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Briere, J. & Scott, C. (2025). Principles of trauma therapy: A guide to symptoms, evaluation, and treatment(3rd ed.). Sage Publications. ISBN: 9781544333557. Chapter 11

MINDFULNESS IN TRAUMA TREATMENT

Mindfulness has been described at various points in this book as potentially helpful for trauma survivors. We explore this component more directly in this chapter, outlining the research, goals, and methodology of mindfulness-relevant trauma treatment. Most intriguing is the possibility that such interventions do not just duplicate the effects of standard therapy, but they also provide new1 or incremental skills and perspectives that are especially suited to those who have had adverse experiences. A growing number of researchers and clinicians have come to integrate mindfulness into therapeutic approaches. In fact, even when mindfulness-based interventions are not specifically employed, various other aspects of Buddhist psychology or practice (e.g., compassion, metacognitive awareness, and appreciation of dependent origination, each discussed in this chapter) can be helpful in work with traumatized people. WHAT IS MINDFULNESS? Mindfulness can be defined as the capacity to maintain ongoing awareness and acceptance of current experience, including internal mental states and aspects of the external world, without judgment. A more psychologically focused definition of mindfulness can be found in Walsh and Shapiro (2006), who refer to a family of self-regulation practices that focus on training attention and awareness in order to bring mental processes under greater voluntary control and thereby foster general mental well- being and development and/or specific capacities such as calm, clarity, and concentration. (pp. 228–229) However defined, the ability to attend to the present moment and view oneself and the world nonjudgmentally—as opposed to being preoccupied with (and affected by) negative aspects of the past or worry about the future—is thought to decrease psychological suffering (Kabat-Zinn, 2003) as well as, we will suggest, allowing certain helpful psychological processes to occur. In Buddhism, mindfulness is one of a variety of activities whose ultimate purpose is to increase existential insight, reduce suffering associated with unnecessary attachments, and, ultimately, provide spiritual enlightenment. Although not without controversy in the Buddhist community, the last several decades have witnessed a more secular application of mindfulness, primarily to reduce psychological symptoms and problems. As we will see, mindfulness-based clinical interventions have been shown in studies to be helpful for a wide range of psychological issues and complaints. Mindfulness is more than psychotechnology, however; we encourage the reader to view the therapeutic applications of mindfulness as a relatively small and excised part of the much broader domain of contemplative psychology, which, we believe, can offer rich existential lessons and insights for traumatized and nontraumatized people alike.

An important component of mindfulness is the capacity for acceptance, which involves acknowledgment of and openness to current experience of oneself and of one’s situation without judgment. In an online interview (Goldstein, 2009), Tara Brach described this as “an honest acknowledgment of what is going on inside you, and a courageous willingness to be with life in the present moment, just as it is” (para. 10). Similarly, Germer (2009) refers to this process as “a conscious choice to experience our sensations, feelings, and thoughts, just as they are, moment to moment” (p. 32). Notably, this version of acceptance should not translate into passivity or helplessness. Hayes and colleagues (2011), for example, notes that mindful acceptance involves an active attempt to embrace oneself and one’s experience, including unwanted states, in the here-and-now. The engaged acceptance component is important, above and beyond the development of attention and awareness skills also found in mindfulness training models. The implicit contradiction involved in embracing acceptance as a way to, in fact, change one’s thoughts or feelings was articulated in another context long ago by Carl Rogers (1961), who said, “The curious paradox is that when I accept myself just as I am, then I can change” (p. 17). The first part of this chapter describes the applications of mindfulness to psychological distress from a science perspective, summarizing research on empirically evaluated mindfulness-based treatments. The second part attempts to apply those aspects of mindfulness most relevant to trauma as well as some of the existential/philosophical lessons of Buddhist psychology. RESEARCH Empirically based, structured mindfulness interventions have been shown to significantly reduce a variety of psychological symptoms and disorders, including many associated with trauma exposure, including the following:

Anxiety and panic Depression, or prevention of relapse into depression Obsessive-compulsive disorder Substance abuse Disordered eating Attention deficit hyperactivity disorder Self-injurious behavior Aggression Low self-esteem and other cognitive distortions Chronic pain Insomnia The psychological effects of cancer and other life-threatening medical conditions Symptoms of fibromyalgia Chronic emotional dysregulation Borderline personality disorder Aspects of bipolar affective disorder

See the following recent reviews or meta-analyses of studies on the clinical efficacy of mindfulness for these and other difficulties: Goldberg et al., 2018; Headman-Lagerlöf & Öst, 2018; Hoffman et al., 2010; Khoury et al., 2013, and a systematic review of 44 meta-analyses of mindfulness RTCs (Goldberg et al., 2021). Current Mindfulness-Based Therapies Several different empirically validated mindfulness interventions have been developed over the last several decades, all of which are relevant to trauma-related distress:

Mindfulness-Based Stress Reduction (MBSR; Kabat-Zinn, 1982) Mindfulness-Based Cognitive Therapy (MBCT; Segal et al., 2013) Mindfulness-Based Relapse Prevention (MBRP; Bowen et al., 2011) ACT (Hayes et al., 2011) Dialectical Behavior Therapy (DBT; Linehan, 1993)

Two of the most popular of these, MBSR and MBCT, are described below as examples of how mindfulness can be taught to clients to good effect. Mbsr Developed at the University of Massachusetts Medical Center by Jon Kabat-Zinn, MBSR is the best known and most employed mindfulness intervention in the West. It typically involves eight weekly group sessions, each lasting approximately two and a half hours, as well as one day-long session during the sixth week. In addition to homework assignments, including readings on MBSR-related topics, participants are asked to meditate 6 days a week for 45 minutes each day. A central component of MBSR is instruction on how to engage in mindfulness meditation, including (a) specific sitting and lying positions; (b) focusing one’s attention on a single target (e.g., the breath, or sensations in the body); and (c) when, inevitably, the mind is distracted by emergent thoughts, emotions, or sensations, noting these intrusions in a nonjudgmental way and then returning to the target of attention. In a related activity, the body scan, participants are led through a guided exploration of sensations arising from the body, starting at the feet and eventually ending at the head. Other exercises include gentle stretching and Hatha yoga positions, and teaching and group discussions on mindfulness, meditation, and mind-related contributions to stress. MBSR has been shown to be effective in many studies of chronic pain and other health conditions, as well as anxiety, depression, sleep disturbance, binge eating, and overall psychological distress. Mbct MBCT is an adaptation of MBSR specifically targeted to preventing relapse in individuals with a past history of major depressive episodes, although it is now applied to other domains as well, including anxiety, obsessive-compulsive disorder and, most relevant here, psychological trauma (e.g., Key et al., 2017; King & Favorite, 2016; Semple & Madni, 2015). This intervention typically involves eight 2.5-hour sessions and a 1-day retreat, and teaches many of the same skills as MBSR, such as mindful, nonjudgmental attention to thoughts, feelings, and sensations, and the development of meditation skills. However, MBCT focuses to a greater extent on participants’ thought processes, based on the well-established fact that cognitive distortions and

negative preoccupations may become self-perpetuating and contribute significantly to the development of depression (Beck, 1995). Participants are especially taught to develop a “decentered” or metacognitive perspective on their thoughts, whereby negative cognitions or depressive thinking patterns are recognized as merely thoughts—not necessarily as evidence of the true state of reality. When they occur, such cognitive intrusions (e.g., “I am a bad person.” “Things are hopeless.” or “I can’t do this.”) are not suppressed, but rather they are noted dispassionately and considered mindfully—that is, as emergent processes of the mind that inevitably come and go, but that do not have intrinsic meaning or truth. Applications to Traumatized Individuals Although studies of mindfulness interventions for trauma survivors have relatively recently appeared in the literature, there are a number of studies evaluating the efficacy of mindfulness training in the treatment of PTSD and other trauma-related symptoms, almost all of which indicate positive outcomes (e.g., Bremner et al., 2017; Davis et al., 2019). As noted by Boyd and colleagues (2017), these studies “suggest that mindfulness-based treatments are effective in reducing symptoms of PTSD, with medium to large within-group effect sizes” (p. 20). Further, at least one mindfulness-based treatment, DBT, has a long track record of success with client populations in which trauma is overrepresented, especially those diagnosed with borderline personality disorder (Kliem et al., 2010; Öst, 2008), and several studies report the effectiveness of mindfulness interventions for those abused as children (Kimbrough et al., 2010; Steil et al., 2011) and other trauma survivors (e.g., Davis et al., 2019; Fiorillo & Fruzzetti, 2015). See Semple and Briere (2020) for a review of this literature with special reference to treating adolescent trauma survivors. Although the mindfulness-based interventions described above have been shown to be helpful for a range of symptoms and concerns, many of which can arise from adverse experience, they have a singular limitation for classic trauma treatment: They are generally not implemented in the context of individual psychotherapy, which is a central modality in work with seriously impacted trauma survivors. In fact, empirically based mindfulness interventions, almost without exception, occur in group settings and tend to be relatively nonclinically oriented, focusing more on skills development (e.g., mindfulness, metacognitive awareness, capacity to meditate) than on individual psychological symptoms. This is entirely appropriate, and skill development groups such as MBSR or MBCT can be very helpful adjuncts in work with traumatized persons, assuming there are no obvious contraindications. At the same time, it is unlikely that a person suffering from some combination of the various issues and problems described in this book would have all or even most of their clinical needs addressed by mindfulness-based groups, or a meditation practice, alone. Finally, because mindfulness is often best learned through meditation, which can be contraindicated for some trauma survivors, the potential impacts of the client’s trauma history—including trauma symptomatology—must be taken into account and monitored on an individual basis, so that, in relatively rare instances, the survivor is not adversely affected. In this context, we suggest a hybrid approach (Briere, 2015, 2019):

1. Screen for the appropriateness of mindfulness (typically meditation) training. Experience suggests that clients who are subject to acutely overwhelmingly intrusive flashbacks,

rumination, easily triggered trauma memories, or other negative states are sometimes more likely to experience at least transient distress or destabilization when meditating (e.g., Cebolla et al., 2017), probably because meditation and mindfulness reduce experiential avoidance and provide greater exposure to internal experience, including memories and painful emotions (Treanor, 2011). Furthermore, as described in Chapter 2, some survivors suffer from reduced emotional regulation/tolerance capacities, meaning that triggered sensory or emotional material may be more challenging once activated in meditation. More obviously, trauma survivors experiencing psychosis, severe depression, mania, significant suicidality, or some instances of substance dependence should typically avoid meditation-based mindfulness training until these symptoms or conditions are resolved or are under better control. See Germer (2005) for common-sense suggestions regarding the use and adaptation of mindfulness practice with symptomatic trauma survivors and Treleaven (2018) for a discussion of trauma-sensitive mindfulness.

Given these concerns, we recommend that clients considering meditation in the context of trauma issues be assessed for possible risk factors beforehand. In most cases, there will not be any psychological impediment, and multiple benefits may accrue. In the remaining instances, the issue may be less that the client cannot ever attempt meditation, but rather that they only do so when they are more stable and/or less debilitated. In cases when mindfulness training is, in fact, contraindicated, other, less activating approaches might be considered, including trauma-sensitive yoga (Emerson & Hopper, 2011), lovingkindness meditations (Salzberg, 1995), and self-compassion exercises (Germer & Neff, 2015).

2. If there are no contraindications, the client is willing, and the clinician has adequate

experience with mindfulness, consider teaching a simple breath-counting meditation procedure. Below is an example of a mindfulness meditation, adapted from Briere (2019). Clinical experience suggests that even this brief activity can be helpful for those who seek a regular way to decrease stress and increase mindful awareness. Note that this is not a replacement for more in-depth mindfulness meditation training, which we describe next.

3. For those who can tolerate it, and wish to learn mindfulness more extensively, refer to an

MBSR or MBCT group, or a qualified meditation training center, where basic meditation skills can be learned.2 Extensive mindfulness training during psychotherapy sessions can be inefficient in some cases, since such skills development usually requires a significant investment of time, during which, presumably, trauma-focused therapy would have to take a back seat. In addition, qualified meditation teachers usually have devoted years of training and experience to acquiring meditation and mindfulness skills, as well as knowledge of how to teach them to others—a background that may not be fully available to many clinicians.

In some lucky circumstances, the therapist will, in fact, be sufficiently experienced in both domains—a situation that may allow the client to receive both therapy and meditation/mindfulness training from the same source. In other contexts, the clinician may introduce elementary mediation instruction, as presented above, for example, to increase relaxation or metacognitive awareness, but not spend an inordinate amount of time doing so. In either instance, the therapist should make sure that trauma-focused psychotherapy is not receiving short shrift by virtue of too much attention given to the development of meditation or mindfulness skills. Although the clinician is unlikely to be the client’s primary meditation teacher, their personal experience with meditation is important. During the period when the client is simultaneously attending psychotherapy and mindfulness training, the meditation-experienced therapist can monitor and inform the process—helping the client to understand and integrate what they are learning and experiencing in both domains and continuing to assess the appropriateness of mindfulness training over time. As the client gains meditation and mindfulness skills, these capacities can be called upon during trauma-focused psychotherapy. Minimally, this may involve the following:

The use of settling skills (Semple & Briere, 2020) learned in meditation. The individual who is able to decrease their anxiety or hyperarousal through meditation—for example, by attending to their breath, engaging the here-and-now, and occupying a less self- identified cognitive perspective—can use these skills at points when therapy involves painful memories and triggered emotional states. Similarly, mindfulness skills involving the ability to let go of intrusive or persistent mental content may be helpful when the client encounters triggered thoughts, feelings, or memories that dominate their experience during trauma treatment. Trauma processing, as described in Chapter 9. Multiple writers (e.g., Germer, 2005; Treanor, 2011) note that the decreased avoidance associated with mindfulness can expose the individual to emotionally laden memories in the context of a relatively relaxed state and a less involved, nonjudgmental, and accepting cognitive perspective—a process that is likely to desensitize and countercondition such material and decrease its power to produce distress. In the therapy session, this process (described by some modern Buddhist writers as “inviting your fears to tea” or “leaning into fear” [Brach, 2003]) may be engaged by asking the client to feel and allow triggered emotions that come up in treatment, while maintaining as mindful a state as possible. Metacognitive awareness, as described in Chapter 7. During therapy, the client can be invited to consider their trauma-related negative cognitions, feelings, and memories as “just” products of the mind that are not especially real in the current context, but, instead, reexperienced memories that—if not suppressed or hung on to—come and go. Although the intent is not to convince the survivor that their thoughts and memories are irrelevant, they may be able to gain from increased awareness that such phenomena represent the reflexive actions of the mind or brain and are not necessarily accurate feedback on the current state of reality. Reduced reactivity and less need to engage in distress-reduction or other avoidance behaviors. The client’s meditation experiences, and mindfulness training may also increase their emotional regulation capacity, essentially by changing their relationship to thoughts, memories, and feelings. For example, as the survivor engages metacognitive awareness either during therapeutically activated trauma memories or in the outside world, there may be less need for them to act on (or emotionally respond to) intrusive trauma-related cognitions such as “He’s disrespecting me.” “I’m in danger.” or “I deserve this because I am a __.” As noted in Chapter 6, the ReGAIN exercise is an example of using mindfulness to reduce reactivity to trauma- or attachment-related triggers, wherein the individual learns to discriminate activated memories from real-world perceptions and to respond to triggered states with metacognitive skills and activities. Similarly, the “urge surfing” skill described in Chapters 6 and 8 and Appendix 4 may be helpful as the client learns to “surf” intrusive thoughts, feelings, and urges from a position of relative calm without having to act on these internal experiences. 4. In the context of ongoing treatment, the therapist can encourage existential insight, potentially changing the client’s perspective on situations and events that otherwise might produce greater distress. Such insight does not have to involve the development of a skill,

as is true for mindfulness, but rather tends to occur as the client explores basic life assumptions in conversations with the clinician or, when relevant, in the context of meditation. Among these notions are attachment, impermanence, and dependent origination. In Buddhist psychology, attachment refers to “grasping” or “clinging,” involving the desire to hang on to or overly invest in things that, ultimately, are impermanent.3 Impermanence refers to the fact that all things are in a state of flux, and that no thing or event lasts forever. The ubiquitous need for things that do not last, or may not even exist, is thought to increase human suffering. As a result, this perspective counsels against excessive preoccupation with possessions or status, or rigid ideas or perceptions about oneself or others, since these things and ideas are inevitably unsustainable and unreliable, resulting in loss, disappointment, and unhappiness (Bodhi, 2005).

Trauma is a powerful threat to attachment, since it often involves loss of people, possessions, social status, beliefs, hopes, self-esteem, and/or well-being. The burn survivor may have to grapple with disfigurement or diminished functioning; the disaster survivor may have lost possessions, property, and perhaps loved ones; someone who has been raped or tortured may suffer the loss of belief in personal safety, justice, or the beneficence of others; and the heart attack survivor may have to confront previously unexamined assumptions about personal immortality. Thus, there may be two sources of distress associated with any given trauma—the event itself, and the interpretations or unhelpful responses that follow from it. The Second Arrow. One of the earliest Buddhist teachings describes this binary aspect of pain and reaction to pain in the parable of a person shot with two arrows, one immediately following the other (Bhikkhu, 1997). The first arrow is the objective pain felt when encountering an adverse event, such as a trauma or loss. The second arrow is the extent to which the pain and loss are exacerbated by attachment to needs and responses that increase suffering—especially those involving nonacceptance, hurtful self-interpretations, and resistance to change. Although it is unlikely that any person can entirely avoid triggered states or resistance when exposed to memories of very hurtful events, mindfulness-informed psychotherapy can reduce this second source of suffering by helping the survivor to (a) loosen their grip on beliefs, needs, and expectations that have been challenged or proven false and (b) redirect their attention to more realistic, nourishing, and accepting ways of being. In effect, the survivor may be able to change what is potentially possible to change—their perspective and understanding—as opposed to what cannot be changed—the trauma or its concrete impacts. Arrow work. In the typical instance, the clinician might encourage the client to explore their thoughts, feelings, and reactions, and provide nondirective opportunities for the whats of the traumatic event and their responses:

What did the client believe about themself before the trauma (e.g., that they were generally safe, they could trust others)? What hurts the most now, after the trauma has passed (e.g., loss, betrayal, awareness of vulnerability)?

What are they resisting that is nevertheless true (e.g., awareness of the impermanence of life, the unpredictability and uncontrollability of the future)? What was the first arrow? What is the second?

Finally, dependent origination holds that all things arise from concrete conditions and sustaining causes, which, themselves, arise from other causes and conditions (Bodhi, 2005). In other words, everything that happens to the survivor, and their response to what has happened, are the logical result of other events—nothing occurs independently or in isolation. This view is in agreement with the basic principles of behavioral science, that people do things because of the influence of other things or processes. Dependent origination and Western psychology both suggest that attributions of intrinsic badness, inadequacy, or even pathology to self or others who do us harm may be due to insufficient information: If we could know about the logical why of a given person’s (or our own) behavior, we would be less likely to judge or blame them or ourselves (Briere, 2012). Importantly, this does not mean that the survivor is coached to forgive or condone an abusive person’s behavior, especially to the extent that doing so implies that the client not entitled to negative feelings and thoughts. Nor should they blame themselves when forgiveness seems impossible. In fact, as noted earlier, social or personal pressure to block or avoid unwanted internal states, including anger and desire for revenge, may inhibit the normal psychological processing necessary for recovery. When this process occurs in the absence of pressure from the clinician to decide on one version versus another, in the context of noncontingent acceptance and support, the client’s detailed analysis may lead to a slow transition from a view of (a) self as weak or pathological to that of someone who was not responsible for what happened and whose responses (then and now) are the logical effects of traumatization, and, in some cases, (b) the perpetrator or abuser as intrinsically evil to that of someone whose behavior, although not acceptable, arose from their own problematic predispositions and adverse history. From this perspective, embracing dependent origination is not necessarily in the service of redeeming the perpetrator, but rather is for the benefit of the survivor (Kornfield, 2008). Mindfulness in Social/Cultural Context Because, as described throughout this book, trauma is often embedded in social and cultural inequality, discrimination, and maltreatment, it is important that mindfulness training and mindfulness-inclusive psychotherapy be adapted to meet the individual’s specific sociocultural context. When mindfulness is taught or employed without reference to the effects of social adversity and cultural differences, or when it limits itself to the experiences and needs of (ironically, given its cultural roots) White middle-class English-speaking individuals, it runs the risk of being irrelevant to the needs of many trauma survivors (Deluca et al., 2018). Treleaven (2018) warns, in this regard, that “if we fail to actively engage with social context, we become a liability in our mindfulness-based work. Absent an understanding of how individual

and social systems interact, we can potentially cause harm, break people’s trust, and perpetuate systems of domination.” (p. 179). THE MINDFUL THERAPIST Not only can it be helpful for the trauma client to increase their mindfulness and existential appreciation, the clinician’s level of functioning in these areas is also important. A therapist who is able to focus their attention on the client in an alert, accepting, and compassionate way will almost inevitably increase the quality of the therapeutic relationship (Bruce et al., 2010; Siegel, 2010). A positive client–therapist relationship, in turn, appears to be one of the most helpful component of treatment. As noted earlier, this may be especially true for the trauma survivor in therapy, where a positive relationship can be both a minimal requirement and a powerful intervention. Several aspects of therapist mindfulness may contribute to the positive therapeutic conditions that assist and comprise trauma therapy, as outlined in Chapter 4. These potentially include empathic attunement, compassion, unconditional positive regard, and reduced transference- related reactivity. Because mindfulness involves the learned capacity to pay close and nonjudgmental attention to internal and external phenomena, it can assist the clinician in maintaining a significant degree of attunement to the client (Morgan & Morgan, 2005). In their discussion of the role of therapist mindfulness in the psychotherapeutic relationship, Bruce et al. (2010, p. 83) note that “through mindfulness practice, a psychotherapist comes to increasingly know and befriend himself or herself, fostering their ability to know and befriend the patient.” Not only does this state increase the capacity of the therapist to understand the client’s ongoing experience, but it may help the client to process negative interpersonal schemas and emotional responses. As described earlier, when attunement is continuously experienced by the client, especially if the clinician’s compassion is also evident, the client may enter a form of attachment activation, engaging psychological and neurobiological systems that encourage openness and connection and increase well-being. As a result, the therapist’s mindfulness and compassion tend to countercondition relational distress, producing an increased likelihood of trust and interpersonal connection. The therapist’s mindfulness not only allows them to foster attunement and compassion toward the client, but it also serves as a partial protection from their own countertransferential reactivity during psychotherapy. By facilitating greater awareness of their internal processes, mindfulness helps the clinician to better understand the subjective and multidetermined nature of their own thoughts, feelings, memories, and reactions to the client—a form of the metacognitive awareness described in Chapter 7. As they are more able to recognize specific emotional and cognitive responses to the client as potentially triggered phenomena—as opposed to perceptions based solely on the client’s clinical presentation—the therapist can place them in proper perspective before they result in significant countertransferential behaviors or vicarious traumatization.

Developing mindfulness in the therapist. If clinician mindfulness and compassion have positive effects, the obvious question is how this capacity can be developed or enhanced. In general, the best answer—as for the trauma client—appears to be a regular meditation practice. Although there are many books available to the clinician that teach about mindfulness, regular meditation, especially in the context of a qualified and supportive teacher or group, provides the structure, repetitive opportunity for skills development, and, eventually, existential insights usually necessary to meaningfully increase mindfulness. Furthermore, most authorities on the clinical application of mindfulness (e.g., Semple & Lee, 2011; Shapiro & Carlson, 2009) requires that the therapist already have a regular meditation practice before attempting to teach mindfulness to others. This does not mean, of course, that important understanding of mindfulness and compassion cannot be gained initially by attending lectures or workshops, or by reading books by teachers such as Brach (2019), Chödrön, (2000), Hahn (1987), and Kornfield (2008). Chapter 12

TREATING THE EFFECTS OF ACUTE TRAUMA: SARAH STOYCOS, HEIDI

ARDERN, JOHN BRIERE, & CATHERINE SCOTT

Although much of this book has been concerned with the treatment of chronic trauma-related distress, the needs of those who have been exposed to more recent adverse events are also important. Unfortunately, there are fewer well-validated treatment strategies for acute stress disorder (ASD). Most current interventions for ASD are modifications of treatments for PTSD, based on the assumption that what is helpful when posttraumatic stress has become chronic will also be helpful for more acute responses. Although this approach has some merit, there are significant differences in how most people experience acute, as opposed to more chronic, traumatic stress. These differences often require somewhat different intervention approaches. This chapter reviews the literature on acute stress and provides an overview of how treatment can be modified to take into account the special needs of the acute trauma survivor. In the context of PTSD, the term acute generally refers to symptoms emerging in the first 3 months following a traumatic event. With the addition of ASD to the diagnostic nomenclature, however, it is also used to describe reactions within the first month. In this chapter, we use the term in its broadest sense, to refer to responses that occur within the first weeks or months following trauma exposure. RESEARCH ON ACUTE TRAUMATIC STRESS Since the introduction of the diagnosis of ASD to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR; American Psychiatric Association, 2000), and following the events of September 11, 2001, there has been a groundswell of research and clinical interest in acute traumatic stress. Initially, most published articles in this area limited their discussion to the phenomenology of ASD and risk factors associated with the development of PTSD. In recent years, however, researchers have focused additionally on targeted intervention strategies or approaches.

