Neurobiological mechanisms underlying delayed expression of posttraumatic stress disorder: A scoping review

Table 5 Overview of review studies

Ref.	Study types	Review focus
Admon et al[11], 2013	Human	Reviews predisposing and acquired neural abnormalities that can be discerned based on PTSD neuroimaging studies that include genetic, environmental, twin, and prospective data
Belda et al[22], 2015	Animal	Reviews sensitization: A phenomenon whereby exposure to a particular stimulus triggers a state of hyperresponsiveness
Kim et al[18], 2019	Human, animal	Reviews influences of chronic exposure to stress on the immune system, resulting in increased proinflammatory cytokine levels. Focuses on changes in the amygdala, hippocampus, PFC, and insula, that are particularly influenced by excess cytokines
McFarlane[17], 2000	Human	Focuses on people who develop PTSD de novo, i.e., without preexisting disorder at the time of the traumatic event that may have acted as a risk factor to the onset of PTSD
McFarlane[23], 2010	Human	Examines the issue of the timing of the onset of PTSD following exposure to traumatic events
McFarlane et al[16], 2002	Human	Reviews the knowledge from neural networks to model a framework for exploring the relationship between neurobiology, cognition, and behavior in PTSD
McFarlane et al[40], 2017	Human	Argues that major advances in the biological treatments of PTSD depend on a more sophisticated classification of PTSD that acknowledges the heterogeneity of this condition
Michopoulos et al[24], 2015	Human	Reviews putative PTSD biomarkers with specific emphasis on the interaction between neurobiological influences on disease risk and symptom progression
Smid et al[38], 2003	Human	Reviews risk factors for delayed PTSD, including combat trauma, stressful events after the trauma and previous emotional problems
Soreq[37], 2010	Human, animal	Reviews effects that are often reported yr after prophylactic treatment with cholinesterase inhibitors for protection under threat of chemical warfare, e.g., during the Gulf War, and their similarity to symptoms of PTSD
Wilker and Kolassa[10], 2013	Human, animal	Reviews genetic risk factors in PTSD etiology from the perspective of a psychobiological model, which proposes that intrusive memories, the core PTSD symptom, result from the formation of an associative neural fear network, which stores sensory-perceptual representations of traumatic memories
Zovkic et al[12], 2013	Human, animal	Discusses epigenetic regulation of PTSD in human studies and in animal models and ways in which these models can be expanded. Reviews the literature that directly addresses the involvement of epigenetics in PTSD and puts it into the broader context of epigenetics in stress and fear learning

PTSD: Posttraumatic stress disorder; PFC: Prefrontal cortex.