Metabolic mapping of deep brain structures and associations with symptomatology in autism spectrum disorders

Doyle‐Thomas, Krissy; Card, Dallas; Soorya, Latha; Wang, A. Ting; Fan, Jin; Anagnostou, Evdokia

doi:10.1016/j.rasd.2013.10.003

Cited by 40 publications

(45 citation statements)

References 51 publications

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“…By contrast, Doyle-Thomas et al (2014) reported that RRBs in general were associated with atypically low choline/creatine in the thalamus, whereas ASD social impairment was not. In addition, Gabriels et al (2013) reported that the general severity of RRBs was inversely correlated with daytime cortisol levels.…”

Section: Does Asd Have Neurobiological Validity?mentioning

confidence: 92%

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?mentioning

confidence: 92%

ASD Validity

Waterhouse

London

Gillberg

2016

Rev J Autism Dev Disord

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“…However, other studies have found decreased glutamate/Glx in ASD in regions including the ACC (Bernardi et al, 2011;van Elst, Maier, Fangmeier, & Endres, 2014) the basal ganglia (Horder et al, 2013); frontal and occipital cortex, the cerebellum (Devito et al, 2007) and white matter (Corrigan et al, 2013). Yet other studies have found no significant differences in glutamate / Glx levels between individuals with and without ASD in several different brain regions including parietal lobes (Horder et al, 2013;Page et al, 2006), frontal lobes (Horder et al, 2013) temporal lobes (Devito et al, 2007), and occipital lobes (Robertson, Ratai, & Kanwisher, 2015); the thalamus (Bernardi et al, 2011;Doyle-Thomas et al, 2014;Hardan et al, 2008); hippocampus (Joshi et al, 2012);and cerebellum (van Elst et al, 2014). Therefore, the literature regarding glutamate/Glx levels in ASD is mixed.…”

Section: Glutamate / Glxmentioning

confidence: 96%

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

2016

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The balance of neural excitation and inhibition (E/I balance) is often hypothesised to be altered in autism spectrum disorder (ASD). One widely held view is that excitation levels are elevated relative to inhibition in ASD. Understanding whether, and how, E/I balance may be altered in ASD is important given the recent interest in trialling pharmacological interventions for ASD which target inhibitory neurotransmitter function.Here we provide a critical review of evidence for E/I balance in ASD. We conclude that data from a number of domains provides support for alteration in excitation and inhibitory neurotransmission in ASD, but when considered collectively, the available literature provide little evidence to support claims for either a net increase in excitation or a net increase in inhibition. Strengths and limitations of available techniques are considered, and directions for future research discussed.3

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“…Hassan et al (2013) 12. Doyle-Thomas et al (2014). HC = healthy control; ASD = autism spectrum disorder; nASD = narrowly defined ASD; bASD = broadly defined ASD; pASD = parents of children with ASD; SV = single voxel; MRSI = magnetic resonance spectroscopic imaging (multi-voxel, aka chemical shift imaging); IQ = intelligence quotient; L = left; R = right;…”

Section: Tablementioning

confidence: 99%

The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment

Rojas

2014

J Neural Transm

171

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Glutamate is the major excitatory neurotransmitter in the brain and may be a key neurotransmitter involved in autism. Literature pertaining to glutamate and autism or related disorders (e.g., Fragile X syndrome) is reviewed in this article. Interest in glutamatergic dysfunction in autism is high due to increasing convergent evidence implicating the system in the disorder from peripheral biomarkers, neuroimaging, protein expression, genetics and animal models. Currently, there are no pharmaceutical interventions approved for autism that address glutamate deficits in the disorder. New treatments related to glutamatergic neurotransmission, however, are emerging. In addition, older glutamate-modulating medications with approved indications for use in other disorders are being investigated for re-tasking as treatments for autism. This review presents evidence in support of glutamate abnormalities in autism and the potential for translation into new treatments for the disorder.

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Metabolic mapping of deep brain structures and associations with symptomatology in autism spectrum disorders

Cited by 40 publications

References 51 publications

ASD Validity

ASD Validity

Measuring neural excitation and inhibition in autism: Different approaches, different findings and different interpretations

The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment

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