Decades of research in psychotraumatology and neuroscience have mapped out how traumatic experiences alter key brain regions and physiological pathways. Researchers have long observed that trauma is “stored in somatic memory and expressed as changes in the biological stress response” (van der Kolk, 1994, p. 253). Intense emotional trauma triggers a cascade of neurochemical and structural changes: stress hormones surge, certain brain areas become overactive while others shut down, and the autonomic nervous system shifts into prolonged defensive states. These changes help explain why trauma survivors often experience hyperarousal, intrusive emotional memories, and bodily symptoms even when the original danger is long past. Below, we outline the major neurobiological systems affected by trauma and how they create a lasting imprint:
Amygdala (Fear Center): The amygdala is an almond-shaped limbic structure crucial for detecting threats and generating fear responses. In trauma exposure and posttraumatic stress disorder (PTSD), the amygdala often becomes hyper-reactive. Neuroimaging studies consistently show heightened amygdala activity when trauma survivors re-experience flashbacks or even process trauma-unrelated emotional cues (Shin et al., 2006). This hyper-responsivity — sometimes called a “smoke detector” on overdrive (van der Kolk, 2014) — means the brain’s alarm system is easily triggered, sounding the alert of danger even in safe situations. Notably, amygdala activation in PTSD correlates with symptom severity (Shin et al., 2006), underscoring that an overactive amygdala is central to the clinical picture of trauma. The amygdala’s reactions are involuntary and pre-conscious, which explains why survivors may feel intense fear or anger before they even think about why they are reacting.
Hippocampus (Memory Encoding): The hippocampus is the brain’s key structure for forming and retrieving explicit memories and for distinguishing past from present. Traumatic stress has been linked to reduced hippocampal volume and impaired hippocampal function (Bremner et al., 1995; Shin et al., 2006). Repeated studies have found that people with chronic PTSD exhibit hippocampal shrinkage – on the order of 8–26% smaller volume in some findings (Bremner et al., 1995). Excess cortisol and excitatory neurotoxicity during trauma are believed to contribute to these changes in the hippocampus (Sapolsky, 1996). Functionally, a compromised hippocampus means difficulty forming coherent contextual memories of the trauma; instead of a story with a beginning, middle, and end, the trauma may be remembered in fragmentary flashbacks, sensations, or emotional states. As van der Kolk (1994) observed, when declarative memory fails, the trauma may be organized on a somatosensory level – as visual images, body sensations, and emotional states – rather than as a verbal narrative. This helps explain why trauma memories often feel timeless and are easily re-lived: the context-tagging and time-stamping function of the hippocampus has been disrupted. The person continually experiences the feeling of the trauma, even when they cannot consciously contextualize it as a past event.
Prefrontal Cortex (Executive Control and Regulation): The prefrontal cortex, especially the medial and orbitofrontal regions, is responsible for executive functions, emotional regulation, and extinction of fear responses. In the neurobiology of trauma, the prefrontal cortex (PFC) is notable for its underactivity during high stress and recollection of trauma. When trauma survivors are triggered or reminded of their trauma, studies show a relative deactivation of the frontal lobes – particularly areas involved in speech and reasoning (e.g., Broca’s area and medial PFC) (van der Kolk, 2014). For example, in a brain imaging study, recalling traumatic memories caused PTSD patients’ left frontal cortex (including Broca’s speech area) to shut down, while limbic regions lit up (van der Kolk, 2014). This neurologically correlates with the common report that during flashbacks or panic, individuals “go blank” or struggle to articulate what they are experiencing. Shin et al. (2006) found not only that the PFC was functionally hyporesponsive in PTSD, but also that some prefrontal areas can be physically smaller in volume following chronic trauma. Diminished frontal regulation leaves the amygdala disinhibited, so the brain’s emotional alarm signals occur unchecked by rational appraisal. In essence, trauma can impair the brain’s natural top-down control, making it harder for a person to consciously calm themselves or distinguish safe present context from traumatic past. This biological pattern — an overactive amygdala with an underactive prefrontal cortex — encapsulates why traumatic reactions are often intense and difficult to consciously control.
Periaqueductal Gray and the Default Mode Network
Beyond the well-known limbic and cortical regions affected by trauma, two additional systems have garnered significant attention in recent research: the periaqueductal gray (PAG) and the Default Mode Network (DMN).
The periaqueductal gray is a midbrain structure that plays a central role in modulating defensive responses, pain perception, and freeze states. Under conditions of inescapable threat, the PAG helps coordinate immobilization responses such as tonic immobility or dissociation (Fanselow, 1991). In trauma survivors, overactivation of the PAG may underpin episodes of shutdown, passivity, or dissociative detachment—especially when the sympathetic fight-or-flight response is not viable. Functional MRI studies have shown increased PAG activation during trauma recall in individuals with dissociative PTSD (Harricharan et al., 2016), highlighting its contribution to autonomic and behavioral shut-down responses. This understanding is particularly relevant in complex trauma and developmental trauma, where freeze and collapse responses are more common than overt hyperarousal.
Closely tied to the PAG’s role in dissociation is the function of the Default Mode Network (DMN), a distributed network of brain regions including the medial prefrontal cortex, posterior cingulate cortex, precuneus, and angular gyrus. This network supports self-referential processing, autobiographical memory, and a coherent sense of self (Buckner et al., 2008). Trauma, particularly early and chronic forms, has been shown to disrupt DMN connectivity, leading to impairments in identity coherence, self-awareness, and autobiographical integration (Lanius et al., 2010).
Ruth Lanius and colleagues have demonstrated through neuroimaging that trauma survivors—especially those with complex PTSD or dissociative subtypes—exhibit hypoactivation and desynchronization within the DMN during resting states and self-related tasks (Lanius et al., 2015). These disruptions are correlated with a loss of self-coherence, emotional numbing, and depersonalization. Lanius et al. (2020) propose that restoring DMN function is critical for reintegration and recovery, as it supports the rebuilding of narrative identity and access to embodied self-awareness. Clinically, this points to the importance of therapies that foster self-reflective capacity, body awareness, and safe re-engagement with autobiographical material.