BACKGROUND The capacity of posttraumatic stress disorder(PTSD)to occur with delayed onset has been documented in several systematic reviews and meta-analyses.Neurobiological models of PTSD may provide insight into the...BACKGROUND The capacity of posttraumatic stress disorder(PTSD)to occur with delayed onset has been documented in several systematic reviews and meta-analyses.Neurobiological models of PTSD may provide insight into the mechanisms underlying the progressive increase in PTSD symptoms over time as well as into occasional occurrences of long-delayed PTSD with few prodromal symptoms.AIM To obtain an overview of key concepts explaining and types of evidence supporting neurobiological underpinnings of delayed PTSD.METHODS A scoping review of studies reporting neurobiological findings relevant to delayed PTSD was performed,which included 38 studies in the qualitative synthesis.RESULTS Neurobiological mechanisms underlying PTSD symptoms,onset,and course involve several interconnected systems.Neural mechanisms involve the neurocircuitry of fear,comprising several structures,such as the hippocampus,amygdala,and prefrontal cortex,that are amenable to time-dependent increases in activity through sensitization and kindling.Neural network models explain generalization of the fear response.Neuroendocrine mechanisms consist of autonomic nervous system and hypothalamic-pituitary-adrenocortical axis responses,both of which may be involved in sensitization to stress.Neuroinflammatory mechanisms are characterized by immune activation,which is sometimes due to the effects of traumatic brain injury.Finally,neurobehavioral/contextual mechanisms involve the effects of intervening stressors and mental and physical disorder comorbidities,and these may be particularly relevant in cases of long-delayed PTSD.CONCLUSION Thus,delayed PTSD may result from multiple underlying neurobiological mechanisms that may influence the likelihood of developing prodromal symptoms preceding the onset of full-blown PTSD.展开更多
Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functi...Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into展开更多
基金Supported by the Danish Working Environment Research Fund from Arbejdsmilj?forskningsfonden(to Bonde JP)。
文摘BACKGROUND The capacity of posttraumatic stress disorder(PTSD)to occur with delayed onset has been documented in several systematic reviews and meta-analyses.Neurobiological models of PTSD may provide insight into the mechanisms underlying the progressive increase in PTSD symptoms over time as well as into occasional occurrences of long-delayed PTSD with few prodromal symptoms.AIM To obtain an overview of key concepts explaining and types of evidence supporting neurobiological underpinnings of delayed PTSD.METHODS A scoping review of studies reporting neurobiological findings relevant to delayed PTSD was performed,which included 38 studies in the qualitative synthesis.RESULTS Neurobiological mechanisms underlying PTSD symptoms,onset,and course involve several interconnected systems.Neural mechanisms involve the neurocircuitry of fear,comprising several structures,such as the hippocampus,amygdala,and prefrontal cortex,that are amenable to time-dependent increases in activity through sensitization and kindling.Neural network models explain generalization of the fear response.Neuroendocrine mechanisms consist of autonomic nervous system and hypothalamic-pituitary-adrenocortical axis responses,both of which may be involved in sensitization to stress.Neuroinflammatory mechanisms are characterized by immune activation,which is sometimes due to the effects of traumatic brain injury.Finally,neurobehavioral/contextual mechanisms involve the effects of intervening stressors and mental and physical disorder comorbidities,and these may be particularly relevant in cases of long-delayed PTSD.CONCLUSION Thus,delayed PTSD may result from multiple underlying neurobiological mechanisms that may influence the likelihood of developing prodromal symptoms preceding the onset of full-blown PTSD.
文摘Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into