Acute Symptoms and Risk for PTSD The development of ASD. A number of risk factors for the development and severity of ASD have been identified in the research, including trait anxiety and posttraumatic cognitions (Suliman et al., 2013), and excessive use of avoidance and dissociation (Hansen et al., 2015). As noted in earlier chapters, a significant proportion of acute trauma survivors recover naturally from trauma exposure; posttraumatic symptoms either never develop, or they decrease—but do not always entirely resolve—over time, even in the absence of treatment (see Galatzer-Levy et al., 2018). In a review of studies, Bryant (2015) summarizes four major trajectory classes (groups) in the development of traumatic stress following trauma:

A resilient class of individuals with consistently few trauma-related symptoms A recovery class with initial distress and then gradual recovery or resolution of symptoms A delayed-reaction class with initially low symptom levels, who then experience increased symptoms over time A chronically distressed class with consistently high levels of posttraumatic stress that often result in PTSD A variety of factors may determine which trajectory an individual’s symptoms take. For example, high levels of depression and anxiety several months after a traumatic event appear to predict a chronic trajectory of symptoms, whereas other factors (e.g., family tension and living in a lower socioeconomic area) may better predict a delayed onset of symptoms (Jones et al., 2019; Shigemoto, 2019).

The transition from acute stress to PTSD. Early research suggested that most trauma survivors whose initial symptoms are severe enough to warrant a diagnosis of ASD would eventually go on to develop PTSD (Bryant & Harvey, 2000). However, it has become clearer that while acute stress reactions bear some relationship to the subsequent development of PTSD, they do not predict PTSD with consistent specificity or sensitivity (Bryant, 2016). Yet, despite this variability, there may be a common path to both ASD and PTSD involving poor fear inhibition (Jovanovic et al., 2013), peritraumatic panic, anxiety sensitivity, avoidance, and negative cognitions about self (Hansen, Armour, Wang et al., 2015; Hansen Armour, Wittmann et al., 2014).

Some research indicates PTSD is correlated with the severity of earlier ASD symptoms whereas other studies suggest that early PTSD symptoms, more than those of ASD, per se, predict chronic PTSD (see Bryant, 2011, for a systematic review). In the first instance, for example, a 2019 study by Giupponi and colleagues found ASD symptoms—along with somatization and a history of other adult traumas—predicted PTSD. In the second instance, although dissociative symptoms were required for a diagnosis of ASD in DSM-IV-TR and have been associated with the later emergence of PTSD (Briere et al., 2005), studies suggest that they may not be as important in the development of PTSD as early onset and continuous hypervigilance, sleep disturbance, irritability, and reexperiencing (Dalgleish et al., 2008; Halpern et al., 2011). The risk of lasting distress (including PTSD) for those trauma survivors who develop ASD and/or early symptoms of PTSD—as well as the psychosocial dysfunction associated with most acute trauma presentations—underscores the need for early intervention in posttraumatic symptomatology. In response, research has begun to identify specific interventions to target ASD

and the early symptoms of PTSD. As noted, these interventions are mostly modifications of treatments originally designed to treat PTSD and remain in the early stages of validation. Certain approaches that have historically been utilized with acutely traumatized populations (e.g., psychological debriefing) have been de-emphasized in favor of strategies with a broader base of empirical support. The Literature on Interventions for Acute Stress Debriefing Psychological debriefing was initially developed as a way to intervene with large numbers of trauma survivors in circumstances where individual evaluation and treatment was not possible, such as during war or after terrorist attacks or natural disasters. As early as World War II, debriefing was described as a method of helping soldiers to “purge” themselves of the distress related to battle experiences (Bisson et al., 2000). Critical Incident Stress Debriefing The most used debriefing approach has been Critical Incident Stress Debriefing (CISD), a structured protocol developed by J. T. Mitchell (1983). CISD has been employed with rescuers, first responders, and law enforcement personnel after major traumatic events. For example, after the terrorist attacks of September 11, 2001, CISD was widely applied to groups of people who were directly exposed to the disaster, who lived or worked nearby, or who were otherwise affected by the attacks but did not witness or experience the event itself. CISD is typically conducted in a group setting with 10 to 20 people, although there are also protocols for individual debriefing. Sessions last anywhere from 1 to 3 hours and are usually conducted within a week of the trauma. Participants are asked to describe in detail their experiences of the trauma, to formulate a cognitive appraisal and interpretation of the event, and to express their emotional reactions. Group sharing is encouraged, with the intention of normalizing stress reactions as well as providing social support. Sessions end with a discussion of coping strategies and psychoeducation regarding possible future consequences of the event (Mitchell, 1983). Unfortunately, CISD offers fewer benefits in reducing current distress or preventing the development of PTSD symptoms than previously thought. Two meta-analyses (Rose et al., 2002; van Emmerik et al., 2002) and a randomized trial (Adler et al., 2008) indicate that single-session debriefing does not prevent PTSD nor does it hasten recovery from already-present symptoms. Non-CISD interventions—or no intervention at all—have sometimes been associated with better outcomes than CISD. In fact, in several studies, debriefing has been found to have potentially detrimental effects, with higher rates of PTSD at long-term follow-up (Mayou et al., 2000), and more misinformation incorporated into memory, more intrusive thoughts, and more confabulation (Paterson et al., 2014). There are several possible reasons why CISD might occasionally have deleterious effects, and why research findings on CISD are so mixed:

CISD in group settings often involves individuals with different trauma exposure histories, levels of distress, symptomatology, and risk for PTSD. In such situations, some people may be retraumatized or additionally distressed by hearing the experiences of others before they have processed and integrated their own reactions. CISD is sometimes used with primary survivors of trauma (e.g., accident survivors), a purpose for which it was not developed. A review of the CISD literature suggests that CISD is more apt to be effective in reducing PTSD risk in the populations for which it was initially intended, primarily emergency services personnel and first responders (Jacobs et al., 2004). Although CISD is intended to normalize and validate emotional responses, in some cases it may lead to stigmatization; for example, certain individuals may have visibly more extreme reactions to the traumatic event than others, and, as a result, perceive themselves (or be perceived by others in the group) as psychologically disturbed. To the extent that CISD is administered to all individuals in a unit or squad who were exposed to a potentially traumatic event, there are likely to be individuals who were not traumatized by the event and who may therefore have negative responses to being treated. The effects of being treated for something that you have not experienced are unclear but might easily be at least mildly problematic.

Proximity, Immediacy, and Expectancy Another form of debriefing—Proximity, Immediacy, and Expectancy (PIE, also referred to as Frontline Treatment; Ritchie et al., 2006)—was used in military settings, with the goal of returning injured soldiers to the front lines of war. PIE emphasizes the need to intervene with injured survivors as close to the front lines as possible (proximity), as promptly as possible (immediacy), and with the expectation of recovery upon return to the military unit (expectancy; Jones & Wessely, 2003). This intervention also includes attention to basic needs and medical care, along with the opportunity for emotional ventilation and expression. The PIE model was used with Israeli soldiers in the 1982 Lebanon War, with some apparent success (Solomon et al., 2005). A more recent study by Potter and colleagues (2009) also provided some evidence for the effectiveness of the PIES (the additional S refers to simplicity) model in treating stress reactions during deployment; however, no recent studies of PIE were found in the extant literature. Regardless of its possible efficacy, the concept of return to duty, which implies a return to the situation and circumstances of the original trauma—as well as to the possibility of further trauma exposure—is somewhat controversial. In the Vietnam War, for example, rapid return to duty was not associated with better mental health outcomes (Shalev, 2002). For some individuals, particularly those who are less traumatized, who have a more resilient underlying biology, or who are otherwise at low risk for posttraumatic symptomatology, it may be true that immediate reexposure hastens psychological recovery. However, for those who are overwhelmed by events, who lack sufficient emotional regulation skills, or who have a biological vulnerability to stress, such reexposure may be retraumatizing and harmful. Other Acute Interventions Defusing

Another, less common form of acute trauma intervention is referred to as defusing. Defusing is a brief (typically 10–30 minutes) “conversational” intervention, intended to provide support, reassurance, and information to trauma-exposed individuals in informal contexts (Ritchie et al., 2006; Young et al., 1998). Although little data are available on this approach, one study of Swedish peacekeepers in Bosnia found that, in combination with peer support, defusing was associated with greater postservice mental health (Larsson et al., 2000). This improvement did not occur, however, for those with the worst preservice psychological functioning. A more recent study of defusing conducted by French mental health disaster responders suggests that the majority of individuals who went through defusing felt “soothed” afterward (Prieto et al., 2018). Although the results of these studies are somewhat encouraging, further research is required to evaluate the efficacy of defusing, especially independent of the effects of peer support. Psychological First Aid and Skills for Psychological Recovery Psychological First Aid (PFA) was developed by the Terrorism Disaster Branch of the National Child Traumatic Stress Network (NCTSN) and the National Center for PTSD. The PFA Field Operations Manual, 2nd Edition—a working document published in response to the need for written materials for those providing assistance after Hurricane Katrina in the Gulf of Mexico region (can be downloaded from https://www.nctsn.org/sites/default/files/resources//pfa_field_operations_guide.pdf). In contrast to debriefing techniques and defusing, PFA is not a specific therapeutic intervention. Instead, it outlines a modular framework for mental health professionals who provide individualized assistance to survivors of natural disasters, terrorism, and other mass traumas. PFA can be delivered in the field in diverse settings (such as shelters, hospitals, and mobile response units) and can be used with children, adolescents, and adults. It is intended to be flexible, and the different components can be tailored to fit the specific needs of the individuals involved. The main goals of the intervention are to decrease the initial distress associated with exposure to trauma and to improve longer-term adaptive functioning. The model emphasizes a nonintrusive, compassionate attitude on the part of clinicians. Notably, PFA avoids trauma debriefing. Clinicians are encouraged to allow traumatized individuals to talk about their experiences as little or as much as they wish, but never to push for information or processing. The core components of PFA focus on giving practical assistance with immediate needs, providing safety and comfort, and establishing connections with primary support networks and social resources. Additionally, the operations manual provides a variety of resources and handouts for several specialized populations, such as unhoused populations. Skills for Psychological Recovery (SPR) is similar to PFA in that it provides a modular framework to assist individuals of all ages, across diverse settings, to decrease early distress related to trauma exposure. However, SPR is more specifically focused on skill-building, with an emphasis on coping with trauma-related symptoms as well as adverse consequences associated with traumatic events or disasters. SPR is designed to be implemented post–PFA, though the timeframe may vary depending upon event and client characteristics. SPR emphasizes the development of problem-solving skills, engagement in positive activities, managing distressing physical and emotional reactions, promoting helpful thought processes, and rebuilding healthy

social connections. The NCTSN offers a free online course on SPR, with access to the field operations manual (https://www.nctsn.org/resources/skills-psychological-recovery-spr-online). Notably, there is very little empirical evidence that PFA, SPR, psychoeducation, or debriefing are especially beneficial immediately posttrauma (Bryant, 2016). Psychoeducation, for example, may prime people to expect symptoms, and may have no impact upon the appraisals people make about the information they’re given. SPR was developed in such a way as to allow for more detailed study, though such research has not yet been published. The Skills for Life Adjustment and Resilience (SOLAR) program represents a more recent foray into the development of a brief, skills-based intervention that can be delivered postdisaster by individuals with little or no mental health training. Although a pilot study (O’Donnell et al., 2020) conducted with 15 wildfire survivors shows promise for the potential of this intervention to reduce psychological distress and trauma-related symptoms, the SOAR intervention awaits more validation. Cognitive-Behavioral Interventions In contrast to the approaches outlined previously, there is empirical evidence from several trials that a course of cognitive-behavioral therapy (CBT) in the weeks following a trauma can reduce the likelihood of subsequent PTSD—immediately posttreatment, at 5 months, 6 months, 9 months, and in one study, at 4 years posttrauma (see Birur et al., 2017 for review). Subsequent meta-analyses and systematic reviews of the literature demonstrate with some consistency that CBT is an efficacious treatment for ASD (Carpenter et al., 2018; Roberts et al., 2019). In a comprehensive meta-analysis of CBT for anxiety disorders, for example, Hofmann and Smits (2008) found a strong effect size for the treatment of acute stress disorder utilizing CBT strategies, and a systematic review by Roberts et al. (2010) found that brief, trauma-focused CBT was more effective than waiting list interventions and supportive counseling; these effects were maintained 6 months later. Roberts et al.’s follow-up meta-analysis in 2019 indicates that individuals diagnosed with ASD and PTSD experienced clinically important benefits from early interventions utilizing trauma-focused CBT, cognitive therapy without exposure, and eye movement desensitization and reprocessing (EMDR). Other reviews and meta-analyses support these findings, in some cases for preventing later PTSD as well as reducing ASD symptoms (e.g., Birur et al., 2017; Carpenter et al., 2018). A clinical trial conducted by Shalev et al. (2012) compared early versus delayed CBT for PTSD and examined the effects of a selective serotonin reuptake inhibitor (SSRI) medication (escitalopram) in the prevention of PTSD. Overall, prolonged exposure and cognitive therapy were found to be equally effective in preventing PTSD over a 9-month period, relative to controls and those receiving escitalopram. Notably, delaying prolonged exposure treatment did not affect the 9-month outcome. These data are important, suggesting that if it is not feasible to provide treatment for ASD/PTSD shortly after a traumatic event or disaster, survivors will still benefit from treatment if it is delayed, and may not be at any higher risk for developing chronic PTSD should this occur. This study also supports targeting for treatment those individuals who meet full diagnostic criteria, as opposed to partial PTSD, since the latter fared well whether or

not they participated in treatment. Notably, as discussed in Chapter 15, the escitalopram group fared the worst after 9 months, with no apparent preventative effect. Although cognitive therapy for ASD appears to be helpful, a study by Bryant and colleagues (2008) highlighted the importance of therapeutic exposure in preventing PTSD. They found that clients who received exposure therapy had a 33 percent rate of PTSD at follow-up, whereas those receiving cognitive restructuring had a rate of 63 percent of PTSD and those who received assessment only had a 77 percent rate. Exposure also led to lower levels of depression and anxiety compared to the other conditions. Further research is indicated in this area, however, especially given that other studies show cognitive processing therapy to be at least as useful as exposure therapy in treating posttraumatic stress (Nixon et al., 2016). Overall, this literature suggests CBT approaches can be effective in reducing symptoms and the risk of later PTSD in at least some of those suffering from ASD, and perhaps that the effect is greatest for CBT approaches that incorporate some aspect of exposure. However, there are several ways to engage patients in exposure and it is not clear that all method are equally effective (Larson et al., 2020). For example, there is preliminary support for EMDR protocols adjusted for ASD (e.g., Shapiro & Laub, 2008), although many have small sample sizes limiting their interpretability. Lastly, it should be noted that the strongest studies of CBT for ASD, with the largest samples, have focused largely on survivors of motor vehicle accidents, disasters, and other noninterpersonal traumas. This makes it harder to generalize the results of such studies to the larger clinical environment, since sexual and physical interpersonal traumas are often more common in clinical caseloads than are noninterpersonal events, can cause particularly severe symptoms, and generally lead to higher PTSD rates. INTERVENING IN ACUTE POSTTRAUMATIC STRESS: AN OVERVIEW The literature reviewed earlier, although generally limited to the treatment of screened samples of noninterpersonal trauma survivors in specialty clinics or, in some cases, battleground environments, provides important guidance for clinicians working with the acutely traumatized—both in terms of what one should and should not do. At the same time, these studies are similar to the cognitive-behavioral literature on treating more chronic posttraumatic disturbance, in that they shed less light on the actual conduct of acute trauma therapy as it occurs in (and is constrained by) general clinical practice. The originators of the most effective interventions described in this chapter are highly trained and specialized clinicians who devote much of their time to the study and treatment of acute trauma, often with relatively pure cases of ASD, in the context of relatively academic environments. In contrast, most real-world clinicians do not have such specialized training and often deal with clients who (1) present with multiple old and new traumas and (2) frequently suffer from a broad range of comorbid psychiatric conditions. In other words, the acute trauma survivor presenting to the average community mental health clinic is often someone who has experienced trauma previously, and who has a variety of needs—psychosocial, psychological, and sometimes physical or medical—for whom intervention ideally involves considerable assessment and carefully monitored treatment.

Given this complexity, and issues related to generalizability, the rest of this chapter is based on our clinical experience with acute trauma survivors in community mental health, emergency, and trauma clinic settings, as informed by the existing psychological literature. The suggestions we offer represent an attempt to balance empiricism with practicality. Fortunately, once certain preconditions are met, much of the treatment of acute trauma parallels the intervention approach described in earlier chapters for more chronic posttraumatic reactions. For example, therapy tends to involve the steps of trauma processing outlined previously; that is, exposure, activation, disparity, counterconditioning, and extinction/resolution, as well as other cognitive-behavioral components, such as psychoeducation and anxiety management. However, when the client is an acute trauma survivor, assessment of readiness for treatment is a considerably larger issue, and the process of therapy requires even more attention to the appropriate focus, intensity, and pace of treatment. Immediate Assessment The evaluation of acutely traumatized individuals follows the general principles of assessment as presented in Chapter 3. It is especially important to remember that individual responses to acute trauma can differ dramatically and that there is no single, typical response—some survivors appear to be relatively unaffected, whereas others may have extreme and dramatic responses characterized by anger, tearfulness, erratic behavior, and distress-reduction activities. Even seemingly asymptomatic responses can be deceiving because an expressionless exterior may reflect dissociation, numbing, and significant internal distress, as well as the possibility of later exacerbation. As a result, a common mistake made by evaluators is to assume that all of those who appear to be “in control” or otherwise euthymic soon after a trauma are necessarily coping well. For some in the acute trauma phase, the traumatic event remains ongoing (e.g., displacement postdisaster upon becoming a refugee or chronic interpersonal abuse/violence), necessitating a façade of coping that helps the person to survive and function at a level that might be deceptively high. At the same time, however, the avoidant trauma survivor should not be forced or coerced into treatment, regardless of their inferred needs. High levels of dissociation or cognitive avoidance soon after a trauma may signal overwhelming distress and/or reduced emotional regulation capacities. As noted in other chapters, too much (or sometimes any) exposure to traumatic memory in such cases may overshoot the therapeutic window and retraumatize. In general, in agreement with PFA, we recommend that clinicians let acutely traumatized individuals talk as little or as much as they wish to during the assessment process. Pushing for details about the trauma or encouraging survivors to talk when they are reluctant to do so should be avoided when possible. Obviously, however, certain issues are a critical part of assessment in the acute phase and may require some potentially intrusive questioning. The goal is to find a balance between providing gentle support while eliciting necessary information in a nonthreatening manner. A qualitative analysis by Brand et al. (2018) suggests that five main stressors negatively impact recovery following a severe injury: (1) Trauma-related psychological reactions, (2) relationship

stress, (3) unsatisfactory services and support systems, (4) reduced functioning, and (5) negative thoughts and emotions in relation to recovery. The same study suggested that the three factors most helpful in recovery were positive coping, professional support, and social support. While treatments such as CBT may address some of these concerns, other critical issues must be assessed in order to determine the timing and potential benefit of treatment: Physical safety. Is there injury requiring medical attention? Does the individual have adequate access to shelter, clothing, and food? Does the survivor of rape or domestic violence have a safe place to go where they cannot be found by the perpetrator? Suicidality. Has the acute experience of personal loss, overwhelming shame, betrayal by an attachment figure, massively reduced functioning, or physical disfiguration resulted in suicidal thoughts and impulses? Is there a suicide plan? Are there methods (e.g., pills, knives, guns) easily available? This is particularly pertinent in light of research showing that individuals with acute stress reactions have a much higher rate of completed suicides (10 times higher than those who do not exhibit such reactions; Gradus et al., 2010). This risk is increased by comorbid substance abuse or depressive symptoms, and in individuals with other pertinent risk factors (e.g., adolescents with a history of exposure to interpersonal violence; Zuromski et al., 2019). Homicidality/potential for violence. Has the trauma increased the likelihood of aggressive behavior, that is, in the service of revenge or punishment? Does the survivor have access to a gun or other weapon? Are they making a credible threat? Do they have a history of violent behavior? Psychosis. Has the trauma resulted in psychotic symptoms, or, equally important, was the client psychotic before the trauma? If so, do these symptoms interfere with the client’s access to resources by impairing cognitive capacities and goal directedness? Do the symptoms place the individual at immediate risk for additional harm by impairing their judgment or understanding? Other psychological comorbidity/debilitation. Is the survivor experiencing severe anxiety, depression, or dissociation, such that their ability to behave in an appropriate, goal-directed manner is impaired? Are they overwhelmed or destabilized, by either extreme emotional distress or highly intrusive or debilitating posttraumatic stress symptoms? Is the individual experiencing significant grief/loss as a result of the event (e.g., losing a loved one, pet, or home due to disaster)? Cognitive symptoms. Is there evidence of deficits in attention, memory, and/or executive functioning? While research does not support changes in brain structure as the result of acute psychological trauma (Szabó et al., 2015), neuropsychological deficits have been found in PTSD. Such deficits, for which time of onset posttrauma often is not clear, may include dysregulated frontotemporal brain functioning (LaGarde et al., 2010) and impaired associative memory (Guez et al., 2013). Family or other sources of social support. Research supports the involvement of family members and others in addressing trauma impacts (e.g., Thompson-Hollands et al., 2021; Vranceanu et al., 2020). Are there relational or social resources available to the survivor that they can access in the acute aftermath of the trauma? Are there family members, friends, or support persons the survivor wants involved in their treatment?

Trauma status. Is the trauma over? The clinician may assume that a given adverse event is now in the past and thus is not a continuing threat. Unfortunately, many forms of interpersonal violence are repetitive and ongoing, resulting in both continuing danger to the survivor and survival responses that may make psychotherapy difficult. Immediate assessment questions should include the following:

Does the perpetrator still have physical access to the survivor? Is the survivor emotionally connected to the assailant in a way that will allow the assailant continuing access to them? If the perpetrator was arrested, were they incarcerated? If so, how long will they be imprisoned? Does the perpetrator have access to outside contacts who could still harm the survivor?

Biological assessment: There is growing literature suggesting that neurobiological assessment posttrauma may add to our ability to predict who may be most vulnerable to developing ASD/PTSD, as well as suggesting avenues for treatment. For example, Marin et al. (2019) assessed for ASD symptoms and cortisol awakening response in a sample of psychiatric hospital employees exposed to workplace trauma. They found a higher cortisol awakening response to be protective against the ASD progressing to PTSD over time. Brain imaging may also hold some clues to assessing likelihood of the development of PTSD following a diagnosis of ASD (see, e.g., Cwik et al., 2020). Currently, such biological assessments are likely too costly to be prevalent, and so most clinicians do not have this type of data at their disposal, but this will likely change in the future. Referral. Based on answers to these questions, immediate intervention may or may not be appropriate. When it is indicated, the clinician’s first function may be that of referral agent. If there are signs of significant psychological, medical, or psychosocial difficulties, the clinician will typically act on assessment by triaging to appropriate resources:

Injured or otherwise medically ill trauma survivors should be referred for immediate medical attention or transported to the nearest emergency room. Those needing shelter, clothing, or food should be offered information about social service agencies and/or shelters, and/or relevant caseworkers should be alerted to the clients’ needs. Survivors of rape and domestic violence should be referred to a local emergency room, crisis center, shelter, or appropriate service agency. If necessary, reports should be made to law enforcement, adult protection services, and/or child abuse agencies. Individuals who are psychotic or otherwise impaired by psychiatric symptoms to the extent that they cannot care for themselves, are at risk of harming themselves or others, or have become suicidal, should be referred for psychiatric hospitalization.

To the extent possible, and within the constraints of any confidentiality issues, attempts should be made to contact family and friends who may be able to assist the traumatized individual.

Treatment Although some form of referral is often indicated for symptomatic individuals who have been exposed to acute trauma, the need for formal psychological treatment (as well as the client’s perception of this need) varies from person to person. The reasons for this include the following:

The time frame may not support psychological interventions. The first days, and sometimes weeks, after a traumatic event often involve emotional responses and symptoms that spontaneously resolve after a period of cognitive adjustment and consolidation—a process that can be interrupted or diverted by ill-timed psychological treatment (Bisson, 2003). Although recent research indicates that individuals who meet criteria for ASD likely benefit from intervention within the first 4 weeks to 3-months posttrauma (e.g., DeRoon-Cassini et al., 2019; Giummara et al., 2018; Roberts et al., 2019), further research is still needed to better understand what the ideal time frame is to intervene with symptomatic acute trauma survivors. Given this, working with acute trauma requires careful attention to the survivor’s motivation and readiness for treatment prior to beginning. As noted earlier, a significant number of people who undergo a potentially traumatic event are not, in fact, traumatized by the event; they may experience few if any lasting posttraumatic symptoms and thus typically should not be treated. For survivors of more severe traumas, when physical injury is involved, medical attention takes priority over mental health intervention. However, evaluation and monitoring of acute stress reactions should occur around the same time as medical intervention and, if present, intervention in the first four weeks postinjury may be indicated (DeRoon-Cassini et al., 2019; Giummara et al., 2018; Visser et al., 2017). Beyond medical treatment, adequate shelter, clothing, and food are usually the first priority for survivors of floods, earthquakes, fires, and other disasters (National Institute for Mental Health, 2002). For many survivors of rape or domestic violence, a major concern may be finding a place to stay that is safe from the perpetrator. In such situations, when physical needs and safety are paramount, psychological treatment is often not an immediate focus.

