Trauma acutely activates the sympathetic nervous system, which is responsible for the body’s immediate fight-flight-freeze response. This system rapidly mobilizes survival energy through the release of catecholamines, primarily adrenaline (epinephrine) and norepinephrine (NE). These neurochemicals increase heart rate, dilate pupils, redirect blood flow to muscles, and sharpen sensory input—preparing the organism to react to danger (Southwick et al., 1999).
While adaptive in the short term, prolonged activation of this system in trauma survivors can result in chronic hyperarousal, studies show that people with PTSD often exhibit elevated norepinephrine levels, which are associated with symptoms such as exaggerated startle response, insomnia, irritability, and persistent anxiety (Geracioti et al., 2001). These neurochemical changes help explain why trauma survivors may feel constantly on edge or hypervigilant, even when no threat is present.
Moreover, trauma-related dysregulation of catecholamines can lead to disturbances in other neurotransmitter systems. For example, trauma has been associated with reduced serotonin, which may contribute to depression, aggression, and emotional lability; altered dopamine, which can impact reward processing and motivation; and imbalances in GABA and glutamate, which regulate the brain’s excitation and inhibition balance (Krystal et al., 2011). Elevated glutamate levels have been particularly implicated in trauma-related excitotoxicity and may play a role in dissociative responses and neurotoxicity (Moghaddam, 2002).
In sum, the sympathetic nervous system’s overactivation and catecholamine imbalances in trauma not only underlie classic PTSD symptoms like hypervigilance and anxiety, but also interfere with sleep, mood, cognition, and autonomic regulation, further entrenching the physiological state of threat.