An unbiased Bayesian approach to functional connectomics implicates social-communication networks in autism

Venkataraman, Archana; Duncan, James S.; Yang, Daniel Y.-J.; Pelphrey, Kevin A.

doi:10.1016/j.nicl.2015.04.021

Cited by 34 publications

(28 citation statements)

References 85 publications

(107 reference statements)

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“…Mayes et al (2015) found that language impairment in children without ASD was associated with atypical structure and function in traditional language regions including the inferior frontal gyrus, posterior superior temporal gyrus, and caudate nucleus. As noted earlier, Venkataraman et al (2015) reported that ASD included impaired brain connectivity in language regions including right temporal pole, left posterior cingulate cortex, left supramarginal gyrus, and left middle temporal gyrus. ASD has also been found with both decreased and increased rightward functional activation of language cortex (Joseph et al 2014).…”

Section: Does Asd Have Neurobiological Validity?supporting

confidence: 60%

“…Counter to both Kitzbichler et al (2015) and Venkataraman et al (2015), though, Redcay et al (2013) reported finding no evidence for atypical connectivity in ASD. Tyszka et al (2014) also stated that their ASD sample showed, Bno evidence at all for altered connectivity at the whole-brain level( pp.…”

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 95%

“…The theory with the most active support argues that ASD results from impaired brain connectivity that is likely to have been preceded by early brain overgrowth Stoner et al 2014;Venkataraman et al 2015). Although the underconnectivity theory has been studied for more than 15 years (Just et al 2004) and has many supporters (Anderson 2013;Dawson 2016;Ecker et al 2015;Green et al 2015;Shen et al 2013), nonetheless, this theory has not become standard because there is as much evidence against the theory as there is for it.…”

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

“…Venkataraman et al (2015) determined that ASD brain malconnectivity occurred in two networks: a language network including temporal lobe areas and a Bsocial-person^network including temporal and parietal areas. Venkataraman et al (2015), however, found no impairment in ASD frontal lobe connectivity. Conversely, Kitzbichler et al (2015) reported that ASD malconnectivity was centered in frontal lobe-linked connections.…”

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

“…Another problem for standardizing the overgrowthmalconnectivity model is that there are so many different versions of this model (Fishman et al 2014;Kennedy et al 2015;Khan et al 2015;Kitzbichler et al 2015;Venkataraman et al 2015). As noted by Kennedy et al (2015), Bthe connectivity hypothesis has been vague ever since its inception… slowly morphing from a theory about underconnectivity in ASD, to one about distal underconnectivity paired with local overconnectivity, to one about atypical connectivity in either direction (or both)^(p. 81).…”

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

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ASD Validity

Waterhouse

London

Gillberg

2016

Rev J Autism Dev Disord

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ASD research is at an important crossroads. The ASD diagnosis is important for assigning a child to early behavioral intervention and explaining a child's condition. But ASD research has not provided a diagnosis-specific medical treatment, or a consistent early predictor, or a unified life course. If the ASD diagnosis also lacks biological and construct validity, a shift away from studying ASD-defined samples would be warranted. Consequently, this paper reviews recent findings for the neurobiological validity of ASD, the construct validity of ASD diagnostic criteria, and the construct validity of ASD spectrum features. The findings reviewed indicate that the ASD diagnosis lacks biological and construct validity. The paper concludes with proposals for research going forward.Keywords DSM-5 . ASD . Autism . Diagnosis . Validity . Comorbidity . HeterogeneityThe goal of the DSM-3 nosology (American Psychiatric Association 1980) was to create reliable and standard categorical psychiatric diagnoses (Robins and Guze 1970). However, in the past 30 years, clinical, genetics, and neuroscience findings have revealed that the DSM diagnoses are not biologically valid. The National Institutes of Mental Health (NIMH) responded by proposing the Research Domain Criteria (RDoC) framework for a brain-based transdiagnostic psychiatric symptom nosology (Cuthbert and Insel 2013;Insel et al. 2010;Lilienfeld and Treadway 2016). Peterson (2015) and Weinberger et al. (2015) argued that the RDoC could not replace the DSM-5 psychiatric nosology (American Psychiatric Association 2013) or the parallel International Classification of Diseases (ICD) psychiatric nosology (World Health Organization 2012). But BFor the foreseeable future, RDoC is not envisioned as a system of psychiatric classification in its own right. Instead, in the near term, RDoC and DSM-ICD are expected to coexist. Nevertheless, RDoC is intended to provide scaffolding for a large-scale research program that will ultimately yield an alternative to DSM-ICD^ (Lilienfeld and Treadway 2016, p. 445).RDoC advocates accept that DSM-5/ICD psychiatric categories remain necessary in clinical practice, but argue that researchers should shift to RDoC study designs immediately. They assert that studying psychiatric categories lacking biological validity blocks the discovery of brain bases for psychopathology and thus cannot lead to effective medical treatments for specific psychiatric symptoms (Cuthbert and Insel 2013;Insel et al. 2010;Lilienfeld and Treadway 2016;Yee et al. 2015). Against this RDoC imperative for biological validity, Weinberger et al. (2015) countered that current DSM-5 psychiatric behavioral diagnoses were valid when they yielded effective medical treatment, clear prognosis, and a life course specific to a diagnosis.Autism spectrum disorder (ASD) research has been productive (Dawson 2016;de la Torre-Ubieta et al. 2016;Szatmari et al. 2016), but no ASD research findings have met the validity criteria of Weinberger et al. (2015). DSM-5 ASD research has found no s...