Lessons from 9/11. To restate, in the context of acute trauma, very early treatment may seem out of place, intrusive, or unhelpful to the extent that it distracts from more immediate concerns. After the terrorist attacks of September 11, 2001, for example, anecdotal reports suggested that the services most immediately appreciated by survivors and their families were emotional support, assistance in locating other family members or survivors, concrete advice, referral to social services, emotional encouragement, and, in some cases, the human contact and warmth associated with donuts, coffee, and blankets at the disaster site. In contrast, however, there were

some complaints that clinicians insisted survivors discuss and process traumatic material despite protestations of not needing or wanting clinical intervention. This latter group tended to characterize the effects of such treatment more negatively. As care providers, it is important that we not be too rigidly attached to providing “clinical” services to acutely traumatized individuals—there are times when the most important thing we can offer is basic human contact, emotional support, logistics, and connection with others. In some cases, as was sometimes true in the 9/11 scenario, requests for mental health treatment do not come from the survivor, but, instead, from family members, clergy, relief workers, or medical and rehabilitation staff. Referral for clinical intervention can be critically important when the survivor is unable or unwilling to seek out needed medical or psychological attention on their own. For example, intervention is clearly indicated when the acute survivor is psychotic, suicidal, unwilling to engage with necessary or life-saving medical treatments, or otherwise at risk for immediate harm. In less extreme instances, however, trauma-exposed individuals may experience uninvited referrals and interventions as intrusive and irrelevant to their immediate concerns. Despite these cautions, there is little question that some people are profoundly and immediately affected by traumatic events and that early psychological intervention for such individuals can be helpful. Recent reviews indicate that, as described earlier, mental health interventions delivered within the first 4 weeks after acute trauma are associated with reduced severity of later traumatic stress symptoms and co-occurring disorders. In summary, we suggest that formal psychological treatment for acute stress be considered if the following criteria are met:

Assessment indicates significant psychological impairment or clinical symptomatology directly related to the traumatic event Significant food, shelter, and life-threatening medical issues are not present or are under control The client indicates a desire to receive treatment

This list runs the risk of making things appear more cut-and-dried than they often are, however. Perhaps most significantly, in some cases where early intervention could be helpful given the survivor’s level of impairment, the survivor either denies significant symptoms or actively avoids treatment. As noted at various points in this book, a frequent aspect of posttraumatic response is some form of emotional or behavioral avoidance. The shock and numbing often associated with an overwhelming event may reduce the survivor’s access to (and therefore description of) their internal state. In some cases, the survivor may feel so overwhelmed by negative feelings that they understandably avoid conversations (e.g., symptom disclosure) and activities (e.g., treatment) that might activate the symptoms of ASD. Survivors may feel embarrassed or frightened by their symptoms, or by the trauma itself, and thus may be reluctant to disclose their experiences. Others may consider emotional expression or help-seeking a sign of weakness, and still others may accept social messages that they should “put their past behind them” or “just get over it,” in the hopes that, if suppressed or unacknowledged, trauma symptoms will remit on their own.

Together, these various responses can result in a conundrum for the clinician: The individual appears traumatized, but denies symptoms and rejects offers of treatment. Ultimately, the decision to disclose or to participate in therapy must be the survivor’s alone. It is rarely wise to insist that even obviously symptomatic individuals enter psychological treatment if they do not want to be treated. On the other hand, when faced with such situations (e.g., with a highly symptomatic rape survivor who demands to be left alone or an emotionally distressed police officer who fears stigmatization if they disclose PTSD symptoms or enters therapy), it is entirely appropriate for the clinician to gently discuss with the individual their current symptomatic state, any risks they are facing, the possible benefits of current or future therapy, and possible solutions to any barriers preventing them from seeking treatment. If it is clear that the survivor is unwilling to engage in treatment, it is usually best not to push further. Instead, the clinician may consider one or more of the following:

Offer information—either verbally or in written form—that describes possible longer- term effects of trauma exposure and outlines ways to receive help in the future, including referrals to community support groups. Make a follow-up appointment for the survivor a month after the current contact, noted on a written appointment slip. With the survivor’s permission, arrange for at least one follow-up phone call from the clinician “just to see how things are going.” With the person’s permission and signed release form, meet with one or more significant others (e.g., a partner or family members) to discuss the survivor’s situation and the future availability of clinical services. Ideally, this is done with the survivor present—in which case release forms may or may not be necessary. Refer the survivor to a prescribing practitioner for evaluation for possible medication. Some individuals, while concerned about possible stigma associated with psychotherapy, may be willing to consider medication to help with distressing symptoms (e.g., sleep disturbance) and may see such intervention as less pathologizing. Medication management, while not affording client the opportunity to fully process trauma, may provide empathic support as well as a safe environment in which to express concerns. It may also open the door to the possibility of future psychological treatment.

In some cases, survivors respond to these additional prompts or supports by eventually requesting psychological assistance, albeit sometimes well after the fact. For example, the individual may keep a flyer or appointment slip “just in case”—and then refer to it when symptoms increase or fail to remit. In other instances, it may be years before the trauma survivor seeks mental health services, if at all. Even in these cases, however, the clinician’s demeanor, helpfulness, and initial information at the time of the trauma may be remembered and may influence later decisions to seek help. CENTRAL COMPONENTS OF TREATMENT FOR ACUTE TRAUMA

Once it has been determined that treatment is both indicated and desired by the client, therapy generally proceeds as described in previous chapters. However, because acutely traumatized individuals are sometimes easily overwhelmed, and may rely to a greater extent on avoidance defenses, treatment must be provided with considerable attention to the principles outlined in this book, especially vis-à-vis the therapeutic window. Following are a series of treatment components often found in effective interventions for acute trauma. Balanced Emotional Support and Compassion As noted earlier, individuals acutely overwhelmed by traumatic events often have significant, immediate needs for human contact, support, and compassion. This need is often so strong that the less responsive clinician may be seen as uncaring or unapproachable, thereby potentially reducing their effectiveness. We suggest that the first moments of interaction with an acute trauma survivor be directed toward making empathic contact and communicating caring. This does not mean that the therapist should be so sympathetic that their attentions suggest pity or pathology, nor should expressions of concern be intrusive. The goal should be to respond in a manner that communicates appreciation of the client’s traumatic situation, provides emotional acceptance and warmth, and yet remains professional and noninvasive. Survivors often remember such caring, professional helper responses, whether in the emergency room or at a disaster site, well into the future. Active Relatedness In classic psychotherapy, the clinician sometimes works to communicate therapeutic neutrality and may respond to client disclosures in a relatively reflective, nondirective manner. In contrast, therapy for trauma survivors, perhaps especially those acutely exposed to traumatic events, is often more active and directly interactive with the client. To paraphrase Herman (1992b), there is rarely a place for therapeutic neutrality in work with survivors of violence or, we suggest, others exposed to major trauma. The potentially overwhelming quality of some acute posttraumatic presentations may require that the therapist provide concrete advice, make direct referrals, and act as a strong relational figure—someone the client can temporarily rely upon. Importantly, active relatedness is typically a shorter-term response to the disorganizing and destabilizing effects of acute trauma exposure. As the client’s immediate needs for structure, access to resources, and therapeutic guidance wanes, so too should the therapist’s directiveness. Greater Than Usual Accessibility In more traditional, less emergent mental health contexts, contact boundaries are often negotiated between the client and therapist, typically limiting when the client may call or otherwise access the therapist. Such understandings discourage excessive dependency and allow the therapist to have uninterrupted periods of time when they are not “on duty.” In acute trauma situations, however, the client may experience crises and/or intermittent episodes of overwhelming distress or grief that require more frequent contact. For this reason, professional assistance should be available to the acute trauma survivor whenever necessary in the days, weeks, and early months following the trauma. In addition to providing the client with phone numbers for emergency rooms, crisis centers, or on-call or back-up clinicians, the emergency/trauma clinician should consider allowing more phone calls or impromptu sessions (ideally during normal work hours)

than would be the case in regular psychotherapy. Of course, it is almost never appropriate for even acute trauma clinicians to be available on a 24-hour basis. If the acute trauma survivor appears to require many mental health contacts within a short period of time, more intensive intervention (e.g., psychiatric hospitalization) should be considered. Case Work and Advocacy As described earlier in this chapter, many acute trauma survivors require medical, social, legal, and other nonpsychological services above and beyond psychological treatment. The logistics inherent in accessing these additional services and resources are often daunting for the recently traumatized person. For example, in the context of loss, posttraumatic stress, and acute dysphoria, the client may have difficulty arranging for clinic appointments, locating appropriate social services (e.g., disaster relief or crime survivor support), housing or economic assistance, insurance personnel, or help with legal issues when law enforcement is (or should be) involved. Although assisting the client in such areas may seem to be beyond the therapist’s job description, it is often difficult to separate case work issues from psychotherapeutic ones when the client’s immediate world has been disrupted (e.g., Young et al., 1998). In such situations, the clinician may need to call or write to governmental, legal, or other agencies to advocate for the client, resolve issues, or cut through red tape that the client could not resolve on their own. Social Connection The psychological effects of trauma include isolation and social disconnection—the survivor may feel that they have undergone experiences that cannot be fully understood or appreciated by others. In disasters and other mass trauma phenomena, there also may be actual disconnection— during the chaos and confusion of acute traumatic events, survivors may be separated from other survivors, families, and friends, and helpers may not be able to reach all survivors quickly or may themselves be affected by the event (Hobfoll et al., 1995; Orner et al., 2006). Additionally, social isolation and lack of perceived social support are associated with the development and maintenance of ASD and later PTSD (Ozer et al., 2008; Visser et al., 2017), whereas social support is a protective factor against the development and persistence of PTSD (Brewin et al., 2000). For these reasons, intervention in acute trauma often includes reconnecting survivors with relational resources (e.g., helping survivors locate and establish contact with family members) and broad sources of social support (e.g., involving clergy, when appropriate, or facilitating access to community resources and groups). In many cases, in fact, increasing social support and mobilizing community resources may be more immediately beneficial to the acute trauma survivor than classic psychological interventions (Orner et al., 2006). Positive social support is a protective factor while relationship stress is a risk factor for development of PTSD. Once the acute trauma survivor is reconnected with social supports, it may be helpful to talk with the survivor, and their support members if they are willing, about any relationship dynamics that appear to hinder recovery. For example, encouraging open and validating communication about experiences posttrauma, rather than constraining conversation to nontrauma topics, may promote natural processing for the survivor, decrease avoidant-coping, and increase positive support (Belsher et al., 2012). Depending on the survivor’s comfort with others’ involvement, this may range from meeting with support members a few times to provide psychoeducation about the nature of acute stress, avoidance, and ways others can promote

natural processing for the survivor, to regular dyadic interventions targeting acute stress and relational support. Recent research supports the potential benefit of including social supports in trauma recovery. Thompson-Hollands and colleagues (2021), for example, tested a brief support member intervention for patients in individual trauma-focused treatment for PTSD and found reduced treatment dropout. Similarly, Brunet and colleagues (2013) and Vranceanu and colleagues (2020) tested intervention protocols that incorporated support members in treatment and reported overall improved psychological outcomes for both the acute trauma survivor and support member. Some survivors’ support persons may have their own strong reactions to their loved one’s suffering, or the history of their relationship may be complex. Yet, other than in instances where such individuals have been abusive or violent, it may be helpful to at least briefly address these issues so that the survivor’s support system can be as helpful as possible. Psychoeducation Most clinicians and researchers view psychoeducation as a critical aspect of treatment for acute trauma survivors. The acutely traumatized client should be provided with information regarding self-care including, when possible, counseling against excessive behavioral avoidance of trauma cues, such as entirely secluding oneself to avoid triggered memories of recent interpersonal violence, or attempting to avoid all conversations, thoughts, or reminders of a traumatic event. Similarly, the excessive use of alcohol or recreational drugs should be discouraged in the first weeks or months after a major trauma, since substance abuse may interfere with trauma processing and reduce inhibitions that otherwise would impede self-destructive behaviors, suicidality, or danger to others. The general message, in this regard, is that excessive avoidance of trauma triggers and memories, although entirely understandable, potentially interferes with psychological recovery by undercutting the normal process of exposure, activation, and processing. In some cases, such advice supports a form of in vivo desensitization. For example, a recent survivor of a motor vehicle accident who drives only when absolutely necessary might be encouraged to drive more often, or to try driving progressively closer to the area where the accident occurred. Similarly, a self-secluding female rape survivor might be asked to consider walking to the local store with a woman friend or, if possible, attending an activity (with a friend) where men are present but interaction with them is limited. In such instances, the clinician ideally does more than advise—they explain the underlying reasons for such advice. In our experience, clients who are advised that they should, in a sense, avoid avoidance are considerably more likely to try to do so if they understand the underlying rationale for such advice. As described in Chapter 5, the client is typically informed of the range of symptoms and problems that may follow acute exposure to traumatic events. This often includes the major symptoms of ASD and PTSD, as well as other cognitive or behavioral responses that seem relevant to the client’s specific situation. By definition, those appropriate for trauma therapy are generally symptomatic, although not all will experience the entire range of posttraumatic disturbance. Nevertheless, gentle, nonalarming education about possible posttraumatic outcomes

can serve to validate and normalize what the client is already experiencing, so that they are less likely to feel stigmatized or mentally disordered. Finally, the survivor may benefit from information on how to identify potentially triggering situations and stimuli so that they can avoid excessive activation when it is problematic. As noted in Chapter 6, the benefit of this information is that the easily overwhelmed client may feel a greater sense of control to the extent that they are able to predict, contextualize, and even sometimes reduce intrusive flashbacks and trauma-related emotional flooding. Attention to the Therapeutic Window Although the relative balance between the effects of trauma memory activation and the client’s level of self-capacity must be attended to in all trauma work, this issue may be especially relevant to treating acute trauma survivors. Because such individuals are often in the midst of major, intrusive posttraumatic symptoms and equally powerful dysphoric states, it may be relatively easy to overshoot the therapeutic window by intervening too quickly or too evocatively. This is probably the most common error made by clinicians working with the acutely traumatized—beginning formal treatment too early and/or providing too much memory exposure and activation with a client who is acutely dysregulated and who has not yet had a chance to consolidate their psychological resources. Because the therapeutic window may initially be quite “small” in such cases, the clinician must approach trauma processing carefully, and only attempt significant exposure activities when it is clear that the client has sufficient internal stability. In many cases, in fact, the various interventions outlined earlier in this chapter and elsewhere (e.g., emotional support, case work, increasing positive social support, psychoeducation, and, in some instances, strengthening self-capacities) may be required before extensive memory processing is considered. This is not to say that therapeutic exposure is contraindicated in work with acute trauma survivors—recent research clearly indicates that it can be quite helpful when appropriate. Instead, the relevant issues are how soon and how intense. Although careful therapeutic exposure soon after a trauma might be most efficient for those acute survivors who can tolerate it, more often the best approach is to assess for emotional stability and then to provide titrated exposure only when indicated, only when the client is ready, and with careful attention to the therapeutic window. Duration of Treatment A final issue that may discriminate treatment of acute traumatic stress from treatment of more chronic posttraumatic states is that of therapy duration. In some cases, survivors of multiple traumatic events that have occurred over a number of years may require extended therapy before they show major and sustained clinical improvement. In contrast, some acute stress survivors respond to a considerably shorter treatment period. For example, Bryant and Harvey (2000) and Ehlers et al. (2003) describe empirically validated cognitive-behavioral treatments for ASD that range from 5 to 12 sessions and Giummara et al., (2018) describe treatments within the first 3 months posttraumatic injury that range from 1 to 12 sessions. Although brief therapy may not always be appropriate, for example when treating acute survivors who have undergone especially invasive or horrific experiences like torture, severe

burns, or war atrocities, have substantial comorbidity, or have a history of unresolved prior traumas, the success of these clinical researchers underscores an important point: Many acutely traumatized individuals do not require extended treatment. As noted earlier, the reasons for this are several. First, many acute trauma responses will resolve, to some extent, on their own—the role of therapy in such cases may be to provide more rapid and/or complete recovery. In contrast, PTSD and other posttraumatic conditions are often more chronic, and thus represent more severe and treatment-resistant phenomena. Second, although chronic posttraumatic stress is associated with multiple risk factors (e.g., inadequate emotional regulation, excessive avoidance), this may not always be the case for some instances of acute trauma. Finally, it is possible, although not yet entirely proven, that early, successful intervention “catches” posttraumatic symptoms before they have a chance to generalize and elaborate over time, and thus less comprehensive intervention is required. Ultimately, as is true for all trauma therapy, the extent of treatment required to resolve a given instance of acute stress should not be determined by the clinician’s preexisting assumptions or by what kind of therapy they habitually provide. In many cases, a positive outcome may result from less treatment than otherwise might be anticipated. SPECIAL ISSUE: TRAUMA WORK IN ACUTE MEDICAL CONTEXTS Emergency Rooms The first stop for many individuals, post-acute trauma, is the emergency room (ER). Although the primary focus of the ER visit is stabilization of critical illness or injury, the ER is also where some survivors will begin to experience psychological effects. Approximately 6 to 37 percent of survivors of traumatic injury develop ASD within (by definition) the first weeks (Love & Zatzick, 2014; Thombs et al., 2005; Visser et al., 2017) and those numbers increase for survivors of interpersonal violence (Ophuis et al., 2018). Further, research suggests that posttraumatic distress present at hospital discharge is often stable at up to 1- and 2-years posthospitalization (McKibbon et al., 2008). Beyond their psychological impacts, ASD and PTSD have deleterious impacts on physical prognosis and health-related quality of life in patients requiring hospitalization. Given these numbers, the American College of Surgeons Committee on Trauma strongly recommend that screening for ASD and PTSD occur in emergency rooms and Level I and II trauma centers and recommend a minimum of brief self-report measures and referrals for outpatient mental healthcare (see DeRoon-Cassini et al., 2019 for a review of screening instruments). However, there are several challenges to implementing assessment and intervention for ASD in emergency rooms. As of 2014, for example, only 7 percent of Level I and Level II trauma centers were screening for PTSD (Love & Zatzick, 2014). ERs are, on the whole, ill- equipped to identify and provide early intervention for individuals suffering from the initial symptoms of an acute stress response. This is not necessarily due to poor organization—in fact, the ER’s focus on prioritizing and triaging for appropriate treatment is ideal for such a task. The challenge appears to be more related to lack of time, lack of mental health trained personnel, difficulty identifying early symptoms of traumatic stress, and a lack of validated pragmatic interventions (e.g., Zatzick et al., 2021).

Despite these challenges, early screening and intervention is important and the emergency room provides a unique opportunity to identify patients that otherwise would miss being connected to mental health services. An ideal approach to this issue is for ERs to be staffed with onsite mental health professionals who can take on the role of identifying patients who may benefit from early intervention for symptoms of acute stress. Additionally, collaborative care interventions or training of non-mental health staff in ASD and PTSD assessment and intervention would likely be useful in administering brief interventions, although further research on pragmatic assessment and intervention is needed (Zatzick et al., 2021; Brunet et al., 2013). Numerous studies of the trauma response have been conducted in ERs and provide valuable information as to strategies to detect early risk factors of ASD and/or PTSD. For example, in a sample of 53 accident survivors, lower levels of salivary cortisol and lower diastolic blood pressure, along with past emotional problems, and greater dissociation predicted PTSD symptoms 6 months after the ER visit (Ehring et al., 2008). Elevated heart rate in the ER has also been found to predict ASD and PTSD symptoms 6 months posttrauma (Kuhn et al., 2006). A review of studies examining PTSD in trauma patients who encountered the emergency department found that being female, younger in age, having financial problems or low income, reduced cognitive functioning, pain, lower social support, hyperarousal, persistent dissociation, and an ASD diagnosis were linked with later PTSD (Visser et al., 2017). Although the average ER is unlikely to be able to test for acute cortisol levels, it may be helpful to integrate heart rate and blood pressure data into bedside trauma assessments. Similarly, routine assessment and monitoring of pain level, dysphoria, traumatic stress, and support systems can assist the clinician in assessing the risk of current or impending ASD. Should an ER patient be transferred to the intensive care unit (ICU), their chance of developing ASD and later PTSD appears to increase. The literature describes widely varying prevalence rates of PTSD (from 5 percent to 63 percent) in ICU patients, though it is likely that the higher rates are overestimates (Jackson et al., 2007). The ICU, itself, independent of demographic factors, premorbid mental health status, and injury characteristics, may contribute significantly to the development of ASD or PTSD (O’Donnell et al., 2010; Righy et al., 2019)—lighting, noises, the sounds of others’ suffering, high ratio of medical staff, and high potential for invasive procedures may be directly traumatic. As suggested by those studies reviewed in this chapter, early psychological interventions in the ICU may decrease the likelihood of later stress disorders. Peris and colleagues (2011), for example, found that ICU patients receiving early clinical psychologist support demonstrated significantly lower risk for PTSD as compared to a control group (21 percent vs. 57 percent). Treatment In general, interventions for trauma survivors in the ER are similar to what has been discussed in this chapter for acute stress, albeit adjusted for the medical emergency context. Often, this will involve the following:

A gentle, supportive, and empathic clinical approach, wherein the patient is treated with dignity and compassion

Limiting the number of team members who ask the patient to describe the traumatic event preceding hospitalization to only essential personnel, and advising the rest of the care team to follow the patient’s lead as to whether they wish to discuss the precipitating event A professional clinical demeanor that does not appear frightened, repulsed, or pitying in the face of what may be very severe physical injuries, burns, blood, significant disfigurement, or the possibility of impending death Collaborative care with the treating team, including potentially advocating for pain management and offering CBT interventions for pain if the patient is willing. Reassurance and optimism, without falsely promising unrealistic recovery Psychoeducation, including—if possible and appropriate—a description and likely timeline of future medical procedures as well as any appropriate information about the patient’s specific injuries, illness, and/or disabilities Cognitive interventions (as adapted from Chapter 7), when indicated, to address guilt, shame, self-blame, or an overly catastrophized view of the immediate future Nonoverwhelming and appropriately timed opportunities for trauma processing, when desired or initiated by the patient, such as titrated descriptions of the traumatic event and the circumstances surrounding it Intervention with family members and significant others in order to increase their capacities for support of the trauma survivor—including psychoeducation, discussions of any inappropriate blaming of the patient, and opportunities to process the trauma themselves so that they will not respond to the patient in alarming or unhelpful ways Appropriate referrals for the patient following discharge from the hospital, potentially including outpatient individual and family/couples’ psychotherapy, support groups, and linkage to social services

Burn Units According to the American Burn Association (2016), approximately 486,000 people per year receive some form of medical intervention for a burn injury, and about 10 percent of these people require hospitalization. Burns recovery often requires weeks or more of hospitalization and several months or more of rehabilitation, often characterized by painful procedures and therapies. As medicine has evolved, the survival rate from severe burns has also increased. Currently, the survival rate for burn injuries is 97 percent. With increased immediate survival, the focus of burn care has shifted to long-term morbidity, disability, and health-related quality of life in survivors (Weichman et al., 2020). The medical and psychosocial needs of burn patients can be extensive. As noted in Chapter 1, survivors of burn injuries face a multitude of challenges, beginning with pain management and

wound treatment (often surgical in nature, e.g., debridement, skin grafts, and, in some cases, amputations), and continuing through a lengthy recovery and rehabilitation process which may include physical and occupational therapy, therapeutic exercise, psychological interventions with the patient and family, medical devices such as pressure garments and prosthetics, and vocational counseling. The most common psychological symptoms exhibited by burn-injured patients are posttraumatic stress and depression (Logsetty et al., 2016). In general, PTSD is thought to affect approximately one third of both the civilian and military burn patient populations (McGhee et al., 2009), although prevalence rates vary from study to study. Several studies of burn patients suggest a clear connection between ASD and not only later PTSD (McKibben et al., 2008), but also poorer physical functioning and health-related quality of life postburn. Further, untreated early symptoms of traumatic stress are unlikely to remit for up to two years postburn (McKibbon et al., 2008), reinforcing the need for early intervention with those who exhibit acute symptoms of posttraumatic stress. Clinical research has identified a variety of risk factors for the development and maintenance of trauma-related symptoms in burn patients. These include the early manifestation of certain symptoms, as described more generally in this chapter, including peritraumatic dissociation and acute stress symptoms (Davydow et al., 2009), as well as a prior psychiatric disorders, substance abuse history, premorbid personality factors (especially high neuroticism), burn injury characteristics (such as visibility of burn injury, disfigurement, or percentage of total body surface area burned), anxiety related to pain, avoidant coping, and blaming others for the injury (Jeschke et al., 2020; Jones & Ollendick, 2005; Spronk et al., 2018). Treatment Although medical and mental health care providers cannot change the circumstances of the burn injury, they may be able to address aspects of the treatment experience that can contribute to trauma-related symptoms (Davydow et al., 2009). Inadequate pain management is a major contributor to trauma-related symptoms in burn patients, leading them to feel vulnerable and without adequate emotional resources to manage other aspects of their recovery (Tengvall et al., 2010). The extent of negative care experiences during burn-related hospitalization (e.g., feelings of uncertainty or powerlessness, fear, and neglect of needs) is associated with more symptoms of PTSD (Wikehlt et al., 2008). It follows, then, that interventions geared toward information sharing and education regarding patients’ injuries and prognosis, improving patients’ sense of safety and control, and helping patients to consider the possibility of acceptance, as described in previous chapters, may reduce trauma-related symptoms. The negative psychosocial and functional impacts of burns is clear and there is a plethora of literature noting that earlier intervention is better for traumatic distress in those hospitalized with burns. However, there are fewer empirically supported treatments targeting distress for burn inpatients. Since the previous edition of this book, only one psychological intervention study for adult burn patients has been published. Fauerbach et al. (2020) conducted a feasibility study of a four-session, individualized, secondary prevention protocol for ASD/PTSD and major depression in adult inpatient burns. This intervention was exposure-based and incorporated anxiety

management training, imaginal exposure, and cognitive restructuring of safety and meaning schema. They found reductions in posttraumatic stress and depression symptoms in the intervention group, compared to nondirective supportive therapy group control. However, they noted significant difficulties associated with recruitment and retention in light of the complexity of burns patients’ medical and physical recovery. Further research is needed to understand how ASD and PTSD may be most effectively and feasibly assessed and treated during hospitalization for burns. It may be important to draw from the larger traumatic injury research that shows promising impacts for stepped collaborative care models (Giummara et al., 2018; Zatzick et al., 2021). As with ASD in other contexts, active processing of the burn-related event before the patient is able to stabilize and self-soothe may produce poor or even harmful results (Fauerbach et al., 2009). However, in many cases, carefully titrated exposure to burn-related memories, per the therapeutic window described in Chapter 8 and by Briere and Semple (2013) may be helpful as soon as desired by the patient. Mental health providers who work with burn patients should be aware of the complex issues burn patients confront during the recovery and rehabilitation process, any or all of which may be addressed in psychological treatment—including grief, loss, pain, role changes, disfigurement, reduced functioning, social stigma, financial concerns, legal issues, difficulty returning to work, and overall diminished quality of life (Davydow et al., 2009; Difede et al., 2009). The issue of disfigurement is especially prominent for many acutely burned patients (Martin et al., 2017; McAleavey et al., 2018). People who have serious facial burns, or severe burns to other visible areas of the body such as the hands, as well as those whose burns resulted in amputation of a limb, may suffer considerable distress associated with stigma and the negative reactions of others, real or presumed. Those with severe facial scarring, reconstructed facial features, or hand burns may have the experience of witnessing repulsion, or at least gaze aversion, by others, which can engender shame, embarrassment, or even, occasionally, self-hatred in the burn survivor. This is experience may be exacerbated by the inability to conceal facial and hand burns. In many cases, intervention in this area involve helping the client to accept themselves as they are, despite a radically changed appearance. Although easier said than done, it may be helpful to support the survivor in developing a model of self-esteem more focused on resilience, internal qualities (e.g., intelligence, humor, caring, or wisdom), and/or relationships with people who are (or eventually become) less affected by superficial appearance, such as invested family members, friends, or other loved ones. Additionally, it is important to monitor the survivor’s avoidance of social interactions outside the home, and to apply the principles of emotional processing, previously discussed, to increase social interactions and reintegration to life outside the home. Given that social isolation is a risk factor for ASD and PTSD, helping the survivor to address barriers to social reintegration may facilitate posttraumatic growth (Martin et al., 2017). It is our experience that some clinicians, despite themselves, may reflexively reject the idea that badly burned and disfigured people can make a reasonable adjustment to life and even may have a chance of lasting happiness. Yet we have seen this outcome on many occasions. Although typically not quantified in the scientific literature, the ongoing psychological survival of severely burned people appears to be a testament to the capacity of humans to successfully integrate

extremely traumatic events when conditions are right. For this reason, it is very important that the clinician not give up on individuals whose physical appearance or medical circumstances seem insurmountable; acceptance, accommodation, and even growth are entirely possible for many physically disfigured or very injured clients, whose recovery might otherwise be limited by therapist or institutional countertransference. Beyond acute psychological interventions, posthospitalization follow-up or referral is especially important for the burn survivor. Burn patients who do not receive treatment for ASD and/or PTSD symptoms are more likely to struggle with physical and psychosocial functioning following discharge from the hospital (Corry et al., 2010). Many burn patients benefit from ongoing psychological interventions after hospital discharge, such as peer support groups and regular follow-up visits, since their return to society is likely to be marked by new challenges (see a review by Won et al., 2021). Importantly, the families of burn patients may also gain from intervention, both in the early stages of their loved one’s injury as well as postdischarge. This may be particularly salient for parents of younger burn survivors, who may be struggling with ASD/PTSD symptoms themselves (Hall et al., 2006). Chapter 13

