The neurocognitive basis of autism

doi:10.1016/S1364-6613(97)01010-3

Trends in Cognitive Sciences

Volume 1, Issue 2, May 1997, Pages 73-77

https://doi.org/10.1016/S1364-6613(97)01010-3 Get rights and content

The cognitive study of the underlying mental abnormalities in autism has advanced rapidly, while the biological study of the underlying brain abnormalities and of putative genetic mechanisms is lagging somewhat behind. However, the linking of cognitive and biological studies has become a real possibility. Developmental cognitive neuroscience has transformed our understanding of this enigmatic disorder, which was once misguidedly thought to be caused by maternal rejection. The hypothesis of a specific theory of mind deficit was a crucial step in this process. It explains the puzzle of the characteristic social and communication impairments of autism and allows for the fact that they can coexist with good general abilities. This hypothesis has been widely accepted and a start has been made at pinpointing the brain basis of theory of mind. The non-social impairments of autism have now become a major focus for cognitive research. One theory proposes dysfunction in executive processes, in an attempt to explain repetitive behaviour and inflexibility. Another theory proposes weak information integration, in an attempt to explain narrow interests and special talents. Autism research has thus stimulated ideas on important mind-brain systems that may be dedicated to the development of social awareness, executive functions and integrative processing.

References (44)

MottronL. et al.
A study of perceptual analysis in a high-level autistic subject with exceptional graphic abilities
Brain Cogn.
(1993)
OzonoffS. et al.
An exploration of right-hemisphere contributions to the pragmatic impairments of autism
Brain Lang.
(1996)
FrithU. et al.
The cognitive basis of a biological disorder
Trends Neurosci.
(1991)
Baron-CohenS. et al.
Does the autistic child have a 'theory of mind'?
Cognition
(1985)
FletcherP.C.
Other minds in the brain: a functional imaging study of 'theory of mind' in story comprehension
Cognition
(1995)
HughesC. et al.
Evidence for executive dysfunction in autism
Neuropsychologia
(1994)
FrithU. et al.
Autism: beyond 'theory of mind'
Cognition
(1994)
CiaranelloA.L. et al.
The neurobiology of infantile autism
Annu. Rev. Neurosci.
(1995)
BaileyA.J. et al.
Autism: integrating clinical, genetic, neuropsychological, and neurobiological perspectives
J. Child Psychol. Psychiatry
(1996)
HappéF. et al.
The neuropsychology of autism
Brain
(1996)

KannerL.

Autistic disturbances of affective contact

Nerv. Child

(1943)

AspergerH.

Autism and Asperger Syndrome

FrithU.

LotterV.

Epidemiology of autistic conditions in young children: I. Prevalence

Social Psychiatry

(1966)

GillbergC. et al.

WingL.

Autistic spectrum disorders: no evidence for or against an increase in prevalence

Br. Med. J.

(1996)

EhlersS. et al.

The epidemiology of Asperger syndrome. A total population study

J. Child Psychol. Psychiatry

(1993)

World Health Organization

American Psychiatric Association

HappéF.

RimlandB. et al.

FrithU. et al.

Language and communication in the autistic disorders

Philos. Trans. R. Soc. London Ser. B

(1994)

