When the Past is Always Present Part 7

Other Consequences of Traumatization.

The consequences of traumatization are extraordinarily varied. As mentioned above, phobias, somatization disorders, panic, chronic pain, chronic emotional states, and PTSD are consequences of traumatization. It is highly likely traumatization impacts other disorders by altering the landscape. Diseases such as depression, anxiety, substance abuse, obsessive-compulsive disorder, and so on, may have some component that relates to traumatization.7 These consequences arise from a maladaptive response to chronic stress. This maladaptive response affects various brain systems, such as the nucleus acc.u.mbens (a.s.sociated with addictive disorders), cingulate gyrus (a.s.sociated with disorders of emotional regulation), and caudate nucleus (a.s.sociated with compulsive disorders).8 Traumatization may even be pa.s.sed to your descendents.9

The Absence of Forgetting.

The persistence of a traumatic memory is puzzling. While it is true that nontraumatized emotional moments can often be recalled, they are not usually so vivid and a.s.sociated with intense emotions. Nor are there somatic and autonomic components. As observed by Janet, traumatized memories are accurate and immutable over time; he believed they are fixed in the subconscious. Nontraumatized memories, on the other hand, can change. When a haven cannot be found or an escape cannot be perceived at the moment of traumatization, we never feel safe; the threat, concomitant vigilance, and feelings are always with us.

One possible explanation is that during initial amygdala activation by a perceived threat, the prefrontal cortex (PFC) is inhibited from sending an inhibitory signal to the amygdala. This inhibitory signal is known to release GABA in the amygdala. When an event is synaptically encoded as a traumatization, there is no perceived escape and no signal is sent to the amygdala from the prefrontal cortex. This lack of signal allows for the potentiation of the glutamate pathway, the moment is encoded and the memory endures, readily available for reactivation. Subsequent recall of a component of a previously traumatized event by thought or other stimuli causes the BLC to send an inhibitory signal to the prefrontal cortex, ensuring that the pathway is not erased.

Treating the traumatized memory requires discovering the origin of the emotional core of a traumatization. Since the emotional distress from recall of a traumatically encoded moment is experienced as if it were occurring for the first time, this suggests that if a neurobiological equivalent of safety can be generated after emotional activation, the pathway can be disrupted.

References.

1. Robertson, J. (1962). Hospitals and children: A parent's-eye view (pp. 5758). New York, NY: Gollancz.

2. Ames, E. W. (1997). The development of Romanian orphanages children adopted to Canada. Ottawa, Canada: Human Resources Development. Retrieved from http://findarticles.com/p/articles/mi_m2248/is_136_34/ai_59810232/ 3. Shekhar, A., Sajdyk, T. S., Keim, S. R., Yoder, K. K., & Sanders, S. K. (1999). Role of basolateral amygdala in panic disorder. Ann. N.Y. Acad. Sci. 747750.

4. van der Kolk, B. A. (1989). The compulsion to repeat trauma. Psychiatr. Clin. North Am. 12(2):389411.

5. Sarno, J. E. (2006). The divided mind, pp. 89128. New York, NY: Regan Books.

6. Smith, A. (1989, September 8). Long Beach Journal: Eyes that saw horrors now see only shadows. Special to the New York Times.

7. Felitti,V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., Koss, M. P., & Marks, J. B. Relations.h.i.+p of childhood abuse and household dysfunction to many of the leading causes of death in adults: The Adverse Childhood Experiences (ACE) Study (1998). Am. J. Prev. Med. 14(4): 245258. For an up to date a.n.a.lysis see http://www.cdc.gov/ nccdphp/ace/ 8. Scaer, R. C. (2005). The trauma spectrum: Hidden wounds and human resiliency. New York, NY: W.W. Norton Press.

9. www.developingchild.networkingpaper#10.

7.

DISRUPTING A TRAUMATIZATION..

Traumatization can be avoided if, during a potentially traumatizing moment, an escape is perceived. If an event is encoded as a traumatic memory, upon recall of the event, providing the individual with a safe haven should disrupt the trauma-induced linkages and erase the emotional response to related stimuli.

Avoiding the Encoding of a Traumatic Memory.

A gang of thugs is chasing you after you inadvertently insulted the leader's girlfriend. They are going to beat you to a pulp after they catch you and you are literally running for your life. You are getting tired and there is no place to hide. The thugs are gaining and your heart is racing as fast as it can to keep you going. They are just about to catch you and all of a sudden you wake up. Sweating, eyes wide open, and heart pumping, you realize it was just a dream and you laugh to yourself, but it's a little hard getting back to sleep. Awakening just in time from a scary dream is a great way to escape the danger and avoid traumatization. Escape is when the danger has permanently pa.s.sed. Hollywood understands this concept. How many endings of scary movies have you seen where the predator, thought to be killed, somehow manages to survive and look the audience in the face? Just when you thought you were safe, that you escaped-it is the stuff nightmares and traumatizations are made of.

