New Pretrauma Prospective Study: Your Brain Is Not Damaged By Trauma

The most decisive evidence about PTSD comes from studies done before trauma.

CATEGORY: CONTROL OF LANGUAGE AND IDEAS

Licia de Voogd, PhD

Source: Biological Psychiatry
Read time: 2.4 minutes
 
This Happened
In a new study, researchers scanned the brains of police recruits before and after active-duty exposure to stressful and traumatic experiences to test the crucial question of whether brain differences related to PTSD pre-exist trauma or are caused by trauma. These types of pretrauma prospective studies are difficult to conduct for a variety of reasons, and therefore are relatively rare. The findings are worth highlighting.
Who Did This?
First author was Licia de Voogd, Ph.D., employed at Radboud University (Netherlands). She has nine first-author and four secondary-author publications, mostly focused on brain imaging related to stress and trauma.
The Premise
One hundred seventy-nine Dutch police recruits had their brains imaged before graduating to active duty (Baseline) and then again after 8 months of active duty (Follow-up). While lying in the brain scanner, they viewed virtual images of a suspect raising a gun at them under two conditions. In the High Threat condition, this threat was paired with an electric shock. In the Low Threat condition, there was no shock.
While on active duty, they experienced an average of five stressful or traumatic events. At Follow-up, 12 individuals met criteria for PTSD, and 61 individuals met criteria for subthreshold PTSD.
The Results
At Baseline, those with relatively greater activation in the left amygdala went on to develop significantly more PTSD symptoms at follow-up.
No significant association was present within the periaqueductal gray region.
At Follow-up, amygdala reactivity showed no alterations in relation to increases in PTSD symptoms.
The authors concluded, “This prospective longitudinal study shows that dorsal amygdala hyperresponsivity during threat anticipation is associated with increased vulnerability for developing PTSD symptoms.”
Analysis
This study adds to the growing list of well-conducted studies showing that trauma and PTSD do not alter the neurophysiology or size of brain centers, i.e., the body does not keep the score. By my count there are now 32 pretrauma prospective studies of neurobiological variables, of which six involve the amygdala. All three literature reviews of these types of studies concluded that differences in neurobiology between those with PTSD compared to those without PTSD existed prior to experiencing any trauma [1-3]. And, there is little to no good evidence that trauma associated with PTSD causes lasting alterations in brain function, brain center volumes, or other neurobiological variables.
The researcher activists who relentlessly promote the narrative that trauma damages brains cite many human studies that seem to support their claim, but those are always weak cross-sectional studies that possess zero ability to determine what came first. The only type of studies that have causal explanatory power are pretrauma prospective studies where the brains and neurobiology are measured both before and after trauma exposure.
What This Means
The central importance of this study lies in what it reveals about the direction of causality—a point that sits at the heart of the “body keeps the score” controversy. If PTSD-related brain differences are largely pre-existing, rather than created by trauma, then the dominant narrative in clinical training, public health messaging, and educational policy is fundamentally misaligned with the best evidence.

For clinical work, these findings argue for a shift away from the assumption that trauma inflicts lasting neurological injury that must be “repaired.”

Instead, clinicians should recognize that individuals come to traumatic events with varying, biologically influenced stress-response profiles. This reframes PTSD not as brain damage, but as a predictable outcome for a subset of vulnerable individuals, which supports more targeted screening, early intervention, and realistic expectations for recovery.

For research, the study underscores the necessity of prospective designs. Cross-sectional studies—still the backbone of trauma neuroscience because they are cheaper and easier—cannot answer causal questions, and their continued use perpetuates misleading interpretations about trauma-induced brain change. Funding priorities should shift toward designs capable of distinguishing vulnerability from consequence.
For social policy, the findings challenge sweeping claims that trauma universally harms the brain. Policies built on that assumption—such as mandated trauma-informed programs or broad neurological narratives in schools—risk oversimplifying human resilience, misallocating resources, and promoting deterministic views of children and adults.
In short, the evidence points toward pre-existing vulnerability, not neurological scarring, with major implications for how society understands and responds to trauma
 

References
[1] Julia A. DiGangi et al. (2013). Pretrauma risk factors for posttraumatic stress disorder: A systematic review of the literature. Clinical Psychology Review 33:728-744.
[2] Andrea Danese et al. (2017). The origins of cognitive deficits in victimized children: Implications for neuroscientists and clinicians. American Journal of Psychiatry 174:349-361.
[3] Michael S. Scheeringa (2020). Reexamination of diathesis stress and neurotoxic stress theories: A qualitative review of pre-trauma neurobiology in relation to posttraumatic stress symptoms. International Journal of Methods in Psychiatric Research 30:e1864. doi: 10.1002/mpr.1864