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Neural responses to heartbeats distinguish self from other during imagination
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Citation Excerpt :
Future studies might investigate potential HER effects in these other domains of perspective taking. This could be particularly relevant in the case of autism, which has been associated with impairments in visuo-spatial perspective taking (Hamilton et al., 2009), theory of mind (Frith, 1997) and empathy (Charman et al., 1997) but also in interoceptive processing (Quattrocki and Friston, 2014). Imagining oneself might entail increased attention to bodily signals including heartbeats.
Imagination is an internally-generated process, where one can make oneself or other people appear as protagonists of a scene. How does the brain tag the protagonist of an imagined scene as being oneself or someone else? Crucially, during imagination, neither external stimuli nor motor feedback are available to disentangle imagining oneself from imagining someone else. Here, we test the hypothesis that an internal mechanism based on the neural monitoring of heartbeats could distinguish between self and other. 23 participants imagined themselves (from a first-person perspective) or a friend (from a third-person perspective) in various scenarios, while their brain activity was recorded with magnetoencephalography and their cardiac activity was simultaneously monitored. We measured heartbeat-evoked responses, i.e. transients of neural activity occurring in response to each heartbeat, during imagination. The amplitude of heartbeat-evoked responses differed between imagining oneself and imagining a friend, in the precuneus and posterior cingulate regions bilaterally. Effect size was modulated by the daydreaming frequency scores of participants but not by their interoceptive abilities. These results could not be accounted for by other characteristics of imagination (e.g., the ability to adopt the perspective, valence or arousal), nor by cardiac parameters (e.g., heart rate) or arousal levels (e.g. arousal ratings, pupil diameter). Heartbeat-evoked responses thus appear as a neural marker distinguishing self from other during imagination.
Correlates of social functioning in autism spectrum disorder: The role of social cognition
2017, Research in Autism Spectrum Disorders
Citation Excerpt :
Recent research indicates that adults with ASD and adults with schizophrenia are quite similar in their social cognition profiles (Couture et al., 2010; Eack, Bahorik et al., 2013) and often fail to pass first- and second-order false belief tasks like individuals with ASD (Bora, Yucel, & Pantelis, 2009), suggesting that these associations found in schizophrenia may also hold in individuals with ASD. Deficits in social cognition may not fully account for deficits in social functioning in ASD, particularly in higher functioning individuals (Frith, 1997), and may be further compounded by a number of associated factors (i.e., motivational, perceptual, and emotional challenges) as well as broader and more general challenges with motor function (Sumner, Leonard, & Hill, in press). Research indicates that individuals with ASD have poorer motor function, with greater clumsiness, more motor coordination abnormalities, greater postural instability, and poorer performance on standardized tests of motor speed such as the finger tap and grooved pegboard tests, with a large effect size for motor coordination deficits identified by a recent systematic review (Fournier, Hass, Naik, Lodha, & Cauraugh, 2010).
Individuals with autism spectrum disorder (ASD) experience marked challenges with social function by definition, but few modifiable predictors of social functioning in ASD have been identified in extant research. This study hypothesized that deficits in social cognition and motor function may help to explain poor social functioning in individuals with ASD.
Cross-sectional data from 108 individuals with ASD and without intellectual disability ages 9 through 27.5 were used to assess the relationship between social cognition and motor function, and social functioning.
Results of hierarchical multiple regression analyses revealed that greater social cognition, but not motor function, was significantly associated with better social functioning when controlling for sex, age, and intelligence quotient. Post-hoc analyses revealed that better performance on second-order false belief tasks was associated with higher levels of socially adaptive behavior and lower levels of social problems.
Our findings support the development and testing of interventions that target social cognition in order to improve social functioning in individuals with ASD. Interventions that teach generalizable skills to help people with ASD better understand social situations and develop competency in advanced perspective taking have the potential to create more durable change because their effects can be applied to a wide and varied set of situations and not simply a prescribed set of rehearsed situations.
Brain mechanisms of plasticity in response to treatments for core deficits in autism
2013, Progress in Brain Research
Citation Excerpt :
Environmental exposure to toxic substances, abnormal immune responses, and adverse prenatal experiences, especially those during critical periods such as the first trimester and parturition, have also been implicated (Gregory et al., 2013; Landrigan, 2010; Rossignol and Frye, 2012). Furthermore, some purport that deficits in specific cognitive processes, such as executive functioning and ToM, that are often present in individuals with ASD may stem from neurological abnormalities in connectivity and structure and may underlie some of the social impairment and restricted behaviors characteristic of the disorder (Frith, 1997, 2012; Minshew and Williams, 2007). Though in the past decades, there have been a plethora of theories about the origins of ASD and specific brain regions have been consistently implicated, we have yet to pinpoint the primary underlying neurobiological causes of the disorder.
