About this Research Topic
Following our previous Research Topic “Neural mechanisms of posttraumatic stress disorder” (2017), we welcome you to contribute to this new Research Topic.
A dizzying number of research lines are leading to advances in our thinking about the mechanisms that drive post-traumatic stress disorder (PTSD), resistance to traumatization and recovery. These include enduring alterations in neuronal systems, glucocorticoid signaling, emotional and autonomic reactivity, sleep and circadian rhythm, brain function and immune function.
In addition to the above, we seek contributions in the following domains:
1. Clinical Implications: Although animal models have traditionally defined PTSD as molecular and behavioral changes in stress responsive circuits following trauma, this concept needs to be further clarified for both research and clinical use. PTSD can be determined by a multifactorial combination of physiological parameters, epigenetic modulators, and neurobiological candidate markers.
2. Tailored treatment: Prospective studies of military populations emergency room patients are providing substantial evidence about the emerging biological abnormalities that precede the full-blown disorder. Implications for selection of interventions tailored to the stage of progression need to be specified. The neurobiology of chronic unremitting PTSD needs to be differentiated from the acute disorder.
3. The joint occurrence of PTSD and other diseases: Because PTSD is a systemic disorder, underpinned not only by the biological dysregulation noted above, the increased rates of cardiovascular and autoimmune disease among PTSD patients should be further explored. Related to this, elevated CRP and other inflammatory changes as risk factors for PTSD need to be better understood.
4. The role of cognitive abnormalities: dysregulated processing of both emotionally relevant and emotionally neutral information underlies some PTSD symptom expression. This processing of emotional memory also occurs during sleep and is likely disrupted in PTSD. Implications for intervention need to be drawn.
Data-based findings that bear on the biological mechanisms of PTSD are preferred, but integrative theoretical pieces will be considered.
A dizzying number of research lines are leading to advances in our thinking about the mechanisms that drive post-traumatic stress disorder (PTSD), resistance to traumatization and recovery. These include enduring alterations in neuronal systems, glucocorticoid signaling, emotional and autonomic reactivity, sleep and circadian rhythm, brain function and immune function.
In addition to the above, we seek contributions in the following domains:
1. Clinical Implications: Although animal models have traditionally defined PTSD as molecular and behavioral changes in stress responsive circuits following trauma, this concept needs to be further clarified for both research and clinical use. PTSD can be determined by a multifactorial combination of physiological parameters, epigenetic modulators, and neurobiological candidate markers.
2. Tailored treatment: Prospective studies of military populations emergency room patients are providing substantial evidence about the emerging biological abnormalities that precede the full-blown disorder. Implications for selection of interventions tailored to the stage of progression need to be specified. The neurobiology of chronic unremitting PTSD needs to be differentiated from the acute disorder.
3. The joint occurrence of PTSD and other diseases: Because PTSD is a systemic disorder, underpinned not only by the biological dysregulation noted above, the increased rates of cardiovascular and autoimmune disease among PTSD patients should be further explored. Related to this, elevated CRP and other inflammatory changes as risk factors for PTSD need to be better understood.
4. The role of cognitive abnormalities: dysregulated processing of both emotionally relevant and emotionally neutral information underlies some PTSD symptom expression. This processing of emotional memory also occurs during sleep and is likely disrupted in PTSD. Implications for intervention need to be drawn.
Data-based findings that bear on the biological mechanisms of PTSD are preferred, but integrative theoretical pieces will be considered.
Keywords: PTSD, etiology, neural circuitry, extinction, inflammation, genetics, neuroimaging, sleep
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
