。我在耳边唠叨个不停，没想到当日我失落地回到家中时，以为心中并不在乎生日，可是眼前的一切，让我心中涌现的喜悦，脸上露出的微笑证明我是在乎的。

爸爸唱的英文生日快乐歌虽然不是很动听，但爸爸对我的那份爱我听得很清楚，妈妈为我做的长寿面，我细细的品尝，吃出了爱的味道。妹妹急忙让我许下三个愿望，嘴里不停的唠叨：我知道你的三个愿望是什么?我问：为什么呀!我们是一家人，心连心呀!她高兴的说。那一刻我才真正解开幸福的密码，感受到了真正的幸福，以前我无法理解幸福，即使身边有够多的幸福也不懂得欣赏，不懂得珍惜，只想拥有更好更贵的，其实幸福比物质更珍贵。那一刻的幸福就是爱的升华，许多时候能让我们感悟幸福不是名利，物质。而是在血管里涌动着的，漫过心底的爱。也许每一个人生的那一刻，就是我们幸运的降临在一个温馨的家庭中，而不是降临在孤独的角落里。家的感觉就是幸福的感觉，幸福一直都存在于我们的身边!

关于我的幸福作文八篇汇总

关于我的幸福作文八篇汇总幸福在每个人的心中都不一样。在饥饿者的心中，幸福就是一碗香喷喷的米饭；在果农的心中，幸福就是望着果实慢慢成熟；在旅行者的心中，幸福就是游遍世界上的好山好水。而在我的心中，幸福就是每天快快乐乐，无忧无虑；幸福就是朋友之间互相帮助，互相关心；幸福就是在我生病时，母亲彻夜细心的照顾我。幸福在世间上的每个角落都可以发现，只是需要你用心去感受而已。记得有一次，我早上出门走得太匆忙了，忘记带昨天晚上准备好的钢笔。老师说了：“今天有写字课，必须要用钢笔写字，不能用水笔。”我只好到学校向同学借了。当我来到学校向我同桌借时，他却说：“我已经借别人了，你向别人借吧！”我又向后面的同学借，可他们总是找各种借口说：“我只带了一枝。”问了三四个人，都没有借到，而且还碰了一鼻子灰。正当我急的像热锅上的蚂蚁团团转时，她递给了我一枝钢笔，微笑的对我说：“拿去用吧！”我顿时感到自己是多么幸福！在我最困难的时候，当别人都不愿意帮助我的时候，她向我伸出了援手。幸福也是无时无刻都在身旁。当我生病的时候，高烧持续不退时，是妈妈在旁边细心

的照顾我，喂我吃药，甚至一夜寸步不离的守在我的床边，直到我苏醒。当我看见妈妈的眼睛布满血丝时，我的眼眶在不知不觉地湿润了。这时我便明白我有一个最疼爱我的妈妈，我是幸福的！幸福就是如此简单！不过，我们还是要珍惜眼前的幸福，还要给别人带来幸福，留心观察幸福。不要等幸福悄悄溜走了才发现，那就真的是后悔莫及了！这就是我拥有的幸福，你呢？悠扬的琴声从房间里飘出来，原来这是我在弹钢琴。优美的旋律加上我很强的音乐表现力让一旁姥爷听得如醉如痴。姥爷说我是幸福的，读了《建设幸福中国》我更加体会到了这一点。儿时的姥爷很喜欢读书，但当时家里穷，据姥爷讲那时上学可不像现在。有点三天打鱼两天晒网，等地里农活忙了太姥爷就说：“别去念书了，干地里的活吧。”干活时都是牛马拉车，也没机器，效率特别低。还要给牲口拔草，喂草，拾柴火，看书都是抽空看。等农闲时才能背书包去学校，衣服更是老大穿了，打补丁老二再接着穿，只有盼到过年时才有能换上件粗布的新衣服。写字都是用石板，用一次擦一次，那时还没有电灯，爱学习的姥爷在昏暗的煤油灯下经常被灯火不是烧了眉毛就是燎了头发。没有电灯更没有电视，没有电视更没有见过钢琴，只知道钢琴是贵族家用的。

