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• W2022797703 endingPage "347" @default.
• W2022797703 startingPage "337" @default.
• W2022797703 abstract "•PTSD is triggered by well-delineated stressors, facilitating causal brain models. •Amygdala and dACC abnormalities confer vulnerability for increased fear upon stress. •Reduced hippocampus–vmPFC connectivity following stress may impair fear inhibition. •The functions of these brain circuits imply a temporal trajectory of PTSD symptoms. Discriminating neural abnormalities into the causes versus consequences of psychopathology would enhance the translation of neuroimaging findings into clinical practice. By regarding the traumatic encounter as a reference point for disease onset, neuroimaging studies of post-traumatic stress disorder (PTSD) can potentially allocate PTSD neural abnormalities to either predisposing (pre-exposure) or acquired (post-exposure) factors. Based on novel research strategies in PTSD neuroimaging, including genetic, environmental, twin, and prospective studies, we provide a causal model that accounts for neural abnormalities in PTSD, and outline its clinical implications. Current data suggest that abnormalities within the amygdala and dorsal anterior cingulate cortex represent predisposing risk factors for developing PTSD, whereas dysfunctional hippocampal–ventromedial prefrontal cortex (vmPFC) interactions may become evident only after having developed the disorder. Discriminating neural abnormalities into the causes versus consequences of psychopathology would enhance the translation of neuroimaging findings into clinical practice. By regarding the traumatic encounter as a reference point for disease onset, neuroimaging studies of post-traumatic stress disorder (PTSD) can potentially allocate PTSD neural abnormalities to either predisposing (pre-exposure) or acquired (post-exposure) factors. Based on novel research strategies in PTSD neuroimaging, including genetic, environmental, twin, and prospective studies, we provide a causal model that accounts for neural abnormalities in PTSD, and outline its clinical implications. Current data suggest that abnormalities within the amygdala and dorsal anterior cingulate cortex represent predisposing risk factors for developing PTSD, whereas dysfunctional hippocampal–ventromedial prefrontal cortex (vmPFC) interactions may become evident only after having developed the disorder. existence of more than one form of the same gene within the population. Each of those gene forms is called an ‘allele’. laboratory fear conditioning is an experimental paradigm used to teach animals or humans to form an association between a neutral stimulus (e.g., a light or a tone) and an aversive unconditioned stimulus (US; e.g., a mild electric shock). The presentation of the now-conditioned stimulus (CS) triggers the organism to exhibit several physiological responses. Most commonly measured conditioned responses are freezing and potentiated startle in rodents, and skin conductance and potentiated startle responses in humans. a training phase in conditioning studies that occurs after fear conditioning. During fear extinction, the cue (the CS) is repeatedly presented in the absence of the US. This extinction training (or within-session extinction learning) leads to decrement of the conditioned responses over trials. Subsequent test of the extinction learning after a delay (i.e., 24 h) is referred to as an extinction recall (or retention) test. a measure of the level of activation synchronization between two or more brain regions as inferred from common changes in their activation over time. Functional connectivity may reflect either an excitatory or inhibitory link between those brain regions in a direct or indirect pathway. an anxiety disorder that may develop following exposure to a traumatic event that involves actual or threatened death, serious injury, or a threat to the physical integrity of oneself or others, to which the person responded with intense fear, helplessness, or horror. Formal diagnosis of PTSD includes three symptom clusters: (i) re-experiencing the original trauma(s), such as through flashbacks or nightmares; (ii) avoidance of stimuli associated with the trauma(s); (iii) and hyperarousal in the form of irritability, hypervigilance, and exaggerated startle." @default.
• W2022797703 created "2016-06-24" @default.
• W2022797703 creator A5044133929 @default.
• W2022797703 creator A5061143819 @default.
• W2022797703 creator A5063798638 @default.
• W2022797703 date "2013-07-01" @default.
• W2022797703 modified "2023-09-27" @default.
• W2022797703 title "A causal model of post-traumatic stress disorder: disentangling predisposed from acquired neural abnormalities" @default.
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