Stress Hormones and Post Traumatic Stress Disorder:: Basic Studies and Clinical Perspectives
de Kloet, E. Ronald; Oitzl, Melly S.; Vermetten, Eric
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Table of contents
- Cover
- List of contributorsv
- Prefacex
- Acknowledgementsxiii
- Contentsxv
- Section I: The Vulnerable Phenotype: Molecules and Cells1
- Chapter 1. Stress-induced changes in hippocampal function3
- Introduction3
- The initial phase of the stress response5
- The late phase of the stress response7
- Relevance for PTSD9
- Abbreviations10
- References10
- Discussion: Chapter 115
- Chapter 2. Glucocorticoids, developmental ’programming’ and the risk of affective dysfunction17
- ’Programming’ and the developmental origins of brain disorders17
- Glucocorticoid programming18
- Stress and glucocorticoid programming of the brain20
- CNS programming mechanisms22
- Glucocorticoid programming in humans23
- Programming and PTSD24
- Overview25
- Abbreviations25
- Acknowledgements25
- References25
- Discussion: Chapter 233
- Chapter 3. Amygdala modulation of memory-related processes in the hippocampus: potential relevance t35
- Amygdala modulation of synaptic plasticity in the hippocampus36
- Post-traumatic stress disorder (PTSD)39
- Summary43
- Appendix45
- Abbreviations46
- Acknowledgments47
- References47
- Discussion: Chapter 351
- Chapter 4. Commentary: neuroendocrine basis53
- Stress mediators53
- Dynamics of the CORT response54
- Long-term control of stress reactivity: a question of balance55
- Acknowledgement56
- References57
- General Discussion: Section I59
- Section II: The Vulnerable Phenotype: Circuits and Behavior63
- Chapter 5. Mice that under- or overexpress glucocorticoid receptors as models for depression or post65
- Introduction65
- The role of glucocorticoid receptors in depression67
- The role of glucocorticoid receptors in PTSD67
- Mice with reduced GR expression68
- Mice with increased GR expression70
- Implications for psychiatry: are results from GR mutant animals transferable?70
- Conclusions72
- Abbreviations73
- Acknowledgments73
- References73
- Discussion: Chapter 577
- Chapter 6. Adrenal stress hormones, amygdala activation, and memory for emotionally arousing experie79
- Introduction79
- Adrenal stress hormone effects on memory consolidation require emotional arousal80
- Role of the amygdala in mediating stress hormone effects on memory consolidation81
- Interactions of the amygdala with other brain regions84
- Role of the amygdala in mediating adrenal stress hormone effects on memory retrieval and working mem87
- Concluding remarks90
- Abbreviations90
- Acknowledgments90
- References90
- Discussion: Chapter 697
- Chapter 7. Adult neurogenesis and systemic adaptation: animal experiments and clinical perspectives99
- Historical overview99
- Biological significance of adult neurogenesis100
- Adult white matter neurogenesis and PTSD103
- Conclusion104
- Abbreviations104
- References105
- Discussion: Chapter 7109
- Chapter 8. Commentary: behavioral phenotype111
- References113
- General Discussion: Section II115
- Section III: The Clinical Perspective: Conceptualization of PTSD and Related Disorders119
- Chapter 9. Transgenerational transmission of cortisol and PTSD risk121
- Introduction121
- The evidence for parental PTSD as a risk factor for PTSD122
- Is parental PTSD a genetic risk factor?122
- Alternative explanations for the association between parental PTSD and PTSD in offspring123
- Biological correlates of parental PTSD: studies of Holocaust offspring124
- Cortisol levels in Holocaust offspring: cause or effect of vulnerability conferred by parental PTSD?125
- Cortisol levels in mothers and babies125
- Are cortisol levels more related to maternal than paternal PTSD?126
- Potential mechanisms for transgenerational transmission126
- Early handling in rats and vulnerability to psychopathology in offspring: a crisis in translation?127
- Characteristics of maternal attachment related to ambient cortisol levels in adult offspring128
- What has been learned?131
- Relevance of epigenetic analyses to PTSD risk131
- Abbreviations132
- Acknowledgments132
- References132
- Discussion: Chapter 9135
- Chapter 10. Early care experiences and HPA axis regulation in children: a mechanism for later trauma137
- Animal models: parental care and HPA activity138
- Human development and the hypothalamic-pituitary axis139
- Conclusions144
- Abbreviations144
- Acknowledgments144
- References144
- Discussion: Chapter 10149
- Chapter 11. The functional neuroanatomy of PTSD: a critical review151
- Introduction151
- Summary and future directions165
- Abbreviations166
- References166
- Discussion: Chapter 11169
- Chapter 12. Structural and functional plasticity of the human brain in posttraumatic stress disorder171
- Introduction171
- Psychological effects of trauma171
- Effects of stress on memory and the hippocampus172
- Stress and neurohormonal systems173
- Neurohormonal modulation of memory174
- Fear conditioning and extinction175
- Effects of treatment on the brain in PTSD176
- Glutamate, dissociation, and PTSD176
- Conclusions178
- Abbreviations178
- References178
- Discussion: Chapter 12185
- Chapter 13. Commentary: biological findings in PTSD „ too much or too little?187
- Introduction187
- Why PTSD?188
- Biological studies of PTSD189
- Genetic studies of PTSD192
- Is the context a noise „ or a signal?192
- Acknowledgment194
- References194
- General Discussion: Section III197