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自吹自擂造句本文是关于好词好句的，仅供参考，如果觉得很不错，欢迎点评和分享。自吹自擂造句 1、暴发户可能挥金如土来提升形象，自吹自擂。而一个国家大概也会面临同样的诱惑。 2、自吹自擂，等于无知。 3、一些所谓专业书者在商业气浪的影响下，开始对自己的作品在自吹自擂中明码标价。 4、爱自吹自擂的人很快就会失去朋友。 5、这个自吹自擂的候选人大谈特谈他的政治野心，使在场的人非常反感。 6、它有可能来作为没有惊讶电影的首都在美国自吹自擂若干个神鬼出没行动剧场中做。 7、如同一场比赛那样，一个运动员或是一个运动队，如果既不充分了解对方的长短，也不自己的长短，只靠关上门自吹自擂，表决心，喊口号，那怎么能有可靠的战胜对手的信心呢？ 8、语序上的差异导致了语义上的高低差别，而语义上的变化与合理思维产生偏离于是诙谐而生，表面上语序的转移，却深刻地讽刺了那些不学无术，自吹自擂的丑陋形象。 9、没有人喜欢自大狂，尽量别大声地自吹自擂。数一数自己的

福气，亲切地接受自己所赢得的掌声。 10、我们这些职业中专也只是在招生宣传会上才会简单的散发一些印刷精美的宣传材料给家长，然后自吹自擂一番。 11、为了你，你的母亲会一直在那里。她会倾听你的烦恼，你的自吹自擂，还有你受的挫折等等。 12、营销战略过于自信自恋，自吹自擂，脱离营销环境，无法实现突围的情况极其普遍。 13、这些作品从来没有经世界银行发表过，它拒绝自我批评的原则，宁愿自吹自擂。 14、美国人可以接受的自吹自擂的广告，在加拿大却被定为是误导性广告而被禁止。 15、中国人反对王婆卖瓜式的自吹自擂，然而中国式的自我谦虚或自我否定却常常使西方人大为不满。 16、这个人喜欢自吹自擂。 17、安东尼自吹自擂他已通过了普通级法语考试，但那有什么了不起，成千上万的人都通过了。 18、你应该改掉自吹自擂的缺点；否则别人会总不相信你。 19、他自吹自擂说能喝十品脱啤酒，但无人理睬他。 20、我认为我不应该为自己的无能而自吹自擂，因为我有一些非常要好的朋友陪在身边。 21、我经常说的是你必须自吹自擂，因为如果连你自己都不去宣传卖弄你自己，谁还会这么去做呢？

小学六年级语文学科毕业专项训练复习资料――词语专项训练[1]

