Pathophysiology of the human locus coeruleus complex in fetal/neonatal sudden unexplained death

Lavezzi, Anna Maria; Alfonsi, Graziella; Matturri, Luigi

doi:10.1179/1743132812y.0000000108

Cited by 17 publications

(24 citation statements)

References 49 publications

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“…Reduction and/or loss of TH staining in the LC has been reported by Lavezzi et al [25,47], while no differences in TH immunoreactivity in SIDS have been found by other authors [73,74]. …”

Section: Discussionmentioning

confidence: 77%

“…Intense TH immunoreactivity in almost all the LC neurons was already observed in the youngest neonate of our sample (aged 25.5 weeks) who belonged to the severe/acute HII group 1. Immunohistochemical studies in human fetal tissues using antibodies against TH and/or dopamine-β-hydroxylase showed that noradrenergic neurons appear in the dorsal pons as early as gestational weeks 5-6 [22,23,24,48], while at birth almost all LC neurons are TH-IR [25], as occurs in the adult [26,27]. The presence of TH immunoreactivity in the adult LC was confirmed by the two adult brain specimens used as positive controls.…”

Section: Discussionmentioning

confidence: 99%

“…TH - the immunohistochemical marker of catecholamine perikarya in the brain - is detectable in LC neurons very early in development, i.e. already from 5-6 weeks of gestation onwards [22,23,24], while at birth almost all the LC neurons appear to be TH immunoreactive (IR) [25], as occurs in adulthood [26,27]. …”

Section: Introductionmentioning

confidence: 99%

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The Effect of Perinatal Hypoxic/Ischemic Injury on Tyrosine Hydroxylase Expression in the Locus Coeruleus of the Human Neonate

Pagida¹,

Konstantinidou²,

Korelidou³

et al. 2015

Dev Neurosci

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We have previously shown that perinatal hypoxic/ischemic injury (HII) may cause selective vulnerability of the mesencephalic dopaminergic neurons of human neonate. In the present study, we investigated the effect of perinatal HII on the noradrenergic neurons of the locus coeruleus (LC) of the same sample. We studied immunohistochemically the expression of tyrosine hydroxylase (TH, first limiting enzyme for catecholamine synthesis) in LC neurons of 15 autopsied infants (brains collected from the Greek Brain Bank) in relation to the neuropathological changes of acute or chronic HII of the neonatal brain. Our results showed that perinatal HII appears to affect the expression of TH and the size of LC neurons of the human neonate. In subjects with neuropathological lesions consistent with abrupt/severe HII, intense TH immunoreactivity was found in almost all neurons of the LC. In most of the neonates with neuropathological changes of prolonged or older injury, however, reduction in cell size and a decrease or absence of TH staining were observed in the LC. Intense TH immunoreactivity was found in the LC of 3 infants of the latter group, who interestingly had a longer survival time and had been treated with anticonvulsant drugs. Based on our observations and in view of experimental evidence indicating that the reduction of TH-immunoreactive neurons occurring in the LC after perinatal hypoxic insults persists into adulthood, we suggest that a dysregulation of monoaminergic neurotransmission in critical periods of brain development in humans is likely to predispose the survivors of perinatal HII, in combination with genetic susceptibility, to psychiatric and/or neurological disorders later in life.

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“…Reduction and/or loss of TH staining in the LC has been reported by Lavezzi et al [25,47], while no differences in TH immunoreactivity in SIDS have been found by other authors [73,74]. …”

Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Effect of Perinatal Hypoxic/Ischemic Injury on Tyrosine Hydroxylase Expression in the Locus Coeruleus of the Human Neonate

Pagida¹,

Konstantinidou²,

Korelidou³

et al. 2015

Dev Neurosci

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“…In contrast, thalamic lesions in stroke are characterized by ‘suspending' in the drowsy state (extended NREM 1), decreased arousal index and no major REM sleep alterations [58], supposedly accompanied by exaggerated sympathetic activation with preserved parasympathetic drive to the cardiovascular system [59]. The possible approach here could be controlling nondipping BP at bedtime (chronotherapy [60,61]) with angiotensin receptor blockers [62,63].…”

Section: Discussionmentioning

confidence: 99%

Nocturnal Deterioration after Ischemic Stroke and Autonomic Dysfunction: Hypothesis and Implications

et al. 2013

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Background: A significant number of patients admitted to hospital after acute ischemic stroke deteriorate clinically. Deterioration is generally noted within the first 48 h after stroke onset. The mechanisms leading to this deterioration are not fully understood. Summary: One potential cause of this deterioration may be altered or impaired autonomic function. We expect the hemodynamic changes regulated by the autonomic nervous system that are dysregulated after stroke to be exaggerated during sleep, resulting in arrhythmia and blood pressure fluctuations in these patients. Such physiological changes could result in worsening the overall outcome of the ischemic stroke patient or in sudden death. Therefore, it is necessary to summarize yet unrelated observations and hypothesize on their individual effects and interactions as they relate to poststroke deterioration. Key Messages: If the hypothesis is correct that dysautonomia occurs to the degree that it affects clinical outcomes negatively, this would have important implications for the prevention of neurological deterioration and sudden death after ischemic stroke.

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“…Other staining materials are Lillie for the neuromelanin pigment (28) and Perl’s Prussian blue for iron in oxygen-transporting heme mechanism (29). …”

Section: Stepwise Proceduresmentioning

confidence: 99%

Updates on the Methodological Approaches for Carrying Out an In-Depth Study of the Cardiac Conduction System and the Autonomic Nervous System of Victims of Sudden Unexplained Fetal and Infant Death

Alfonsi

Crippa

2016

Front. Med.

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This article contains a set of protocols for histopathological techniques that can be used for carrying out in-depth studies of cases of sudden infant death syndrome and sudden intrauterine unexplained fetal death syndrome. In order to enable researchers to advance hypotheses regarding the causes of the unexpected death of infants and fetuses, the authors propose three innovative and accurate methodologies for studying the cardiac conduction system, the peripheral cardiac nervous system, and the central autonomic nervous system. Over the years, these protocols have been developed, modified, and improved on a vast number of cases which has enabled pathologists to carry out the microscopic analyses of the structures which regulate life, in order to highlight all the possible morphological substrates of pathophysiological mechanisms that may underlie these syndromes.In memory of our research professor Lino Rossi (1923–2004).

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Pathophysiology of the human locus coeruleus complex in fetal/neonatal sudden unexplained death

Cited by 17 publications

References 49 publications

The Effect of Perinatal Hypoxic/Ischemic Injury on Tyrosine Hydroxylase Expression in the Locus Coeruleus of the Human Neonate

The Effect of Perinatal Hypoxic/Ischemic Injury on Tyrosine Hydroxylase Expression in the Locus Coeruleus of the Human Neonate

Nocturnal Deterioration after Ischemic Stroke and Autonomic Dysfunction: Hypothesis and Implications

Updates on the Methodological Approaches for Carrying Out an In-Depth Study of the Cardiac Conduction System and the Autonomic Nervous System of Victims of Sudden Unexplained Fetal and Infant Death

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