Psychophysiology of Trauma

Psychophysiology of Trauma

The how’s and why’s of posttraumatic stress, subse­quent symptoms, and symptom resolution can be un­derstood in relation to the events that occur in the brain during and after a traumatic event. What follows is a brief (emphasis on brief) description of the se­quence of events during and after a trauma. It is helpful to recognize that your symptoms are part of the body and mind’s natural response to extreme events. For a more complete understanding of the neurological sequence involved with trauma, you are referred to Sapolsky, 1997; Scaer, 2006; van der Kolk, McFarlane & Weisaeth, 1996; Rothschild, 2000; and Johnson, 2003.

When a person experiences a traumatic event, the in­formation is registered in the brain along two pathways. The first and quickest path sends sensory information (i.e., scent, related objects, sounds, sights, etc) to the amygdala, where a fear response is triggered and the information is cataloged as important for sur­vival. From the amygdala, the information proceeds to other areas of the brain (e.g. the stria terminalis and the locus ceruleus) responsible for preparing the body for flight or fight and a subsystem of the Autonomic Nervous System (the sympathetic nervous system) is activated. The information is eventually stored in the hippocampus as a memory important for survival. Thereafter, anything that stimulates that sensory memory trace will also potentially stimulate the body to prepare for survival (fear/anxiety/arousal). In other words, when an individual is exposed to related cues to the memory (i.e., scent, related objects, sounds, sights, etc) these sensory reminders re-ignite the associated strong feelings. Interestingly enough, the memory of the traumatic event itself may or may not be recalled. This can leave you feeling as if you were in danger but not necessarily knowing why.

This variability in memory can be understood by following the second pathway for information processing. This second and much longer path for the information proceeds through the thalamus, which routes sensory information to appropriate parts of the neo-cortex to be analyzed. This information is processed through various areas in the neo-cortex where language is used to organize and generate responses (a declarative memory is formed), associations to other information are made, and meaning is created. It is, then, routed to and stored in the hippocampus. It is also the case that the neo-cortex contains inhibitory areas that are ca­pable of inhibiting or turning down the survival/fear response generated by the information passed through the amygdala. In other words, the neo-cortex can po­tentially change the meaning of the original memory trace and alter or modulate the survival response.

Under conditions of extreme stress, the brain pro­duces stress hormones such as cortisol that interfere with the consolidation of the information from the neo-cortex. This also interferes with the possible in­hibitory responses that would ameliorate the anxiety of the survival response. Memories that are formed under conditions of trauma often become fragmented. They remain out of context and are, thus, left unincor­porated and unassociated with other memories. The result is that whenever the memory trace is stimu­lated, the body reverts to survival mode, which is ex­perienced as anxiety. Since the traumatic memories are often unconsolidated, it is sometimes difficult for a survivor to make the link between earlier traumatic experi­ences and the current feeling of anxiety. You might then be­gin to perform behaviors to relieve the anxiety (i.e., not driving after you were in a transportation accident; not returning to work if that is the place where you were physically injured). If these behaviors work to relieve the anxiety (i.e. remove a noxious condition), they are negatively reinforced to occur again.

These information storage pathways account for the development of many trauma related symptoms. In the example of someone who was injured in an accident, a large number of sensory cues are recorded such as the smell of exhaust fumes, heavy traffic, and dim light. This sensory information is recorded in such a manner that even without actually remembering the original accident, the person in the accident might find themselves becoming extremely anxious at the smell of exhaust fumes or being in heavy traffic at dusk. Since a person might not necessarily make a connection to a previous accident when smelling exhaust fumes it might be difficult to make sense of feelings of anxiety in the current moment. This is often a confusing task, especially if there isn’t anything particularly threatening at the time that you might be feeling upset about. A person might just assume they are having an “anxiety attack” and attribute it to a physiological problem. Or you might simply begin to perform behaviors to reduce feelings of anxiety such as self-medicating with drugs or alcohol or avoiding driving.

The initial neurological response of the brain is quite likely the mechanism by which the immediate learning of the traumatic response is accomplished. In one-trial learning the sensory stimuli are sent to the midbrain and recorded as a threat to survival. The brain attaches the emotions of fear and anxiety to these stimuli and prepares the body for flight, fight or freeze. Very little cognitive processing occurs at this stage, since the neo-cortex has been flooded with cortisol and other cortico-steroids, which interfere with memory consolidation. The fact that memories are unconsolidated and un­connected results in the failure to normally resolve the fear/anxiety/arousal response. In other words, the brain has failed to unhook the sensory information from the fear/anxiety/arousal response. Later behav­iors are operationally learned as a way to alleviate this fear/anxiety/arousal.

Subsequent stimulation of this memory trace will potentially re­activate the survival routines until the neo-cortex has been allowed to process the information and inhibit the response. Relaxation in the face of expo­sure facilitates access to neo-cortical functions (de­clarative memory, meaning generation and anxiety inhibition). Recent research suggests that this may be mediated by a decrease in cortisol under conditions of relaxation (Benson, 1997; Luecken,, Dausch, Gulla, Hong & Compas, 2004; Mason, Giller, Kosten & Harkness, 1988). Strictly behavioral inter­ventions pair the memory trace with responses (relax­ation, self soothing) that are inconsistent with the sur­vival mode (fear/anxiety/arousal), expanding the re­sponse set. Cognitive interventions specifically work to pair the memory trace with more fully processed (and hence more meaningful) information that has the ability to inhibit the survival response.

Think of what might happen to someone who has experienced an automobile accident. The sensory stimuli are sent to the midbrain and recorded as a threat to survival. The brain attaches the emotions of fear and anxiety to these stimuli and prepares the body for flight or fight. As expected, little cognitive processing occurs at this stage, and the neo-cortex becomes flooded with cortisol and other cortico-steroids essentially inhibiting the ability to consolidate and fully store memories. Future reminders of the memory will re-ignite the poorly stored memory trace of the event resulting in survival strategies being engaged. Survival responses will continue to occur until neo-cortical processing of the traumatic memory has adequately allowed for re-storage of the memory while concurrently extinguishing the emotional distress associated with the memory. An in vivo (on-site) behavioral intervention would teach relaxation techniques and then pair relaxation with the sensory stimulus. In this example, the person would be relaxed and then perhaps be instructed to imagine driving on the highway or preparing to take a road trip until anxious feelings ignite. At that point, the individual would be instructed to initiate relaxation exercises until the symptoms of anxiety begin to reduce. This might require many exposures or sessions until the person no longer feels anxious when thinking of or engaging in the previously fearful memory or activity. Cognitive interventions often require teaching relaxation techniques and re-experiencing the event. Initial sessions, often involve discussions of memories peripheral to the actual trauma and subsequent beliefs about the event. Eventually trauma reduction sessions would involve the direct memory of the event (again, under conditions of relaxation) and the ability to describe the event without anxiety. Finally, cognitive restructuring would address distorted beliefs and behaviors previously learned and used to keep safe.

Offering post-trauma care that addresses the impact of the trauma on our brain functioning requires that the clinician assist the client to slow down the reactivity ignited when exposed to trauma reminders that set-off old emotions. It is the gap between exposure to trauma reminders and reactivity that opens the door to change. It is pausing in that gap with calm reflection that allows us to inform and reform our reactivity creating a new storage of the trauma memory associated with a more reflective and less reactive or emotionally strained response. Our goal in Trauma Practice is to find the route to retraining the brain along with the body, mind and emotion.