REMOTE TREATMENT OF TRAUMA: TELETHERAPY PRINCIPLES

The era of COVID-19 and its variants—as well as the likelihood that there will be other pandemics in the future—has significantly increased clinicians’ interest in and use of teletherapeutic interventions. Typically involving smart phones, video tablets, and computers, teletherapy allows clients and therapists to interact without the risk of disease transmission. Clinicians have recently adapted teletherapy principles to the treatment of trauma survivors, some of whom have additional needs and concerns relevant to this modality. A variety of studies indicate that teletherapeutic interventions are about as effective as in-person therapy, both generally and for trauma-exposed populations (e.g., Turgoose et al., 2017; Varker et al., 2019). However, specific adaptations for teletherapy in the era of COVID are not yet common, especially for trauma clients. Presented below are references to platforms, websites, and written resources on teletherapy for mental health practitioners, followed by a list of principles for remote trauma treatment. Although this chapter is most relevant to psychotherapy during COVID and other pandemics, it can be adapted when the issue is not safety from infection but when teletherapy is indicated for nonmedical reasons—for example for trauma survivors in geographically remote or logistically challenging environments. It is also helpful for those who otherwise might forgo psychotherapy based on social avoidance or fear of stigmatization. The U.S. Veterans’ Administration, for example, has conducted versions of teletherapy since the Vietnam war and has found it useful for, among others, those in rural environments and those who eschew in-person mental health contacts (e.g., Kruse et al., 2018; Turgoose et al., 2018). ACCEPTABLE TELETHERAPY PLATFORMS

Once teletherapy is chosen as the appropriate modality, the next question is what platform or program to employ. An important concern in this regard is whether confidentiality and privacy can be assured, especially whether the platform is compliant with the Health Insurance Portability and Accountability Act (HIPAA) of 1996, which protects sensitive patient health care information from being disclosed without the patient’s consent (https://www.cdc.gov/phlp/publications/topic/hipaa.html). Currently, common HIPAA-compliant (or HIPAA configurable) telehealth platforms include, but are not limited to

Zoom (https://zoom.us) or Zoom for Healthcare (https://zoom.us/healthcare) Doxy.me (https://doxy.me) WebEx (https://www.webex.com) Thera Nest (https://theranest.com) Simple Practice (https://simplepractice.com) Thera-LINK (https://www.thera-link.com) Microsoft Teams (https://www.microsoft.com/en-us/microsoft-teams) Updox (https://www.updox.com/) VSee (https://www.updox.com) Google Meet (https://meet.google.com)

Note that this list does not include FaceTime, Skype, or Facebook Messenger, which were not HIPAA compliant at the time of this writing. However, these platforms are included in an emergency notice by the U.S. Department of Health & Human Services (HHS; 2021) (https://www.hhs.gov/hipaa/for-professionals/special-topics/emergency- preparedness/notification-enforcement-discretion-telehealth/index.html), allowing their use “during the COVID-19 nationwide public health emergency.” HHS notes, however, that “providers are encouraged to notify patients that these third-party applications potentially introduce privacy risks, and providers should enable all available encryption and privacy modes when using such applications.” Because this exemption expired on August 9, 2023, the reader should investigate the HIPAA acceptability of any teletherapy platform they consider using and determine what policies are currently in effect. TELETHERAPY GUIDANCE FOR MAJOR PROFESSIONAL GROUPS A number of professional groups have issued guidelines or advisories on the use of teletherapy by their members. Although similar to one another in some ways, each group has recommendations or requirements specific to their mental health specialty. The most common of these are the following: For psychologists—https://www.apa.org/practice/guidelines/telepsychology; https://www.apa.org/topics/covid-19 For social workers—https://www.socialworkers.org/About/Legal/HIPAA-Help-For-Social- Workers/Telemental-Health For therapists and counselors—https://amftrb.org/wp-content/uploads/2017/05/Proposed- Teletherapy-Guidelines-DRAFT-as-of-09.12.16.pdf

For psychiatrists— https://www.psychiatry.org/psychiatrists/practice/telepsychiatry/toolkit/practice-guidelines ARTICLES AND GUIDES ON TELETHERAPY PRACTICE We recommend the following sources for detailed information and guidance on how to implement teletherapy in different contexts and situations, including pandemics: Briere et al., 2020; Moring et al., 2020; and Stewart et al., 2017. TELETHERAPY PRINCIPLES Self-Care As noted, teletherapy provides certain benefits to the clinician in terms of reducing fear of infection or of spreading diseases to family members and others, as well as eliminating the need for travel to the clinic or therapy office. At the same time, delivering teleservices during a pandemic can be stressful for the therapist, both because social distancing and isolation can have significant effects, and because teletherapy, itself, can be challenging and often requires new skills. Often, providing remote treatment from home during a pandemic means addressing new problems and issues, including, in some cases, the following:

Having to provide childcare and educational activities for children unable to attend school The almost unavoidable likelihood of revealing aspects of one’s appearance or home environment when working via video platforms Potential exposure to the client’s environment, for example hearing angry or intoxicated voices or seeing or hearing verbal/physical altercations in the background Technological challenges associated with teletherapy, including setting up video cameras, installing and configuring teletherapy platforms The relative absence of support, consultation, supervision, and collegial interactions often available in face-to-face clinic environments

Teletherapists report a number of strategies to reduce stress and increase self-care during the COVID-19 crisis. Differentiating Home and Office Environments and Activities Most guidance and clinical feedback stress the importance of explicitly separating one’s work and home environments so that there is less leakage between one’s personal and professional life, which many people report is distracting and sometimes stressful. Based on clinical experience, suggestions by therapists, and a review of published materials in this area, we suggest that the clinician

Create, when possible, a home working space that is physically separate from their living space. This may involve, for some, a separate home office, whereas for others it may be a

private corner of a room where teletherapy equipment can be placed and privacy is possible. Formally delineate a regular schedule and routine for each workday, with work starting and ending at approximately the same times as they would in nonteletherapy contexts. This also means that, when possible, the therapist does not schedule anything but emergency sessions outside normal worktimes. Basically, using teletherapy should not mean that one works outside normal hours, thereby insuring that protected downtime is possible. Changing one’s clothes before and after work hours, that is, dressing for work as normally would be the case, and changing into “home” clothes once the workday is done. Although this recommendation might seem excessive, clinicians report that the clothes one wears helps signal the role one is inhabiting, whether at work or leisure. As well, clients appear to appreciate that their therapists continue to maintain a professional appearance despite the other changes they are likely experiencing. If children or adolescents are in the home, ensuring breaks from caretaking responsibilities while working. Generally, this means either delegating childcare to other adults in the home, or, when possible, arranging for daycare or babysitting with pandemic-protections in place.

Establishing Clear Boundaries Between Sessions Just as explicit work and nonwork boundaries decrease the stress of inadvertent overlap, it is suggested that the clinician intentionally take 10 to 15-minute breaks between sessions, to reset their focus and attention for the next session. In many cases, this may mean 45- to 50-minute sessions with 10- to 15-minute breaks in between. The clinician should be mindful of any tendency to let sessions run longer than usual and use up this downtime. During these brief breaks, the therapist may choose to take a short walk around the house or immediate neighborhood; engage in a brief mindfulness, stretching, or relaxation exercise; play with pets, or—ideally if it can be done without prematurely reentering the parent–caretaker role during work--checking-in with children, partners, or others. Although the clinician may need to write therapy notes during some of this time, we recommend that they be limited to short references to the most important aspects of the session, which can then be formally completed at times during the day when there are not back-to-back appointments. Regarding this last point, clinicians often note that back-to-back teletherapy sessions should be avoided, when possible, since they can contribute to “Zoom overload” and reduced time to recover before the next session begins. Reducing “Zoom Fatigue” Research (e.g., Fauville et al., 2021; Lee, 2020) supports clinician reports that regular, extended use of remote platforms can be stressful and create fatigue beyond whatever effects accrue from regular in-person sessions. For this reason, it is recommended that teletherapists take up (or

devote more time to) some form of regular contemplative or destressing activity during nonworking times in their daily life. This may include daily yoga, meditation, prayer, or mindfulness exercises, and use of phone apps such as CALM (www.calm.com) or Headspace (www.headspace.com). Other options listed by those surveyed are in Briere et al. (2020):

Going outside several times a day, whether on walks or hikes or simply sitting in one’s backyard or public park spaces breathing the air and appreciating nature Beginning a new hobby or extracurricular activity Reading books (but limiting one’s exposure to news media) Creative pursuits such as cooking, gardening, writing, playing a musical instrument, or an art activity Regular exercise, whether jogging, walking, dancing, recreational activities, or bicycling Journaling If desired, attendance in one’s own therapy or support group

Also recommended during pandemics are intentional, regular contacts with others, whether by phone, video chats, or in in-person meetings if not constrained by pandemic restrictions. This ideally involves frequent conversations with family and friends, but also includes professional debriefing times with colleagues, consultants, or supervisors on a regular basis. Clinicians also suggest that therapists stay engaged in their professional environments by attending virtual professional activities, such as grand rounds, clinical meetings, webinars, conferences, or networking workshops and trainings. Focus on Client Safety As noted throughout this book, effective trauma therapy requires that, to the extent possible, the client feel safe during the psychotherapy session. Physical safety may be relatively easy to insure when the client is seen in the clinician’s office. This may be less true in teletherapy contexts. The client is often at home, where there may be dangers ranging from ongoing abuse by family members to community violence. COVID-related factors may increase the likelihood of danger by isolating people in their living spaces, where domestic violence may be ongoing, social and financial challenges may increase family stress, substance abuse may be more prevalent, and police or other authority response times may be lengthened by pandemic-related issues. Unfortunately, at the very time that these factors are potentially present, the clinician’s ability to assess and intervene in client danger is reduced by their physical distance and the limiting aspects of interacting through electronic media. Finally, the actual teletherapy process may be affected by a lack of client privacy associated with crowded home conditions and potentially lessened interpersonal boundaries. Some clients, of course, are safer than others. People who live in stable, supportive home environments may not require as much therapist attention to safety, whereas the unhoused person receiving teletherapy in a shelter or the home-bound victim of ongoing partner conflict or violence will need more focus on safety issues. Even this dichotomy may be overly simplistic, however. Some clients may appear to be in a safe living environment when, in fact, there is undisclosed danger from sexual or physical abuse. For this reason, we recommend that safety not be assumed in any case, and that it be reassessed whenever necessary.

Logistics One of the first requirements of trauma-focused teletherapy involves joint decisions about when and where therapy is to take place. Timing should reflect not only when the clinician is available, but also when the client is most able to engage in regularly scheduled sessions. The optimal location for sessions should also be agreed upon beforehand—generally the safest, most private place in the client’s environment, for example, a bedroom or another room where the door can be closed and the client can be alone. Some clients in crowded or nonsafe environments may choose to use a parked car, a bathroom, a laundry room, or a safe outdoor space. In other cases, when family members or others are nondangerous and supportive, there may be an arrangement between the client and others that there will be specific, scheduled times when they need privacy, or that specific actions signal their need to be alone, such as going into the bedroom and closing the door, draping a dishcloth on a doorknob, or even hanging a sign to indicate that therapy is about to begin. Assessment and Communication Around Immediate Danger Although it may seem redundant or even unnecessary in some circumstances, clients for whom potential danger has been previously identified should be asked about their immediate environment at the beginning of each teletherapy session: both (a) their actual physical location/address and phone number, and (b) whether there is any impending or possible danger from others. We recommend this because there have been occasions when clients were in danger, but they were at a different location than usual and were unable to communicate where to send help without alerting the potential abuser. Given this possibility, a two-step process is recommended. First, when there is some likelihood that the client might be in danger in their home, the client and therapist should agree beforehand, ideally in the first session, on a code phrase that the client can use to signal that they are unsafe because a potentially violent or abusive person is present. The phrase should be something that might naturally occur in a conversation, such as “I don’t feel well today” or “I don’t feel like talking much today.” In some cases, there may be two different codes, one for immediate danger and one indicating that someone is in the immediate area and therefore the call is not private. When the client uses the code phrase, the clinician should ask specific questions about whether there is immediate danger and whether anyone else is present, answerable in a yes/no format so that any listener cannot determine the question or the meaning of the answer. Upon being notified by the client, the therapist may then do whatever they and the client have previously decided upon in such instances. In many cases, this will involve notifying the police or other authorities, or the client escaping the house, meeting the authorities outside, or going to a safe place (see Safety Planning, below). In some instances, the client may have prior negative experiences with discrimination, violence, or disrespect from authorities (especially law enforcement), may not have legal immigration status, or may fear arrest based on a prior crime. As a result, the clinician must be careful to ascertain who the client trusts and views as safe, and not suggest safety plans that are unlikely to be followed. Safety Planning

Initially developed for women who were exposed to intimate partner violence (Logan et al., 2006), safety planning is a proactive tool that the client can use when they and the therapist have identified danger, as described above, or in any other instance when the survivor is confronted with a potentially violent person or situation. Safety planning typically involve specific strategies for exiting the home or environment and gaining assistance from others who can intervene to provide safety. Much of the benefit of safety planning resides in preplanning specific actions, so that when escape is necessary the client can immediately turn to a defined strategy. Such plans are perhaps even more important during pandemic-related social distancing, since the client may be confined to a specific environment where there is a risk of violence and may feel they have less permission to run to a neighbor or friend’s house or reach out to a stranger. Calling police or other authorities—in addition to its associations with danger for some socially marginalized clients—may be even more difficult for the client who is under the control of an abuser or other dangerous person. While these concerns make safety planning more complex, it is crucial that the clinician have safety conversations on a regular basis with any client who is in potential danger. Optimizing Rapport As described earlier, there are numerous studies indicating that trauma-focused teletherapy can be as effective as in-person treatment. Yet, concerns are often voiced by clients and clinicians that remote treatment can interfere with the therapeutic relationship by decreasing rapport. When this occurs it is problematic, since the quality of the therapeutic relationship is one of the most powerful predictors of improvement in psychotherapy. Some clients (and therapists) complain that video-based therapy seem distant and artificial and note that subtle cues and responses between client and therapist can be harder to perceive. This potential lack of full connection can be triggering for the client and may lead to perceptions of therapist nonattunement. The potentially narrower bandwidth of teletherapy relative to face-to-face treatment also may cause the clinician to miss indications of client distress, such as facial expressions or changes in breathing or body movement, potentially leading them to insufficiently titrate aspects of the therapeutic process. As well, technical difficulties a (e.g., moments when the video image freezes, distorts, or pixilates; the connection abruptly terminates; or data-lagging causes one party to inadvertently speak over the other) can be frustrating and highlight the perceived artificiality of the teletherapy process. Although client and therapist concerns about decreased therapeutic rapport and relatedness are often not born out (Germain et al., 2010), there is little question that some clients suffer from the limitations of remote treatment. Presented below are some ways in which teletherapy can be adjusted to increase the client’s sense of rapport and alliance with the therapist.

Normalize and problem-solve the teletherapy process.

The therapist should explicitly discuss and normalize the teletherapy process, generally by discussing beforehand any potential problems and inadequacies of the process and providing the client with an opportunity to discuss any discomfort or reservations about receiving therapy in this manner. Such discussions should be supported throughout therapy, so that the client

perceives any negative reactions as due to teletherapy, per se, not their personal failings or sensitivities.

Plan for possible session disruptions.

Given the vagaries of internet and cyber technology, it is important that the therapist and client agree beforehand on a plan for how the teletherapy session can be resumed should either party’s internet or phone connection fail or the session is otherwise interrupted. When this is not done, an interrupted session may not be successfully reinitiated, leaving the client feeling abandoned and potentially exacerbating any negative feelings toward teletherapy or even the therapist. For example, the fallback plan might be to try to reconnect for a specific time period (e.g., 5 minutes), and then, if that is unsuccessful, the therapist attempting to contact the client through previously established phone numbers, or vice versa. In such cases, of course, HIPPA constraints must be taken into account.

When Appropriate, Maintain Eye Contact. When possible and culturally appropriate, maintain as much eye contact as is reasonable with the client, as opposed to regularly glancing away to one’s phone or objects in one’s room. In many cases, eye contact tends to increase rapport and helps the client to feel seen despite the constraints of remote treatment. This is not always true, however. Some clients avoid extensive eye contact because it is threatening or because their culture interprets too much eye-to-eye contact as rude or intrusive. In other cases, reduced eye contact is a way for the survivor to lessen the intensity of the session, either because it reduces trauma activations or because they are generally shy or socially avoidant. In such instances eye contact may be titrated to the client’s level of comfort or existing defenses.

Be aware of camera placement. The client’s and therapist’s distance from their phone or computer camera may cause the client to feel that the clinician is too close (i.e., potentially intrusive or threatening) or too far away (i.e., potentially disengaged or emotionally distant). In some cases, the client’s camera may not be centered midscreen, but instead is placed to the side, making it difficult to maintain eye contact. For this reason, the client and therapist should explicitly discuss camera placement at the outset of treatment, so that they can determine the optimal distance and focus. In any case, it is important that the therapist’s face be sufficiently visible that their facial expressions are readily observable by the client and vice versa.

Monitor the need for greater therapeutic connection. By virtue of the limited amount of stimuli that can be transmitted through video technology, teletherapy may occasionally attenuate the degree and quality of interpersonal connections between client and therapist. For this reason, it may be helpful for the clinician to consciously heighten the interactive quality of any given telesession. Within the bounds of authenticity, this often means that the clinician

Intentionally increases their verbal expressiveness on video calls

Avoids monotonous speech Encourages interactions, including asking more questions and facilitating more feedback than might be the case for in-person sessions verbalizes appreciation of the survivor’s willingness to participate in teletherapy communicates acceptance, compassion, and support on a regular basis

Be Attuned to Transference.

In some cases, teletherapy technology may reduce the client’s access to accurate, moment-by- moment information on the therapist and their reactions. For example, lower bandwidth, sporadic audiovisual feed, or reduced volume may lessen the visibility of the therapist’s compassionate or empathic reactions to client disclosures. Especially for survivors who require greater levels of interpersonal support or validation, including those who have been exposed to disattuned or punitive attachment figures in the past, this seeming lack of response may appear to reflect rejection, abandonment, or disrespect. Given the potential for such miscommunications, the clinician should be alert to inaccurate perceptions of them during treatment and encourage clarifying—but not defensive—discussions about what the client believed happened in the session, what actually took place, and what the clinician meant to convey. However, the client triggered by perceived disattunement will rarely respond to verbal information alone—there should also be visible therapist empathy, compassion, and positive regard. Fortunately, these responses tend to fade as the client adjusts to teletherapy and is less likely to respond to diminished information with expectations based on earlier victimization or neglect. It is virtually impossible to predict the future of mental health services delivery at the time of this writing. Although stabilizing in some locations, COVID-19 and new variants continue to be widespread. Some epidemiologists predict additional waves of this or related diseases (e.g., Wise, 2020), especially given the waxing and waning of the general population’s enthusiasm for testing, social distancing, and preventative hygiene. This uncertainty will likely continue until vaccines and treatment for COVID-19 and future diseases are widely available, broadly accepted, and reliably used by the populace. Even then, the likelihood of future viral pandemics suggests the need for permanent modifications in how health and mental health services are provided, including how psychotherapy will be delivered to traumatized populations. Fortunately, clinicians and clients are proving to be resilient and creative in the face of, and new evidence-based teletherapeutic approaches and protocols continue to be developed. PART III PSYCHOBIOLOGY AND PSYCHOPHARMACOLOGY OF TRAUMA

This last book section briefly describes the underlying psychobiology of trauma impacts (Chapter 14) and a review of the psychopharmacology of trauma-relevant medications (Chapter

15). While Chapter 14 is presented for all interested students and practitioners, Chapter 15 is intended for clinicians and clinicians-in-training who either (a) prescribe psychiatric medications

or (b) provide psychotherapy for those who may require such medications.

Chapter 14

NEUROBIOLOGY OF POSTTRAUMATIC STRESS: CATHERINE SCOTT, JOHN BRIERE, & JANELLE JONES

We include a chapter here on the neurobiology of posttraumatic stress as a reference to the neurophysiology and neuroanatomy of the human posttraumatic stress response, and as a source of information on the neurobiology underlying the efficacy (or nonefficacy) of psychiatric medications described in Chapter 15. The last several decades have witnessed substantial interest in the biology of posttraumatic stress. This growing research base indicates that multiple systems and neurotransmitters are involved in posttraumatic disturbance, although some of the evidence is contradictory and sometimes difficult to interpret. There are several implications of this complexity, including the following:

There are multiple biological pathways to posttraumatic stress, and it is likely that no one model will suffice to describe the entire physiology involved. PTSD, as it is currently described, may not represent a single disorder, but rather a collection of outcomes that vary depending on individual differences in genetics, underlying neurophysiology, stress response, and exposure to traumatic events.

THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS AND THE ADRENERGIC SYSTEM When stressed, the normal response of the body is to activate both the adrenergic and the glucocorticoid systems, releasing (among other compounds) norepinephrine and cortisol (Sherin & Nemeroff, 2011). Under healthy conditions these two systems regulate one another—cortisol appears to act as a “brake” on the adrenergic system, preventing sustained sympathetic activity. In PTSD, this balance is not maintained, and the responses of both systems become dysregulated (Raison & Miller, 2003). The adrenergic system, also known as the sympathetic nervous system (SNS), is responsible for what is classically referred to as the fight-or-flight response. It is associated with maintaining arousal and attention and with the consolidation of certain types of memories. Under conditions of stress or threat, the brain increases the synthesis and release of norepinephrine—primarily in the locus coeruleus and reticular activating system—to allow an appropriate response to the situation (e.g., running away or fighting). Under normal conditions. when the stressor is no longer present, the adrenergic system ideally returns to its usual baseline state. This return to normal levels of arousal appears to be disrupted in PTSD. Adrenergic hyperactivity—involving the release of multiple neurotransmitters and neurohormones such as acetylcholine, epinephrine, and norepinephrine, as well as their metabolites—has been demonstrated in individuals with PTSD. Such excessive and sustained activation is associated with multiple posttraumatic symptoms, including hyperarousal, reexperiencing, dissociation, aggression, and both

generalized anxiety and panic attacks. In addition, increased adrenergic activity appears to assist in the encoding of emotionally laden memories (McIntyre & Roozendaal, 2007). The adrenal glands, which are the end organs of the HPA axis, release both cortisol and adrenergic compounds. The cascade that results in cortisol production begins at the hypothalamus, which secretes corticotropin releasing factor (CRF). CRF stimulates the pituitary to secrete adrenocorticotropin hormone (ACTH), which, in turn, controls the release of cortisol by the adrenals. Cortisol is a hormone with multiple functions, including regulation of immune and stress responses. It has been proposed that this substance, along with other compounds such as neuropeptide Y (NPY), may serve to modulate the activity of the adrenergic system (Sah & Geracioti, 2013). NPY is an endogenous anxiolytic that appears to act in concert with cortisol (Kask et al., 2002). At moderate or levels of stress, this means that blood levels of cortisol and NPY are typically high. At such levels, NPY appears to be a protective neurosteroid that confers additional resiliency, acting as a buffer in the brain to protect against the development of PTSD when exposed to trauma (Sah & Geracioti, 2013). However, when an individual is overwhelmed by a traumatic event, this system may be overwhelmed as well, leading to a drop in levels of cortisol and NPY. The result is a limitation on the brain’s capacity to down-regulate sympathetic arousal and a vulnerability to PTSD. In support of the above argument, decreased cortisol and NPY levels have been demonstrated in individuals living under chronically stressful conditions. Several lines of research have also demonstrated lower cortisol and NPY in individuals with PTSD (Yehuda, 2002). Exposure to trauma sensitizes the HPA, resulting in some alteration of cortisol levels, whether or not an individual goes on to develop the full spectrum of PTSD symptoms (de Kloet et al., 2007). In addition, low levels of these neurochemicals after a trauma are predictive of later PTSD (Morgan et al., 2001). Although most studies indicate that those with PTSD have lower levels of cortisol (both morning and 24 hour) than controls without PTSD (see a meta-analysis by Schumacher et al., 2019), not all agree. For example, in a systematic review and meta-analysis of 37 studies, Meewisse and colleagues (2007) report no systematic differences in basal cortisol between those with and without PTSD, but subgroup analyses revealed variations as a function of gender, time of cortisol sampling, and type of trauma exposure. As well, several studies indicate that childhood trauma is an important moderator in the relationship between low cortisol and adult PTSD (e.g., Galatzer- Levy et al., 2017). The HPA axis self-regulates by means of a negative feedback loop. Under normal circumstances, a low cortisol level would provide feedback to the hypothalamus and pituitary, resulting in higher levels of CRF and ACTH—ultimately stimulating the adrenals to secrete more cortisol and balance the system. However, in PTSD there appears to be enhanced negative feedback of the HPA axis—ultimately resulting in higher CRF without a resultant increase in cortisol (e.g., Raison & Miller, 2003). In addition, individuals with PTSD appear to hypersuppress cortisol upon dexamethasone challenge (Yehuda et al., 2004). These data suggest that glucocorticoid receptors may become hypersensitive in some traumatized individuals, leading to lower baseline levels of cortisol and, therefore, increased sympathetic nervous system activity (Yehuda & Seckl, 2011).

