ArticleInternational journal of environmental research and public health2013
Proposed toxic and hypoxic impairment of a brainstem locus in autism.
Article in International journal of environmental research and public health, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Gasotransmitters and their influence on autism spectrum disorders - a systematic review.Molecular biology reports · 2025Pooled it
- Methylation-reprogrammed Wnt/β-catenin signalling mediated prenatal hypoxia-induced brain injury in foetal and offspring rats.Journal of cellular and molecular medicine · 2018Article
- Association of Autism with Maternal Infections, Perinatal and Other Risk Factors: A Case-Control Study.Journal of autism and developmental disorders · 2018Article
- Ellagic acid improves electrocardiogram waves and blood pressure against global cerebral ischemia rat experimental models.Electronic physician · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Electrophysiological findings implicate site-specific impairment of the nucleus tractus solitarius (NTS) in autism. This invites hypothetical consideration of a large role for this small brainstem structure as the basis for seemingly disjointed behavioral and somatic features of autism. The NTS is the brain's point of entry for visceral afference, its relay for vagal reflexes, and its integration center for autonomic control of circulatory, immunological, gastrointestinal, and laryngeal function. The NTS facilitates normal cerebrovascular perfusion, and is the seminal point for an ascending noradrenergic system that modulates many complex behaviors. Microvascular configuration predisposes the NTS to focal hypoxia. A subregion--the "pNTS"--permits exposure to all blood-borne neurotoxins, including those that do not readily transit the blood-brain barrier. Impairment of acetylcholinesterase (mercury and cadmium cations, nitrates/nitrites, organophosphates, monosodium glutamate), competition for hemoglobin (carbon monoxide, nitrates/nitrites), and higher blood viscosity (net systemic oxidative stress) are suggested to potentiate microcirculatory insufficiency of the NTS, and thus autism.
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Registered trials
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.