Treatment guidelines for post-traumatic stress disorder (PTSD) have changed little in 20 years. In real-world settings, dropouts from exposure-based treatments are common, and remission is often incomplete. While many patients have a significant decrease in symptoms with currently recommended treatments, most are left with residuals of the disorder1. Hence, there is a need for a conceptual shift. Current treatments tend to focus on the impact of a specific trauma, but ignore critical elements of the phenomenology and neurobiology of traumatic stress. Most traumatized patients do not suffer from the effects of one single trauma, but from the neurobiological consequences of cumulative traumatic experiences. Problems with affect regulation, concentration, and excessive reactivity interfere with being able to deal effectively with the ordinary demands of daily life. Particularly individuals with histories of child abuse (developmental trauma) tend to experience significant defects in a variety of transdiagnostic mental processes, including an inability to modulate or tolerate distress, being unable to notice internal states (alexithymia), and a lack of a coherent sense of self. All of these aspects have been shown to correlate with poor treatment outcome2. While the role of fear circuitry in PTSD has been well established, little attention has been paid to the central role of sensory processing and affect regulation in the pathophysiology of the disorder. Back in 1872, C. Darwin already described how intense emotions are registered in physical sensations – for instance, heart-breaking feelings in the chest and gut-wrenching sensations in the abdomen (mediated by the vagus nerve, which he called the pneumogastric nerve). Contemporary research has confirmed that traumatic re-experiencing is more than a memory or an emotion. It is a full body physiological and sensory reaction to images, sounds, touch and other internal or external sensory input. These physical sensations are poorly seriated in time and place, and are often experienced without context or insight as to their origins. Trauma's neurobiological imprints vary significantly across the lifespan, shaped by neurodevelopmental stages, hormonal shifts, and the brain's evolving capacity to process threat. From infancy to late adulthood, the same traumatic event can ignite starkly different biological cascades – a reality underscored by mounting research into age-specific trauma responses3 and our increasing understanding of critical periods of brain development. Epidemiological studies consistently find that individuals with probable or subsyndromal PTSD report significantly higher rates of somatic symptoms – such as chronic pain, gastrointestinal complaints, cardiovascular symptoms, and fatigue – compared to those without PTSD. For example, in a population-based military sample, somatic disorder was present in 59.6% of those with probable PTSD, compared to only 5% in those without PTSD4. There is a direct correlation between the intensity of PTSD symptoms and the number and severity of somatic complaints, with a clear gradient observed in individuals exposed to multiple traumatic events5. These data suggest that somatic symptoms are not peripheral but core features of PTSD, that stem from trauma-induced biological changes. The somatic symptoms associated with trauma exposure are due, at least in part, to dysregulated sensory processing and altered interoceptive capacities. The imprints of trauma often defy narrative. Instead, sensory fragments combined with intense emotional arousal or numbing bypass cognitive processing and are expressed as somatic states and behavioral reactivity5. Problems in discriminating whether sensory input is dangerous or safe are central features of PTSD5. Trauma survivors experience intrusive flashbacks not as coherent memories but as disjointed sensations: a flash of light, a muffled scream, the pressure of a hand. Significantly, in patients with PTSD, these sensory disturbances occur not only in response to trauma-related stimuli, but also to neutral sensory information, such as spatial navigation and scene perception6. In particular, children exposed to chronic trauma exhibit altered sensory modulation patterns and deficits in general sensory processing, independent of emotional context, which usually persist in adulthood7. Adults with histories of child abuse have elevated rates of autoimmune disorders, cardiovascular disease, and fibromyalgia – physical echoes of childhood hypothalamic-pituitary-adrenal (HPA) axis dysfunction7. Childhood trauma has been associated with reduced hippocampal volume, impairing memory integration, and a hyperreactive insula that magnifies bodily sensations (e.g., interpreting muscle fatigue as impending collapse)7. PTSD is associated with alterations in both the structure and function of sensory brain regions, such as lower gray matter volume in temporal, parietal and occipital regions, including the superior temporal gyrus, which helps integrate audiovisual information from emotional stimuli; the superior parietal gyrus, involved in dorsal visual processing stream for spatial and movement information; and the bilateral orbitofrontal gyrus, involved in guiding sensory attention and integrating inputs from sensory and limbic structures6, 7. Altered connectivity between subcortical (e.g., amygdala, hippocampus) and cortical (e.g., prefrontal cortex, sensory cortices) regions impairs top-down (conscious) regulation, allowing bottom-up sensory and affective signals to predominate5. The resulting sensory overload further contributes to somatic distress, and promotes hypervigilance and feeling emotionally overwhelmed, as expressed in behavioral agitation, panic reactions and loss of impulse control7. On the other hand, hypo-responsivity, the result of emotional overmodulation, is associated with increased activation of medial prefrontal cortex and rostral anterior cingulate regions8, reflected in dampening of bodily awareness, dissociative symptoms, numbness, and feeling detached from reality. A study comparing PTSD patients with and without the dissociative (depersonalization/derealization) subtype documented that the former group showed greater amygdala connectivity to prefrontal regions during resting state8. Somatic symptoms and lack of sensory regulation are central, not peripheral, to the clinical presentation of PTSD. They reflect complex neurobiological and psychological mechanisms9. Recognizing and addressing these somatic correlates is essential for comprehensive assessment and effective treatment of PTSD. Traditional trauma-focused therapies, while effective for many, do not fully address the sensory dysregulation and somatic symptoms experienced by a substantial subset of patients. When considering whether emerging treatments – such as mindfulness approaches, stellate ganglion block, neurofeedback, and psychedelic-assisted psychotherapies – offer novel therapeutic benefits, it is important to evaluate their effect on the somatic and sensory domains of PTSD, and to investigate which treatments can reverse or repair these long-term neurobiological imprints of trauma.
Kolk et al. (Fri,) studied this question.