Given this information, it has been proposed that the deficit in PTSD is one of impaired glucocorticoid signaling rather than simply a problem of too little cortisol, per se (Raison & Miller, 2003). And because dexamethasone challenges (and adequate levels of CRF) fail to result in expected ACTH elevations in those experiencing PTSD, the trouble in the HPA system is thought to lie in the pituitary (Ströhle et al., 2008). Interestingly, as we describe in the next chapter, research suggests that it may be helpful to give a treatment such as hydrocortisone to restore the HPA axis’s ability to dampen subjective distress, both as a way to prevent PTSD and, perhaps, as a way to treat it. Taken together, the above findings suggest that there is a neurobiological window for optimal stress response, within which various brain compounds (such as NPY and cortisol) operate to inhibit the release of norepinephrine so that the sympathetic nervous system does not overshoot (Southwick et al., 2005). In posttraumatic stress, there appears to be a co-occurrence of increased adrenergic activity with decreased glucocorticoid (cortisol) and NPY modulation. This imbalance may lead to the rapid and powerful consolidation of emotionally laden traumatic memories, which, under conditions of ongoing adrenergic stimulation, become intrusive and overwhelming, and lead to symptoms of hyperarousal, agitation, anxiety, and dissociation. THE ENDOCANNABINOID (ECB) SYSTEM The eCB system is among the most ubiquitous of signaling systems in the human brain, and strongly influences the connection between the prefrontal cortex and the amygdala and HPA axis (Mayo et al., 2021). The CB1 receptor within the eCB system is specifically involved in the consolidation and extinction of fear-related memories in the basolateral amygdala, generally by suppressing corticosterone secretion (Hill et al., 2009). PTSD is associated with dysregulation of the eCB system, primarily through altered CB1- mediated anandamide signaling (Neumeister et al., 2013). As described in the next chapter, the cannabinoids tetrahydrocannabinol (THC) and cannabidiol (CBD), probably among others, impact the eCB system by both facilitating the extinction of fear-related memories and blocking their reconsolidation (Hill et al., 2018). As described later, eCB research has heightened scientific interest in exogenous cannabinoids as novel treatments for PTSD (Mayo et al., 2021). OTHER BIOLOGICAL CORRELATES OF PTSD As the above discussions indicate, the biology of trauma is highly complex, with multiple systems and circuits, which overlap and interact with each other in a variety of ways. In the coming years, we will undoubtedly learn more from this area of research. PTSD has been associated with changes in serotonin levels, serotonin transporters, opioid dysregulation, and high-normal thyroid hormone levels (Friedman, 2000), as well as altered immune functioning that also may contribute to some of the pathophysiology of the disorder (Pace & Heim, 2011). Low levels of gamma-aminobutyric acid (GABA, the primary inhibitory neurotransmitter in the brain, responsible for regulating neuronal excitability) have been implicated in PTSD (Rasmussen et al., 2006), potentially as mediated by insomnia (Meyerhoff et

al., 2014). Kindling, in which repeated stress is thought to sensitize limbic neurons so that reactions are set off by stimuli that were once sub-threshold, has also been proposed as a model for the development of PTSD (McFarlane, 2010), especially in conditions of chronic stress such as child abuse (Weiss & Post, 1998). An emerging body of research in neurobiology, which may explain the hippocampal changes seen in neuroimaging (described next) is that of neurogenesis—the production of new cells within the nervous system. It appears that PTSD, as well as other anxiety and affective disorders, may be related to impaired neurogenesis in the hippocampus. Until recently, it was thought that adult brains could not create new cells; however, in the 1990s, neurogenesis was first demonstrated in the brains of adult rodents (see a description by Takemura & Kato, 2008). Neurogenesis appears to be affected by levels of stress and is associated with learning and memory processes (Takemura & Kato, 2008). In fact, it appears that under stressful situations cortisol modulates neurogenesis, with higher levels leading to cell atrophy and lowers levels correlating with cell growth (Odaka et al., 2017). Boldrini et al. (2009) examined on autopsy the hippocampal tissue of individuals with untreated depression, depression treated with selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants (TCAs), and a set of controls. They found greater numbers of dividing cells in the treated group, compared to both untreated and control subjects. However, the effects of SSRIs may be more varied than merely increasing available serotonin or enhancing hippocampal growth, indicating an even greater complexity of the underlying biology. Serotonergic agents also have effects on the locus coeruleus, where the adrenergic cell bodies reside—a possible mechanism for SSRIs to affect the HPA axis. In addition, it has been suggested that one of the actions of the serotonergic agents in PTSD is to increase levels of the neurosteroid allopregnanolone, an endogenous anxiolytic. Allopregnanolone, in turn, impacts anxiety by activating GABA and thus down-regulating neural excitability (Pinna, 2010). FINDINGS FROM NEUROIMAGING STUDIES Recent advances in neuroimaging technology allow us to view the brain as it functions in vivo, opening a window into how trauma affects both neuroanatomy and neurophysiology. In general, PTSD has been associated with amygdaloid hyperactivity, smaller brain white and gray matter, smaller hippocampal volumes, and smaller anterior cingulates (Chen et al., 2018). Accelerated brain atrophy appears to occur in patients with worsening rather than improving symptoms (Cardenas et al., 2011). Small hippocampal volume has also been found in survivors of child abuse, irrespective of PTSD diagnostic status (see a systematic review by Ahmed-Leitao et al., 2016). This volume loss correlates with the severity of the abuse, the severity of PTSD symptoms (Fennema-Notestine et al., 2002), and, in some cases, with memory disturbance (Tischler et al., 2006). In one study, even new onset PTSD was associated with decreased hippocampal and parahippocampal density and volume (Zhang et al., 2011). A question that remains to be answered is whether smaller hippocampal volume might predate the trauma and therefore predispose an individual to develop PTSD, or whether the volume decrease occurs as a result of the neurobiological response to a traumatic event (Nelson &

Tumpap, 2017; Woon et al., 2010). To further complicate the picture, it is possible that both of these processes may occur in an overlapping fashion in some individuals (Apfel et al., 2011). Imaging also has demonstrated decreased activation of the hippocampus during verbal memory tasks in individuals with PTSD (Carrión et al., 2010), a finding that makes sense given that the hippocampus plays an important role in the consolidation of memory. Interestingly, treatment with the selective serotonin reuptake inhibitors (such as Prozac) has been shown to improve verbal memory as well as increase hippocampal volume (Anacker et al., 2011). Similarly, researchers have found decreased recruitment of the anterior cingulate—an area of the brain thought to be associated with emotional responsiveness and affect regulation—during trauma triggering and recall (Stevens et al., 2011). Research also indicates that, in the wake of a trauma, the dorsolateral prefrontal cortex (DLPFC) appears to increase in size (Lyoo et al., 2011), possibly compensating with increased activity to help reduce symptoms stemming from other areas of the brain. The increased thickness of the DLPFC appears to correlate with greater symptom reduction during recovery and may return to baseline over time (Lyoo et al., 2011). INTEGRATING BIOLOGICAL MODELS WITH PSYCHOLOGICAL TRAUMA THEORY The psychobiological models presented here are focused on nervous system pathology, as opposed to the more adaptation-oriented psychological conceptualizations described in earlier chapters. Biological theories tend to suggest that the symptoms of posttraumatic stress arise from excessive activation of the sympathetic nervous system, probably in combination with dysregulation of the HPA axis and related systems, such that traumatic memories become overconsolidated, easily activated, and overwhelming in their capacity to produce negative emotions. Further, the continuous activation of the sympathetic system is thought to result in sustained autonomic arousal and, in the presence of repeated stressors, hyper-reactivity to subsequent stimuli. In contrast, the psychological model described in earlier chapters suggests that posttraumatic reexperiencing (e.g., flashbacks and intrusive trauma-related thoughts) represents, at least in part, a normal psychobiological process—the mind’s attempts to desensitize traumatic memory by repeatedly evoking it in the context of safety (i.e., the concepts of exposure, disparity, and extinction/inhibition discussed in Chapter 9). Although the integration of these two perspectives remains speculative, we suggest that it is possible. We hypothesize that the normal exposure-disparity-extinction/inhibition process works only to the extent that reexperiencing phenomena (e.g., intrusive thoughts and memories) do not exceed the individual’s capacities to regulate and tolerate the associated painful states. These emotional regulation capacities, in turn, are likely to be partially a function of psychobiological phenomena such as the ability of the HPA axis to modulate sympathetic arousal. Thus, it is possible that chronic PTSD and other posttraumatic responses arise when the natural exposure/processing system is derailed—that is, when the emotional impacts of a stressor exceed

the individual’s existing emotional regulation “window.” This is perhaps especially true in those who already have a sensitive or dysregulated nervous system. In cases where reexperiencing appears to be effective—that is, when traumatic memories are successfully exposed and extinguished or inhibited—we might expect to find fewer overwhelming stressors, a less excitable nervous system (and, therefore, more effective modulation via cortisol), higher levels of NPY, and less overall limbic sensitization. Given the preceding discussion, successful treatments for PTSD and other stress disorders would probably involve some combination or subset of the following:

1. Carefully titrated exposure to traumatic memory, so that even compromised biological and psychological systems are not overwhelmed

2. Attempts to increase emotional/stress regulation through the psychological interventions described in Chapter 6, but also, in some instances, through medications thought to stabilize the limbic system and HPA axis

3. A reduction in the overall anxiety/arousal “load” (that is, overactivity and hypersensitivity of the sympathetic nervous system) through relaxation training, meditation, or memory desensitization, as well as dampening of sympathetic activation, when indicated, through medications that treat anxiety

4. Use of medications to reduce comorbid anxiety, depression, or psychosis that otherwise add to overall distress or interfere with emotional regulation, and to mitigate the effects of fear conditioning and hyperconsolidation.

Although, as noted in the next chapter, currently available medications are rarely sufficient to permanently resolve posttraumatic stress, some trauma survivors suffer from such high levels of anxiety, hyperarousal, and comorbid symptoms that psychotherapy alone is unlikely to be fully effective. And some impacts of severe trauma reside in dysregulated neurobiology that seemingly only responds to pharmacological agents. As a result, successful treatment of posttraumatic states—especially in the case of severe or chronic symptoms—may sometimes involve both psychological and pharmacological interventions. Chapter 15 PSYCHOPHARMACOLOGY OF TRAUMA: CATHERINE SCOTT, JANELLE JONES, & JOHN BRIERE This chapter is intended for both prescribing and nonprescribing practitioners and trainees. Of necessity, some of the material presented here is relatively technical in nature, and at first glance may seem less relevant to the nonmedical therapist. However, many trauma survivors who are in psychotherapy take psychiatric medications of one type or another, and the nonprescribing clinician is often the professional most aware of the client’s week-to-week psychological state and general physical functioning. In contrast, medical practitioners may only have a fraction of an hour, perhaps once a month or even less often, to evaluate medication effects. This ready access to the client’s clinical state allows the pharmacologically informed therapist to refer clients for medication when appropriate and help them detect drug side effects or emergent need for medication changes which can then be communicated to the prescribing clinician.

This chapter includes an overview of the major trauma-relevant medications and their general indications and contraindications for posttraumatic symptom patterns in adults. It also discusses strategies for medication management in the context of comorbidity and as an adjunct to trauma- focused psychotherapy. New to this edition, we also review important findings on the clinical use of ketamine, psilocybin, the cannabinoids, and MDMA with trauma survivors. Although in its relative infancy, this research suggests that medication-assisted psychotherapy can lead to trauma recovery rates that exceed what is usually found for either medication or psychotherapy alone. Importantly, the current chapter is limited to the use of medications with adult survivors. Because psychopharmacology for children and adolescents is a specialized area, the reader is referred to the American Academy of Child and Adolescent Psychiatry (2015) and Keeshin et al. (2020) for more information on the use of medication with this group. Medication management. As discussed throughout this volume, posttraumatic outcomes can be extremely complex. Similarly, tailoring treatment—whether it be psychotherapy, psychopharmacology, or a combination of the two—to a given individual’s particular circumstances may be far from simple. Although the medications indicated for the specific treatment of PTSD and related disorders are relatively few in number, the practice of using them and encouraging compliance requires considerable knowledge and attention. It is rarely sufficient to write a prescription and tell the client to return in a month for follow-up. Specific concerns associated with using medications with trauma survivors include the following:

Compliance. Trauma survivors often have a difficult time remembering to take their medications—the result of distractibility, high levels of emotional activation, and, sometimes, dissociation. This may be even more of a concern if a medication regimen requires pills at multiple time points during the day. Anxiety. Many of the antidepressant medications used to treat PTSD can increase the levels of anxiety that some individuals experience in the initial days of treatment, and in some instances can precipitate panic attacks. Trauma survivors who are highly dissociated, somatically preoccupied, and anxious, or who present with panic attacks, are likely to respond to these medications with more anxious symptoms than are other, less traumatized individuals. Sedation. Certain psychotropic medications can cause feelings of dullness, sedation, or of “not being myself” in some individuals. Trauma survivors, in particular, may feel that these side effects impair their ability to sense and respond to danger. Paradoxically, although hypervigilance can be an extremely debilitating component of posttraumatic stress, many individuals do not want to lose the sense of control and safety that hyperalertness provides them. Sleep. Similarly, although trauma survivors frequently report disturbed and erratic sleep, they may resist taking sleep medications for fear that they will sleep through potential danger.

Memory processing. Some medications, particularly the benzodiazepines, may interfere with the psychological processing of traumatic memories, as described later in this chapter. As a result, the costs and benefits of using such drugs should be carefully considered when the client is undergoing psychotherapy or otherwise addressing traumatic material. Substance abuse. Excessive or otherwise problematic substance use is highly comorbid with posttraumatic stress and may intensify or interfere with certain medications. Distrust of authority. Many trauma survivors, especially victims of interpersonal violence, may be distrustful of authority figures, including—in some cases—therapists or physicians, and may therefore be reluctant to take prescribed medications. For example, they may fear that the clinician is trying to sedate or control them through drugs. Overmedication. The chronic and extreme distress that some trauma survivors experience may induce helplessness and frustration in the clinician, leading them to medicate clients more aggressively than is appropriate or to overprescribe addictive anti-anxiety medications.

Given these concerns, we make the following recommendations:

Close follow-up of traumatized clients, preferably within a week of starting a new medication Patience regarding the client’s occasional unwillingness to take medications—it may take more than one visit for them to develop the trust necessary to start a psychotropic regimen Slow dose increases to avoid side effects that may decrease compliance Adequate education about potential side effects, so that, if they occur, they do not surprise or alarm the client or cause them to prematurely discontinue medication that ultimately would be tolerable Gentle encouragement and support around fears of being overmedicated and therefore less responsive to danger Careful consideration of any potential for abuse or overdose when prescribing medications for relief of anxiety As always, documentation of informed consent is necessary when prescribing psychiatric medications

PSYCHOTHERAPY AND PSYCHOPHARMACOLOGY Throughout this volume, we focus on the importance of processing traumatic material in the context of a supportive therapeutic relationship. In some instances, however, posttraumatic symptoms may be so overwhelming that the individual is unable to participate in therapy altogether or becomes so anxious and distressed with even low levels of activation that therapy proceeds at a very slow pace. In other situations, comorbid psychological conditions (most commonly depression) interfere with the client’s ability to participate fully in psychotherapy. In

the worst case, the client may drop out of treatment after a very few sessions, often without explanation, and without returning clinician phone calls. Psychotropic medications can be a useful adjunct to trauma-focused psychotherapy under such conditions, especially in the early phase of treatment. Appropriate pharmacological intervention can provide some initial relief of intense distress—partly via medication effects on posttraumatic symptomatology and partly via the placebo effect. Medication that improves sleep may be particularly helpful, since sleep disturbance is often one of the most debilitating symptoms of posttraumatic stress. When some initial symptom reduction can be gained through the use of medication, clients may be more able and willing to engage in the often-difficult work of trauma-focused psychotherapy. For clients who question the efficacy of treatment, the experience of an initial benefit may help to improve the therapeutic alliance; for those whose negative experiences have caused them to believe there is no possibility of recovery, the demonstration of early symptom relief may provide a glimmer of hope for the future. Seen in this light, pharmacotherapy can be a steppingstone in the process of helping clients to recover—a way to help them both enter into and stay engaged with psychotherapy. Overall, however, medications are rarely curative by themselves and, although helpful, can have less of a therapeutic effect than psychological treatment. For example, a network meta-analysis of the trauma treatment literature indicates benefits of both pharmacotherapy and psychotherapy but concludes that (a) psychotherapy appears to be more effective than medication in the treatment of PTSD, and (b) pharmacological outcomes can be improved by adding psychotherapy to the treatment context (Merz et al., 2019). While there are potential methodological problems associated with such comparisons, there is no evidence to support the idea that pharmacotherapy for posttraumatic stress is intrinsically more effective than psychotherapy. Nevertheless, in our experience, some individuals may miss out on the potential benefits of psychotherapy because their level of symptomatology means that they cannot tolerate—and therefore must avoid—even low levels of activation and distress. For these individuals, medication can be a powerful method of engaging them in psychological treatment, and thus may increase the possibility of recovery. Apropos of the Merz et al. (2019) analysis, a handful of studies looking at the combination of psychotherapy and pharmacology in PTSD have shed some light on this complex topic. Simon et al. (2008), in a trial of paroxetine augmentation in individuals refractory to prolonged exposure therapy, found that medication was not superior to placebo in reducing residual symptoms. Rothbaum et al. (2006) compared sertraline continuation treatment to prolonged exposure in a group of patients already on sertraline for 10 weeks. Interestingly, those patients who had responded well to the medication initially experienced no further benefit from either treatment. However, those who were partial medication responders had a further reduction in PTSD symptoms with the addition of psychotherapy. Lastly, Shalev et al. (2012) compared prolonged exposure, cognitive therapy, medication with citalopram, and placebo in survivors of acute trauma. Results were consistent with the data reported in earlier studies: At 5-month follow-up, 20 percent of the individuals who had received psychotherapeutic interventions had PTSD,

compared to 60 percent of those on medication, and 58 percent of those receiving placebo. These four studies, all carried out by different investigators, with different groups of patients, confirm a remarkably consistent trend: Psychotherapy in all cases produced greater symptom reduction than did psychiatric medications. Treatment Outcome Studies and the Limitations of Medications in Posttraumatic Stress This chapter reviews the medications used to treat posttraumatic symptoms, their indications and side effects, and the major clinical trials (if any) investigating their use in traumatized individuals. There are, however, several limitations of this research that warrant mention. Many studies of treatment outcome in PTSD, whether involving medication or psychotherapy, have examined relatively “pure” PTSD, often associated with adult traumas of little complexity. Individuals with comorbid diagnoses of major depression, personality disorders, obsessive- compulsive disorder, and other anxiety disorders are often excluded from such trials (Spinazzola et al., 2005). In addition, many studies exclude those who abuse substances, are suicidal, or have significant dissociative symptoms. Even despite these exclusions, dropout rates approach 30 percent in many studies (Spinazzola et al., 2005). Finally, many (especially older) studies lack randomization and control group comparisons. In this chapter, we focus on randomized controlled trial (RCT) studies rather than these more limited investigations, unless a non-RCT study provides important information. Unfortunately, in the general population (i.e., in nonscreened, nonresearch settings), PTSD is highly comorbid with other psychiatric diagnoses (Brady et al., 2000). In fact, estimates place the comorbidity of PTSD with other disorders, summing across sex, at up to 80 percent (Kessler et al., 1995). Thus, it is not always easy to generalize the results of treatment outcome studies to the actual environment in which most clinicians practice—a world in which clients often present with a complex array of symptoms and may respond less robustly to treatment or take longer to respond than the studies suggest. Overall, there is considerable evidence that psychoactive medication is sometimes necessary, but it is rarely sufficient in the treatment of PTSD and other trauma-related states. However, these limitations should not preclude the appropriate use of such medications in clinical practice. Pregnancy and Lactation As noted in Chapter 1, women are overrepresented among trauma survivors, and are at a higher risk for victimization when they are pregnant or postpartum (James et al., 2013). Pregnancy is a time of increased vulnerability, both mentally and physically, as well as potentially a time of role change and financial stress. As a result, psychological stability, physical safety, and social support become especially important during pregnancy and the immediate postpartum period. A trauma history, especially childhood sexual abuse, as well as a diagnosis of PTSD, are associated with risky behaviors and negative outcomes in pregnancy (e.g., Seng et al., 2009). As well, childbirth itself can be a trauma that leads to subsequent posttraumatic symptoms and distress, especially in women who have prior histories of childhood sexual abuse (e.g., Dekel et al., 2017).

Estimates of PTSD prevalence in pregnant populations range from 0 percent to 21 percent, depending on the study and the demographics of the individuals participating (Khoramroudi, 2018; Ross & McLean, 2006). A survey of pregnant women found PTSD in 4.1 percent of never abused women, 11.4 percent of women abused as adults, 16 percent of women abused in childhood, and 39.2 percent abused in both childhood and adulthood (Seng et al., 2008). Given the above, it is important to consider both pregnancy and the potential for pregnancy in women of childbearing age when working with traumatized women. Unfortunately, there have been no studies to date evaluating either (1) the specific efficacy of medications in the treatment of PTSD in pregnancy or (2) the course of PTSD treatment in the perinatal period. Thus, clinicians must extrapolate from the available studies of medications during pregnancy in women with depression, anxiety, and schizophrenia. Prescribing practices during pregnancy vary widely, and a review of the literature reveals a variety of opinions, ranging from encouraging clinicians to aggressively treat psychiatric symptoms in pregnancy, to the view that medications clearly have the potential for harm and should be used only as a last resort. Most medications used to treat PTSD were classified by the Food and Drug Administration (FDA) prior to 2015 as pregnancy Category C, indicating possible adverse effects on the unborn child. Certain medications are more clearly contraindicated in pregnancy relative to others. Therefore, the decision to treat a pregnant woman with psychotropic medication involves a careful risk-benefit analysis. For example, are the symptoms severe enough that a woman is at risk for harming herself or her baby? Is the risk for harm due to intentional injury or self-neglect greater than the risk posed by use of a medication? The antidepressants, especially the selective serotonin reuptake inhibitors (SSRIs), generally have been prescribed quite widely during pregnancy. However, in December 2005, the FDA changed the SSRI paroxetine (Paxil) from pregnancy Category C (Risk cannot be ruled out) to D (Positive evidence of risk). This change occurred as a result of preliminary data suggesting that exposure to this drug during the first trimester may increase the chance of congenital malformations, especially cardiac anomalies (Food & Drug Administration [FDA], 2005). It is unclear whether this finding might be a more general SSRI-related effect as opposed to one simply connected with paroxetine. Nonetheless, this change illustrates that there is much we still do not know about this class of medications. In addition, there have been several studies indicating that SSRIs taken in the third trimester of pregnancy can lead to premature birth as well as complications immediately after delivery, including difficulties with breathing and feeding, jitteriness, and need for extended care, collectively described as a “neonatal behavioral syndrome” (Jordan et al., 2008). For this reason, all SSRIs carry a warning regarding third- trimester exposure. Mood-stabilizing medications, sometimes used in patients with PTSD, are overwhelmingly not recommended in pregnancy due to teratogenicity (causing malformations in the fetus). For example, lithium taken in the first trimester can cause cardiac malformations, while valproic acid has been associated with spina bifida and neural tube defects, as well as craniofacial malformations.

