Zimmerman / Connors Maternal Influences on Fetal Neurodevelopment

Clinical and Research Aspects
1. Auflage 2010
ISBN: 978-1-60327-921-5
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 166 Seiten

Novel Approaches into the Origins of Neurodevelopmental Disorders: The Fetal Physiology Foundation Over the past two decades, autism, a neurodevelopmental disorder that is defined by behavior and was once believed to be rare, became recognized in increasing numbers of children and recently received distinction as an 'epidemic' [1]. While numbers of affected children have steadily increased, our knowledge is still ins- ficient to explain autism's diverse causes and broad range of presentations. Despite remarkable progress in research, available medical diagnostic testing applies only to a small minority of affected children. Thus, scientifically based explanations with which physicians can diagnose and treat the majority of children with autism and advise their parents are quite limited. Our society and scientific community were unprepared for the rise in autism, which explains our present inability to understand most of its causes. Researchers in neurodevelopmental disorders have long been aware of other disorders that, despite extensive efforts, have not yielded clear genetic or environmental origins, and autism has become symbolic of the need for new approaches to research into these complex conditions. Although autism has captured our attention in recent years, the prevalence of other neurodevelopmental disorders such as attention de- cit hyperactivity disorder (ADHD) and bipolar disorder, among others, also has been increasing [2-4].

Autoren/Hrsg.

Zimmerman, Andrew W.

Connors, Susan L.

