Gaia Scerif

Executive Functioning as a Predictor of Children's Mathematics Ability: Inhibition, Switching, and Working Memory

Childrens mathematical skills were considered in relation to executive functions. Using multiple measures-including the Wisconsin Card Sorting Task (WCST), dual-task performance, Stroop task, and counting span-it was found that mathematical ability was significantly correlated with all measures of executive functioning, with the exception of dual-task performance. Furthermore, regression analyses revealed that each executive function measure predicted unique variance in mathematics ability. These results are discussed in terms of a central executive with diverse functions (Shallice & Burgess, 1996) and with recent evidence from Miyake, et al. (2000) showing the unity and diversity among executive functions. It is proposed that the particular difficulties for children of lower mathematical ability are lack of inhibition and poor working memory, which result in problems with switching and evaluation of new strategies for dealing with a particular task. The practical and theoretical implications of these results are discussed, along with suggestions for task changes and longitudinal studies that would clarify theoretical and developmental issues related to executive functioning.

Task-Related Default Mode Network Modulation and Inhibitory Control in ADHD: Effects of Motivation and Methylphenidate.

BACKGROUND Deficits characteristic of attention deficit/hyperactivity disorder (ADHD), including poor attention and inhibitory control, are at least partially alleviated by factors that increase engagement of attention, suggesting a hypodopaminergic reward deficit. Lapses of attention are associated with attenuated deactivation of the default mode network (DMN), a distributed brain system normally deactivated during tasks requiring attention to the external world. Task-related DMN deactivation has been shown to be attenuated in ADHD relative to controls. We hypothesised that motivational incentives to balance speed against restraint would increase task engagement during an inhibitory control task, enhancing DMN deactivation in ADHD. We also hypothesised that methylphenidate, an indirect dopamine agonist, would tend to normalise abnormal patterns of DMN deactivation. METHOD We obtained functional magnetic resonance images from 18 methylphenidate-responsive children with ADHD (DSM-IV combined subtype) and 18 pairwise-matched typically developing children aged 9-15 years while they performed a paced Go/No-go task. We manipulated motivational incentive to balance response speed against inhibitory control, and tested children with ADHD both on and off methylphenidate. RESULTS When children with ADHD were off-methylphenidate and task incentive was low, event-related DMN deactivation was significantly attenuated compared to controls, but the two groups did not differ under high motivational incentives. The modulation of DMN deactivation by incentive in the children with ADHD, off-methylphenidate, was statistically significant, and significantly greater than in typically developing children. When children with ADHD were on-methylphenidate, motivational modulation of event-related DMN deactivation was abolished, and no attenuation relative to their typically developing peers was apparent in either motivational condition. CONCLUSIONS During an inhibitory control task, children with ADHD exhibit a raised motivational threshold at which task-relevant stimuli become sufficiently salient to deactivate the DMN. Treatment with methylphenidate normalises this threshold, rendering their pattern of task-related DMN deactivation indistinguishable from that of typically developing children.

Autism, language and communication in children with sex chromosome trisomies

Purpose Sex chromosome trisomies (SCTs) are found on amniocentesis in 2.3–3.7 per 1000 same-sex births, yet there is a limited database on which to base a prognosis. Autism has been described in postnatally diagnosed cases of Klinefelter syndrome (XXY karyotype), but the prevalence in non-referred samples, and in other trisomies, is unclear. The authors recruited the largest sample including all three SCTs to be reported to date, including children identified on prenatal screening, to clarify this issue. Design Parents of children with a SCT were recruited either via prenatal screening or via a parental support group, to give a sample of 58 XXX, 19 XXY and 58 XYY cases. Parents were interviewed using the Vineland Adaptive Behavior Scales and completed questionnaires about the communicative development of children with SCTs and their siblings (42 brothers and 26 sisters). Results Rates of language and communication problems were high in all three trisomies. Diagnoses of autism spectrum disorder (ASD) were found in 2/19 cases of XXY (11%) and 11/58 XYY (19%). After excluding those with an ASD diagnosis, communicative profiles indicative of mild autistic features were common, although there was wide individual variation. Conclusions Autistic features have not previously been remarked upon in studies of non-referred samples with SCTs, yet the rate is substantially above population levels in this sample, even when attention is restricted to early-identified cases. The authors hypothesise that X-linked and Y-linked neuroligins may play a significant role in the aetiology of communication impairments and ASD.