The use of antipsychotic medications in pregnancy presents challenges. Haloperidol (Haldol, one of the first and most extensively used antipsychotics) is the most commonly used in pregnancy, primarily because it has been around the longest. However, there have been multiple reports of malformations with the use of antipsychotics, as well as increased risk for gestational diabetes in the mother, perinatal complications, and movement disorders in the infant (Gentile, 2010). To the extent possible, it is recommended that psychotropics be avoided during the first trimester, since this is when the most crucial neurological development occurs in the fetus. If medication must be used, it should follow an honest discussion with the patient about the potential risks and side effects of whatever pharmacologic agent is being considered. If a patient becomes pregnant while on medication, then a careful consideration must follow of the need to change medication, and the possibility that the fetus will be exposed to more than one agent if a change is made. If a patient remains on medication through the third trimester, attention is necessary close to labor and delivery, as the infant may need a higher level of care in order for neonatal complications to be addressed. Most psychotropic medications are secreted in breast milk. The data on the effects of medications taken in by newborns through breast milk is minimal, and there have been no controlled trials of psychotropic medications in lactating women and their infants. Therefore, in circumstances where new mothers have symptoms severe enough to require pharmacological intervention, the most prudent choice is to avoid breastfeeding. That being said, prescribing practices for lactating women vary widely, and some have suggested that when a patient takes medication during pregnancy, the baby receives far less of the drug through milk than in utero, and therefore may continue taking it while breastfeeding. As always, a thoughtful risk-benefit analysis is required. While antidepressants may in some cases be acceptable during lactation, antipsychotics and mood stabilizers have the potential for more serious side effects in the baby, and if a mother needs to be on such medication, formula rather than breastfeeding is recommended. In a review of antidepressant medications in pregnancy, Payne and Meltzer-Brody (2009) suggest the following “clinical pearls” when working with pregnant and lactating women:

Assume all women of reproductive age will get pregnant and plan ahead. All medication changes should be carried out before pregnancy, if possible. Ideally, the patient should be stable psychiatrically for at least 3 months before attempting pregnancy. Limit the number of exposures for the baby; consider active psychiatric symptoms in the mother an exposure. Use medications that we know more about: Older generally means better. Consider breastfeeding when planning for pregnancy.

If a baby was exposed to a medication during pregnancy, it may not make sense to discontinue the medication (or alternatively not breastfeed) for breastfeeding. Every case is unique—there are no rules. Use a team approach.

Given that there are significant gaps in our knowledge of how medications affect both the course of pregnancy and fetal development, we recommend a cautious approach. To the extent possible, women with PTSD and other sequelae of trauma should be offered psychotherapy as a first treatment option. If a careful risk-benefit analysis suggests that medication is warranted, patient education, fully informed consent, and close monitoring throughout the perinatal period are essential. Complementary and Alternative Medicine and Psychotropic Medications Complementary and alternative medicine (CAM) is comprised of a rather loosely defined group of therapeutic modalities that are not often taught in medical schools or available in hospitals. Alternative therapy is generally distinguished from “conventional medicine” and includes such disparate therapies as herbal remedies, homeopathy, massage, chiropractic, acupuncture, equine therapy, vitamins, and “energy healing,” among others. We explore the use of alternative therapies in this chapter because there is considerable anecdotal evidence that some trauma survivors avail themselves of nontraditional remedies instead of (or in addition to) prescribed psychiatric medication. Often, such remedies are used in concert with changes in lifestyle such as yoga, meditation, or other mindfulness or spiritual practices. As described in greater detail in Chapter 11, mindfulness and yoga can be powerful tools in work with traumatized individuals. In addition, a growing body of research on spirituality, religion, and coping indicates that spiritual beliefs and positive religious coping mechanisms (such as prayer, engaging in good deeds, receiving help from clergy, among others) can be associated with more positive psychological outcomes (e.g., Ahrens et al., 2010). Over the past several decades, the use of alternative therapies has become increasingly widespread in the United States. While some forms of alternative therapies are provided by licensed practitioners, others are entirely unregulated. For example, herbal supplements, nutritionals, and vitamins, many of which can have significant side effects, and may interact with other drugs, are sold over the counter and are not regulated by the FDA. In addition, some faith-based approaches to healing have crossover with CAM. Spiritual healers often are greatly respected within their communities, and their opinions can carry significant weight. Sometimes, they will give herbs or other substances to take as part of a healing ritual or will advise patients to stop all other mainstream treatments in order for their rituals and treatments to be effective. Demographic studies have repeatedly indicated that individuals who seek out alternative forms of health care have higher rates of anxiety, depression, and chronic pain (e.g., J. R. T. Davidson et al., 1998). Possible reasons for this include diffuse, ill-defined physical complaints not well

addressed by conventional medicine, attempts to find “natural” remedies for both physical and psychiatric complaints, and frustration with the health care system, among others. Whatever the reason, it is important for mental health providers to be aware that their clients may be using alternative remedies and that they are often reluctant to share this information with their doctors and/or therapists. An exhaustive discussion of the literature on alternative treatments is beyond the scope of this chapter. However, there is a growing literature on the use of alternative remedies more generally for symptoms of depression and anxiety. These include acupuncture, St. John’s wort (or Hypericin), kava kava, SAMe (s-adenosyl-methionine), omega fatty acids, passionflower, valerian root, aromatherapy, and homeopathy. In addition, there is an abundance of scientifically unsubstantiated information available on the internet regarding the use of vitamins, tryptophan, and other supplements to treat psychiatric symptoms. Although not all of these remedies and interventions are necessarily safe or helpful, there are studies indicating that some alternative treatments can have positive results. In a randomized trial, acupuncture was as effective as group CBT in reducing symptoms of PTSD (Hollifield et al., 2007). In a small pilot study, omega-3 fatty acids were helpful for PTSD after a natural disaster (Matsuoka et al., 2011). Some trials have shown that St. John’s wort is an effective treatment for mild to moderate depression in adults (e.g., Sarris & Kavanagh, 2009), and that omega fatty acids and SAMe may be beneficial as an adjunct to antidepressant treatment (Cuomo et al., 2020). Among alternative remedies, kava kava has shown the most potential as an anxiolytic (Larzelere et al., 2010), but no studies known to the authors have examined its efficacy for PTSD. In a double-blind randomized trial, inositol (a vitamin-like substance found in the human body that has been synthesized in the laboratory) was found to improve depressive symptoms in individuals with PTSD but had no effect on the PTSD itself (Kaplan et al., 1996). Similarly, there is no meta-analytic support for the use of homeopathy in anxiety or other disorders (Mathie et al., 2017). A few critical points regarding safety are worth mentioning:

St. John’s wort (Hypericin) is an herbal supplement available over the counter for treatment of depression and often recommended by alternative providers. It has some SSRI activity, which is presumed to be its mechanism of action. Therefore, it is critical that clients not take St. John’s wort concurrently with an SSRI, since this would increase the risk of serotonin syndrome (see the section on SSRIs for a description of the SSRIs and serotonin syndrome). There are similar potential risks with the use of supplements containing tryptophan, a serotonin precursor. Some natural remedies act as stimulants and activate the sympathetic nervous system (for example, ephedra/ephedrine used for weight control, and yohimbine used for energy and male impotence). As described previously, trauma survivors frequently experience increased sympathetic nervous system activity and are at risk of increased posttraumatic symptoms if they use stimulants. We therefore recommend that traumatized individuals avoid herbal or other nonprescribed stimulants.

Some clients may take supplements that do not come in labeled packaging or that come from other countries. Such supplements may be prescribed by herbalists, for example, or by faith or indigenous healers, as described earlier. If psychotropic medications are indicated, it is imperative to have a frank discussion with the client about additional remedies they are taking. We recommend asking clients to bring all pills and supplements, along with the packaging in which they came, to their appointments, so that the clinician can be as informed as possible about potential problems/interactions. There are several online databases of herbs, supplements, and other natural remedies that can provide useful information on mechanisms of action, side effects, and drug interactions. (e.g., About Herbs from Memorial Sloan Kettering Hospital, https://www.mskcc.org/cancer-care/diagnosis-treatment/symptom- management/integrative-medicine/herbs/search?letter=A)

Although some of these alternative drugs and remedies may have real benefits, others are less efficacious and, in fact, may be dangerous when used in combination with other drugs. The potential risks of combining mainstream medications with nontraditional drugs and remedies must be conveyed to the client as well as documented in the medical record. However, maintaining a supportive, nonjudgmental attitude is essential during any such discussion. Often, clients believe that they will be penalized for using certain drugs or seeing alternative providers and are afraid to report what they are taking. In such situations, open communication among the nonprescribing therapist, the psychiatrist or other medical practitioner, and the client can be extremely useful. In the current atmosphere of increasing interest in alternatives to mainstream medicine, we will undoubtedly learn more about these and other alternative approaches to mental health treatment. And as patients become more highly informed consumers of health care, and have more and more access to information via the Internet, clinicians will need to stay informed in order to deliver the safest and most effective care. We recommend an open-minded, but vigilant, approach on the part of clinicians. As will be discussed later in this chapter, several drugs previously thought to be largely recreational or psychedelic in function are increasingly being employed by trauma survivors to self-medicate trauma-related symptoms, and clinicians and scientists are beginning to document significant benefits associated with their use. Among these are cannabis, hallucinogenic mushrooms, ketamine, and MDMA. We discuss each of these later in this chapter and describe their potential application in a hybrid clinical intervention, drug-assisted psychotherapy. A Note on the Uses and Limitations of This Chapter Much of what we present in the following sections is well-known, easily available information regarding the mechanism of action, side effects, and contraindications of various psychotropic medications. However, in the interest of brevity—and ease for the reader—we have not presented exhaustive general information about each medication. Prescribing clinicians should view this chapter primarily as a guide to the literature on the use of psychopharmacology in trauma; they are referred to more complete and authoritative texts, as well as their own clinical knowledge, for specifics regarding the use of psychiatric medications in actual practice. In no

case should the clinician prescribe or determine medication dosages or determine risk, including for pregnant clients, based solely on information provided here. MEDICATIONS FOR PTSD Antidepressants Selective Serotonin Reuptake Inhibitors (SSRIs) Most of the research on medications for PTSD has focused on the use of SSRIs. This is logical: SSRIs have demonstrated efficacy for the treatment of depression, generalized anxiety, and panic. Therefore, their use for PTSD, which includes symptoms that overlap with these disorders, is a natural extension. The results of research on SSRIs and PTSD have generally been encouraging (see a meta-analysis by Stein, 2021), leading to the widespread use of these medications to treat posttraumatic stress. For example, SSRIs are listed as the first-line medication for PTSD in the Treatment Recommendations for PTSD made by the International Society for Traumatic Stress Studies (Friedman et al., 2009). And the only medications the FDA has approved for treatment of PTSD are SSRIs—sertraline (Zoloft) and paroxetine (Paxil). On the other hand, several recent meta-analyses indicate that the SSRIs have relatively small effects on PTSD (e.g., Cipriani et al., 2018), with only 20 to 30 percent of PTSD suffers achieving full remission of symptoms (Berger et al., 2009). There have been several RCTs of SSRIs in PTSD, using paroxetine (Paxil; e.g., Marshall et al., 2007), sertraline (Zoloft; e.g., Panahi et al., 2011), and fluoxetine (Prozac; e.g., Martenyi & Soldatenkova, 2006). Results of this research indicate that SSRIs reduce symptoms in all three of the core symptom clusters of PTSD (i.e., reexperiencing, hyperarousal, and avoidance). Two SSRIs, citalopram and escitalopram, have not been studied in RCTs, other than in a small study of the former (Tucker et al., 2003) which demonstrated some effectiveness on PTSD symptoms. Both have shown efficacy for treating PTSD in small open-label trials, but larger RCT studies are needed in order to validate and replicate these findings. The newest SSRI, Vilazodone, has been examined in a single RCT, where it was found to be ineffective in treating PTSD and comorbid depression (Ramaswamy et al., 2017). Most studies have followed patients over a relatively short 12-week treatment period. One trial of sertraline followed patients for 28 weeks following the acute phase of the study to assess efficacy in preventing relapse (J. R. T. Davidson et al., 2001). The results suggested that sertraline is relatively effective in preventing relapse of PTSD. There have been two placebo- controlled trials of relapse prevention of PTSD with fluoxetine. The first was a 24-week extension of a 12-week study in which fluoxetine was superior to placebo in preventing relapse (Martenyi et al., 2002). The second confirmed these findings over a longer period: In a 6-month open trial of fluoxetine followed by 6 months of randomization to placebo control, 22 percent of those taking fluoxetine relapsed, compared to 50 percent of those receiving placebo (J. R. Davidson et al., 2005). In addition, time to relapse was longer with fluoxetine than placebo. These studies suggest that, in order for SSRI treatment to be effective over the long term, it must be maintained for a longer period of time than the usual 12-week duration of most clinical trials.

In fact, for PTSD that lasts more than 3 months, it appears that treatment with an SSRI for 9 months to a year after symptom remission may be more appropriate (J. R. T. Davidson, 2004). It is important to note that SSRIs, while sometimes helpful in PTSD, typically are not curative. In most studies, although 50 to 60 percent of participants responded to some extent, only 20 to 30 percent of them no longer met criteria for PTSD by the end of the study (Spinazzola et al., 2005). Put another way, this means that 70 to 80 percent of individuals in these studies still had PTSD after treatment, albeit perhaps in an attenuated form. In addition, despite studies indicating the efficacy of SSRIs in treating PTSD, some research has suggested a less than robust response to these medications, or cite the presence of comorbidities, overall lower doses of medication, or surprisingly high placebo response as confounders (e.g., Martenyi et al., 2007). What this means for clinical practice is that medications for trauma cannot be prescribed in a cookie-cutter fashion: It is essential for clinicians to take into account the entire presentation of the patient and to be especially aware of comorbidities and complexities that may attenuate a given individual’s response to any given treatment. In some studies of SSRIs in PTSD, treatment appears to be less successful in war veterans and in men than in civilians and women (Friedman et at., 2007). There has been much discussion about why this might be the case. The negative studies involved male Vietnam-era participants with PTSD lasting many years—a cohort with, almost by definition, a particularly treatment-resistant form of the disorder. In addition, many Vietnam-era veterans suffer from longstanding, severe substance dependence, which complicate the picture. However, more recent studies in civilians have demonstrated no sex difference in response to these medications. In addition, studies with veterans from other combat areas have shown that SSRIs can be effective in PTSD related to war trauma. For example, Zohar et al. (2002) found that sertraline was superior to placebo in Israeli combat veterans with PTSD, albeit with a smaller effect size than in civilians. In addition, an RCT study of fluoxetine in male veterans traumatized in the Yugoslavian civil war demonstrated significant improvement across all three PTSD symptom clusters (Martenyi & Soldatenkova, 2006). More research is required to clearly elucidate the relationships between type of trauma, chronicity, and substance use. There are some interesting data suggesting that SSRIs may actually have direct effects on the anatomy and neurophysiology that underlie posttraumatic stress, which are described in Chapter 14. In a small group of patients with borderline personality disorder, fluvoxamine (Luvox) was found to decrease the hyper-responsiveness of the HPA axis (as measured by dexamethasone challenge) in individuals with a history of childhood abuse (Rinne et al., 2003). Another study showed a 5 percent increase in hippocampal volume in individuals with PTSD who were treated for a year with paroxetine (Bremner & Vermetten, 2004). This information, while still preliminary, supports the notion that treatment with SSRIs may be most effective when used over a more extended period of time. At the time of publication of this book, there are seven SSRIs available on the market. They have been found to be somewhat effective in reducing symptoms and improving quality of life across most clinical trials for various DSM-IV or -5 diagnoses (e.g., Mace & Taylor, 2000), although not inevitably so. As discussed later in this chapter, they differ primarily in terms of side effects. This is an important consideration in choosing a medication for trauma survivors, because

noncompliance is especially high in this population. At this time, only sertraline and paroxetine have received FDA approval for the treatment of PTSD. However, as the SSRIs are generally equally effective across disorders, decisions regarding choice of one medication over another are primarily based upon the judgment of the clinician. SSRIs are generally considered to be safer than the older antidepressants (the tricyclics and monoamine oxidase inhibitors, described later in this chapter) and less lethal in overdose. However, they have been associated with a potentially life-threatening condition known as serotonin syndrome that results from excess central nervous system serotonin. Symptoms can range from tremor and diarrhea to delirium, neuromuscular rigidity, and hyperthermia. Serotonin syndrome can occur in cases of overdose, drug-drug interactions, or, in rare instances, during therapeutic drug use. Generally, SSRIs are well tolerated and have the benefit of being relatively nonlethal in overdose (as compared to, e.g., the tricyclic antidepressants, which can be fatal when taken in quantities equaling a 15-day supply). However, they all share some potential side effects. These include anxiety, nervousness, sweating, headache, gastrointestinal upset (nausea, diarrhea, dyspepsia), dry mouth, somnolence, insomnia, and disruption of all phases of sexuality (erections in men, and libido and orgasms in both men and women). Although SSRIs treat symptoms of anxiety and are indicated for the treatment of anxiety disorders, they frequently increase anxiety in the initial days of treatment and can sometimes precipitate panic attacks. There are certain side effects that are associated more with some SSRIs than others. Fluoxetine tends to be activating and is generally prescribed to be taken in the morning. Paroxetine (as well as fluvoxamine) tends to be more sedating and is typically taken in the evening. Paroxetine can also cause weight gain. Sertraline, escitalopram, and citalopram are more side-effect neutral, with fewer effects on sleep and weight. However, recent data showing an association of high dose citalopram with prolongation of the QTc interval on EKG led to a decrease in the maximum recommended dose from 60mg daily to 40mg, and a caution regarding those with risk for QT abnormalities. In addition, all SSRIs carry a “black box” warning regarding risk for increased suicidality in children, adolescents, and young adults (age less than 24 years). Some clinicians make decisions about which SSRI to give an individual client based upon the most advantageous use of these side effects, a strategy that we have found anecdotally to increase compliance. For example,

Paroxetine in a nonpregnant client who is highly anxious and unable to sleep and is not bothered by potential weight gain Fluoxetine in a client who is tired and apathetic and has a hard time “getting going” in the morning Sertraline, citalopram, or escitalopram in a client who is particularly concerned about side effects

Given the potential side effects discussed, client education is essential. It is important to warn very anxious and hyperaroused clients that their anxiety may increase initially and that this is a normal response to the medication. It is also crucial to inform clients about possible sexual side effects and to assure men that erectile difficulties will resolve if the medication is stopped. In addition, it is essential to inform clients that antidepressants do not take effect immediately. Often, it takes up to 2 weeks for an initial response to occur; a full response may not take place until an individual has been taking a therapeutic dose for 4 to 6 weeks. SSRIs also have the potential to cause significant symptoms if they are stopped abruptly, known as discontinuation syndrome. Vomiting, diarrhea, nausea, anorexia, dizziness, headache, insomnia, irritability, disturbances of vision, fatigue, and tremor, as well as “electric shock” sensations in the back and arms have all been reported (e.g., Coupland et al., 1996). Paroxetine, with its short half-life, has been noted to cause discontinuation symptoms more frequently than the other SSRIs (Barr et al., 1994). Fluoxetine, with a long half-life, rarely causes such difficulties, and in fact is sometimes used short-term to assist in tapering clients off of other SSRIs. Again, educating clients about the potential symptoms associated with stopping SSRIs is important—they should be encouraged to discontinue such medications only when tapered under the supervision of a prescribing clinician. Other Serotonergic Agents There has been a dramatic increase in the number of antidepressant medications available to clinicians over the past 15 years. In addition to the SSRIs, several newer medications have come onto the market that have effects on other neurotransmitters as well as serotonin. These have been demonstrated to be effective antidepressant medications in their own right; however, we know less about their efficacy in treating posttraumatic stress. Venlafaxine (Effexor) Venlafaxine is a potent serotonin-norepinephrine reuptake inhibitor (SNRI) that has been found to be effective in the treatment of depression and anxiety. Its side effect profile is similar to that of the SSRIs. It tends to be activating rather than sedating and has a relatively high likelihood of causing sexual side effects and discontinuation syndrome (both of these are due to its serotonergic activity and are similar to the side effects described above for the SSRIs). The regular form of venlafaxine was associated with elevations in blood pressure in some individuals; this is seen less with the extended-release form of the medication, venlafaxine XR. It is nevertheless appropriate to monitor blood pressure in individuals taking venlafaxine. Given its similarity to the SSRIs, one would expect venlafaxine to be a useful treatment for PTSD. In fact, a 24-week placebo-controlled study of venlafaxine in PTSD, venlafaxine was superior to placebo in alleviating reexperiencing and avoidance/numbing, but not hyperarousal (J. R. Davidson et al., 2006). This is not surprising given venlafaxine has noradrenergic effects and tends to be activating. In a second RCT, venlafaxine was compared to both sertraline and placebo (J. R. T. Davidson, Pearlstein et al., 2001). In this trial, venlafaxine and sertraline were equivalent in reducing PTSD symptoms, however the placebo response was also relatively high and the effect sizes for both venlafaxine and sertraline were small. In a larger 6-month multisite

RCT, the extended-release formulation of this drug was found to be helpful in both short-term and continuation treatment of PTSD (Davidson, Baldwin et al., 2006). Overall, it appears that venlafaxine is a useful medication for PTSD, similar to the SSRIs, but perhaps not an ideal medication for those with high levels of hyperarousal. Duloxetine (Cymbalta) Duloxetine is another SNRI, often used to treat depression and chronic pain. Two open trials (Villarreal et al., 2010; Walderhaug et al., 2010) indicate apparent efficacy for PTSD, the latter of which also decreased depressive symptoms and improved sleep. As yet there are no RCTs of Duloxetine in the treatment of PTSD. Bupropion (Wellbutrin) Bupropion is unrelated to any other antidepressants. Its precise mechanism of action is unknown—it weakly inhibits the reuptake of serotonin and epinephrine, and more potently inhibits the reuptake of dopamine. It appears to have stimulant-like effects, and therefore it is usually recommended that bupropion be taken before 5 p.m. to prevent insomnia. In line with this activation, a substantial portion of individuals treated with bupropion experience agitation or restlessness, a side effect that must always be kept in mind when treating trauma survivors, who may already complain of autonomic arousal. The most concerning side effect with bupropion is a 0.4 percent risk of causing seizures, which is four times that of other antidepressants. This risk is increased in patients with bulimia, and the medication is therefore contraindicated in those with a prior history of seizure disorder or a history of bulimia. Because some survivors of childhood abuse may engage in distress reduction behaviors, including bingeing/purging (as described in Chapter 2), it is important to ask about a history of eating disorders. There are only two reports in the literature on the use of bupropion in PTSD. This may reflect concerns that bupropion could be too activating in those with significant posttraumatic distress and anxiety. In an open trial of 17 combat veterans with PTSD, bupropion was found to decrease hyperarousal but have no effect on intrusions or avoidance, or, in fact, on measures of overall PTSD severity (Canive et al., 1998). However, in an RCT with a relatively small sample size of 43, bupropion was not found to be helpful for either symptoms of depression or PTSD (Becker et al., 2007). More research is needed before any definitive recommendations can be made regarding the use of this medication in PTSD, but initial reports are not particularly encouraging. Mirtazapine (Remeron) Mirtazapine is another unique medication that has activity on both serotonin and norepinephrine, as well as some presynaptic alpha-adrenergic blockade. It has antagonism at some serotonin receptor sites, which is hypothesized to be the reason that it has fewer serotonergic side effects than do the SSRIs, including less sexual side effects. It is sedating and is usually given at night to help with sleep. Unfortunately, it also can cause significant weight gain. There have been several open trials and one small RCT indicating good response to mirtazapine in PTSD (Alderman et al., 2009; Conner et al., 1999; J. R. T. Davidson et al., 2003), although another RCT found no effects for veterans (Davis et al., 2020). One open RCT in Korean War veterans found

mirtazapine to be superior to Zoloft in reducing symptoms of PTSD (Chung et al., 2004), one found that mirtazapine effective in the continuation treatment of PTSD (Kim et al., 2005); and one found that mirtazapine augmented the effects of sertraline for both PTSD and depressive symptoms (Schneier et al., 2015). There have also been case reports of the efficacy of mirtazapine for PTSD-related nightmares and sleep disturbance (Lewis, 2002). It has been suggested that this may be due to alpha blockade, a topic that is discussed later in this chapter. Trazodone (Desyrel) Trazodone is another serotonergic antidepressant that has alpha-adrenergic blocking activity. It is highly sedating and is used most frequently in psychiatry as a sleep agent. There have been a few case reports and open trials investigating the use of trazodone in PTSD, however there are no RCTs currently available. Significant side effects, aside from sedation, include dry mouth, blurred vision, gastrointestinal upset, and in males, risk of priapism (painful sustained erection that may require emergent medical intervention). Monoamine Oxidase Inhibitors Monoamine oxidase inhibitors (MAOIs) are antidepressants that have largely been replaced by SSRIs because of their considerable side effects and the dietary restrictions that must be followed when taking them. They are generally used for treatment of depression (especially the melancholic type) when other medications have failed. MAOIs inhibit the action of the enzyme monoamine oxidase, which breaks down epinephrine, norepinephrine, serotonin, and dopamine, thereby increasing the available levels of these neurotransmitters. MAOIs have significant side effects, including dizziness, headache, somnolence, weight gain, constipation, dry mouth, and sexual disturbances. MAOIs can also cause hypertensive crisis, especially in those individuals taking other sympathomimetic agents (such as cold preparations, decongestants, and weight reduction medications) or who eat tyramine-containing foods. The dietary restrictions are critical, as monoamine oxidase also breaks down tyramine. When tyramine is not metabolized, it displaces epinephrine and norepinephrine in the nervous system and adrenal glands, which can lead to severe headache, sweating, neck rigidity, palpitations, and dramatic blood pressure elevations. On rare occasions, MAOI-induced hypertensive crisis can lead to cardiac arrhythmias and cerebral hemorrhage. Therefore, individuals taking MAOIs must avoid foods containing tyramine. Clearly, MAOIs are not simple to take, and compliance can be very difficult. There have been three RCTs of phenelzine in PTSD. One showed efficacy in reducing reexperiencing symptoms and in global improvement, superior to both imipramine and placebo (Kosten et al., 1991). Two others were not superior to placebo at all (Frank et al., 1988; Shezatsky, et al., 1988). Open trials of phenelzine have had similarly equivocal results (e.g., Lerer et al., 1987). Finally, two RCTs of the reversible MAOI brofaromine reported no statistically significant effect on PTSD symptoms (Baker et al., 1995; Katz et al., 1994). Tricyclic Antidepressants The tricyclic antidepressants (TCAs) were introduced in the 1950s as a treatment for depression and were the mainstay of pharmacotherapy for depression until the introduction of the SSRIs in the 1980s. TCAs have been used less frequently over the past two decades due to their side

effects, which can be quite debilitating, and because of their potential lethality when taken in overdose. Common side effects of TCAs include sedation, dry mouth, gastrointestinal discomfort, constipation, blurry vision, sexual dysfunction, and weight gain. TCAs can also cause prolongation of the QTc interval on EKG and can, in some instances, lead to cardiac arrhythmias. There have been four RCTs of TCAs in PTSD and multiple open trials. Both imipramine and amitriptyline have shown effectiveness in reducing the reexperiencing and avoidant symptoms of PTSD, but not hyperarousal (Kosten et. al, 1991). One study with desipramine showed no efficacy (Reist et al., 1989). Overall, TCAs appear to be less effective for PTSD than are the SSRIs or the MAOIs (Friedman et al., 2009). However, all of the RCTs have involved veterans, not civilians, which may have affected the results. Like the SSRIs, TCAs can cause a discontinuation syndrome. This is thought to be due to cholinergic excess after the blockade of acetylcholine is removed. Discontinuation symptoms can include abdominal pain, nausea, vomiting, anorexia, chills, diaphoresis, diarrhea, fatigue, headache, malaise, myalgia, and weakness (Lejoyeux et al., 1996). Note that the above antidepressant medications carry the same “black box” warning regarding suicidality in children, adolescents, and young adults (age < 24 years) that the SSRIs do. Benzodiazepines Benzodiazepines are highly addictive medications that are used in psychiatry and general medicine for the treatment of anxiety and for sedation during procedures. They act on GABA and have many similarities to alcohol—in fact, they are used as the primary treatment in alcohol detoxification to prevent withdrawal. Their use is fraught with controversy due to the potential for abuse and dependence, as well as their ineffectiveness (if not harmfulness) in the treatment of posttraumatic stress (Guina et al., 2015). Benzodiazepines are often used in combination with illegal recreational substances, as well as with alcohol, and can be purchased “on the street” as drugs of abuse. Concerns about abuse are especially relevant in the treatment of trauma survivors, who often present complaining of intense, overwhelming anxiety that appears to require immediate relief. For such individuals, benzodiazepines may initially seem a godsend—the only thing that seems to dramatically reduce their level of arousal and/or address their panic. However, in the longer term, many people develop tolerance to the drugs’ effects, requiring higher and higher doses to achieve the same result. Some individuals develop physiological and psychological dependence and find that these medications are extremely difficult to discontinue. As mentioned earlier, benzodiazepines have similar actions to alcohol—including a withdrawal syndrome that can be potentially fatal if not managed properly. Although benzodiazepines are excellent antianxiety medications, they are only a short-term solution—they treat anxiety when it happens and for as long as the drug remains active in the bloodstream. Unlike SSRIs and other antidepressants that treat anxiety only after a therapeutic blood level has built up over several weeks, benzodiazepines only work “in the moment.”

