Healing Trauma, page 30
The Hormonal Response in Post Traumatic Stress Disorder
In well-functioning people, stress produces rapid and pronounced hormonal responses. However, chronic and persistent stress inhibits the effectiveness of the stress response and induces desensitization (Axelrod, 1984). PTSD develops following exposure to events that overwhelm the individual’s capacity to re-establish homeostasis. Instead of returning to baseline, there is a progressive kindling of the individual’s stress response. Initially, only intense stress is accompanied by the release of endogenous, stress-responsive neurohormones such as Cortisol, epinephrine, and norepinephrine (NE), vasopressin, oxytocin and endogenous opioids. In PTSD, even minor reminders of the trauma may precipitate a full-blown neuroendocrine stress reaction: It permanently alters how an organism deals with its environment on a day-to-day basis, and it interferes with how it copes with subsequent acute stress.
While acute stress activates the HPA axis and increases glucocorticoid levels, organisms adapt to chronic stress by activating a negative feedback loop. Counterintuitively, people with PTSD have low levels of serum Cortisol. In a study by Resnick and colleagues (1998), the investigators collected blood samples from 20 acute rape victims and measured their cortisol response in the emergency room. Three months later, a prior trauma history was taken, and the subjects were evaluated for the presence of PTSD. Victims with a prior history of sexual abuse were significantly more likely to have developed PTSD three months following the rape than rape victims who did not develop PTSD. Cortisol levels shortly after the rape were correlated with histories of prior assaults: the mean initial cortisol level of individuals with a prior assault history was 15 μg/dl, compared to 30 μg/dl in individuals without such a history. These findings can be interpreted to mean either that prior exposure to traumatic events results in a blunted cortisol response to subsequent trauma, or in a quicker return of cortisol to baseline following stress.
These results show that cortisol basically functions as an “anti-stress” hormone: It shuts off the other biological reactions that were initiated by the stress response. Simultaneous activation of catecholamines and glucocorticoids stimulates active coping behaviors, while increased arousal in the presence of low glucocorticoid levels would provoke undifferentiated fight or flight reactions.
Trauma and the Central Nervous System
The Disintegration of Experience
In a series of studies we have demonstrated that traumatic memories initially have few narrative elements: When PTSD patients have their flashbacks, the trauma is relived as isolated sensory, emotional and motoric imprints of the trauma, without a storyline. We have shown this in victims of childhood abuse (van der Kolk & Fisler, 1995), assaults and accidents in adulthood (van der Kolk, Burbridge, & Suzuki, 1997), and in patients who gained awareness during surgical procedures (van der Kolk, Hopper, & Osterman, 2001). These studies support Janet’s 1889 observations and confirm the notion that what makes memories traumatic is a failure of the CNS to synthesize the sensations related to the traumatic memory into an integrated semantic memory. Sensory elements of the experience are registered separately and are often retrieved without the patient appreciating the context to which this sensation or emotion refers.
These observations lead to the notion that in PTSD, the brain’s natural ability to integrate experience breaks down. A variety of CNS structures have been implicated in these integrative processes:
(1) the parietal lobes are thought to integrate information between different cortical association areas (Damasio, 1989),
(2) the hippocampus is thought to create a cognitive map that allows for the categorization of experience, and its connection with other autobiographical information (O’Keefe & Nadel, 1978),
(3) the corpus callosum allows for the transfer of information from both hemispheres (Joseph, 1988), integrating emotional and cognitive aspects of the experience,
(4) the cingulate gyrus is thought to play a role of both amplifier and filter that help to integrate the emotional and cognitive components of the mind (Devinsky et al., 1995), and
(5) the dorsolateral frontal cortex, which is where sensations and impulses are “held in mind” and compared with previous information to plan appropriate actions.
The frontal lobes, in general, are thought to function as a “supervisory system” for the integration of experience (Shallice, 1988). Recent neuroimaging studies of patients with PTSD have suggested a role for most of these structures in the neurobiology of PTSD.
Neuroimaging Studies in PTSD
As of 1999, there have been seven published studies utilizing neuroimaging of patients with PTSD (Rauch et al., 1996; Gurvits et al., 1998; Bremner et al., 1995, 1999; Stein et al., 1996; Liberson, 1999; Shin et al., 1999). Four studies have used MRI to measure hippocampal volume in individuals with PTSD and three studies have used positron emission tomography (PET) (Rauch et al., 1996; Shin et al., 1999; Bremner, 1999) to measure differential activation of the CNS in response to traumatic and nontraumatic scripts in patients with PTSD.
