A Summary of Amy Banks, M.D.’s
October 2, 2004 Presentation
Relational Approach to the Neurobiology
of PTSD and Dissociation:
By Patricia Papernow
Amy Banks is a psychiatrist in private practice and Director of Advanced Training at the Jean Baker Miller Institute of Wellesley College. Beginning with a quick summary of the Relational/Cultural theory of Jean Baker Miller, Judith Jordan et al, Amy treated us to a fascinating tour of the brain chemistry of trauma and its effects on relationships. I liked being reminded of Jean Baker Miller’s “Five Good Things” in a growth fostering relationship and its opposite, “Five Bad Things” in an abusive relationship (see boxes). Two other nuggets from her opening summary: Parents provide relational resilience by helping a child to stay within “optimal” levels of arousal; and, when acknowledging limits with our borderline patients, we are most helpful when we communicate our own boundaries to them, rather than by telling them what their limits should be.
Turning to neurobiology, Amy described several lines of research, which help us to more deeply understand the highly triggered responses of our traumatized patients to relational events. She concluded with a thorough overview of medications that help treat the symptoms of PTSD and DID.
She began with studies of “inescapable shock” in rats, which help illuminate the physiological nature of the “triggered” responses we see in our PTSD patients. Traumatic experience results in the release of the neurotransmitter, norepinephrine, creating the familiar fight/flight/freeze trauma response. These responses travel between cells by a process in which neurotransmitters connect with receptor cells. As the amount of neurotransmitters increases, the number of receptor cells decreases. Conversely, when the amount of neurotransmitters decreases, the number of receptor cells increases. In healthy organisms, the number of receptor cells remains elastic, enabling the system to control the flow of alarm messages. However, when rats are exposed to repetitive shock, we see an over production of receptor cells, and these receptors lose their plasticity, remaining stuck in the “up-regulated” pattern. Thus, when an apparently “small” trigger, dumps neurotransmitters into the system, it is all received by “up-regulated” receptor cells, the overwhelming physiological experience we call “triggering.”
In a fascinating twist on this literature, Shelley Taylor’s “Tend and Befriend” studies at UCLA found that women under stress release the hormone oxytocin, creating an increased urge for connection with other people. It is unclear how this chemical response changes in women who have been abused. Men under stress release the hormone, testosterone, leading to the fight/flight response.
Neuro-imaging studies of brain structure provide another source of information about the brain’s response to trauma. The hippocampus, a part of the brain that plays a central role in learning and memory, filters signals from the amygdala, helping us to assess: “Does this cue signal danger? Or not?” Brain scan studies show decreased hippocampal volume in combat veterans and in survivors of childhood sexual abuse. It remains unclear whether those who develop PTSD began with lower hippocampal volume. However, it is believed that neurotransmitters released in traumatized individuals, may decrease hippocampal volume. A small study has also found that hippocampal volume is higher in DID patients, post-integration. These findings, of course, raise fascinating questions about the interplay of biological vulnerability and environmental challenge.
Next, Amy turned to the medial pre-frontal cortex, another area of the brain that exercises regulatory control over the amygdala. This area includes the orbitofrontal cortex and the anterior cingulate. When it is damaged, we see a decrease in self -reflection and self-awareness. Alan Schore’s groundbreaking work with infants has shown that the orbitofrontal cortex remains immature at birth and develops in children as the result of healthy relationships! Research has shown that lesions in the anterior cingulate result in emotional instability and apathy. Conversely, increased activity in the anterior cingulate correlates with higher emotional awareness. When an apparently triggering event is not indeed dangerous, a properly functioning anterior cingulate sends messages to the amygdala saying, “Cool down. We don’t need you.” It provides an aid in the extinction of fear conditioning, and allows us to engage the cognition: “We’re OK here in the present.” In PTSD, we see a decrease or failure of the anterior cingulate’s ability to send messages to the amygdala. In addition, PTSD patients show a more irritable and exaggerated response of the amygdala at baseline, before any triggering material even appears.
Another fascinating piece of information illuminates the truth of the experience of being “scared speechless.” In fact, Broca’s area, the motor area of the brain responsible for speech, shuts down in the face of trauma. Amy noted that it is precisely at these moments of intense triggering when anxious therapists are mostly likely to flood their patients with intrusive questions. Clearly this is a moment when pressure for a verbal response becomes useless and even destructive and reminds of the need for nonverbal approaches to trauma.
Dissociative Identity Disorder (DID) remains, biochemically, less well understood than PTSD. Amy quoted a DID patient saying, “The worst thing was not that my father hit us, but that he denied that he did it,” breaking not only bones but the connection between memory and reality. Research on various pathways of the neurotransmitter, glutamate, sheds some light on the neurobiology of these processes of disconnection. It appears that trauma creates high levels of glutamate, the main excitatory neurotransmitter in the brain. (Dopamine, serotonin, norepinephrine and GABA are inhibitory neurotransmitters). Organized perception requires a balance of both excitatory and inhibitory neurotransmitters. High levels of glutamate result in impaired perception at the time of trauma, as well as altered coding of memory. Over time, high glutamate levels may also be toxic to hippocampal cells, decreasing the functioning of that critical area. All of these processes may contribute to the disrupted perception of self we see in DID patients.