Another concern with the use of benzodiazepines in trauma survivors, aside from the problems related to abuse and dependence, is the alteration in consciousness that they produce. Benzodiazepines not only treat anxiety and panic, but they may cause euphoria, disinhibition, sedation, diminished response to threat, impaired coordination, and feelings of being “zoned out” or “disconnected.” It might appear, at first glance, that this reduction in arousal would be useful in the context of trauma-related psychotherapy. One might imagine, for example, that decreased arousal could reduce the likelihood that the client would be overwhelmed when discussing emotionally laden, traumatic material. However, this is not borne out in clinical practice. Instead, regular use of benzodiazepines may interfere with the processing of traumatic material (Makkar et al., 2010), including in therapy (Guina et al., 2015; van Minnen et al. 2002). Research has clearly demonstrated that benzodiazepines affect both learning and memory performance. Triazolam has been shown to affect memory for emotional content, in a manner consistent with difficulties seen in those who have damage to the amygdala (Buchanan et al., 2003). Other studies have shown that lorazepam can cause impairment in the ability to learn behavioral strategies, a finding that may be due to impaired consolidation of long-term memory while under the influence of the medication (Matthews et al., 2002). Similar impairments in learning and memory have been found for alcohol (e.g., Mattila et al., 1998). These findings are not surprising, given that benzodiazepines are known amnestics and are used as such for sedation and in anesthesia. There are similar data regarding the effects of alcohol on memory and performance that may be generalizable to benzodiazepines, given its similar effects on GABA. Studies with alcohol have shown that information learned while under the effects of alcohol is best retrieved under the same conditions. Research suggests that alcohol disrupts hippocampal-dependent information processing (see a review by White et al., 2000). This finding might explain why it is difficult to remember specific experiences that occurred while under the influence of alcohol. It is important to educate clients early on about these concerns if they are taking benzodiazepines. When clients are informed about the potential for addiction and possible longer-term impacts on trauma processing, those not yet addicted are often more careful in how they use medications. In addition, those trauma survivors who are concerned about having less ability to sense danger often appreciate being informed about the potential for benzodiazepines to sedate and impair responsiveness. It may also be helpful to explain to patients that benzodiazepines work only in the short term—much as drinking a glass of wine will help to alleviate acute anxiety but will not treat it longer term. Unfortunately, when trauma survivors present to medical emergency rooms with complaints of intense anxiety and panic, they are often prescribed benzodiazepines as sole agents, without being provided adequate information about potential problems. All too frequently, the medication prescribed is alprazolam (Xanax), one of the most addictive of this class of medication (Ait- Daoud et al., 2018). Alprazolam also produces a type of euphoria that heightens the potential for psychological addiction and is associated with a particularly bad withdrawal syndrome with rebound panic and, sometimes, seizures (Ait-Daoud et al., 2018; Pecknold et al., 1988). The frequent use of alprazolam in emergency room settings means that trauma therapists and mental

health professionals often find that they need to intervene and educate clients who have already developed a problem with this medication. A systematic review and meta-analysis of 18 trials and observational studies found that benzodiazepines are ineffective for PTSD treatment and prevention, and risks associated with their use tend to outweigh potential short-term benefits. In addition to adverse effects in general populations, BZDs are associated with specific problems in patients with PTSD: worse overall severity, significantly increased risk of developing PTSD with use after recent trauma, worse psychotherapy outcomes, aggression, depression, and substance use. (Guina et al., 2015, p. 281) Specifically, two RCTs have found that Alprazolam failed to reduce symptoms of PTSD or lessen the likelihood of developing the disorder (Braun et al., 1990) and had no effect in reducing sleep disturbance associated with PTSD (Cates et al., 2004). In an open study of clonazepam and alprazolam administered within the first week posttrauma, benzodiazepine-treated patients showed a decrease in heart rate over time, but no other benefit was found at 6 months. In fact, more of the patients who received medication met diagnostic criteria for PTSD at 6 months than those who did not receive a benzodiazepine (Gelpin et al., 1996). Temazepam, given at bedtime for a week in victims of acute trauma, improved sleep and appeared to decrease symptoms of PTSD 1 week after discontinuation; however, there was no long-term follow-up (Mellman et al., 1998). Clonazepam, given at bedtime in a small RCT, was not superior to placebo across multiple sleep measures in combat-related PTSD (Cates et al., 2004). Finally, Girard and colleagues (2007) followed patients who had been mechanically ventilated in an intensive care unit. Six months out, those who received lorazepam during their ICU stay were more likely to have PTSD, and the total dose of lorazepam received correlated with the severity of symptoms. Apropos of these concerns, the Veterans’ Administration/Department of Defense Practice Guidelines for the Management of PTSD (U.S. Department of Veterans Affairs, 2017) strongly recommends against the use of benzodiazepines in the treatment of PTSD in veterans. At the present time, we advise that benzodiazepines be used with traumatized individuals only for the management of intense anxiety and panic attacks for which there is no other appropriate intervention. If used, these medications should be prescribed short term, and the initial treatment plan should include a discussion of risks and side effects as well as a plan for discontinuation. In addition, the clinician should have a discussion with the client regarding treatment with a less addictive, more long-term medication for intense, ongoing symptoms, such as an SSRI. Ideally, treatment with an SSRI would begin concomitantly with the benzodiazepine, with the benzodiazepine being tapered over the first 10 to 14 days of treatment. Close follow-up by the prescribing clinician is essential. In emergency settings, dispensing only enough medications to last 4 or 5 days is recommended as well—this ensures that the patient will not develop dependence before follow-up can occur. Mood Stabilizers As mentioned earlier, kindling has been hypothesized as one of the mechanisms by which PTSD develops under conditions of chronic stress. Because kindling theory was developed as a way to explain seizure disorders, this sparked interest in the use of mood stabilizing and anti-epileptic medications in PTSD. These medications have also been used to treat aggression and irritability

in PTSD and other psychiatric conditions. Only two medications have been FDA approved as mood stabilizers: lithium and valproic acid. Despite the fact that lithium is generally considered to be the “gold standard” for the treatment of classical bipolar disorder, there have been no clinical trials investigating its use in PTSD. Recently, there has been increased interest in using the atypical antipsychotic medications as mood stabilizers, and in fact there are now indications for their use in certain phases of bipolar disorder. These medications and their indications are discussed in the section on antipsychotics. Lithium There are some studies suggesting that lithium may be helpful for the treatment of PTSD-related irritability and aggression (e.g., Kitchner & Greenstein, 1985), but there have been no RCTs investigating the use of this medication for PTSD. Lithium can cause weight gain, tremor, rash, kidney failure, and thyroid problems; it is also potentially fatal in overdose. Lamotrigine (Lamictal) Lamotrigine is an anticonvulsant that affects N-methyl-D-aspartate (NMDA). In a small cohort of patients, lamotrigine was associated with improvements over placebo in the reexperiencing and avoidance/numbing symptoms of PTSD (Hertzberg et al., 1999). Given the small sample size of this study, little can be extrapolated from these findings until more research has been done. Lamotrigine is well documented as an effective mood stabilizer, as well as having antidepressant effects. Its most concerning potential side effect is Stevens-Johnson syndrome, a rare but life-threatening form of erythema multiforme that presents as a rash over the body, particularly the palms, soles, and backs of hands and feet. It can also involve lesions of the mucous membranes, and in severe cases, the kidneys, lungs, and digestive tract. For this reason, it must be slowly titrated with close observation. Valproic Acid (Depakote) Of all the mood stabilizers, valproic acid is probably the agent most commonly used for the control of aggression and irritability. In one RCT, valproic acid was not found to be superior to placebo, although this may have been due in part to small sample size and the fact that participants were veterans with refractory PTSD (Hamner et al., 2009). A systematic review and meta-analysis (Adamou et al., 2007) concluded that there is some evidence valproic acid can be effective in the treatment of PTSD and associated mood symptoms. Valproic acid can cause weight gain, mental dullness, and liver damage. It can also be fatal in overdose. Carbamazepine (Tegretol) Carbamazepine is another anticonvulsant frequently used as a mood stabilizer, although it is not FDA approved as such. It decreases excitability in the brain by stabilizing sodium channels; it also potentiates GABA receptors. In several small open trials, but no RCTs, carbamazepine was effective in reducing all three PTSD symptom clusters (e.g., Looff et al., 1995). Carbamazepine is generally well tolerated, although it can cause bone marrow suppression that may have serious consequences. It can also cause a significant drop in serum sodium levels. Blood counts and

electrolytes, as well as liver and kidney functions, therefore, need to be monitored periodically. Common side effects include gastrointestinal upset, weight gain, and sedation. Carbamazepine can be lethal in overdose. Topiramate (Topamax) Topiramate is an anticonvulsant that is used as an add-on mood stabilizer. It has the added benefit of assisting with weight loss, a notable effect as most of the more commonly used mood stabilizers can cause significant weight gain. The exact mechanism of action is unknown, although topiramate, like other anticonvulsants, appears to have some activity on GABAergic neurons. In a meta-analysis of five RCTs, topiramate had little effect on reexperiencing or avoidance symptoms of PTSD, and a small but significant effect on hyperarousal symptoms (Varma et al., 2018). Its most notable side effect is cognitive dulling, which some individuals find intolerable. Gabapentin (Neurontin) Gabapentin is another anticonvulsant that is used frequently in psychiatry as an add-on mood stabilizer, and as an adjunct in the management of anxiety and aggression. While gabapentin was designed to have effects on GABA, its exact mechanism of action is unknown. It has the benefit of having relatively few side effects and being less risky in overdose. Unfortunately, to date there have been only case reports and retrospective chart reviews of its use as an adjunct to other medications for PTSD. Levetiracetam (Keppra) Levetiracetam is another novel antiepileptic that has unique binding in the nervous system. It is thought to reduce neural transmission through its effects on calcium channels. In a small retrospective study of SSRI nonresponders, levetiracetam was reported effective in reducing symptoms of treatment-refractory PTSD (Kinrys et al., 2006). It remains to be seen whether these results are reproduced in larger controlled studies. Levetiracetam is generally well tolerated, with minimal adverse effects. The most common side effects are irritability, somnolence, and dizziness; in high doses it can cause some psychotic symptoms. Tiagabine (Gabitril) Tiagabine is an antiepileptic that enhances the activity of GABA in the brain. There have been two small trials of tiagabine in PTSD. The first was a double-blind extension of an open trial— responders in the initial phase were randomized to either drug or placebo. Relapse rates were not significantly different between the groups, but tiagabine treatment was associated with greater likelihood of eventual remission, and the authors concluded there was a possible role for tiagabine in the treatment of PTSD (Connor et al., 2006). However, in a later RCT, tiagabine was found to be no more effective than placebo (J. R. Davidson et al., 2007). The most common side effects of tiagabine are dizziness, headache, and nausea. Rarely, it has been associated with seizures in those without a history of epilepsy; it also has been reported to cause depression and other psychiatric symptoms.

Given the lack of adequate data regarding the use of mood stabilizers, they cannot be recommended as a first-line treatment for PTSD. They are probably most appropriate for use in those who do not respond adequately to treatment with SSRIs or other antidepressants, and in those who have significant behavioral disturbances due to aggression or agitated hyperarousal. Adrenergic Agents As described earlier in this chapter, dysregulation of the adrenergic system is clearly part of the biological underpinning of PTSD and other posttraumatic outcomes. Despite research that has demonstrated adrenergic hyperactivity in these states, there has been surprisingly little investigation of the use of antiadrenergic compounds in the treatment of posttraumatic stress. Beta-Adrenergic Blockade Propranolol (Inderal). Propranolol is a nonselective beta-adrenergic blocking agent that has effects on both the central and peripheral nervous systems. While primarily used in general medicine as an antihypertensive and antiarrhythmic medication, propranolol is also used in psychiatry to treat aggression, social phobia, performance anxiety, and akathisia. There are two potential uses of propranolol in the treatment of trauma survivors. First, propranolol has been administered soon after a trauma in the hopes of preventing the later development of PTSD. This approach is based on the theory that that blocking epinephrine and norepinephrine release following a trauma would reduce subsequent hyperconsolidation of trauma memories and reduce fear conditioning (Southwick et al., 1999). The second, more recent, use of propranolol has been to administer it prior to reactivating trauma memories, so that the memories are reexperienced in the absence of (propranolol-blocked) fear conditioning and are then reconsolidated/rewritten without the fear component, leading to a subsequent reduction in PTSD symptoms upon triggering (Brunet et al., 2018). In a comprehensive review of four prior meta-analyses, three RCTs, and one non-randomized study, Young and Butcher (2020) found little evidence that administration of propranolol soon after trauma exposure had any meaningful impact on the subsequent development of PTSD or ASD. However, when propranolol was administered along with reactivation of trauma memory, substantial reductions occurred in PTSD severity and autonomic hyperreactivity, and cognitive functioning was improved. This latter group of findings supports the possibility that propranolol- assisted psychotherapy might be a significant advancement in the future treatment of PTSD and ASD. Notably, frequent side effects of beta-blockers include gastrointestinal upsets (nausea, vomiting, diarrhea, abdominal pain), cold extremities and exacerbation of Raynaud’s phenomenon, sleep disturbance, dizziness, and fatigue. Beta-blockers can also cause congestive heart failure and bronchospasm; they are therefore contraindicated in individuals who have preexisting congestive heart failure, bronchospasm, and bronchial asthma, as well as those who have sinus bradycardia or first-degree heart block. In overdose, propranolol can lead to significant cardiac damage.

Alpha-Adrenergic Blockade Clonidine (Catapres). Clonidine, a presynaptic alpha 2-adrenergic agonist, suppresses the release of norepinephrine both centrally and peripherally. It is used as an antihypertensive agent and as an adjunct in the treatment for the autonomic symptoms associated with opiate withdrawal. The absence of RCTs for this drug, however, precludes definitive conclusions about its effectiveness in PTSD. The most common side effects of clonidine include dry mouth, drowsiness, sedation, dizziness, and constipation. Clonidine acts relatively rapidly and can cause severe hypotension acutely, within 30 to 60 minutes after administration. It must therefore be carefully dosed and monitored. Clonidine should not be given to those with severe cardiovascular disease, and care should be taken on discontinuation to avoid rebound hypertension. A significant problem with the use of clonidine is the development of physiological tolerance, leading to a gradual return of symptoms that sometimes do not respond to higher doses. Prazosin (Minipres). Prazosin is used more commonly than clonidine in psychiatric practice due to its more favorable side effect profile and the fact that, unlike clonidine, it does not lead to tolerance. Prazosin is an antihypertensive agent that blocks alpha1-adrenergic receptors centrally and peripherally. A small placebo-controlled trial in noncombat PTSD found that prazosin was effective at increasing time asleep as well as decreasing nightmares and awakenings (Taylor et al., 2008). Similarly, in two small RCTs in veterans, prazosin was superior to placebo in improving sleep, changing dream content away from trauma-related material, and improving overall PTSD symptoms (Raskind et al., 2007; Raskind et al., 2003). However, in one multisite RCT study of military veterans with chronic PTSD there was no difference between those treated with prazosin and those administered a placebo in terms of alleviating nightmares or improving sleep quality (Raskind et al., 2018). The most common side effects of prazosin are nausea, dizziness, headache, drowsiness, weakness, lack of energy, and palpitations. Prazosin has been noted to cause syncope (sudden loss of consciousness), which is believed in most cases to be due to hypotension. There are no absolute contraindications; however, care must be taken in patients who have preexisting heart disease, and blood pressure must be closely monitored. In overdose, alpha-blockers can cause significant cardiac problems, as well as fatality in very high doses. Guanfacine (Intuniv, Tenex). Guanfacine is a selective agonist of the alpha-2 adrenergic receptor, most often used to treat ADHD and hypertension. In the only RCT of this drug with adults, guanfacine had no therapeutic effect on PTSD symptoms, disordered sleep, or depression, although it did lower blood pressure (Neylan et al., 2006). A Final Note on Adrenergic Agents Although there are some research data suggesting that alpha- and beta-adrenergic blockers can be useful adjuncts in the treatment of some aspects of posttraumatic stress, with a few exceptions the investigations to date have been limited to case reports, open trials, and a handful of RCTs with relatively few subjects. Overall, these data suggest that beta-blockers may be helpful in

treating those individuals who suffer from intense symptoms of hyperarousal, but not in preventing ASD or PTSD, while alpha-blockers may be most helpful in those with intractable sleep disturbance and nightmares. The data are more encouraging for the use of propanol in psychotherapy, given several RCTs indicating its efficacy in blocking reconsolidation following trauma memory activation. Practical precautions to take with patients when prescribing these medications include the following:

Explaining the nature of and rationale for treatment with these agents, including the fact that their use in psychiatry is “off label” Communicating with and obtaining clearance from patients’ internists regarding using blood pressure–lowering agents Close monitoring of vital signs, especially in the first few weeks of treatment Caution regarding risk for falls in elderly or otherwise medically compromised individuals

Antipsychotics The antipsychotics are medications that block dopamine in the central nervous system. They differ from each other primarily in the extent of dopamine blockade, the specific receptors that they affect, and their side effects. The “typical” antipsychotics, (e.g., haloperidol [Haldol], fluphenazine [Prolixin], chlorpromazine [Thorazine]) were seen as a miracle cure for schizophrenia when they were first introduced in the 1950s. However, because they affect dopamine, they have potentially serious and debilitating motor side effects. These extrapyramidal symptoms (EPS—so called because they are thought to originate from the basal ganglia, rather than from the motor pyramids of the brainstem) occur often in the first few days or weeks of treatment, and manifest in three ways: (1) Parkinsonism—tremor, rigidity, shuffling gait; (2) akathisia—the subjective experience of feeling restless and unable to sit still; and (3) dystonia— stiffening of the limbs, jaw, or neck, often occurring quite acutely and requiring immediate medical intervention. Tardive dyskinesia (TD) can occur after long-term treatment with antipsychotics, although it has also been reported both early in treatment and after treatment is terminated. TD is characterized by rhythmic involuntary movements of the mouth, jaw, tongue, and lips (such as chewing, smacking, and pursing) as well as the extremities. The typical antipsychotics have also been associated with a condition known as neuroleptic malignant syndrome (NMS), a potentially life-threatening reaction that is characterized by altered mental status, autonomic dysfunction, fever, and muscle rigidity. In overdose, they can cause arrythmias and can be fatal. In the 1980s, a new class of antipsychotics was developed, referred to as “atypical” to distinguish them from the older medications. These newer medications, as a class, have significantly less risk of motor side effects. They also are relatively benign in overdose. Because of this lower risk, they are being used for an increasingly wide spectrum of nonpsychotic psychiatric disturbances, including mania, depression, severe anxiety, personality disorders, aggression, insomnia, and posttraumatic stress.

The use of these medications in nonpsychotic individuals, nonetheless, remains controversial. While the incidence of movement disorders and NMS is greatly reduced with atypical antipsychotics, the risk is not eliminated. The annual incidence of TD with typical antipsychotics has been estimated to be 5 percent in adults; for the atypicals, the annual incidence is around 0.8 percent (Correll et al., 2004). However, several lines of research have suggested that individuals with mood disorders have a higher likelihood of developing TD from antipsychotics than do those who have primary psychotic disorders. In one study, depressed individuals treated with typical antipsychotics developed TD at an annual rate of 13.5 percent (Kane, 1999). Such data have yet to be replicated using the newer generation of medications. However, given the high comorbidity of PTSD and depression, it might be reasonable to extrapolate from these data that traumatized individuals could also be at higher risk for these debilitating side effects. Given this potential risk, caution is warranted when using antipsychotics for this broader array of symptoms. Another emerging concern with the use of the atypicals is metabolic syndrome—a clustering of obesity, impaired glucose tolerance, hypertension, and increased lipids. Metabolic syndrome has been noted to be higher in those with severe mental illnesses than in the general population (for a variety of reasons, including lifestyle and poor self-care, among others) but has also been associated with psychotropic medications, particularly olanzapine, clozapine, and quetiapine. Recent studies have shown high discontinuation rates with all antipsychotics, and researchers and clinicians are beginning to reevaluate the risk-benefit profiles associated with their use (e.g., Huhn et al., 2019). Antipsychotics for PTSD Five of the atypical antipsychotics have been evaluated for efficacy in trauma. These are risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), ziprasidone (Geodon) and aripiprazole (Abilify). Lurasidone (Latuda), asenapine (Saphris), paliperidone (Invega), and iloperidone (Fanapt) are newer to the market, and it is likely that, in the coming years, their use in trauma will be investigated as well. Risperidone (Risperdal). There have been five RCTs of risperidone in PTSD. In the largest and most recent of these, a 6-month multicenter trial with over 300 subjects, adjunctive risperidone was evaluated in combat veterans with chronic PTSD. Surprisingly, risperidone was not associated with a reduction in symptoms of anxiety, depression, or PTSD in this population (Krystal et al., 2011). However, adverse events were more common with risperidone vs placebo, including self-reported weight gain, fatigue, somnolence, and hypersalivation. The authors suggest that the lack of efficacy for risperidone in this population may have been in part due to the fact that most participants were taking other medications, such as trazodone or quetiapine, which have similar actions and might have reduced the observed effect. They also question the widespread practice of using risperidone as a treatment for chronic PTSD and suggest care when it is prescribed in such situations. The other RCTs of risperidone were limited by some combination of small sample size, the presence of significant comorbidity, and the use of other psychotropic medications. Two of these