Autism spectrum disorders (ASD) are neurodevelopmental disorders characterized by social communication impairments and repetitive behaviors. Although the prevalence of ASD is estimated at 1 in 88, understanding of the neural mechanisms underlying the disorder is still emerging. Regions including the amygdala, superior temporal sulcus, orbitofrontal cortex, fusiform gyrus, medial prefrontal cortex, and insula have been implicated in social processing. Neuroimaging studies have demonstrated both anatomical and functional differences in these areas of the brain in individuals with ASD when compared to controls; however, research on the neural basis for response to treatment in ASD is limited. Results of the three studies that have examined the neural mechanisms underlying treatment response are promising; following treatment, the brains of individuals with ASD seem to “normalize,” responding more similarly to those of typically developing individuals. The research in this area is in its early stages, and thus a focused effort examining the neural basis of treatment response in ASD is crucial.
Disordered connectivity in the autistic brain: Challenges for the 'new psychophysiology'
2007, International Journal of Psychophysiology
In 2002, we published a paper [Brock, J., Brown, C., Boucher, J., Rippon, G., 2002. The temporal binding deficit hypothesis of autism. Development and Psychopathology 142, 209–224] highlighting the parallels between the psychological model of ‘central coherence’ in information processing [Frith, U., 1989. Autism: Explaining the Enigma. Blackwell, Oxford] and the neuroscience model of neural integration or ‘temporal binding’. We proposed that autism is associated with abnormalities of information integration that is caused by a reduction in the connectivity between specialised local neural networks in the brain and possible overconnectivity within the isolated individual neural assemblies. The current paper updates this model, providing a summary of theoretical and empirical advances in research implicating disordered connectivity in autism. This is in the context of changes in the approach to the core psychological deficits in autism, of greater emphasis on ‘interactive specialisation’ and the resultant stress on early and/or low-level deficits and their cascading effects on the developing brain [Johnson, M.H., Halit, H., Grice, S.J., Karmiloff-Smith, A., 2002. Neuroimaging of typical and atypical development: a perspective from multiple levels of analysis. Development and Psychopathology 14, 521–536].We also highlight recent developments in the measurement and modelling of connectivity, particularly in the emerging ability to track the temporal dynamics of the brain using electroencephalography (EEG) and magnetoencephalography (MEG) and to investigate the signal characteristics of this activity. This advance could be particularly pertinent in testing an emerging model of effective connectivity based on the balance between excitatory and inhibitory cortical activity [Rubenstein, J.L., Merzenich M.M., 2003. Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior 2, 255–267; Brown, C., Gruber, T., Rippon, G., Brock, J., Boucher, J., 2005. Gamma abnormalities during perception of illusory figures in autism. Cortex 41, 364–376]. Finally, we note that the consequence of this convergence of research developments not only enables a greater understanding of autism but also has implications for prevention and remediation.
Development of theory of mind and executive control
1999, Trends in Cognitive Sciences
Several recent studies have demonstrated a developmental link, in the age range of 3–5 years, between the acquisition of a ‘theory of mind’ and self control. In this review, we consider the existence of such a link in assessing five competing theoretical hypotheses that might help us to understand the nature of this developmental advance: (1) executive control depends on theory of mind; (2) theory of mind development depends on executive control; (3) the relevant theory of mind tasks require executive control; (4) both kinds of task require the same kind of embedded conditional reasoning; (5) theory of mind and executive control involve the same brain region. We briefly describe these theoretical accounts and evaluate them in the light of existing empirical evidence. At present, only account (3) can be ruled out with some confidence.
Towards an Autism Spectrum Disorder (ASD) care agent for social interaction
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Trends in Cognitive Sciences

ReviewThe neurocognitive basis of autism

Brain Cogn.

Brain Lang.

Trends Neurosci.

Cognition

Cognition

Neuropsychologia

Cognition

The neurobiology of infantile autism

Annu. Rev. Neurosci.

Autism: integrating clinical, genetic, neuropsychological, and neurobiological perspectives

J. Child Psychol. Psychiatry

The neuropsychology of autism

Brain

Autistic disturbances of affective contact

Nerv. Child

Autism and Asperger Syndrome

Epidemiology of autistic conditions in young children: I. Prevalence

Social Psychiatry

Autistic spectrum disorders: no evidence for or against an increase in prevalence

Br. Med. J.

The epidemiology of Asperger syndrome. A total population study

J. Child Psychol. Psychiatry

Language and communication in the autistic disorders

Philos. Trans. R. Soc. London Ser. B

Review
The neurocognitive basis of autism