Double dissociations in developmental disorders? Theoretically misconceived, empirically dubious.

Single dissociations are the bread and butter of neuropsychologists, and double dissociations their chocolate cake! So it is unsurprising that developmental psychologists working on genetic disorders find the concept of double dissociations an attractive one. The following quotations bear eloquent witness to this: “... the study of mental retardation would profit from the application of the framework of cognitive neuropsychology” ... In cognitive neuropsychology, one key question running through the investigator’s mind is «Is this process or mechanism intact or impaired in this person?”. (Baron-Cohen, 1998, p. 335) “...overall, the genetic double dissociation is striking ... The genes of one group of children [SLI] impair their grammar while sparing their intelligence; the genes of another group of children [WS] impair their intelligence while sparing their grammar” (Pinker, 1999, p. 262). We argue that the use of the double dissociation method in developmental disorders is not only inappropriate theoretically, but also erroneous empirically, often based on a dubious choice of control groups. It rests on a false assumption: that the brain of an infant with a genetic disorder comprises a pattern of neatly segregated, “intact/impaired cognitive modules”. In doing so, it neglects one vital factor: the actual process of ontogenetic development (Karmiloff-Smith, 1998). The effects of a genetic mutation during embryogenesis and postnatal brain growth are likely to be widespread across the developing system. Some domains may be more affected than others due to the features of their particular problem space, but in-depth studies reveal subtle impairments in domains that originally seemed “intact” (Karmiloff-Smith, 1998; Karmiloff-Smith et al., 2002). As Dunn and Kirsner (2003, this issue) highlight, the notion of “intact” performance depends on the sensitivity of the measurement scale. In sum, an uneven pattern in the cognitive profile of a genetic disorder cannot be taken for granted to imply impaired versus totally preserved abilities. All domains may be impaired, some more subtly than others. The case is different for adult neuropsychology patients. In their previously normal brains, specialisation and localisation of function had already stabilised, so selective impairments might emerge if pure cases exist. But what about the double dissociation claimed above for Specific Language Impairment (SLI) and Williams syndrome (WS)? Empirical data show that absolutestatements about “sparing” of intelligence or grammar should actually

Delineation of early attentional control difficulties in fragile X syndrome: Focus on neurocomputational changes

Fragile X syndrome (FXS) is due to the silencing of a single X-linked gene and it is associated with striking attentional difficulties. As FXS is well characterised at the cellular level, the condition provides a unique opportunity to investigate how a genetic dysfunction can impact on the development of neurocomputational properties relevant to attention. Thirteen young boys with FXS and 13 mental-age-matched typically developing controls performed a touch-screen-based search task that manipulated the similarity between targets and distractors and their heterogeneity in size. Search speed, path and errors were recorded as multiple measures of performance. Children did not differ in overall search speed or path when searching amongst distractors, but striking error patterns distinguished children with FXS from controls. Firstly, although clear markers of previously found targets remained on screen, children with FXS perseverated on touching previous hits more than typically developing controls, consistent with the well-documented inhibitory deficits in adults with the disorder. Secondly, they could accurately discriminate single target-distractor pairs, but, when searching a complex display, they touched distractors more often than control children when distractors were similar to targets and especially so when these were infrequent, highlighting difficulties in judging relative size and allocate attentional weight independently of stimulus frequency. Thirdly, their performance was also characterised by inaccuracies in pointing, suggesting additional motor control deficits. Taken together, the findings suggest that fragile X syndrome affects the early development of multiple processes contributing to efficient attentional selection, as would be predicted from an understanding of the neurocomputational changes associated with the disorder.

The dawn of cognitive genetics? Crucial developmental caveats

Attempts to bridge genetics and cognition are rapidly coming to the forefront of cognitive neuroscience. It is therefore crucial to evaluate the current state of knowledge about disorders of known genetic origin as a way of assessing whether, and if so how, links between genotype and cognitive phenotype can be drawn, however indirect these links might be. We review recent empirical findings from research on genetic disorders at three levels of description--cognitive, neural systems, and cellular--that caution against simple genotype-phenotype mappings at all levels. Most importantly, interdisciplinary efforts to integrate human genetics and cognition will need to operationalize the mechanisms driving both typical and atypical developmental processes over time.

The attentive brain: insights from developmental cognitive neuroscience

Visual attention functions as a filter to select environmental information for learning and memory, making it the first step in the eventual cascade of thought and action systems. Here, we review studies of typical and atypical visual attention development and explain how they offer insights into the mechanisms of adult visual attention. We detail interactions between visual processing and visual attention, as well as the contribution of visual attention to memory. Finally, we discuss genetic mechanisms underlying attention disorders and how attention may be modified by training.

