When the Past is Always Present Part 6

Why did Joseph have chronic back pain that does not respond to treatment?

Why was Samantha unable to stop mourning her mother's death?

Why did Frank stutter?

While all aspects of life can be affected by traumatization, there are six named disorders where the primary pathology can be traced to being encoded in the amygdala. We call these disorders of traumatization or amygdala-based disorders.

Amygdala-Based Disorders Phobias Panic PTSD.

Pathological emotions.

Pain.

Somatization.

Phobias.

Phobias provide a model for the simplest form of amygdala-based traumatization. A phobia produces a fear response to objects and situations that are not inherently threatening. There is no evolutionary advantage to be terrified of public speaking or escalators or the number 13. Certainly airplanes, cars, tunnels, and bridges did not exist during early human evolution, so why do some people become terrified at the mere thought of these objects or circ.u.mstances? Since there is no innate danger a.s.sociated with these objects or situations, phobias should be considered learned (see Appendix C for details of phobia generation).

The generation of a phobia permanently links fear to a stimulus. Perception of this stimulus releases stress neurochemicals and hence meets our definition of traumatization. Phobias are related to the responses that are generated from an unconditioned fear stimulus (UFS). These UFS are nonspecific, falling into broad categories that can be applied to many situations. As described earlier, such stimuli are reflective of the many ways we can be killed or hurt and are hardwired in the brain. They include fear of the unknown (novel situations), heights (falling), closed s.p.a.ces (being trapped), being unable to run, open places (no place to hide), creepy-crawly slithery things (land-based predators), and something coming from outside of our visual field (air-based predator). As mammals we also can develop a fear of being abandoned, of being alone, known as autophobia.

Phobia Generation and Generalization.

Phobia generation requires the four elements to be present. You are riding along in a car and go over a bridge; you look down and see how high you are off the ground. In the susceptible individual, the height, a UFS, produces an innate fear response. In addition, you are unable to escape because you are riding in a car on the bridge. However, since you are consciously aware you are crossing a bridge, the bridge then becomes a.s.sociated with the fear response generated by the UFS. In a bridge phobia, the rational prefrontal cortex is unable to shut off the fear because it is not the bridge (the conditioned stimulus) that is activating the fear response; it is the fear of heights (the UFS).

When crossing another bridge, because of a similarity of overlap of the surroundings, your fear of bridges generalizes.

Pattern Recognition and Generalizability.

Why does a traumatized fear generalize? Why does someone who is afraid of crossing a bridge become afraid of all bridges? Then become afraid of tunnels, crowds, flying, and eventually develop agoraphobia, the fear of being outside? There are two reasons. The first is that traumatization begets traumatization. A traumatized landscape is primed for further traumatization, but not all go on to this end. The other reason, which is the topic of this essay, is that by nature's design, the mind seeks similarities in situations. This allows for rapid a.s.sessment of a potentially threatening situation. While our mind searches a novel situation for similarities, our vigilance system is activated and prepares us. If there are similarities, previously encoded responses are activated. A phobia of bridges activates the fear system for any bridge. This widening of the traumatization occurs by pattern recognition processing. Even a small piece of this novel situation overlapping with the original encoding event may be enough to activate the amygdala.

A plant is perceived because it has a stem, a flower, leaves, color, smell, and comes up from the ground. The perception is the sum of these various component parts, sent via the thalamus to the various brain areas dealing with specific sensory information, and then, somehow, binds to become a plant in our consciousness. Seeing only pieces of a flower, a petal, a leaf, a stem, can produce in the mind the entire flower. This can be conceptualized as the brain performing a rapid matching function, looking for similar pieces already stored in the brain. We often say that this looks or smells or tastes like something familiar. (Lots of stuff tastes like chicken!) Indeed, we ill.u.s.trate much of life with simile. Our brain seeks these congruent patterns in unfamiliar circ.u.mstances. Part of why we experience deja vu is because of pattern overlap that provides a sense of familiarity.

Pattern recognition is the way in which the brain matches sensory input to create a perception. A percept is a high-level representation of part of the world as imaged by the brain based on a set of rules. This percept is then amplified or diminished by our current state of attention and previous experience. Pattern recognition processing, from sensory input to perception to response, occurs for both conscious and subconscious patterns. If the pattern has enough overlap with an encoded event, it may elicit a fear response from the amygdala. This const.i.tutes a potential mechanism for the generalization of a fear response.