Hippocampal Volume
Three different studies have shown that people with chronic PTSD have decreased hippocampal volumes, ranging from 8% (Bremner et al., 1995, Stein, 1997) to 26% (Gurvits et al., 1998). The fact that the only prospective study of acutely traumatized individuals, (Shalev, personal communication, 1999) failed to identify correlation between hippocampal volume and PTSD severity, suggesting that this hippocampal shrinkage is a function of chronicity. Recent research suggests that the hippocampal changes may not be irreversible. (McEwen, 1999, Starkman & Cushing, 1999). In animals, decreased hippocampal functioning has been shown to cause behavioral disinhibition (Gray, 1982) and makes animals more likely to define incoming stimuli as emergencies and react with fight or flight responses. If the same is true for humans, this might contribute to the problems of PTSD patients with “taking in” and processing arousing information, and to learn from such experiences. The decreased size of the hippocampus might play a role in the ongoing dissociation and misinterpretation of information in the direction of threat. Their altered biology would make them vulnerable to react to newly arousing stimuli as a threat, and to react with aggression, or withdrawal, depending on their premorbid personality (Ademac et al., 1991).
Symptom Provocation Studies
Rauch, van der Kolk and colleagues conducted a PET scan study in which patients with PTSD were exposed to vivid, detailed narratives of their own traumatic experiences (Rauch et al., 1996). During exposure to the script of their traumatic experiences, these subjects demonstrated heightened activity only in the right hemisphere—specifically, in the areas that are most involved in emotional arousal: the amygdala, the insula, and the medial temporal lobe. During exposure to their traumatic scripts there was a significant decrease in activation of the left inferior frontal lobe: Broca’s area, which is thought to be responsible for translating personal experiences into communicable language. A study by Shin and colleagues (1999), utilizing a slightly different paradigm, essentially confirmed these findings in a different trauma population. In another study, Lanius and colleagues (submitted) exposed six subjects with PTSD and six controls to a traumatic script, measuring their responses with MRI scans. This investigator consistently found decreased activation of the thalamus and the dorsolateral prefrontal cortex in PTSD patients during exposure to their trauma scripts.
These early neuroimaging studies of patients with PTSD present us with a range of surprising findings which force us to re-evaluate our previous concepts of the pathophysiology of PTSD. Of the various findings, increased activation of the amygdala in response to traumatic scripts is the least surprising. After all, it has been well established that the amygdala is centrally involved in the interpretation of the emotional valence of incoming information, and that confrontation with feared stimuli activates the amygdala and related structures (LeDoux, 1992). Exposure to traumatic scripts frequently provokes autonomic activation of patients with PTSD (e.g., Pitman et al., 1987; Keane, 1998), and this is likely mediated by activation of the amygdala and related structures. It is well-understood that the information evaluated by the amygdala is passed on to areas in the brain stem that control autonomic and neurohormonal response systems. By way of these connections, the amygdala transforms sensory stimuli into emotional and hormonal signals, thereby initiating and controlling emotional responses.
High level stimulation of the amygdala can also interfere with hippocampal functioning (Ademac, 1991; Squire & Zola-Morgan, 1991). Thus, extreme emotional arousal may prevent the proper evaluation and categorization of experience by interfering with hippocampal functions. It is possible that, when this occurs, sensory imprints of experience are stored in memory,-however, because the hippocampus is prevented from fulfilling its integrative function, these various imprints are not combined into a unified whole (van der Kolk, 1994). The experience is laid down, and later retrieved as isolated images, bodily sensations, and smells, and sounds that feel alien and separate from other life experiences. Decreased hippocampal functioning is likely to interfere with the localization of incoming information in time and space, and to cause continued fragmentation of experience. The recent findings of decreased dorsolateral frontal cortex activation would further provide a neurobiological explanation of why people with PTSD plunge into re-experiencing their trauma with limited consciousness; they are simply remembering elements of experiences belonging to the past. In our pilot study, using single-photon emission tomographty (SPECT) as an outcome measure of eye movement desensitization and reprocessing (EMDR) treatment subjects had increased activation of the dorsolateral prefrontal cortex following effective treatment.
Hemispheric Lateralization
The finding of hemispheric lateralization in subjects exposed to their personalized trauma scripts indicates that there is differential hemispheric involvement in the processing of traumatic memories. This may have important implications for understanding the nature of PTSD. The right hemisphere, which developmentally comes “on-line” earlier than the left hemisphere, is involved in the expression and comprehension of global non-verbal emotional communication (i.e., tone of voice, facial expression, visual/spatial communication), and allows for a dynamic and holistic integration across sensory modalities (Davidson, 1989). This hemisphere is particularly integrated with the amygdala, which assigns emotional significance to incoming stimuli and helps to regulate the autonomic and hormonal responses to that information. While it is exquisitely sensitive to emotional nuances, it has, at best, a rudimentary capacity to think or communicate analytically, to employ syntax, or to reason (Henninger, 1992; Davidson, 1989).
In contrast, the left hemisphere, which mediates verbal communication and organizes problem-solving tasks into a well-ordered set of operations and processes information in a sequential fashion (Davidson, 1989), seems to be less active in PTSD. It is in the area of categorization and labeling of internal states that people with PTSD seem to have particular problems (Krystal, 1978; van der Kolk, McFarlane, & Weisaeth, 1996). It is conceivable that failure of left hemisphere function during states of extreme arousal is responsible for the derealization and depersonalization reported in acute PTSD (Marmar et al., 1995; Shalev et al., 1996).