词语专项练习一、写出下列词语的反义词与近义词。近义词：轻蔑（轻视）充足（充裕。充沛）目不转睛（聚精会神）商议（商量）歉疚（内疚）能耐（本领）推辞（推托）抱怨（埋怨）反义词：怀疑（相信）陈旧（新颖）果断（缠绵）苏醒（昏晕）消失（存在）降低（升高）善良（恶毒）仰望（俯视）二、词语的搭配。 1、用“正”字组词并与括号后面的词语搭配。（修正）错误（端正）态度（改正）缺点（摆正）位置 2、用“保”字组词并与括号后面的词语搭配。（保护）财产（保卫）祖国（保全）性命（保守）秘密 3、在括号里填上合适的词语。开展（活动）保持（秩序）维持（生命）肯定（成绩）端正（态度）明确（目标）养成（习惯）稳定（增长）三、用“√”选出正确的字。（川穿）山岩（拨拔）琴弦一（番翻）宏论慈（详祥）（映印）像枯（燥躁）（住驻）军淡（装妆）浓抹（竟竞）然银（装妆）素裹四、选词填空。 1、继续相继陆续 ①随后，数十头麋鹿被（相继）盗往欧洲，在伦敦、巴黎和柏林等地动物园里展出。 ②后来，流落在国外的迷麋鹿大部分（陆续）死去。 2、争持争夺 ①清政府刚提出修筑的计划，一些帝国主义国家就出来阻挠，他们都要（争夺）这条铁路的修筑权。 ②帝国主义者谁也不肯让谁，事情（争持）了好久得不到解决。 3、融化溶化熔化 ①把白糖放到水里，让它慢慢地（溶化。 ②春天来了，河里的冰慢慢（融化）。 4、品位品味 ①中央电视台春节联欢会的艺术（品位）很高。 ②他经过细细（品味），才明白了那句话的含义。 5、截止截至 ①网站的人气很旺，（截至）8月底，累计点击已达50万人次。 ②音乐美术班报名在昨天已经（截止）。 6、临近邻近 ①我家（邻近）有几棵大榕树。 ②（临近）毕业考试了，大家都在紧张的复习。 7、仰望眺望俯视 ①夏天的夜晚，我常常在阳台上（仰望）天空中璀璨的群星。 ②清晨，我推开窗户，（眺望）着远方的山峰和田野。 ③春游那天，同学们站在南山顶上（俯视）着山脚下翻腾的江水，真有一番情趣。五、根据词语的不同意思造句。 1、骄傲①（自豪）我们应以我们是中国人而自豪。 ②（不谦虚）虽然我学习好，但是我不能骄傲。 2、结实①（身体很强壮）因为我经常锻炼，所以我身体很结实。 ②（坚固耐用）爸爸自制了一张书桌很结实。 3、回味①（食物吃过后的余味）正宗的新疆烤羊肉真是好吃，很让人回味！ ②（对经历过的事情重新体味）李叔叔的一番话很是让我回味。六、在括号里填入由“望”字组成的词。 1、成功举办2008年北京奥运会是全国人民的（愿望）。 2、每年圣诞节，我都（盼望）着圣诞老人的礼物。 3、今年我一定好好学习，因为我（希望）在毕业考试中取得优异成绩，不辜负爸爸妈妈对我的（期望）。七、风有各种各样的：寒风、劲风、金风、疾风、和风、朔风、狂风、微风、暴风……在下边的句子中，该填什么风呢？ 1、（疾风）知劲草，路遥知马力。 2、天高云淡，（金凤）送爽，大雁排着队往南方飞去。 3、一阵（狂风）刮来，飞沙走石，人们难以行走。 4、雨住了，天边出现了一道彩虹，（清风）习习，人们感到舒服极了。 5、（朔风）吹，林涛吼，峡谷震荡。 6、冬天，（寒风）凛冽，吹到脸上像刀割一样。八、皇浦东新进了一批货物，但他不知道怎么摆放。你能帮他把货物分类吗？请将类别写在后面的括号里。水彩笔足球瓜子钢笔牛奶脸盆鞋子篮球手套杯子羽毛球圆珠笔话梅象棋花生袜子衬衫铅笔牙膏筷子 1、水彩笔钢笔圆珠笔铅笔（文具类） 2、足球篮球羽毛球象棋（体育类） 3、瓜子牛奶话梅花生（食物类） 4、脸盆杯子牙膏筷子（生活类） 5、鞋子手套袜子衬衫（服饰类）九、在括号里填上合适的关联词。（4分） 1、（尽管）今天的天气很热，他（还是）坚持干到底。 2、（即使）风再猛，雨再大，（也）阻挡不了我们前进的步伐。 3、小琴（不但）不嫌弃这只破脚的小狗，（而且）真心地喜欢它。 4、（虽然）只是一句平常的问候，（但是）让我感到无比地温暖。 5、他（不是）马虎地把考卷看一遍，（而是）认真地检查。 6、（与其）拖延时间被妈妈责怪，（不如）现在就动手做 7、吴王（之所以）准备出兵攻打楚,（是因为）看到自己国家的军事实力比楚国强大。 8、大臣们认为攻打楚国（虽然）取胜的希望很大，（如果）其他诸侯国乘虚而入，后果（就）不堪设想。（但是）大臣们都不同意吴王的主张。十、按要求写词。 1、喜出望外（含有褒义感情色彩的成语）吐气扬眉欢天喜地兴高采烈 2、负隅顽抗（含有贬义感情色彩的成语）仗势欺人得以忘形胡作非为十一、给下列词语分类。同仇敌忾哭爹喊娘恼羞成怒气势汹汹慷慨激昂载歌载舞惊恐万状奋起还击褒义词：同仇敌忾慷慨激昂载歌载舞奋起还击贬义词：哭爹喊娘恼羞成怒气势汹汹惊恐万状十二、用日常交往中常用的词语填空。久违劳教高见请教包涵拜托恭喜借光打扰赐教请问留步1、表哥考进了北京大学，我见到他便笑嘻嘻地说：“（恭喜）你考上了名牌大学！” 2、我不知道新近开放的动物园在哪里，就问一位老伯伯：“（请问），去动物园怎么走？” 3、来我校考察的客人要走了，汪校长对客人说：“照顾不周，请各位多多（包涵）” 4、我到隔壁刘老师家去问一道数学题，刘老师连忙关掉电视，热情地给我解答。临走时我对刘老师说：“（打扰）您看电视了，真不好意思。谢谢您！”

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小学六年级语文学科毕业专项训练复习资料――词语专项训练[1]