- Section IV: The Clinical Perspective: Targets for Therapy in PTSD201
- Chapter 14. Models of PTSD and traumatic stress: the importance of research ‘‘from bedside to be203
- Implications of epidemiology and psychology of PTSD for neurobiological models of PTSD204
- Animal models205
- Human brain studies of traumatic stress and PTSD: potential biomarkers and novel therapeutic targets209
- Conclusion211
- References211
- Discussion: Chapter 14215
- Chapter 15. What is it that a neurobiological model of PTSD must explain?217
- Clinical features of PTSD217
- Insights from risk factors218
- Explaining flashbacks and nightmares: sensory versus verbal memory219
- Evidence for dual representations of trauma220
- A possible neural substrate for trauma memories222
- Conclusions: implications for a neurobiological model of PTSD223
- Acknowledgments224
- References224
- Discussion227
- Chapter 16. Post-traumatic stress disorder in somatic disease: lessons from critically ill patients229
- Incidence of PTSD after critical illness229
- Traumatic memories from the ICU and PTSD development after severe illness230
- Use of stress hormones as therapeutic agents in the ICU and traumatic memories in patients after cri230
- Glucocorticoids and PTSD development in patients after ICU treatment232
- Conclusions234
- Abbreviations234
- References234
- Discussion: Chapter 16237
- Chapter 17. Glucocorticoid-induced reduction of traumatic memories: implications for the treatment o239
- Traumatic memories in post-traumatic stress disorder239
- Glucocorticoids and memory retrieval240
- Glucocorticoids reduce traumatic memories in PTSD241
- Possible mode of action of glucocorticoids in the reduction of traumatic memories242
- Role of endogenous cortisol in PTSD243
- Conclusions243
- Abbreviations244
- Acknowledgment244
- References244
- Discussion: Chapter 17247
- Chapter 18. Commentary: synthesis and perspectives249
- References251
- General Discussion: Section IV253
- Section V: Short Communications255
- Chapter 19. Strain specific fear behaviour and glucocorticoid response to aversive events: modelling257
- Introduction257
- Methods258
- Results258
- Discussion260
- Abbreviations261
- Acknowledgements261
- References261
- Chapter 20. Interaction of endogenous cortisol and noradrenaline in the human amygdala263
- Introduction263
- Methods and procedure264
- Results265
- Discussion266
- Abbreviations267
- References267
- Chapter 21. Corticosteroid hormones, synaptic strength and emotional memories: corticosteroid modula269
- References270
- Chapter 22. Does trauma cause lasting changes in HPA-axis functioning in healthy individuals?273
- Introduction273
- Hypothesis274
- Study groups274
- Abbreviations275
- References275
- Chapter 23. Need for alternative ways of phenotyping of mood, anxiety, and somatoform disorders in b277
- Introduction277
- Phenotype: diagnosing MAS disorders278
- Endophenotype: the crucial link in between278
- A model to study dimensions of mood, anxiety, and somatisation and HPA-axis functioning279
- Abbreviations279
- References279
- Chapter 24. The HPA-axis and immune function in burnout281
- Introduction281
- Results282
- Discussion283
- Abbreviations284
- Acknowledgments284
- References284
- Chapter 25. Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic s287
- Introduction287
- Methods288
- Results290
- Discussion290
- Abbreviations291
- References291
- Chapter 26. Precuneal activity during encoding in veterans with posttraumatic stress disorder293
- Introduction293
- Methods294
- Results295
- Discussion296
- Abbreviations296
- Acknowledgments297
- References297
- Chapter 27. Posttraumatic stress disorder with secondary psychotic features: neurobiological finding299
- Introduction299
- Methodology300
- Results300
- Pathophysiological hypotheses301
- Discussion301
- Conclusion302
- Acknowledgments302
- References302
- Chapter 28. Neuroendocrine dysregulations in sexually abused children and adolescents: a systematic303
- Introduction303
- Methodology303
- Results304
- Discussion and conclusion305
- Abbreviations306
- References306
- Chapter 29. Volume of discrete brain structures in complex dissociative disorders: preliminary findi307
- Introduction307
- Methods308
- Results308
- Discussion309
- Abbreviations310
- References310
- Chapter 30. Epilogue311
- Subject Index315
Book details
- Vendor Elsevier S & T
- SKU 9780444531407
- ISBN-13 9780080556475
- Author de Kloet, E. Ronald; Oitzl, Melly S.; Vermetten, Eric
- Category Medical
- Subject Neuroscience
Do you have questions about this book?
Post-traumatic stress disorder (PTSD) arises from the experience of severe stressors and trauma. The disorder is characterized by recurrent recall of intrusive memories to the event, nightmares with insomnia, emotional numbing, hyperarousal, which are all long-lasting and relatively resistant to therapy. The focus of this book is on the question of how stress hormones are involved in PTSD. Recent evidence suggests that a dysregulation in stress hormones promotes the precipitation of PTSD and that correction of these hormones may ameliorate the disorder. This book combines state-of-the-art basic research on stress hormones from gene to behaviour with clinical research demonstrating the progress in understanding via imaging techniques, genetics, vulnerable phenotypes and co-morbidity with other disorders and physical illness.
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