At the beginning of a potentially traumatizing event, when specific pathways are being created, it is unclear whether the criteria for inescapability will be met. At this moment, dopamine, norepinephrine, and cortisol are elevated, preparing us to do what needs to be done to survive. If we survive and find a haven we calm down. To calm down, we need to inhibit the release of norepinephrine from the locus coeruleus (LC) and inhibit the central nucleus (Ce) from further activating our physiology. In the LC, serotonin via its effect on GABA neurons prevents the release of norepinephrine.1 The prefrontal cortex, on perceiving the threat has pa.s.sed, inhibits the Ce via GABA interneurons. The amygdala is now quiet and the event fades. But things are different if an event is encoded as a trauma.

Disrupting an Encoded Trauma.

Once an event has been encoded as a traumatization, the subsequent finding of a haven does not disrupt the pathways. How, then, do we de-encode a traumatic memory? The answer is to disrupt the synaptically encoded glutamate-specific pathways in the basolateral complex (BLC). To do so, we must seek the event that leads to their activation, for as we have mentioned earlier, once activated, the glutamate receptors become vulnerable to disruption. Then, once activated, fool the brain into thinking a haven has been found. To promote this, we must also inhibit the cognitive component from further activating the amygdala. The path to a cure is outlined below: Retrieval of emotional component Working memory Hippocampus Activate BLC Sensory input of the event to the amygdala by distraction Havening Disrupt the encoded emotional BLC pathway by depotentiation of glutamate receptors De-link the components of the traumatization Traumatization cured

Preventing the Pa.s.sage of a Retrieved Component From Working Memory to the Amygdala.

Conscious/subconscious retrieval of a traumatized component en route to the amygdala pa.s.ses through a system known as working memory (WM) (Figure 7.1). The working memory system (generally considered to be part of the prefrontal cortex) receives the stored memories and sends this information to the hippocampus. If this information has been encoded as part of a traumatization, it is forwarded to the Figure 7.1 Working memory. (Courtesy of Ronald Ruden and Steve Lampasona.).

amygdala. The WM system is a limited-capacity store for retrieving and retaining information over the short term that allows for performing mental operations on the contents of the store. According to Baddeley,2 working memory has, at minimum, two components, a phonological loop that is concerned with auditory and speech-based information, and the visual-spatial sketchpad that maintains and manipulates visual and spatial information. His model also postulates a central executive that directs what working memory pays attention to and supervises these two components. The central executive's role is to regulate attention, and it does not readily allow working memory to hold dissimilar items simultaneously.

Displacing From Working Memory a Stimulus That Activates the BLC.

Working memory is the system to which retrieved components of the traumatic memory are first brought. In order to keep the component in working memory, it must be rehea.r.s.ed or augmented by an emotional feeling. The ability of an emotion-producing stimulus to sustain the item in working memory is the reason feelings can overwhelm rational thought. However, even emotion-producing stimuli that enter the working memory system can be displaced if the mind is distracted. Displacement can be accomplished by simultaneously attending to other cognitive or physical tasks. Using Baddeley's model, after entry into the working memory, having the individual attend to verbal commands that activate the visual-spatial sketchpad (having them imagine walking downstairs while counting the steps) or the auditory loop (hum "Take Me Out to the Ball Game") can displace the component. It is nearly impossible for the mind to sustain two different items in working memory. Try for yourself by adding two 3-digit numbers in your head while humming the "Star Spangled Banner." For the moment, this displacement stops the retrieved traumatic memory from activating the amygdala and producing a response. However, it requires a concentrated effort to do so.

Working memory can only hold one item.

Traumatic component in WM Displacement from WM /////// Hippocampus ////// BLC activation No response.

The displacement of the traumatic component from working memory temporarily extinguishes the response.

If the working memory is holding an event that activates the emotional component, it is difficult to dislodge it, and even if dislodged, it returns at another time. Nonetheless, if one can displace the event, activation of the BLC will cease. Thus, for example, for someone who is snake phobic, bringing into working memory an image of a slithering, sliding snake will cause the release of norepinephrine and a fear response. Distraction by thinking of something else stops this conscious activation of the BLC. However, bringing another snake to WM will reactivate the BLC and cause the person to reexperience the fear response.

Shakespeare expressed the idea that retrieval of traumatic memories causes us to reexperience the feelings as if for the first time, and that we can alter these feelings by displacement from working memory: Sonnet 30.

When to the sessions of sweet silent thought.

I summon up remembrance of things past,

I sigh the lack of many a thing I sought,

And with old woes new wail my dear time's waste:

Then can I drown an eye, unused to flow,

For precious friends hid in death's dateless night,

And weep afresh love's long since cancelled woe,

And moan the expense of many a vanished sight.

Then can I grieve at grievances foregone,

And heavily from woe to woe tell o'er

The sad account of fore-bemoaned moan, Which I new pay as if not paid before.

But if the while I think on thee, dear friend, All losses are restored and sorrows end.

Activating Traumatic Components So They Can Be Treated.