New Directions for Treatment
For over a century it has been understood that traumatic experiences can leave indelible emotional memories. Contemporary studies of how the amygdala is activated by extreme experiences dovetail with the laboratory observation that “emotional memory may be forever” (LeDoux et al., 1991). The accumulated body of research suggests that patients with PTSD suffer from impaired cortical control over subcortical areas responsible for learning, habituation, and stimulus discrimination. The concept of indelible subcortical emotional responses, held in check to varying degrees by cortical and hippocampal activity, has led to the speculation that delayed onset PTSD may be the expression of subcortically mediated emotional responses that escape cortical, and possibly hippocampal, inhibitory control (van der Kolk & van der Hart, 1991; Pitman et al., 1993; Shalev et al., 1992).
The early neuroimaging studies of PTSD showed that, during exposure to a traumatic script, there was decreased Broca’s area functioning and increased activation of the right hemisphere. This would imply that it is difficult for traumatized individuals to verbalize precisely what they are experiencing, particularly when they become emotionally aroused. They may experience physiological arousal, and fragments of memories may be activated, but they often seem to be too hyper- or hypo-aroused to be able to “process” and communicate what they are experiencing. A relative decrease in left hemispheric representation provides an explanation of why traumatic memories are experienced as timeless and ego-alien: The part of the brain necessary for generating sequences and for the cognitive analysis of experience is not functioning properly. Our research (Rauch et al., 1996) can be interpreted as showing that during activation of a traumatic memory, the brain is “having” its experience. The person may feel, see, or hear the sensory elements of the traumatic experience, but he or she may be physiologically prevented from being able to translate this experience into communicable language. When they are having their traumatic recall, victims may suffer from speechless terror in which they may be literally “out of touch with their feelings.” Physiologically, they may respond as if they are being traumatized again. Particularly when a victims experience depersonalization and derealization they cannot “own” what is happening, and thus cannot take steps to do anything about it.
To help traumatized individuals process their traumatic memories, it is critical that they gain enough distance from their sensory imprints and trauma-related emotions so that they can observe and analyze these sensations and emotions without becoming hyperaroused or engaging in avoidance maneuvers. The selective serotonin reuptake inhibitors (SSRIs) seem to be able to accomplish exactly that. Studies in our laboratory have shown that SSRIs can help PTSD patients gain emotional distance from traumatic stimuli and make sense of their traumatic intrusions (van der Kolk et al., 1995). The apparently relative decrease in left hemisphere activation while re-experiencing the trauma suggests that it is important to help people with PTSD find a language in which they can come to understand and communicate their experiences. It is possible that some of the newer body-oriented therapies, dialectical behavior therapy, or EMDR may yield benefits that traditional insight-oriented therapies may lack.
To make meaning of the traumatic experience usually is not enough. Traumatized individuals need to have experiences that directly contradict the emotional helplessness and physical paralysis that accompany traumatic experiences. In many people with PTSD, such helplessness and paralysis becomes a habitual way of responding to stressful stimuli, further weakening their feelings of control over their destiny. The critical steps in treating PTSD can be summarized as follows (for more details see: van der Kolk, McFarlane, & van der Hart, 1996):
1. Safety. When people’s own resources are inadequate to deal with threat, they need to rely on others to provide them with safety and care. After having been traumatized, is critical that the victim re-establish contact with his or her natural social support system. If this system is inadequate to ensure the safety of the patient, institutional resources need to be mobilized to help the patient find a place to recover.
2. Anxiety management. After the patient’s safety has been assured, there may be a need for a variety of psychological interventions. They need to learn to name the problems they face, and learn to formulate appropriate solutions. Assault victims must learn to distinguish between the real life threats and the haunting, irrational fears which are part of PTSD. If anxiety dominates, victims need to be helped to strengthen their coping skills. Practical anxiety management skills training may include deep muscle relaxation, breathing control, role-playing, covert modeling, thought stopping, and guided self-dialogue.
3. Emotional processing. To put the event(s) in perspective, the victim needs to re-experience the event without feeling helpless. Traditionally, following Freud’s notion (Breuer & Freud, 1893–1895/1955) that words can substitute for action to resolve a trauma, this has been done by helping people to talk about the entire experience. They are asked to articulate what they think happened, and what led up to it; their own contributions to what happened; their thoughts and fantasies during the event; what was the worst part of it; and their reactions to the event in detail, including how it has affected their perceptions of themselves and others. Such exposure therapy is thought to promote symptom reduction by allowing patients to realize that: (a) remembering the trauma is not equivalent to experiencing it again; (b) that the experience had a beginning, a middle, and an end, and that the event now belongs to one’s personal history.
In recent years, a variety of new techniques has been developed that have the potential of desensitizing patients with PTSD without fully engaging them in a verbal reliving of the traumatic experience. Of these treatments, EMDR has been best studied (Chemtob et al., 2000). Although traditional exposure therapy can be very helpful in overcoming traumatic intrusions, it needs to be applied with care. Some patients, on recalling their trauma, may become flooded with both the traumatic memories and memories of previously forgotten traumas. Increased activation of traumatic memories may be associated with increased shame, guilt, aggression, and increase in alcohol and drug use.