Inhaltsverzeichnis

1;Maternal Influences on FetalNeurodevelopment;3
1.1;Copyright;4
1.2;Preface;5
1.2.1;References;8
1.3;Contents;9
1.4;Contributors;11
1.5;Chapter 1: Brave New World: The Intrauterine Environment as the Biological Foundation for the Lifespan;13
1.5.1;The Developing Brain;14
1.5.2;Disorders in the Offspring and the Intrauterine Environment;15
1.5.3;Future Research;16
1.5.3.1;Developmental, Not Only Intrauterine, Environment;16
1.5.3.2;Public Health Implications of Developmental Programming;17
1.5.3.3;Manipulating the Environment to “Optimize” Outcomes;17
1.5.3.4;Intrauterine Environmental Deprivation;17
1.5.3.5;Fetal Learning;18
1.5.3.6;Conclusions: View from Mt. Barcroft;18
1.5.4;References;19
1.6;Chapter 2: In the Beginning;21
1.6.1;Fetal Neurobehavioral Development;22
1.6.2;Prenatal to Postnatal Continuities;24
1.6.3;Within Domain Relations;24
1.6.4;Cross-Domain Associations;25
1.6.5;Summary;26
1.6.6;References;27
1.7;Chapter 3: Maternal Influences on the Developing Fetus;30
1.7.1;Contemporaneous Associations Between Maternal Psychological Functioning and Fetal Neurobehavior;31
1.7.2;Fetal Response to Experimental Manipulation of Maternal State;33
1.7.3;Temporal Associations Between Maternal and Fetal Functioning;36
1.7.4;Relationship Between Maternal Psychological State During Pregnancy and Postnatal Developmental Outcomes;38
1.7.5;Summary and Future Directions;40
1.7.6;References;40
1.8;Chapter 4: Implications of Maternal Programming for Fetal Neurodevelopment;44
1.8.1;Programming the Maternal Brain;44
1.8.1.1;Alterations in Maternal Attachment and Care Giving;45
1.8.1.2;Alterations in Stress Responsiveness;45
1.8.1.3;Alterations in Cognitive Performance;47
1.8.1.4;Alterations in Brain Structure and Function;48
1.8.1.5;Maternal Programming Effects Are Cumulative and Persistent;48
1.8.2;Maternal Programming Mechanisms;49
1.8.2.1;Estrogens;50
1.8.2.2;Oxytocin;50
1.8.2.3;Glucocorticoids;52
1.8.3;Emerging Possibilities for Fetal Participation in Prenatal Programming of Maternal Brain;52
1.8.3.1;Placental CRH;53
1.8.3.2;Fetal Sex;53
1.8.3.3;Fetal Behavior;54
1.8.3.4;Fetal Microchimerism;54
1.8.4;Implications for the Study of Prenatal Influences on Neurodevelopment;55
1.8.4.1;Fetal Programming;55
1.8.4.2;Rationale for an Integrated Model of Fetal and Maternal Programming;56
1.8.5;References;57
1.9;Chapter 5: Maternal Thyroid Function During Pregnancy: Effects on the Developing Fetal Brain;65
1.9.1;Introduction;65
1.9.2;Basic Thyroid Physiology;66
1.9.3;Thyroid Hormones in Pregnancy;68
1.9.4;Thyroid Hormones and Fetal Brain Development;70
1.9.5;A Historical Perspective on Maternal Hypothyroidism;74
1.9.6;Studies on Outcome Following Maternal Hypothyroidism;76
1.9.7;Does Maternal Hypothyroidism Contribute to Childhood Developmental Disorders?;79
1.9.8;Conclusions;80
1.9.9;References;80
1.10;Chapter 6: Obstetric Factors Related to Perinatal Brain Injury;88
1.10.1;Introduction;88
1.10.2;Definitions and Epidemiology;88
1.10.3;Pathophysiology;90
1.10.4;Intrapartum Complications;91
1.10.4.1;Placental Abruption;91
1.10.4.2;Uterine Rupture;91
1.10.4.3;Umbilical Cord Prolapse;92
1.10.4.4;Preeclampsia;93
1.10.4.5;Fever and Chorioamnionitis;94
1.10.4.6;Shoulder Dystocia;94
1.10.4.7;Breech Delivery;95
1.10.5;Intrapartum Identification of Asphyxia;95
1.10.6;Neonatal Markers of Hypoxic Injury;98
1.10.7;Interventions to Reduce Perinatal Brain Injury;100
1.10.8;References;101
1.11;Chapter 7: Activation of the Maternal Immune System as a Risk Factor for Neuropsychiatric Disorders;105
1.11.1;Introduction;105
1.11.2;Risk Factors Contributing to Schizophrenia and Autism;106
1.11.3;Maternal Infection: An Environmental Risk Factor;107
1.11.4;Animal Models of Immune Activation;108
1.11.4.1;Maternal Influenza Infection;108
1.11.4.2;Maternal Immune Activation;108
1.11.4.3;Maternal Poly(I:C) Administration;109
1.11.4.4;Maternal LPS Administration;109
1.11.4.5;Other Protocols for Maternal Immune Activation;110
1.11.5;Mechanisms Underlying MIA-Induced Behavioral Abnormalities;110
1.11.6;The Immune System in Neuropsychiatric Disorders;113
1.11.6.1;Immune Activation in the Human Brain;113
1.11.6.2;Inflammation and Drug Treatment;113
1.11.6.3;Mechanisms for Chronic Inflammation and Abnormal Behavior;115
1.11.7;Conclusion;117
1.11.8;References;117
1.12;Chapter 8: Prenatal Infections and Schizophrenia in Later Life – Focus on Toxoplasma gondii;124
1.12.1;Introduction;124
1.12.2;Methods for the Study of Perinatal Infections and Risk of Schizophrenia;125
1.12.2.1;Case Control Studies;125
1.12.2.2;Prospective Cohort Studies;126
1.12.2.3;Population-Based Studies;128
1.12.2.4;Register-Based Studies;128
1.12.3;Perinatal Infectious Disease Exposures Associated with Schizophrenia;129
1.12.4;T. gondii and Risk of Schizophrenia;130
1.12.4.1;The T. gondii Organism;130
1.12.4.2;Maternal Antibodies During Pregnancy;132
1.12.4.3;Toxoplasma Antibodies in Adults;134
1.12.5;Prevention and Treatment;135
1.12.6;Unanswered Questions Relating to Toxoplasma and Schizophrenia;135
1.12.6.1;Individual Variation in Response to Toxoplasma Infection;136
1.12.6.1.1;Genetic;136
1.12.6.1.2;Immunogenetic;136
1.12.6.2;Geographic Differences in Antibody Prevalence;137
1.12.7;Conclusion;138
1.12.8;References;139
1.13;Chapter 9: Maternally Acting Alleles in Autism and Other Neurodevelopmental Disorders: The Role of HLA-DR4 Within the Major H;144
1.13.1;Introduction;144
1.13.2;Early Examples of Maternally Acting Alleles;145
1.13.2.1;Rh Incompatibility;145
1.13.2.2;Maternal Phenylketonuria;148
1.13.3;More Recent Reports of Maternally Acting Alleles;149
1.13.3.1;Choice of a Study Design to Document Maternally Acting Alleles;149
1.13.3.2;Case Control Studies of MHC Gene Alleles and Autism;151
1.13.3.3;Non-inherited Maternal Alleles in Rheumatoid Arthritis;152
1.13.3.4;Documentation of Maternally Acting Alleles Using More Direct Study Designs;153
1.13.3.5;Known Maternally Acting Alleles;154
1.13.4;Reports of HLA-DR4 Studies in Autism;154
1.13.4.1;The Major Histocompatibility Complex;154
1.13.4.2;Case–Control Studies of HLA-DR and Autism;155
1.13.4.3;Case-Parent Study of Autism (Table 9.1, #4);156
1.13.5;Possible Modes of Action by Which HLA-DR4 Might Contribute to Autism;157
1.13.5.1;Inflammation and Oxidative Stress;158
1.13.5.2;Synaptic Pruning and the MHC;159
1.13.5.3;HLA-DR4, High Relative Birth Weight and Possible Relevance to Autism;160
1.13.5.4;Maternal Antibodies and Autism;160
1.13.5.5;Non-inherited Maternal Allele HLA-DR4 in Rheumatoid Arthritis;161
1.13.6;Future Studies of HLA Markers and Autism;161
1.13.7;References;162
1.14;Index;168