Paul had a phobia of statues. This bizarre phobia arose when, as a child, he saw a bust of the head of the crucified Christ, complete with a crown of thorns and showing His immense suffering. This traumatized him. This is an example of vicarious traumatization. He then generalized this fear to all statues.

Panic Attacks.

A panic attack is characterized by sudden attacks of terror, usually accompanied by a pounding heart, weakness, faintness, or dizziness. During these attacks, people may feel flushed or chilled; their hands may tingle or they may feel numb. They may become short of breath, experience chest pain, and feel they are going to die. They often experience a sense of unreality, a fear of impending doom and imminent death, or a fear of losing control of their mind. Individuals who experience panic attacks can't predict where or when an attack will occur and will always avoid a situation where an attack has happened. Many worry intensely about the next attack. Panic attacks can occur at any time, even during sleep. They are a frequent cause for emergency room visits.

Panic attacks most often begin in late adolescence and are more common in women than men. Not everyone who has a panic attack goes on to have multiple attacks that lead to a diagnosis of panic disorder. A strong tendency to inherit this disorder is known. Some people with panic disorder become so restricted by their fears that they avoid normal activities, such as grocery shopping or driving. About one-third become housebound or are able to confront a feared situation only when accompanied by a spouse or other trusted person. Both phobias and panic disorder produce irrational fears.

The remarkable aspect of panic disorder is the lack of any warning and the absence of any cognitive cue. This is unusual because a fear response is usually generated in preparation for escape from something we are aware of. This does not happen here. Thus, the stimulus that initiates the panic attack is subconscious. It is likely that fear of an unantic.i.p.ated attack plays a major role in sensitizing the individual and making the situation worse. In this disorder, there truly is no haven.

What role does the amygdala play in panic disorder?3 Research shows that most of the neurons in to the basolateral complex (BLC) of the amygdala inhibits the flow toward the central nucleus (Ce). It is speculated that in panic disorder, this inhibition is somehow diminished and activation of Ce occurs at a much lower threshold. Thus, mild, anxiety-provoking internal stimuli, such as a rapid heartbeat, chest pain, or lightheadedness, which would not normally engage the amygdala, do so, causing the Ce to activate other areas of the brain, producing a fear response. Since no "predator" is seen, the situation is inescapable. People experience great dread because they cannot locate the source of fear. This repeating cycle of subconscious stimuli and severe fear landscapes the amygdala and produces a more generalized fear of the outside world. It is notable that being at home seems to prevent these attacks, except perhaps when sleeping, during which the mind can experience anything.

Posttraumatic Stress Disorder (PTSD).

PTSD is considered to be the prototype of traumatization. Individuals with PTSD present with a complex array of symptoms that include: Reexperiencing the trauma.

Emotional numbing.

Avoidance.

Increased arousal (hypervigilance).

Diminished capacity for problem solving.

Nightmares, flashbacks, and intrusive thoughts.

Repet.i.tion compulsion.

Since some of these symptoms seem opposite from the others, this disorder seems puzzling. How can one be emotionally numb at one moment, then experience increased arousal at the next? PTSD may be diagnosed months after an event has been traumatized, as the internal response to subconscious and conscious cues or other events causing chronic stress altering the landscape of the brain allows for the production of symptoms. According to our model, for a traumatization to occur, only the conditions outlined earlier need to be met; however, some researchers feel that PTSD has a unique aspect: The individual often is unable to give a complete narrative of the event causing the disorder. PTSD contains a cognitively mental imprint of sensory and affective elements of the traumatic experience.

Most researchers believe the components of the traumatic memory are stored in different memory systems. That is, the cognitive, emotional, and somatosensory components are not anatomically located together. The complete picture must be a.s.sembled from different parts of the brain. It is felt the amygdala is the structure that establishes a.s.sociations between these components. In fact, traumatization can be looked upon as a disorder of permanent a.s.sociation and, in extreme cases like PTSD, a disorder of partial a.s.sociation or, in other words, dissociation. It is by disrupting the normal amygdala/hippocampal function to protect us from encoding consciously available memories that are too horrible that we develop PTSD. It has been suggested earlier that very high levels of cortisol at the time of the event are the cause of a disrupted narrative, making some memories unavailable to conscious recall. It may be that disordered retrieval is at the heart of PTSD. PTSD is often progressive, as more of the narrative is revealed from the subconscious in flashbacks, intrusive thoughts, and dreams. Unless this process can be disrupted, the extreme fear arising from this activation of the amygdala often makes things worse. One important and interesting consequence of PTSD is a disorder called repet.i.tion compulsion.

Repet.i.tion Compulsion.

