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.
Highlights
In this article, we present a hypothesis for autism via primary impairment of nucleus tractus solitarius (NTS)
A recent study suggested that heart rate, electrodermal activity, and skin temperature measurements point to an atypical autonomic response to anxiety in ASDs that is consistent with sympathetic overarousal and parasympathetic under-arousal [107]
The hypothesis inverts the prevailing neurobiological construct, which attributes ASDs to primary dysfunction of multiple regions of the higher brain, or their connections. It certainly accommodates collateral dysfunction of these higher structures, from perinatal hypoxia affecting the NTS, or cerebrovasculature dysregulation stemming from functional impairment of the NTS
Summary
We present a hypothesis for autism via primary impairment of nucleus tractus solitarius (NTS). The broad class of hydrophilic neurotoxins that circulate in blood as charged ions is more likely to have direct contact with the cell membranes of CVOs than other regions of the brain after one year of age The ubiquity of these hydrophilic neurotoxins in the autism era is indisputable, and it is intriguing to speculate that these primary toxicities affecting the CVOs may contribute to development of ASDs. Given the phenotypic similarity of early-onset and regressive ASDs, it is logical to consider how the same toxin or toxins may trigger ASDs by affecting the same region or regions of the brain, but at different times. Evidence suggests that elevated exposures to metals and other neurotoxins in the CVOs do occur, laying the groundwork for the idea that such exposures may contribute to the development of ASDs
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