To Look or Not to Look? Typical and Atypical Development of Oculomotor Control

The ability to inhibit saccades toward suddenly appearing peripheral stimuli (prosaccades) and direct them to contralateral locations instead (antisaccades) is a crucial marker of eye movement control. Typically developing infants as young as 4-month-olds can learn to inhibit reflexive saccades to peripheral stimuli, but they do not produce antisaccades, whose development later in infancy and its underlying neural computations remain unexplored. Here we tested oculomotor control in typically developing toddlers and toddlers with fragile X syndrome (FXS), a disorder of known genetic origin that allows the investigation of the neuro-computational properties contributing to the development of saccadic control. Typically developing toddlers decreased looking toward peripheral cues that predicted contralateral rewards, whose appearance they anticipated. Furthermore, this correlated with age, indicating a gradual development of saccadic control. In contrast with the typical case, toddlers with FXS did not decrease their looks to peripheral onsets that predicted contralateral events. Importantly, the atypical pattern of performance was also evident in the elimination of the correlation with mental or chronological age found in controls. Taken together, the findings suggest that control of saccades and its developmental trajectory is atypical in toddlers with FXS, consistent with inhibitory deficits previously shown at later ages in this condition. Potential implications for the neural mechanisms underlying the typical and atypical development of oculomotor control are discussed.

Effects of Motivation and Medication on Electrophysiological Markers of Response Inhibition in Children with Attention-Deficit/Hyperactivity Disorder

Background Theories of attention-deficit/hyperactivity disorder (ADHD) posit either executive deficits and/or alterations in motivational style and reward processing as core to the disorder. Effects of motivational incentives on electrophysiological correlates of inhibitory control and relationships between motivation and stimulant medication have not been explicitly tested. Methods Children (9–15 years) with combined-type ADHD (n = 28) and matched typically developing children (CTRL) (n = 28) performed a go/no-go task. Electroencephalogram data were recorded. Amplitude of two event-related potentials, the N2 and P3 (markers of response conflict and attention), were measured. The ADHD children were all stimulant responders tested on and off their usual dose of methylphenidate; CTRLs were never medicated. All children performed the task under three motivational conditions: reward; response cost; and baseline, in which points awarded/deducted for inhibitory performance varied. Results There were effects of diagnosis (CTRL > ADHD unmedicated), medication (on > off), and motivation (reward and/or response cost > baseline) on N2 and P3 amplitude, although the N2 diagnosis effect did not reach statistical significance (p = .1). Interactions between motivation and diagnosis/medication were nonsignificant (p > .1). Conclusions Motivational incentives increased amplitudes of electrophysiological correlates of response conflict and attention in children with ADHD, towards the baseline (low motivation) amplitudes of control subjects. These results suggest that, on these measures, motivational incentives have similar effects in children with ADHD as typically developing CTRLs and have additive effects with stimulant medication, enhancing stimulus salience and allocation of attentional resources during response inhibition.

Attention across modalities as a longitudinal predictor of early outcomes: the case of fragile X syndrome.

BACKGROUND   Fragile X syndrome (FXS) is an early diagnosed monogenic disorder, associated with a striking pattern of cognitive/attentional difficulties and a high risk of poor behavioural outcomes. FXS therefore represents an ideal model disorder to study prospectively the impact of early attention deficits on behaviour. METHODS   Thirty-seven boys with FXS aged 4-10 years and 74 typically developing (TD) boys took part. Study 1 was designed to assess visual and auditory attention at two time-points, 1 year apart. Study 2 investigated attention to multimodal information. Both tested attention markers as longitudinal predictors of risk for poor behaviour in FXS. RESULTS   Children with FXS attended less well than mental-age matched TD boys and experienced greater difficulties with auditory compared to visual stimuli. In addition, unlike TD children, they did not benefit from multimodal information. Attention markers were significant predictors of later behavioural difficulties in boys with FXS. CONCLUSIONS   Findings demonstrate, for the first time, greater difficulties with auditory attention and atypical processing of multimodal information, in addition to pervasive global attentional difficulties in boys with FXS. Attention predicted outcomes longitudinally, underscoring the need to dissect what drives differing developmental trajectories for individual children within a seemingly homogeneous group.