Proposed Toxic and Hypoxic Impairment of a Brainstem Locus in Autism

Woody R. McGinnis, Tapan Audhya and Stephen M. Edelson
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Woody R. McGinnis: Autism Research Institute, 4182 Adams Avenue, San Diego, CA 92116, USA
Tapan Audhya: Division of Endocrinology, Department of Medicine, New York University Medical School, New York, NY 10016, USA
Stephen M. Edelson: Autism Research Institute, 4182 Adams Avenue, San Diego, CA 92116, USA

IJERPH, 2013, vol. 10, issue 12, 1-46

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.

Keywords: autism; nucleus tractus solitarius; blood-brain barrier; autonomic; baroreflex; toxins; hypoxia; perfusion; adrenergic; A 2 neurons (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2013
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