Evidence map›Paper›PMID 24062668›Full record

ReviewFrontiers in human neuroscience2013

Exploring Links between Genotypes, Phenotypes, and Clinical Predictors of Response to Early Intensive Behavioral Intervention in Autism Spectrum Disorder.

Valsamma Eapen, Rudi Crnčec, Amelia Walter

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in human neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed.

  1. Efficacy and Safety of AltibrainCurrent pharmaceutical design · 2025
    Trial
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. ERP evidence of semantic processing in children with ASD.Developmental cognitive neuroscience · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Sleep in Children with Autism Spectrum Disorder.Current psychiatry reports · 2017
    Review
  16. Review
  17. Early identification of autism spectrum disorder: Do we need a paradigm shift?The Australian and New Zealand journal of psychiatry · 2016
    Article
  18. Observational
  19. Does the cognitive architecture of simplex and multiplex ASD families differ?Journal of autism and developmental disorders · 2016
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Valsamma EapenAcademic Unit of Child Psychiatry South West Sydney, South Western Sydney Local Health District , Liverpool, NSW , Australia ; School of Psychiatry, University of New South Wales , Sydney, NSW , Australia.
Rudi Crnčec
Amelia Walter

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is amongst the most familial of psychiatric disorders. Twin and family studies have demonstrated a monozygotic concordance rate of 70-90%, dizygotic concordance of around 10%, and more than a 20-fold increase in risk for first-degree relatives. Despite major advances in the genetics of autism, the relationship between different aspects of the behavioral and cognitive phenotype and their underlying genetic liability is still unclear. This is complicated by the heterogeneity of autism, which exists at both genetic and phenotypic levels. Given this heterogeneity, one method to find homogeneous entities and link these with specific genotypes would be to pursue endophenotypes. Evidence from neuroimaging, eye tracking, and electrophysiology studies supports the hypothesis that, building on genetic vulnerability, ASD emerges from a developmental cascade in which a deficit in attention to social stimuli leads to impaired interactions with primary caregivers. This results in abnormal development of the neurocircuitry responsible for social cognition, which in turn adversely affects later behavioral and functional domains dependent on these early processes, such as language development. Such a model begets a heterogeneous clinical phenotype, and is also supported by studies demonstrating better clinical outcomes with earlier treatment. Treatment response following intensive early behavioral intervention in ASD is also distinctly variable; however, relatively little is known about specific elements of the clinical phenotype that may predict response to current behavioral treatments. This paper overviews the literature regarding genotypes, phenotypes, and predictors of response to behavioral intervention in ASD and presents suggestions for future research to explore linkages between these that would enable better identification of, and increased treatment efficacy for, ASD.

Indexed as

autism spectrum disorderearly interventiongenotypephenotypetreatment response

Identifiers

PMID24062668
PMCPMC3769633

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.