In order to disrupt a traumatic memory, it must first be retrieved and brought into working memory. Then it must activate the BLC. This activation corresponds to the release of glutamate in the BLC-specific pathway that was produced during encoding. It is this ability of stimuli to activate the BLC pathway that must be de-encoded. This prevents a signal from being sent to the Ce (which in turn activates the locus coeruleus and releases norepinephrine) and the other areas of the brain where the linkages are stored. In the case of subconscious stimuli that activate somatosensory and autonomic symptoms, bringing the symptom into working memory followed by havening may rid the individual of the symptoms, but it will not eliminate the synaptic pathway through the BLC that encodes the emotional response. The ability to reencode these nonemotional components exists and relapse remains possible. Sarno3 has observed this in many of his patients, symptoms returning or appearing elsewhere if the emotional core was not disrupted.

To de-traumatize an event we must search for its emotional origin so that it can be activated. A diagnosis of an amygdala-based disorder should make us seek the encoding event. Chronic pain and other somatic symptoms should cause us to search for a traumatizing event or unresolved anger. PTSD has both cognitive and subconscious stimuli that activate the emotions, and all should be sought. Phobias directly enter into working memory by cognitive processes and activate a fear response. Trying to recall the first time it happened is helpful. Pathological emotions arising from distressing events can be directly activated by conscious effort. If no origin can be found, such as in panic attacks, one can still generate emotions for panic disorder by thinking about the last time it occurred and how fearful we are that it will happen again. Even events that are not cognitively stored, such as those from early childhood, can be de-traumatized if we can recreate the felt sense, the emotion and/or some sensory feeling. If the traumatizing event can be found and activated, this affords an opportunity to alter the BLC pathway. How can this be accomplished?

Early Successful Trauma Treatments.

Early attempts at treating the consequences of a traumatization by talk therapy were generally unsuccessful. Most researchers felt that a traumatization permanently encoded the event, and that cognitive cues or subconscious triggers of the event caused emotional, somatosensory, and visceral responses derived from the original trauma. Professionals in this field thought that a cure was not possible. As we shall see, this has proved to be wrong.

Dr. Roger Callahan first described his tapping approach to cure trauma in 1985.4 This was followed by eye movement desensitization and reprocessing (EMDR), described by Dr. Francine Shapiro.5 Both therapies involve imaginal reexposure to the event and followed by various forms of sensory input. Dr. Callahan's approach was to evoke the memory of the trauma, then tap on various acupuncture points. This would be interspersed with a distracting process called a Gamut procedure. EMDR has eight phases. These phases include reexposure and maintenance of the images while attending to other forms of stimulation in the form of repeated sets of eye movements, tones, and taps. The goal is to focus on the information, as it is currently stored. In well-controlled trials, EMDR was shown to cure PTSD in a significant percentage of patients.

Somatic experiencing is a method for the treatment of trauma described by Dr. Peter Levine.5 He focused his therapeutic efforts on the moments when a traumatizing event is encoded and uses an escape metaphor to describe his theory. It is of interest here because he recognizes that finding an escape is critical for the resolution of a traumatized event. According to Levine,6 "Traumatic symptoms are not caused by the triggering event itself. They stem from the frozen residue of energy that has not been resolved and discharged; this residue remains trapped in the nervous system where it can wreck havoc on our bodies and spirit. It occurs because we cannot complete the process of moving in, through and out of the 'immobility' or freezing state." (Dr. Levine and Dr. Scaer (see below) use the term freeze state to denote flaccidity.) He uses the animal model of "freeze discharge" to free the individual from the traumatic event. After attempting escape and being caught, an animal becomes flaccid. If somehow the animal survives, it begins to move its legs as if it were running. This is the freeze discharge. After a few moments, the animal is then able to get up and walk away.

Traumatization occurred when the animal could not experience a freeze discharge. For Levine, the animal is psychologically and physically frozen in time. How does one escape from this state? Levine says this is possible by accessing the "felt sense," that which is stored in the procedural memory system. This can be done by a variety of ways, not always requiring the recall of the event. Just sensing the inescapability may be sufficient. Levine7 uses Eugene Gendlin's term felt sense, which "is not a mental experience but a physical one. Physical. A bodily awareness of a situation or person or event. An internal aura that encompa.s.ses everything you feel and know about the given subject at a given time-encompa.s.ses it and communicates it to you all at once."

This felt sense is the gut feeling, the knowing without knowledge, the experience of correctness or incorrectness; it is somatosensory information without interpretation. It is the physical aspects of emotion without cognition. The same pathway that is activated by cognitive generation of emotions is also activated and experienced as a felt sense.

The first step in somatic experiencing is to retrieve the feeling aspect of the event. The next step is to complete an escape that liberates the undischarged energy. In his seminal story, Levine encourages the patient to run when fear arises. This completes the escape, a freeze discharge has occurred, albeit in the client's imagination, and the person is cured. His discovery story is wonderfully instructive8: As I began with this patient she began to relax. Suddenly, without warning, she panicked. Terrified, and with no notion of what to do, I had a fleeting image of a tiger jumping towards us. It appeared dreamlike, and at the time, I had no idea where it had come from.