Given these powerful neuro-biological
responses, how can medication help our patients get their chemistry back in line
enough to be more available to the healing possibilities of relationship?
Unfortunately no drugs exist yet to specifically treat the dysregulation that
occurs in the Hypothalmic Pituitary Adrenal (HPA) Axis as a result of PTSD.
In addition, most patients with PTSD carry up to an 80% rate of co-morbid diagnoses. Furthermore, it is entirely possible, Amy feels, that effective treatment will require longer trials at higher doses. We may need 12 weeks to determine whether a medication is effective in trauma
The SSRIs remain the “treatment of choice” for PTSD, as they have the most global impact. Nonetheless we are looking at response rates of 30 to 50 % reduction in symptoms! (The “best” drugs for the “easiest” drug target, depression, are only 70% effective). Amy generally starts with an SSRI first, then after 4 to 12 weeks, thinks about what needs to be added. She notes that drug preferences are specific to the psychiatrist: “Everyone has their favorite.” Prozac, Zoloft, and Lexapro are somewhat more stimulating, which can be helpful to some, but create too much agitation at start-up for others. Paxil and Zoloft are FDA approved for PTSD, but Amy notes, that does not mean that they are actually any better. Celexa and Paxil are more sedating, and so are more useful for patients who suffer from insomnia and agitation. She has had more mixed results with Lexapro. Amy does not usually start with Effexor, despite its double action on both norepinephrine and serotonin, as she finds more people get agitated on this drug. Effexor also adds blood pressure risk. Luvox has been marketed as an OCD drug, however, it is quite sedating and interacts with too many other drugs. Any drugs that increase serotonin will help with OCD. A reminder: It is critical, with SSRI’s, to monitor closely for agitated depression.
Unfortunately 50 to 90% of patients on SSRIs experience sexual dysfunction. This is especially problematic at later stages in recovery when patients are healthy enough to re-enter relationship. Furthermore, many experience weight gain, at the level of 5-10 lbs over all. Sometimes Amy likes to add a little Wellbutrin to an SSRI. Wellbutrin, which works through the dopamine system, has no sexual side effects but is not good for treating generalized anxiety disorder. Remeron is another dual action drug with lower sexual side effects. However, because many patients experience a significant weight gain (20 pounds in a month!) it is not a good place to start .
MAO Inhibitors (Nardil, Parnate) remain “really good treatment,” worth thinking about for patients who have had no luck with SSRIs. They require the discipline to avoid certain foods or face a stroke risk, though the list is far less restrictive than had been thought.
TheTricyclics are trickier ( Norpramine (desipramine), Elavil (amitriptyline), Sinequan (doxepine) and Pamelor.) They do treat some of the symptoms, but are so potentially lethal “it is like handing a patient a loaded gun.”
Mood stabilizers form another class of drugs that can be useful when PTSD is co-morbid with depression or bi-polar disorder. Depakote is a long-standing choice that requires close monitoring of blood levels as it can suppress bone cell production. Lithium, which remains “a good antidepressant and mood stabilizer,” requires extensive fluid intake and monitoring for a toxic level. Lamictal increases GABA (an inhibitory neurotransmitter) which blocks glutamate. It has few side effects and often has a global effect that relieves symptoms missed by SSRIs. Although it can create a fatal rash, which begins with mouth sores, Amy uses it a lot including with her DID patients, and finds that her patients really like it and can stay on it a long time. Neurontin works on the GABA system—it has “saved the lives” of some patients and works not at all for others. It also has some use for anxiety. Topimax decreases production of glutamate, but even a 100mg can result in cognitive impairment. Because some people lose weight on them, Amy sometimes combines these drugs with others that create weight gain.
Note: Using Benzodiazepines (Klonopin, Ativan, Xanax, Valium) in the immediate aftermath of a trauma may increase the chances of developing PTSD.
Atypical antipsychotics include Seroquel, Risperidal , Zyprexa, Geodon and Abilify. Some work through serotonin and some through blocking glutamate, damping the “scared to death” experience. “Better to be knocked out than to relive over and over again.” Weight gain with Zyprexa is unfortunately extreme. Geodon and Abilify are atypical antipsychotics without the weight gain and do not have sedating qualities.
Finally, in the “Other” category, we have: Clonidine can be very helpful in relieving nightmares and flashbacks and other intrusive recollections. Although it may lower blood pressure, it is not extremely dangerous at this dosage range--just “don’t bolt out of bed.” Trazodone (Desyrel) is a somewhat more sedating SSRI that helps with sleep and decreases nightmares. Naltrexone is an opiod antagonist, which helps block the benefit of self-injurious behaviors. Note: In a 15 subject study, 5 got better, 5 got worse, and 5 stayed the same!
Amy began her presentation with the hope that fuller understanding of neurobiological process can deepen our empathy for the intense challenges we see in our patients with PTSD in intimate relationships, including the psychotherapy relationship. She ended remarking on the extraordinary resilience we see in the brains and bodies of trauma survivors. I left Amy’s presentation marveling at how, yet again, the trauma field teaches us that mind and body, and physiology and relationship, are inextricably intertwined.