Brain Weight and Sudden Infant Death Syndrome

Falck, Geir; Rajs, Jovan

doi:10.1177/088307389501000212

Cited by 17 publications

(16 citation statements)

References 10 publications

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“…Several groups have examined brain weight in SIDS [7][8][9][10][11][16][17][18][19][20]. The majority of these investigators have reported that the brain (either in isolation, or expressed as a ratio of brain weight : body weight) is heavier in SIDS than either a control population or published 'normal' data [7][8][9][10][16][17][18][19].…”

Section: Discussionmentioning

confidence: 99%

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Brain weight in sudden unexpected death in infancy: experience from a large single‐centre cohort

Bamber

Paine

Ridout³

et al. 2015

Neuropathology Appl Neurobio

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Section: Discussionmentioning

confidence: 99%

“…Brain weight : body weight ratio Brain weight [7] 79 and reference data 79 Reference data -SIDS heavier [16] 261 and reference data 208 53 and reference data -SIDS heavier [17] 150 61 89 -SIDS heavier [8] 227 and reference data 227 Reference data No difference SIDS heavier [9] 163 and reference data 125 38…”

Section: Number Of Sids Cases Number Of Control Casesmentioning

confidence: 99%

Brain weight in sudden unexpected death in infancy: experience from a large single‐centre cohort

Bamber

Paine

Ridout³

et al. 2015

Neuropathology Appl Neurobio

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“…When organ weights are measured as a function of body weight (not age) some studies show significant differences between cases of SIDS [77,78] and non-SIDS while others contradict these [79]. Reasons for the discrepancies between the studies relate to features of the control groups (presence of infection, gestational age, changes in infant nutritional status with socioeconomic development, and so on).…”

Section: Discussionmentioning

confidence: 99%

A perspective on SIDS pathogenesis. The hypotheses: plausibility and evidence

Goldwater

2011

BMC Med

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Several theories of the underlying mechanisms of Sudden Infant Death Syndrome (SIDS) have been proposed. These theories have born relatively narrow beach-head research programs attracting generous research funding sustained for many years at expense to the public purse. This perspective endeavors to critically examine the evidence and bases of these theories and determine their plausibility; and questions whether or not a safe and reasoned hypothesis lies at their foundation. The Opinion sets specific criteria by asking the following questions: 1. Does the hypothesis take into account the key pathological findings in SIDS? 2. Is the hypothesis congruent with the key epidemiological risk factors? 3. Does it link 1 and 2? Falling short of any one of these answers, by inference, would imply insufficient grounds for a sustainable hypothesis. Some of the hypotheses overlap, for instance, notional respiratory failure may encompass apnea, prone sleep position, and asphyxia which may be seen to be linked to co-sleeping. For the purposes of this paper, each element will be assessed on the above criteria.

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“…A previously published study demonstrated that one specific AQP4 variation (rs2075575) can be related to increased brain weights in SIDS infants, suggesting that this variation may predispose the development of cerebral edema (15). The association of an increased brain weight and SIDS, however, is controversial because some studies reported an increased brain weight in SIDS infants compared with gender-and agematched controls, whereas others could not confirm such a correlation (16)(17)(18)(19). Therefore, one might speculate that an increased brain weight is not a general indicator for SIDS but is only seen in combination with genetic or environmental risk factors (15,19).…”

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confidence: 85%

Aquaporin-4 polymorphisms and brain/body weight ratio in sudden infant death syndrome (SIDS)

2014

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Background: Failure in the regulation of homeostatic water balance in the brain is associated with severe cerebral edema and increased brain weights and may also play an important role in the pathogenesis of sudden infant death syndrome (SIDS). We genotyped three single-nucleotide polymorphisms in the aquaporin-4 water channel-encoding gene (AQP4), which were previously shown to be associated with (i) SIDS in Norwegian infants (rs2075575), (ii) severe brain edema (rs9951307), and (iii) increased brain water permeability (rs3906956). We also determined whether the brain/body weight ratio is increased in SIDS infants compared with sexand age-matched controls. Methods: Genotyping of the three AQP4 single-nucleotide polymorphisms was performed in 160 Caucasian SIDS infants and 181 healthy Swiss adults using a single-base extension method. Brain and body weights were measured during autopsy in 157 SIDS and 59 non-SIDS infants. results: No differences were detected in the allelic frequencies of the three AQP4 single-nucleotide polymorphisms between SIDS and adult controls. The brain/body weight ratio was similarly distributed in SIDS and non-SIDS infants. conclusion: Variations in the AQP4 gene seem of limited significance as predisposing factors in Caucasian SIDS infants. Increased brain weights may only become evident in conjunction with environmental or other genetic risk factors. s udden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an infant younger than one year of age, which remains unexplained even after a complete investigation of the circumstances of death (1). According to the triple risk model proposed in 1994, the occurrence of SIDS involves three overlapping classes of SIDS-associated risk factors, namely (i) a vulnerable infant, (ii) a critical developmental period, and (iii) exogenous stress factors (2,3). While many of the exogenous stress factors, such as prone sleeping position, overheating, or maternal smoking during pregnancy, are well described, the genetic pathogenesis of SIDS remains poorly understood (4-8).Aquaporin-4 (AQP4) water channels are the main water transporters in the brain and are responsible for the active transport of water and small solutes across cell membranes at the blood-brain and brain-cerebrospinal fluid barriers (9). The highest density of AQP4 is expressed in astrocytic endfeet membranes and allows bidirectional transport of water to regulate the brain volume and ion homeostasis depending on the level of neuronal activity (10,11). Failure in the regulation of the homeostatic water balance can result in osmotic expansion of astrocytes, known as cytotoxic edema, which is typically accompanied by brain swelling (12). The involvement of AQP4 in the formation of brain edema was demonstrated in AQP4-deficient mice that experienced less astrocytic swelling and improved survival after acute water intoxication than wild-type mice (13). Water permeability assays further demonstrated that even partial knock-down variations in the AQP4 gene could reduc...

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Brain Weight and Sudden Infant Death Syndrome

Cited by 17 publications

References 10 publications

Brain weight in sudden unexpected death in infancy: experience from a large single‐centre cohort

Brain weight in sudden unexpected death in infancy: experience from a large single‐centre cohort

A perspective on SIDS pathogenesis. The hypotheses: plausibility and evidence

Aquaporin-4 polymorphisms and brain/body weight ratio in sudden infant death syndrome (SIDS)

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