Hyperthermia in utero due to maternal influenza is an environmental risk factor for schizophrenia.
Identifieur interne : 001F23 ( Main/Exploration ); précédent : 001F22; suivant : 001F24Hyperthermia in utero due to maternal influenza is an environmental risk factor for schizophrenia.
Auteurs : Marshall J. Edwards [Australie]Source :
- Congenital anomalies [ 0914-3505 ] ; 2007.
Descripteurs français
- KwdFr :
- Carence en vitamine D (), Complications de la grossesse et maladies infectieuses, Deuxième trimestre de grossesse, Effets différés de l'exposition prénatale aux facteurs de risque, Encéphale (anatomopathologie), Encéphale (embryologie), Encéphale (malformations), Environnement, Exposition maternelle, Facteurs de risque, Femelle, Fièvre (anatomopathologie), Grippe humaine (anatomopathologie), Grossesse, Humains, Schizophrénie (), Schizophrénie (étiologie).
- MESH :
- anatomopathologie : Encéphale, Fièvre, Grippe humaine.
- embryologie : Encéphale.
- malformations : Encéphale.
- étiologie : Schizophrénie.
- Carence en vitamine D, Complications de la grossesse et maladies infectieuses, Deuxième trimestre de grossesse, Effets différés de l'exposition prénatale aux facteurs de risque, Environnement, Exposition maternelle, Facteurs de risque, Femelle, Grossesse, Humains, Schizophrénie.
English descriptors
- KwdEn :
- Brain (abnormalities), Brain (embryology), Brain (pathology), Environment, Female, Fever (pathology), Humans, Influenza, Human (pathology), Maternal Exposure, Pregnancy, Pregnancy Complications, Infectious, Pregnancy Trimester, Second, Prenatal Exposure Delayed Effects, Risk Factors, Schizophrenia (complications), Schizophrenia (etiology), Vitamin D Deficiency (complications).
- MESH :
- abnormalities : Brain.
- complications : Schizophrenia, Vitamin D Deficiency.
- embryology : Brain.
- etiology : Schizophrenia.
- pathology : Brain, Fever, Influenza, Human.
- Environment, Female, Humans, Maternal Exposure, Pregnancy, Pregnancy Complications, Infectious, Pregnancy Trimester, Second, Prenatal Exposure Delayed Effects, Risk Factors.
Abstract
A hypothesis is presented that the association between maternal influenza and other causes of fever during the second trimester of pregnancy and the subsequent development of schizophrenia in the child is due to the damage caused by hyperthermia to the developing amygdalohippocampal complex and associated structures in the fetal brain. Hyperthermia is a known cause of congenital defects of the central nervous system and other organs after sufficiently severe exposures during early organogenesis. The pathogenic mechanisms include death of actively dividing neuroblasts, disruption of cell migration and arborization and vascular damage. In experimental studies, hyperthermia during later stages of central nervous system development also caused damage to the developing brainstem that was associated with functional defects. This damage usually results in hypoplasia of the parts undergoing active development at the time of exposure. Recent studies have shown no evidence of direct invasion of the fetus by the influenza virus. Factors that might interact with hyperthermia include familial liability to schizophrenia, season of birth, maternal nutrition, severe stress and medications used to alleviate the symptoms of fevers. The time of the development of the fetal amygdalohippocampal complex and the changes found in its structure and associated areas of the brain are compatible with the known effects of hyperthermia.
