The Activity of 2′,3′‐Cyclic Nucleotide 3′‐Phosphohydrolase in the Corpus Callosum, Subcortical White Matter, and Spinal Cord in Infants Dying from Sudden Infant Death Syndrome

Carey, Eric M.; Foster, Peter C.

doi:10.1111/j.1471-4159.1984.tb12692.x

Cited by 10 publications

(8 citation statements)

References 24 publications

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“…[8,[14][15][16]29], astroglial proliferation in the brainstem has been observed to be increased in some of the SID victims [11,19,28]. Furthermore, in about 50% of SID cases a reduced cyclic nucleotide phosphorylase activity has been found, and oligodendroglial cell numbers were reduced before the onset of myelination in the corpus callosum [5]. Cases with prolonged neonatal respiratory insufficiency had similar patterns [5].…”

Section: Discussionmentioning

confidence: 62%

“…Furthermore, in about 50% of SID cases a reduced cyclic nucleotide phosphorylase activity has been found, and oligodendroglial cell numbers were reduced before the onset of myelination in the corpus callosum [5]. Cases with prolonged neonatal respiratory insufficiency had similar patterns [5]. Leukomalacia has also been described in about 21% of the SID cases [27].…”

Section: Discussionmentioning

confidence: 95%

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Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Storm

Rognum²,

Saugstad

et al. 1993

Eur J Pediatr

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Beta-endorphin (BEND) may induce respiratory depression. Elevated levels of beta-endorphin immunoreactivity (BENDI) in the CSF are found in children with apnoea and in about 50% of sudden infant death (SID) victims. Premortal hypoxia in SID victims has been indicated by elevated hypoxanthine (HX) levels in the vitreous humour (VH). In this study we correlated BENDI in CSF with HX in VH in SID victims (n = 19) and controls (n = 18). BEND in CSF was measured by RIA, and HPLC was used for identification of BENDI. HX in VH was measured by HPLC. All the SID victims had elevated levels of HX in VH. The BENDI in CSF divided the SID victims into two subpopulations (P < 0.01); one with undetectable levels (< 4.3 fmol/ml) (n = 10) and one with high levels (160-400 fmol/ml) (n = 9). In the SID subpopulation with high levels of BENDI in CSF, we found a correlation between BENDI in CSF and HX in VH (r = 0.92). Control infants who died a stressful death, such as during heart operations (n = 2), had high levels of BENDI in CSF and low levels of HX in VH. Controls who died of infections (n = 11) had low levels of BENDI in CSF and elevated levels of HX in VH. Because hypoxia in itself does not increase BENDI in CSF, increased BENDI in CSF is probably not secondary to hypoxia but may be of aetiological significance.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 95%

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Storm

Rognum²,

Saugstad

et al. 1993

Eur J Pediatr

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“…In this work, analogous differences were not found in the medullary nuclei, although a possible confounding role of age cannot be excluded. Subtle abnormalities have also been reported in central and peripheral centers involved in cardiorespiratory regulation (Carey and Foster, 1984;Filiano and Kinney, 1992;O'Kusky and Norman, 1992;Kinney et al, 2002;Macchi et al, 2002;Porzionato et al, 2008b). In particular, O' Kusky and Norman (1992) found lower neuronal density in XII in SIDS cases with respect to controls without significant changes in total neuron numbers.…”

Section: Discussionmentioning

confidence: 98%

Morphometric Analysis of Infant and Adult Medullary Nuclei Through Optical Disector Method

