Recent Trauma Exposure Linked to Increased V1 Thickness, Independent of PTSD Symptoms

Posttraumatic stress disorder (PTSD) is a complex condition that can develop after trauma exposure, affecting a significant number of individuals [1, 2]. The efficacy of standard treatments like selective serotonin reuptake inhibitors can be modest, with a standardized mean difference of only -0.23 (95% CI -0.33 to -0.12) in symptom reduction [3]. This has prompted investigation into the underlying neurobiology of trauma's impact on brain structure [4, 5, 6]. A central challenge is differentiating neural changes caused by trauma exposure itself, such as increased thickness in the primary visual cortex [7], from changes specific to the chronic pathophysiology of PTSD. Clarifying this distinction is essential for identifying individuals at high risk and understanding the neural basis of resilience.