DOI: 10.1111/j.1741-4520.2007.00151.x
PubMed: 17688466
Affiliations:
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Edwards</name><affiliation wicri:level="4"><nlm:affiliation>Faculty of Veterinary Science, University of Sydney, New South Wales, Australia. ava104@tpg.com.au</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Faculty of Veterinary Science, University of Sydney, New South Wales</wicri:regionArea><orgName type="university">Université de Sydney</orgName><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author></analytic><series><title level="j">Congenital anomalies</title><idno type="ISSN">0914-3505</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (abnormalities)</term><term>Brain (embryology)</term><term>Brain (pathology)</term><term>Environment</term><term>Female</term><term>Fever (pathology)</term><term>Humans</term><term>Influenza, Human (pathology)</term><term>Maternal Exposure</term><term>Pregnancy</term><term>Pregnancy Complications, Infectious</term><term>Pregnancy Trimester, Second</term><term>Prenatal Exposure Delayed Effects</term><term>Risk Factors</term><term>Schizophrenia (complications)</term><term>Schizophrenia (etiology)</term><term>Vitamin D Deficiency (complications)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Carence en vitamine D ()</term><term>Complications de la grossesse et maladies infectieuses</term><term>Deuxième trimestre de grossesse</term><term>Effets différés de l'exposition prénatale aux facteurs de risque</term><term>Encéphale (anatomopathologie)</term><term>Encéphale (embryologie)</term><term>Encéphale (malformations)</term><term>Environnement</term><term>Exposition maternelle</term><term>Facteurs de risque</term><term>Femelle</term><term>Fièvre (anatomopathologie)</term><term>Grippe humaine (anatomopathologie)</term><term>Grossesse</term><term>Humains</term><term>Schizophrénie ()</term><term>Schizophrénie (étiologie)</term></keywords><keywords scheme="MESH" qualifier="abnormalities" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Encéphale</term><term>Fièvre</term><term>Grippe humaine</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Schizophrenia</term><term>Vitamin D Deficiency</term></keywords><keywords scheme="MESH" qualifier="embryologie" xml:lang="fr"><term>Encéphale</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="malformations" xml:lang="fr"><term>Encéphale</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Fever</term><term>Influenza, Human</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Schizophrénie</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Environment</term><term>Female</term><term>Humans</term><term>Maternal Exposure</term><term>Pregnancy</term><term>Pregnancy Complications, Infectious</term><term>Pregnancy Trimester, Second</term><term>Prenatal Exposure Delayed Effects</term><term>Risk Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Carence en vitamine D</term><term>Complications de la grossesse et maladies infectieuses</term><term>Deuxième trimestre de grossesse</term><term>Effets différés de l'exposition prénatale aux facteurs de risque</term><term>Environnement</term><term>Exposition maternelle</term><term>Facteurs de risque</term><term>Femelle</term><term>Grossesse</term><term>Humains</term><term>Schizophrénie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A hypothesis is presented that the association between maternal influenza and other causes of fever during the second trimester of pregnancy and the subsequent development of schizophrenia in the child is due to the damage caused by hyperthermia to the developing amygdalohippocampal complex and associated structures in the fetal brain. Hyperthermia is a known cause of congenital defects of the central nervous system and other organs after sufficiently severe exposures during early organogenesis. The pathogenic mechanisms include death of actively dividing neuroblasts, disruption of cell migration and arborization and vascular damage. In experimental studies, hyperthermia during later stages of central nervous system development also caused damage to the developing brainstem that was associated with functional defects. This damage usually results in hypoplasia of the parts undergoing active development at the time of exposure. Recent studies have shown no evidence of direct invasion of the fetus by the influenza virus. Factors that might interact with hyperthermia include familial liability to schizophrenia, season of birth, maternal nutrition, severe stress and medications used to alleviate the symptoms of fevers. The time of the development of the fetal amygdalohippocampal complex and the changes found in its structure and associated areas of the brain are compatible with the known effects of hyperthermia.</div></front></TEI><affiliations><list><country><li>Australie</li></country><region><li>Nouvelle-Galles du Sud</li></region><settlement><li>Sydney</li></settlement><orgName><li>Université de Sydney</li></orgName></list><tree><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Edwards, Marshall J" sort="Edwards, Marshall J" uniqKey="Edwards M" first="Marshall J" last="Edwards">Marshall J. Edwards</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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