Porzionato

Macchi

Parenti

et al. 2009

The Anatomical Record

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In the literature, comprehensive and comparative morphometric studies of infant and adult medullary nuclei performed with unbiased methods are still lacking. In this study, the unbiased quantitative method of the optical disector was applied to analyze neuronal densities, nuclear volumes, and total neuron numbers of the hypoglossal nucleus (XII), dorsal motor nucleus of the vagus (DMNV), nucleus tractus solitarii (NTS), medial vestibular nucleus (MedVe), cuneate nucleus (Cu), nucleus of the spinal trigeminal tract, principal inferior olivary nucleus (PION), medial inferior olivary nucleus (MION), and dorsal inferior olivary nucleus (DION) in adults (16 male, six female; mean age: 37 years) and infants (five male, five female; mean age: 5 months). In both infants and adults, higher neuronal densities were found in the more ventrally located nuclei of the spinal trigeminal tract (mean values (coefficient of variation): 20,947 (0.29) and 8,990 (0.18) neurons/mm 3 , respectively) and inferior olivary complex (PION: 20,010 (0.15) and 9,076 (0.10); MION: 18,667 (0.20) and 9,989 (0.13); DION: 22,424 (0.17) and 10,986 (0.20), respectively) than in the nuclei of the medullary tegmentum, that is, XII (2,747 (0.39) and 1,026 (0.31)), DMNV (2,876 (0.19) and 1,553 (0.26)), NTS (7,993 (0.17) and 2,877 (0.13)), MedVe (7,010 (0.17) and 2,918 (0.12)), and Cu (2,563 (0.23) and 1,038 (0.16)). All the medullary nuclei showed higher volumes and lower neuronal densities in adults than in infants, without statistically significant differences in total neuron numbers, probably because of postnatal development of the neuropil and microvascularization. Anat Rec, 292:1619Rec, 292: -1629Rec, 292: , 2009. V V C 2009 Wiley-Liss, Inc.Key words: morphometry; optical disector; medulla oblongata; human; infantThe medulla oblongata is involved in many different and complex functions as it contains nuclei involved in cardiac and respiratory control, nervous centers providing sensory and motor innervation of peripheral structures, groups of neurons receiving inputs related to the special senses of hearing, vestibular function and taste, or providing/receiving efferent/afferent cerebellar projections. There have been a few studies in the literature detailing morphometric parameters, such as neuronal density, nuclear volume, and total neuron number, in the medullary nuclei considered in this study (e.g

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“…The number of oligodendroglial cells, which are programmed with the ability to myelinate fibers in the CNS, 577 was investigated in the spinal cord, subcortical white matter and the corpus callosum of SIDS and non-SIDS infants [172]. Also investigated was the enzyme 2',3'cyclic nucleotide 3'-phosphohydrolase (CNPase), which is believed to mark differentiation of glioblast into oligogendrocyte.…”

Section: White Matter Changesmentioning

confidence: 99%

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

Sparks

Hunsaker

2002

Childs Nerv Syst

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Background: The agonizing enigma of sudden infant death syndrome (SIDS) endures. Contemporary research concentrates on the central nervous system (CNS) as the prime cause. Review and discussion: What follows is a review of the neuropathology of SIDS. A persuasive, but as yet unproved, hypothesis is that the lethal pathophysiologic derangement or mechanism in SIDS involves dysfunction of sleep-related cardiorespiratory homeostatic controls or failure to arouse or both. Neuropathological investigation of SIDS continues to be closely linked to the study of specific anatomic structures and regions of the CNS. The structures in these regions underpin and regulate normal cardiorespiratory function. It follows that dysfunction of one or more of these loci probably precipitates SIDS. Under this large umbrella review we include histological, immunohistochemical, and biochemical markers in the cerebrospinal fluid (CSF), ce-rebrum, cerebellum, brain stem, pituitary gland, and pineal gland. With variable effect, these regions are deemed to mediate the functionality of cardiorespiratory activity and the diurnal rhythms of sleep/arousal. The following factors, which (a) are associated with altered electrochemical or neural transmission and biochemical changes in the CNS and (b) predispose to systemic derangements that most probably precipitate SIDS, are subjects of ongoing investigation: evidence of delayed development; ischemic insult; degenerative changes; and synaptic alterations. Conclusion: On the basis of current data, we add to these theoretical constructs by postulating that apoptotic neurodegeneration constitutes the anatomic substrate accounting for the pathophysiologic mechanism and proximate cause of SIDS.

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The Activity of 2′,3′‐Cyclic Nucleotide 3′‐Phosphohydrolase in the Corpus Callosum, Subcortical White Matter, and Spinal Cord in Infants Dying from Sudden Infant Death Syndrome

Cited by 10 publications

References 24 publications

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Elevated beta-endorphin immunoreactivity in the cerebrospinal fluid in victims of sudden infant death correlates with hypoxanthine in vitreous humour

Morphometric Analysis of Infant and Adult Medullary Nuclei Through Optical Disector Method

Neuropathology of sudden infant death (syndrome): literature review and evidence of a probable apoptotic degenerative cause

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