The range of problems traumatization can produce is remarkable. One of the most extraordinary is the compulsive self-exposure of the traumatized individual to the experience of trauma again. Research shows that physically abused children are more likely to reexperience a similar trauma later in life. Some become abusers themselves. Many prost.i.tutes have been s.e.xually molested as children. Repet.i.tion compulsion4 is about the individual subconsciously reenacting the trauma. This underscores the power of the homeostatically driven need to heal. Sadly, because the person is unsure why he or she is being driven to exhibit this behavior, a safe haven can never be found. This repet.i.tion does not help a person gain mastery of the situation; rather, it often reinforces the insolvability of the problem, making the need to reenact even more powerful.

PTSD, as well as the other amygdala-based disorders, appears to require a certain landscape for symptoms to occur. Thus, symptoms may be delayed by days, months, or even years after a traumatizing event. This landscape can be created by the addition of chronic stress.

In the case of PTSD, this landscape can be the result of the event itself or other unrelated life stressors.

Chronic Pain.

Most Western medicine is end-organ driven. That is, if you have a back problem, the problem is considered to be in the back; a pelvic problem must originate in the pelvis. Indeed, Western medicine names these problems by the end organ; thus, we have "lower back pain" and " pelvic floor dysfunction." This approach is called physicalism. Therefore, if a patient experiences a physical problem, the problem must have a physical origin. Of course, surgery and other traditional Western approaches can definitely treat many physical problems, but pract.i.tioners also find problems for which no, or only partial, solutions are available from a physical standpoint.

That chronic pain can be psychological in origin is hard for most people to comprehend. It makes sense that when we touch a spot that feels tender, the cause of the pain must arise somewhere near that spot. This is not always true. The somatic parts (pain, burning, temperature alterations, and tenderness) of a trauma can be stored in the brain to be retrieved by exposure to subconscious stimuli, processed through the BLC, and reperceived.

Subconscious stimuli BLC Ce Pain.

The Ce of the amygdala has a pain center called the nociceptive amygdala. It is here that pain signals arriving from other parts of the brain are modulated. During flight, fight, or rage, inhibition by norepinephrine of the nociceptive (pain-perceiving) portion of the Ce prevents the pain from being experienced.

If one consciously evokes a painful traumatic event and generates the emotional component, the somatic pain experience is not elicited due to the release of norepinephrine (NE) and its effect on the Ce. Thus, thinking about the event does not cause pain. This is what makes this pain syndrome so confusing.

Consciously evoked emotional event-related stimuli BLC Ce NE No pain Regardless of the exact network of neurons involved, the pain occurring during the traumatizing event is stored as a memory in the brain. This was first described in the late 1800s by Charcot, Janet, Freud, and Breuer who believed subconscious stimuli could cause pain and other somatic symptoms. They believed the pain was coencoded with a psychological trauma but cognitively dissociated from conscious awareness. Accordingly, pain relief would occur only when the trauma was brought to conscious awareness and treated.

In addition to traumatically encoded fearful events as a cause of pain and other somatic sensations, John Sarno5 suggests that symptoms arise to prevent traumatically encoded subconscious rage and other negative emotions from reaching consciousness. The inability to express strong negative emotions can come from fear of punishment, helplessness, the need to be in control, and the need to be seen as the 'good one.' It is interesting to note that the areas where pain is most commonly described are the back, neck, head, and upper limbs. Many of these individuals also grind their teeth and clench their jaws. Remarkably, these are also the locations of the muscles described for use during defensive rage. This triad of neck pain, back pain, and temporomandibular joint syndrome is very common in clinical practice.

On the Origin of Chronic Psychogenic Pain.

This essay attempts to produce a model for understanding chronic pain as it occurs in traumatization. Quite often, during a traumatizing event where bodily injury occurs, we do not experience pain. The question then arises: If pain was not experienced at the time of the event, how does chronic pain based on the event develop later? The case in which a woman's hand was hurting for three months is ill.u.s.trative. The patient was injured in a taxi accident in London, where the vehicle overturned. As the car tumbled, her hand swung wildly in the car. The back of her hand was badly bruised, but she did not experience the pain at the time of the accident. The pain and tenderness returned 15 years later, when she had decided to return to London to live.

The physiology at work here can be explained as follows. During the event, norepinephrine was secreted into the amygdala from the locus coeruleus. Flight was not possible during the event, and the four criteria, including inescapability, were present, which led to a traumatization. Norepinephrine (NE) release at the time of the event inhibited the nociceptive Ce from signaling pain to consciousness (Pain from hand goes to brain NE Ce // Consciousness). From a survival point of view this makes sense, as her first priority was to escape from the overturned vehicle. Each and every time she would consciously recall the event, norepinephrine would be released, inhibiting the conscious awareness of pain.

