Hypoplasia and neuronal immaturity of the hypoglossal nucleus in sudden infant death

Ottaviani, Giulia; Matturri, Luigi; Mingrone, Rosaria; Lavezzi, Anna Maria

doi:10.1136/jcp.2005.032037

Cited by 33 publications

(18 citation statements)

References 17 publications

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“…However, alterations in the breathing-related modulation of hypoglossal motoneurons have been considered to be involved in sleep obstructive apnea [28][29][30]. Previous studies have shown that during specific experimental conditions, such as hypercapnia-hypoxia or lung inflation, the XII rhythmic activity might not be perfectly coupled to other respiratory motor outputs such as phrenic motoneurons [31,32].…”

Section: Discussionmentioning

confidence: 99%

Gasping Generation in Developing Swiss–Webster Mice In Vitro and In Vivo

et al. 2008

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During hypoxia the respiratory network produces gasping in vivo and in vitro. To understand the mechanisms involved in such response and to validate in vitro findings, correlative studies are necessary. During perinatal age gasping generation is robust and then declines during postnatal development, possibly due to changes in either the rhythm generator (the pre-Bötzinger complex, PBC) and/or its motor outputs. We tested this hypothesis by recording respiratory response to hypoxia in vivo and in vitro during postnatal development. We found that postnatal age influences: (1) The hypoxia-induced pattern change in the PBC bursts, (2) The coupling between the PBC and the XII nucleus during prolonged hypoxia and (3) The ability of mice to gasp and autoresuscitate from hypoxic conditions. We conclude that the inability of mice to gasp during late postnatal development might be determined by a progressive uncoupling between the respiratory rhythm generator and its motor outputs in hypoxia.

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Section: Discussionmentioning

confidence: 99%

Gasping Generation in Developing Swiss–Webster Mice In Vitro and In Vivo

et al. 2008

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“…This explains sudden death from snake bites [321,322], vaccines [323][324][325][326][327][328][329][330][331][332][333], and cocaine [215], in otherwise healthy people, as examples. Depending on their surfactant property and their position within the Hofmeister series, environmental biological or chemical intoxicants of virtually any type can provide the EIWS to induce SDS.…”

Section: Discussionmentioning

confidence: 99%

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Davidson¹,

Seneff²

2012

Entropy

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Abstract:In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade.Keywords: inflammation; serum sickness; colloidal instability; interfacial water stress; bio-sulfates; Shwartzman phenomena; sudden death syndrome Glossary of TermsAnaphylaxis a severe, rapidly progressing, life-threatening, generalized allergic reaction. Biological equipoise a stable, non-equilibrium, dissipative system synonymous with life. Cholesterol sulfate (Ch-S)quantitatively the most important known sterol sulfate in human plasma where it regulates the activity of the serine proteases, in cell membranes where it has a stabilizing role, and in platelet membranes where it supports platelet adhesion. Coherence domain (CD)a water CD is a collection of liquid water molecules which oscillate in unison in tune with a self-trapped electromagnetic field at a well-defined frequency. The coherent oscillations produce an ensemble of quasi-free electrons, able to collect noise energy from the environment and transform it into high-grade coherent energy in the form of electron vortices. This high-grade energy may then activate biomolecules resonating with the water CD. Colloidal instabilitya property attributed to a colloidal suspension that develops when stabilizing repulsive steric and electrostatic forces between colliding particles are insufficient to prevent their natural tendency to aggregate into masses large enough to precipitate.Colloidal suspension a colloid that has a continuous liquid phase in which a solid is suspended in a liquid, e.g., our flowing blood. Exclusion zone (EZ)a glass-like, gel phase consisting of water CDs resonating in-phase, adjacent to hydrophilic surfaces, several hundred micrometers wide which excludes colloi...

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“…The arcuate nucleus is an important cardiorespiratory center in the medulla and hypoplasia of this nucleus has been detected in over 50% of infants dying of SIDS (105). Alterations in another brainstem nucleus have also been demonstrated (85, 107–112). Some of these nuclei (e.g., nucleus ambiguus, parabrachial nucleus) also participate in the reflex arc of TCR (40, 42).…”

Section: Role Of Tcr In Sudden Infant Death Syndromementioning

confidence: 94%

Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review

et al. 2016

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Sudden infant death syndrome (SIDS) is an unexplained death in infants, which usually occurs during sleep. The cause of SIDS remains unknown and multifactorial. In this regard, the diving reflex (DR), a peripheral subtype of trigeminocardiac reflex (TCR), is also hypothesized as one of the possible mechanisms for this condition. The TCR is a well-established neurogenic reflex that manifests as bradycardia, hypotension, apnea, and gastric hypermotility. The TCR shares many similarities with the DR, which is a significant physiological adaptation to withstand hypoxia during apnea in many animal species including humans in clinical manifestation and mechanism of action. The DR is characterized by breath holding (apnea), bradycardia, and vasoconstriction, leading to increase in blood pressure. Several studies have described congenital anomalies of autonomic nervous system in the pathogenesis of SIDS such as hypoplasia, delayed neuronal maturation, or decreased neuronal density of arcuate nucleus, hypoplasia, and neuronal immaturity of the hypoglossal nucleus. The abnormalities of autonomic nervous system in SIDS may explain the role of TCR in this syndrome involving sympathetic and parasympathetic nervous system. We reviewed the available literature to identify the role of TCR in the etiopathogenesis of SIDS and the pathways and cellular mechanism involved in it. This synthesis will help to update our knowledge and improve our understanding about this mysterious, yet common condition and will open the door for further research in this field.

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Hypoplasia and neuronal immaturity of the hypoglossal nucleus in sudden infant death

Cited by 33 publications

References 17 publications

Gasping Generation in Developing Swiss–Webster Mice In Vitro and In Vivo

Gasping Generation in Developing Swiss–Webster Mice In Vitro and In Vivo

The Initial Common Pathway of Inflammation, Disease, and Sudden Death

Sudden Infant Death Syndrome – Role of Trigeminocardiac Reflex: A Review

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