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Section: Does Asd Have Neurobiological Validity?supporting

confidence: 60%

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 95%

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 99%

See 3 more Smart Citations

ASD Validity

Waterhouse

London

Gillberg

2016

Rev J Autism Dev Disord

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Social Brain Functional Maturation in Newborn Infants With and Without a Family History of Autism Spectrum Disorder

et al. 2019

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Key Points Question Are changes in the maturation of the social brain in infants associated with vulnerability to neurodevelopmental conditions such as autism spectrum disorder? Findings In this cohort study of 36 neonates with and without a family history of autism spectrum disorder, newborns with a family history of autism spectrum disorder had significantly higher neural activity in the right fusiform and left parietal cortex. In addition, the pattern of age-related changes in spontaneous activity in the cingulate and insula was disrupted in infants with a family history of autism spectrum disorder. Meaning Atypical development of functional activity patterns in key regions responsible for social processing may be a vulnerability mechanism for autism.

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Subregional differences in intrinsic amygdala hyperconnectivity and hypoconnectivity in autism spectrum disorder

et al. 2015

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LAY ABSTRACT Autism research indicates that there may be similar brain circuits affected in both individuals with autism and individuals with mood disorders such as major depression. However, psychotropic medications, while widely prescribed in individuals with autism, have been largely unsuccessful in treating core autism symptoms, indicating that etiology of co-existing psychiatric and autism symptoms may differ. In this fMRI study, the relationship between brain activity in the amygdala, a small, almond-shaped structure located deep within the brain, and activity in other parts of the brain were examined in 25 individuals with autism and 28 individuals without autism, during rest. This study provides the first evidence that connections between the amygdala and other brain regions are not uniformly atypical in autism, but differ depending on the subregion under investigation. In autism we observed weaker connections from the laterobasal subregion of the amygdala, a group of nuclei involved in social behavior and emotion, and, stronger connections from the centromedial and superficial subregions, which are involved in emotional arousal and olfaction. Additionally, we found that connectivity patterns related to autism symptoms were different from connectivity patterns related to mood symptoms. This finding suggests that despite occurring frequently in individuals with autism, mood disorders may involve separate neural mechanisms. This finding may also help explain why psychotropic medications are generally ineffective at treating autism symptoms. SCIENTIFIC ABSTRACT Background The amygdala is a complex structure with distinct subregions and dissociable functional networks. The laterobasal subregion of the amygdala is hypothesized to mediate the presentation and severity of autism symptoms, although very little data are available regarding amygdala dysfunction at the subregional level. Methods In this study, we investigated the relationship between abnormal amygdalar intrinsic connectivity, autism symptom severity, and anxiety and depressive symptoms. We collected resting state fMRI data on 31 high functioning adolescents and adults with autism spectrum disorder and 38 typically developing (TD) controls aged 14–45. 25 participants with ASD and 28 TD participants were included in the final analyses. ASD participants were administered the Autism Diagnostic Interview–Revised and the Autism Diagnostic Observation Schedule. Adult participants were administered the Beck Depression Inventory II and the Beck Anxiety Inventory. Functional connectivity analyses were conducted from three amygdalar subregions: centromedial (CM), laterobasal (LB) and superficial (SF). In addition, correlations with the behavioral measures were tested in the adult participants. Results In general, the ASD group showed significantly decreased connectivity from the LB subregion and increased connectivity from the CM and SF subregions compared to the TD group. We found evidence that social symptoms are primarily associated with under-conn...

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An unbiased Bayesian approach to functional connectomics implicates social-communication networks in autism

Cited by 34 publications

References 85 publications

ASD Validity

ASD Validity

Social Brain Functional Maturation in Newborn Infants With and Without a Family History of Autism Spectrum Disorder

Subregional differences in intrinsic amygdala hyperconnectivity and hypoconnectivity in autism spectrum disorder

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