Her desire to return to London had enough overlap with the context of the event to stimulate the BLC regarding the event. Norepinephrine was not generated because the thought of retuning to London was not in and of itself threatening. Not only did she experience pain, but she also felt tenderness of the area, suggesting that local effects were being produced. Since she was not consciously thinking of the event, her clues that would a.s.sociate the event with the pain were absent.

It appears that coencoded subconscious contextual stimuli can selectively activate the pain pathway without activating either the emotional or cognitive components of the traumatizing event. Havening the emotional component of distress on recall of the taxi accident broke the linkages that BLC Event and BLC Pain had in common. As the coencoded subconscious stimulus used this pathway to produce pain, her pain disappeared after havening.

If one consciously thinks about the pain and applies havening, it may be possible to inhibit the BLC pathway responsible for that specific pain. If, however, the cognitive-emotional linkage is not broken, the potential exists to reexperience pain encoded, often elsewhere in the body. This model is also true for chronic pain involving rage. Unrelated events that produce anger or stress may overlap with the encoded rage and reproduce the neck, jaw, and lower back muscle tension.

Somatosensory conditions that can be coencoded with trauma include: Low back pain.

Neck and upper back pain.

Sciatica.

Somatization disorders.

Radiculopathies.

Phantom limb pain.

Temporomandibular joint syndrome.

Chest pain.

Nonetheless, for both patients and health care professionals, this chronic pain is perceived as arising from peripheral sites. Thus, much therapeutic effort is directed to these areas, including treatments with opioid a.n.a.lgesia, surgery, and physical therapy. Unfortunately, these meet with little success.

Pathological Emotions.

The pathological emotions, including guilt, shame, jealousy, grief, and so on, are reflective emotional states. They require a strong degree of attachment. Guilt, as in Lady Macbeth's cry to remove the blood from her hands, can be experienced in dreams or in the awake state.

At first Sandra did not understand their young daughter's diagnosis of autism, given to her by her pediatrician. When she heard it the second time from an expert, she was landscaped for traumatization. She felt guilty she may have done something wrong during pregnancy (she did not), she experienced anger about this happening to her child, and she experienced fear that her child would need lifelong care. She experienced grief over the loss of the expectations of this new relationship. These emotions were her daily fare. She used food as a way to treat her emotions. She gained over 100 pounds during the next several years. Nonetheless, she functioned as a loving, caring mother, but with a heavy heart (and body).

The traumatization of pathological emotions may seem like a normal response to a tragedy, but these emotions produce chronic stress and alter the nature of all relationships. They may prevent the mourning process from occurring. This maladaptive behavior continues as long as the cue and content, in this case her guilt, fear, and subconscious anger, stimulate the amygdala and release stress hormones. These pathological emotions produce a landscape of the brain that sets the stage for further traumatization.

Somatization.

There is another form of an amygdala-based disorder described in the psychiatric literature. It produces an astonishing array of symptoms. These symptoms are called somatization responses and represent a somatosensory/autonomic response to the event. For example, survivors who witnessed the killings by the Khmer Rouge lost their ability to see.6 All were women who witnessed violent acts, such as seeing their daughters being raped and beaten to death by soldiers, or their husbands or sons being executed in front of them.

Some somatic symptoms can be very puzzling, such as stigmata. Here, the markings of Christ on the cross appear on the body of the individual. It is not a leap of faith to see how someone can be traumatized by seeing an image of the Crucifixion. Clearly, these individuals are highly susceptible. Stigmata may appear on the body as the somatic response to subconscious retrieval of a traumatizing memory (imagine the fear that must be generated in children when seeing a crucified man on a cross and who are too young to understand it) and be expressed via the autonomic nervous system as vasomotor dysregulation in the areas of Christ's injuries.

Somatization of a traumatic event can produce blindness, paralysis, stuttering, copious v.a.g.i.n.al secretions, pelvic floor dysfunction, vomiting, stuffy nose, and literally an almost endless array of distressing problems. These symptoms should always initiate a search for a traumatic event. It is here that a cure may be found.

After being s.e.xually a.s.saulted, Stephanie developed copious v.a.g.i.n.al secretions, up to 50 cc/day, that prevented her from leaving the house. She ultimately required surgery to remove the v.a.g.i.n.al wall.