found that low-dose risperidone was helpful in the treatment of irritability and intrusive reexperiencing (Monnelly et al., 2003; Reich et al., 2004), and another found efficacy on the hyperarousal subscale of the CAPS (Bartzokis et al., 2005). Similarly, an RCT of risperidone in the treatment of PTSD symptoms among 20 female sexual assault and domestic violence survivors indicated significant reductions in PTSD, anxiety, and depression symptoms (Padala et al., 2006). However, another study investigated the use of risperidone in veterans with PTSD who also had psychotic symptoms and found a modest improvement in their psychotic symptoms but no statistically significant reduction in PTSD symptoms (Hamner et al., 2003). Of the atypicals, risperidone has the highest risk of extrapyramidal symptoms, in that sense it is the most “typical” of the atypicals. Risperidone also carries some risk of weight gain, sedation, and increase in prolactin levels, which can be a problem especially in women of childbearing age. Olanzapine (Zyprexa). There have been two small RCTs using olanzapine as an adjunctive treatment in nonpsychotic combat veterans with PTSD, and one as a monotherapy in a sample of noncombat-related chronic PTSD. The first indicated moderate response in symptoms of PTSD compared to placebo, but no significant difference in clinical global improvement (Stein et al., 2002). The second found a high placebo-response rate and no statistical benefit to olanzapine over placebo (Butterfield et al., 2001). Finally, an RCT of olanzapine monotherapy in 28 men and women found significant reduction in PTSD (Carey et al., 2012). The authors note that although olanzapine was well tolerated, substantial weight gain was reported nearly half of the participants in the olanzapine group. Olanzapine-related weight gain can be intolerable for some patients, and has been associated with the development of diabetes and metabolic syndrome. It is also quite sedating, and it may cause hypotension in some individuals. Quetiapine (Seroquel). An RCT of 80 military veterans found that quetiapine was effective in reducing PTSD symptoms, especially those involving reexperiencing and hyperarousal (Villareal et al., 2016). The authors of this study suggest that quetiapine may an effective monotherapy in the treatment of military PTSD. Quetiapine can cause significant weight gain and sedation and has been identified as a risk factor for the development of metabolic syndrome. Seroquel has attained a “street value” among substance-addicted individuals and for this reason has been taken off formulary in some clinical settings such as prisons. Aripiprazole (Abilify). There have been no RCTs of aripiprazole as a monotherapy for PTSD, although one trial (Naylor et al., 2015) tested its effectiveness as an adjunctive agent. In this study of 14 VA patients with SSRI-resistant PTSD there was no statistically significant benefit of adding aripiprazole to patients’ preexisting regimen, although the authors nevertheless suggested their findings held promise for the use of aripiprazole as an adjunctive treatment strategy. In the absence of RCTs, however, there have been several open trials and chart reviews examining the efficacy of aripiprazole. In an open-label augmentation trial, overall PTSD

symptoms improved—especially those involving avoidance/numbing symptoms—in contrast to risperidone and olanzapine which appear to be most useful in targeting reexperiencing and hyperarousal (Robert et al., 2009). A retrospective chart review of patients with PTSD and depression found that both PTSD and depressive symptoms improved with aripiprazole augmentation, with depressive symptoms improving slightly more (Richardson et al., 2011). Aripiprazole as monotherapy appeared to be effective in two open trials, with up to two thirds of the participants showing significant symptom improvement. However, in these trials one fourth and one third of the subjects, respectively, dropped out due to adverse side effects (Villareal et al., 2007). Aripiprazole is a unique medication, billed as a “dopamine equalizer”—it blocks dopamine in some areas of the brain, while increasing its activity in others. This can lead to paradoxical activation in some individuals, along with sedation and gastrointestinal upset. In studies of PTSD and aripiprazole there appear to be more dropouts due to adverse effects than with other antipsychotics. It may be that the activation is intolerable to some already-hyperaroused trauma survivors. Aripiprazole does not appear to cause significant weight gain, and it carries less risk of metabolic syndrome. Ziprasidone (Geodon). One RCT of ziprasidone was discontinued due to participant dropout— the cases were unblinded and it turned out that all of the dropouts receiving ziprasidone suffered adverse events (Kellner et al., 2010). In a second RCT of 30 patients with PTSD and comorbid depression, no significant effect of ziprasidone was found for any symptom cluster (Ramaswamy et al., 2016). Notably, Ziprasidone has a good metabolic profile, with little weight gain. It must be taken with food, as this increases its absorption into the blood by a factor of 2. The above data regarding antipsychotics suggest that, for treatment-refractory PTSD, particularly when there are psychotic symptoms present, atypical antipsychotics can be a useful addition to pharmacotherapy. In fact, in clinical practice, antipsychotics appear to be prescribed for symptoms of hyperarousal, insomnia, and aggression in significant quantities. However, given the high risk of side effects, the limited number of RCTs to guide their use, and the limited amount of data regarding their true efficacy for nonpsychotic posttraumatic stress, caution is recommended. It may be particularly difficult to convince highly anxious, distrustful individuals, especially those who do not want to be sedated, that antipsychotics are a reasonable alternative. At the present time, there is little indication that the antipsychotics are as effective as the SSRIs for PTSD, nor is there much evidence to suggest that antipsychotics represent a first-line choice for PTSD (Friedman et al., 2009). For those instances in which an antipsychotic is clinically warranted, the literature indicates some trends that may prove useful:

Atypicals are likely to be most helpful in patients with symptoms that have not responded or have partially responded to other pharmacologic interventions.

Olanzapine and risperidone appear to be most effective for symptoms of reexperiencing, intrusion, and hyperarousal. Quetiapine appears to be particularly effective in improving sleep and reducing nightmares. Aripiprazole may be most useful for patients with significant numbing/avoidance and/or comorbid depression.

Medications for Trauma-Related Psychosis As noted earlier in this volume, posttraumatic stress is occasionally accompanied by psychosis. Severe trauma can lead to brief psychotic disorder with marked stressors (BPDMS), and it can exacerbate symptoms in those with an underlying psychotic disorder such as schizophrenia. Some individuals may have intense reexperiencing symptoms that can be very difficult to distinguish from psychotic symptoms; others may have trauma-associated fear and avoidance responses that generalize to a wide range of stimuli and are hard to discriminate from paranoid delusions. Although there is no DSM-5 category for “PTSD with psychotic features,” there do appear to be some individuals with PTSD who have psychotic symptoms, who do not appear to have another underlying psychotic disorder, and who do not meet criteria for psychotic depression. (See Chapter 2 for a more complete discussion of this issue and the diagnostic dilemma involved.) In instances when trauma leads acutely to psychosis, the recommended treatment is antipsychotic medication. Often, as in BPDMS, the psychotic symptoms resolve over a relatively brief time period. In such situations, the antipsychotic may be tapered off over a course of several weeks, with close monitoring for recurrence as well as for the development of other posttraumatic symptomatology. The literature on BPDMS (and on its predecessor in DSM-III [American Psychiatric Association, 1987], Acute Reactive Psychosis) is extremely sparse, and there are no clinical trials investigating the use of medications specifically for this condition. Major depression with psychotic features, a not uncommon disorder in trauma survivors (see Chapter 2), is a particularly difficult condition both to diagnose and treat. When PTSD occurs comorbidly with psychotic depression, treatment with both an antidepressant (generally an SSRI) and an antipsychotic is indicated (see Farahani & Correll, 2012 for a review). Tricyclic antidepressants as monotherapy have generally been found to be ineffective for psychotic depression, as have SSRIs and antipsychotic medications (Wijkstra et al., 2015). Overall, response rates with the combination of an SSRI and an atypical antipsychotic have ranged in the area of 50 to 60 percent. Over the course of treatment, the symptoms of PTSD, depression, and psychosis should be followed closely. The decision to continue antipsychotic medication once psychotic symptoms have resolved must be made on an individual basis. This involves an assessment of risk of recurrence, prior history of psychosis, severity of depression, current levels of stress, and presence or absence of debilitating medication side effects. Research indicates that treatment with an antipsychotic for at least 4 months after remission is associated with a decreased risk of relapse (Flint et al., 2019).

There is an emerging literature on the use of medications that inhibit the HPA axis, such as mifepristone, for psychotic depression (e.g., Block et al., 2018). This practice is based on the finding that psychotic depression appears to be associated with abnormal HPA axis activity and elevated cortisol levels (Schatzberg, 2003). Note that the reconciliation of this finding with the generally low HPA axis activity and low cortisol associated with PTSD, as described in Chapter 14, is as yet unclear. Some recent research has suggested that nonpsychotic depression associated with trauma is biologically (in terms of HPA axis activity) more similar to PTSD than it is to “regular” depression that is not associated with trauma (Yehuda et al., 2004). Perhaps, as research continues, we will find a similar biological difference between psychotic depression that is associated with trauma and PTSD and psychotic depression that occurs in the absence of trauma. This conundrum, again, illustrates the complexity associated with studying and treating trauma. As of yet, there are no RCT data examining the use of HPA inhibition in psychotic depression that is comorbid with PTSD. For those situations where PTSD is accompanied by psychotic symptoms in the absence of depression or another psychiatric disorder, the literature provides little in the way of direction. Clinical and anecdotal experience suggest that, as for PTSD with comorbid psychotic depression, treatment with an antidepressant and an antipsychotic is indicated, with similar close follow-up and assessment of the need for ongoing medication. In our experience, antipsychotics are rarely helpful when the reexperiencing symptoms of PTSD mimic psychosis. Medications for Acute Traumatic Stress As described in Chapter 12, there is a relative dearth of literature on the pharmacological treatment of acute stress disorder (ASD). Instead, when treating acute trauma victims, clinicians often extrapolate from the literature on PTSD. There are, however, a larger number of studies examining the efficacy of medication in preventing posttraumatic stress disorders. Preventing Acute Stress or Early PTSD As described previously, two drugs have been evaluated for their ability to prevent the development of a stress disorder following exposure to a trauma. The first of these, propranolol, has been administered immediately posttrauma in a number of studies in the hopes that blocking adrenergic release would reduce the consolidation of trauma memories, thereby preventing the development of a stress disorder (Southwick et al., 1999). However, a comprehensive review of four previous meta-analyses (Young & Butcher, 2020) concluded that there was little evidence that administration of propranolol soon after a trauma served to prevent ASD or PTSD. Hydrocortisone also has been administered posttrauma as a potential prevention agent for acute traumatic stress. This approach is based on the notion that since PTSD is associated with a dysregulated HPA axis, and administration of a low dose glucocorticoid (dexamethasone) appears to interfere with the recall and reconsolidation of traumatic memories, the use of an exogenous glucocorticoid might reduce adrenergic release and thus prevent the hyperconsolidation of trauma memories (Yehuda & Golier, 2009).

A recent meta-analysis indicated that in contrast to propranolol, administration of hydrocortisone posttrauma had a modest effect in preventing PTSD and reducing the severity of emerging PTSD symptoms (Astill Wright et al., 2019). However, because hydrocortisone appears to be only mild preventative and is associated with serious potential side effects, including congestive heart failure, hyperglycemia, hypernatremia, and infection/septic shock, the authors counseled against its routine use pending further study. Treating Acute Stress A variety of medications have been used to mitigate or treat the acute effects of trauma. Their effectiveness is discussed below. Benzodiazepines. As described earlier, the benzodiazepines, although technically effective for the amelioration of acute anxiety, are not useful treatments for acute trauma and, in fact, may increase symptom severity and associated substance abuse, interfere with psychotherapy, and increase the risk of developing PTSD. Nevertheless, there are situations in which extreme distress (e.g., following a gang rape or witnessing the murder of a family member), especially in the emergency room setting, can only be adequately addressed by using a benzodiazepine. Under these circumstances, cautious use is acceptable, preferably in conjunction with beginning an SSRI or other antidepressant. However, because of the especially high risk for abuse and dependence associated with alprazolam, its use is not recommended. Antidepressants. There is only sparse data on the use of antidepressants in the acutely traumatized. In a single, small open trial of imipramine in pediatric burn victims who met ASD criteria, moderate improvement across all three symptom clusters was seen after 7 days (Robert et al., 1999). Surprisingly, there has been no research on the use of SSRIs in acute traumatic stress, despite the fact that SSRIs are the first-line medication treatment for PTSD and appear to have efficacies for all three of its symptom clusters. Notwithstanding the absence of empirical data, in actual clinical practice clinicians often prescribe SSRIs for those individuals who have been diagnosed with ASD, or who are otherwise experiencing acute posttraumatic symptoms, particularly panic attacks. In addition, SSRIs are often prescribed in the hope that they will prevent the development of lasting posttraumatic disturbance. The use of SSRIs in ASD seems reasonable, given the fact that the DSM-5 criteria for ASD are similar to those for PTSD and the data mentioned earlier suggesting that SSRIs may reregulate the HPA dysfunction thought to be involved in posttraumatic stress. For these reasons, the SSRIs are a reasonable choice for those individuals suffering from ASD who require intervention with medications. In light of the problems associated with the use of benzodiazepines, an SSRI is probably the best candidate for treating the acute anxiety of ASD, since these medications are efficacious in the treatment of both generalized anxiety and panic attacks, in addition to PTSD. Adrenergic Agents. As described earlier, the use of adrenergic medications in trauma is theoretically promising, depending on the context in which they are used. Most research indicates that propranolol is not helpful in reducing the risk of PTSD, nor is it especially useful

as a stand-alone medication for PTSD. However, as noted later in this chapter, it may be more effective when it is used in the context of psychotherapy to block reconsolidation of activated fear conditioning. Other Agents. As with the SSRIs, there is very little literature on the use of other psychotropic agents in ASD. More research is necessary to evaluate the use of medications to treat ASD, as well as the potential utility of mood stabilizers used early on to interfere with the kindling that might lead to PTSD. Medications for Sleep Disturbances of sleep can be one of the most distressing and debilitating aspects of posttraumatic stress. Trauma survivors often complain of initial insomnia, frequent nighttime wakenings, nightmares, early morning wakenings, and subjective feelings of being not rested even when they have slept. Sleep studies have been inconclusive in terms of the underlying physiological mechanisms of disordered sleep in traumatized individuals. Although some research has indicated that trauma leads to disordered rapid eye movement (REM) sleep and that nightmare sufferers have more frequent nighttime wakenings (Mellman et al., 2014), other studies have found no correlation between subjective complaints of sleep disturbance and abnormalities on polysomnographic sleep studies in the laboratory (e.g., Hurwitz et al., 1998). Regardless, sleep problems remain a frequent complaint in trauma survivors. Finding medication that improves the quality and quantity of sleep without causing daytime drowsiness or oversedation can be challenging. The literature on treating PTSD-related sleep disturbance is limited. However, many of the medications that improve posttraumatic symptomatology can help with sleep—including the mood stabilizers, the antipsychotics, the tricyclics, and some antidepressants. Many of these medications are also sedating, and clinicians can take advantage of this side effect by prescribing them to be taken at night. Although the SSRIs as a class may improve symptoms across all three clusters of PTSD symptomatology, they can sometimes cause an increase in levels of anxiety and activation, especially in the first few weeks of treatment, and often require the addition of a sleep agent. Trazodone (Desyrel) Trazodone, as discussed earlier, is a highly sedating antidepressant. In fact, it is used more commonly as a sleep agent in low doses than as a treatment for depression. Trazodone is an effective hypnotic, and it does not cause dependence or withdrawal. However, it can cause a feeling of being hungover and daytime drowsiness that some patients cannot tolerate. Several studies and reports indicate that trazodone is a useful sleep agent for PTSD survivors (e.g., Ashford & Miller, 1996). As a sleep agent, there is an optimal “window” of effectiveness—it is generally recommended to go to bed within 1 to 1.5 hours after taking trazodone in order for it to effectively bring on sleep. Trazodone is generally considered a safe adjunct to other psychotropics. Antihistamines

Beyond a single study supporting the use of hydroxyzine (Ahmadpanah et al., 2014), there is no specific literature on antihistamines for PTSD. However, diphenhydramine (Benadryl, which is available over the counter), and hydroxyzine (Atarax, Vistaril) are used commonly as sleep agents because of their sedating properties (Ringdahl et al., 2004). They have relatively few side effects, little risk associated with overdose, and little potential for abuse or dependence. Importantly, however, their chronic use is contraindicated, since extended (i.e., over 3 years) use of anticholinergic medication increases the risk of dementia, including Alzheimer’s disease, in older people (Gray et al., 2015). The major acute side effects associated with their use as sleep agents are dry mouth and the potential for morning drowsiness. Nonbenzodiazepines Zolpidem (Ambien). Zolpidem is a commonly prescribed nonbenzodiazepine sleep agent. It has a rapid onset of action and causes minimal daytime sedation, due to a short half-life of about 2.5 hours. Compared to benzodiazepines, it has significantly fewer effects on cognition and memory (Terzano et al., 2003) and appears to have less risk of abuse. However, a review of pharmacological treatments for PTSD concluded that “non-benzodiazepine hypnotics such as zolpidem appear ineffective in treating PTSD-related sleep disturbance” (Lipinska et al., 2016). Caution is warranted when using this medication, as the manufacturer notes the potential for tolerance and rebound insomnia in some individuals, as well as psychological dependence, and recommends limiting the use of this medication to no more than 3 weeks. The main side effects associated with zolpidem are headache, drowsiness, fatigue, and dizziness. Zolpidem has also been noted to cause perceptual disturbances shortly after administration; this is thought to be due to the rapid induction of a hypnotic or dreamlike state associated with peak plasma levels. It is also available in a controlled-release formulation (Zolpidem CR), which has a longer length of action. Zaleplon (Sonata). Zaleplon is another nonbenzodiazepine hypnotic. It is ultra-short-acting, with a half-life of about 1 hour. There have been no studies investigating its use in PTSD. However, because of its short length of action, zaleplon may be a good choice for those traumatized individuals who are particularly concerned about sedation and decreased responsiveness to threats. Conversely, for individuals who suffer from early wakening, or who wake frequently throughout the night due to trauma-related nightmares, the effects of zaleplon may not be long- lasting enough. The main side effects associated with zaleplon are headache, nausea, and dizziness. Zaleplon can also cause a hypnagogic state similar to that caused by zolpidem (Terzano et al., 2003). Eszopiclone (Lunesta). Eszopiclone, another nonbenzodiazepine sleep agent, is related to zolpidem and zaleplon. It appears to be generally well tolerated. In an RCT of 24 patients, eszopiclone decreased sleep disturbance associated with PTSD (Pollack et al., 2011). However, another RCT found no effects of eszopiclone on PTSD-related sleep relative to a placebo (Dowd et al., 2020). The main side effects are a bad taste in the mouth on waking, which some report as intolerable, and headache, as well as the possibility of a hypnagogic state, as described earlier. Benzodiazepines

As discussed earlier, there are significant risks associated with the use of benzodiazepines. If at all possible, clinicians should try other agents before using benzodiazepines as sleep agents. The risk for physiological and psychological dependence is high, as is the potential for abuse. This being said, there are times when no other treatment for the severe insomnia associated with posttraumatic stress is adequate. In such cases, benzodiazepines should be prescribed for short periods of time only, and with careful monitoring of patterns of use and reported need for dose increases. Melatonin Melatonin, and the melatonin agonist ramelteon (Rozerem) are used increasingly widely in clinical practice to assist with sleep initiation. These agents have minimal side effects and no potential for tolerance or abuse, and therefore are potentially promising agents for sleep disturbance in PTSD. Unfortunately, there is no literature on these medications for PTSD. Melatonin is available over the counter, while ramelteon is a prescription medication. Strategies for Medicating Sleep Disturbances in Posttraumatic Stress The recommendations for medicating posttraumatic sleep disturbance can be summarized as follows:

Maximize use of current psychotropic regimen for sleep efficacy (for example, paroxetine, TCAs, trazodone, mirtazapine, antipsychotics, mood stabilizers). Often this can be accomplished by switching from twice daily to once daily at bedtime dosing. If necessary, add a nonaddictive sleep agent such as trazodone or an antihistamine. In those individuals with nightmares as well as sleep disturbance, consider prazosin. Switch to one of the nonbenzodiazepine hypnotics such as zolpidem or zaleplon. If these are ineffective, judicious use of a benzodiazepine may be supportable.

Medications for Dissociation The literature on pharmacological approaches to the treatment of dissociative symptomatology is extremely sparse, and many clinicians make the presumption that medications will not be helpful for dissociation. To some extent, this is correct; currently available medications do not do much for such symptoms as amnesia, cognitive disengagement, depersonalization, rapid switching from one state to another, or losing track of time. However, because dissociative symptoms do appear to intensify under stress, much of the literature encourages treatment of the conditions that may occur comorbidly with dissociative disorders, including depression, anxiety, and PTSD. A few open trials (e.g., Bohus et al., 1999) have suggested that naltrexone may help to reduce dissociative symptoms and posttraumatic flashbacks in borderline patients, while others have described its effectiveness in reducing self-injurious behavior in dissociative identity disorder (Loewenstein, 2005). The differentiation of posttraumatic reexperiencing from psychotic hallucinations (as described in detail in Chapter 3) can be particularly difficult in highly dissociated individuals. Unfortunately, some clients are treated unnecessarily, sometimes for long periods of time, with

antipsychotics that have little effect and have significant side effects, because they were incorrectly judged to be psychotic. Some clinicians find that low doses of antipsychotics are helpful in treating the anxiety and intrusive symptoms of PTSD that can accompany dissociation (Loewenstein, 2005). However, in our anecdotal experience there are times when such medications can in fact increase dissociative responses by decreasing awareness of the environment, much in the way benzodiazepines do. C. A. Morgan and colleagues (2003), in a review, suggest several approaches that might be beneficial for dissociation, given what we know about the biology of dissociative states: (1) treatment of hyperarousal with adrenergic blockers, as traumatized individuals often dissociate when stressed or overwhelmed; (2) treatment with medications that affect GABAergic neurons, such as SSRIs; and (3) use of medications that affect N-methyl-D-aspartate (NMDA), such as lamotrigine. However, these recommendations are based on presumptions about biology rather than clinical outcome data. Our general approach to the treatment of dissociation involves psychotherapy as the primary intervention; in the best-case scenario, as clients process trauma and learn skills that assist with emotional regulation and interpersonal relatedness, dissociation recedes as part of the clinical picture. However, when dissociating clients have significant posttraumatic, depressive, or other anxiety symptoms, treatment with pharmacotherapy may be appropriate. Medications for Other Comorbid Disorders As described in Chapter 2, PTSD is highly comorbid with other psychiatric disorders, including depression, other anxiety disorders, and psychotic disorders. The trauma-focused clinician should not presume that psychotherapy for traumatic stress, alone, will necessarily address this broader range of symptoms. In cases where clients present with one or more comorbid disorders, appropriate pharmacological treatment for these conditions is recommended. Fortunately, when depression or other anxiety symptoms are involved, SSRIs are the treatment of choice, and symptoms of posttraumatic stress can be treated simultaneously. As described earlier, clear psychotic symptoms require the addition of an antipsychotic medication. The general principles of medication management in trauma survivors, described earlier in this chapter, especially regarding side effects and concerns about overmedication, are relevant when treating comorbidities as well as when treating posttraumatic stress. Larger-Picture Treatment Strategies In Effective Treatments for PTSD: Practice Guidelines from the International Society for Traumatic Stress Studies, Bisson and colleagues (2020) highlight the general understanding that the SSRIs are the first-line treatment for PTSD. They offer an algorithm-based approach consisting of three steps:

1. If the client and their clinician agree on the use of medication, prescribe fluoxetine, paroxetine, or sertraline.

2. If Step 1 is ineffective, replace or cross-taper the initial drug with one of the other two SSRIs, or initiate treatment with venlafaxine.

3. If Step 2 does not yield an adequate response, augment with either prazosin or risperidone, or, if risperidone is not well-tolerated, consider quetiapine.

They note that if none of these steps produce an adequate response, other less evidence- supported medications may be used, including amitriptyline, mirtazapine, phenelzine, or an anticonvulsant. The treatment guidelines of the American Psychiatric Association (APA) work group on ASD and PTSD (Ursano et al., 2004) recommend that

1. SSRIs be used as first-line treatment 2. benzodiazepines may be helpful for anxiety and sleep, but caution is warranted

regarding dependence and potential for increased PTSD symptoms 3. atypical antipsychotics may be useful adjunctive therapy in those refractory to SSRIs 4. anticonvulsant medications may be useful in individual cases, but data for

recommending them are lacking The Department of Veterans Affairs and the Department of Defense (2023) guidelines caution more strongly against the use of atypical antipsychotics and benzodiazepines. They recommend initial monotherapy with paroxetine, sertraline, or venlafaxine, which have the strong support in the literature for efficacy in treating PTSD. They note that while there is insufficient evidence for most antipsychotics as pharmacotherapy for PTSD, the recent findings regarding lack of efficacy of risperidone as adjunctive therapy indicate that the metabolic risks of this medication outweigh any potential small benefit. A review from the Harvard Psychopharmacology Algorithm Project suggests a slightly different approach (Bajor et al., 2011). The authors propose that antidepressants may not in fact be the best first-line treatment in all cases. Instead, the most effective initial use of psychopharmacology might be to target sleep, nightmares, and reexperiencing through the use of prazosin or trazodone. Next, a trial of SSRI for ongoing symptoms of PTSD would be warranted. The authors suggest that antipsychotics be reserved for PTSD-related psychosis, or as augmentation for residual symptoms. Our approach to trauma clients incorporates elements of the above recommendations, the literature reviewed in this chapter, and our practical experience with patients. Generally, the psychopharmacological treatment algorithm we recommend is as follows: First-line treatments

1. For patients with significant posttraumatic symptoms, use an SSRI or SNRI. 2. If sleep disturbance or nightmares are prominent, trazodone or prazosin may be

started concurrently with an SSRI. Alternatively, a sedating agent such as mirtazapine may be used to help with sleep difficulties.

3. In patients with overwhelming hyperarousal, treatment with an alpha- or beta-blocker may be considered.

4. When clear psychosis is present, an atypical antipsychotic should be started concurrently with an SSRI.

Second-line treatments for refractory symptoms or partial responders

1. In patients who do not respond to an SSRI, or who have a partial response, a trial of a second antidepressant is warranted.

2. If prominent symptoms still remain, adjunctive low-dose antipsychotic medication may be initiated.

3. When significant aggression is present that is refractory to SSRI treatment, or when antipsychotic medication is contraindicated or unacceptable to the patient, treatment with a mood stabilizer should be considered.

4. As described above, benzodiazepines should be reserved for cases of overwhelming anxiety and/or acute distress that requires immediate, short-term down-regulation.

Once a treatment response is obtained, ideally medication should be continued for 1 year to maintain benefits. SPECIAL TOPIC: REPURPOSED DRUGS AND DRUG-ASSISTED PSYCHOTHERAPY As noted earlier in this chapter, two drugs with long track-records in other medical domains, propranolol and hydrocortisone, have been repurposed to potentially prevent or treat PTSD. However, research indicates that propranolol does not appear to prevent ASD or PTSD whereas hydrocortisone may be slightly more effective. More encouragingly, propranolol appears to have some efficacy in the treatment of posttraumatic stress when administered just prior to psychotherapy sessions, as described below. In addition, several recreational drugs have been found to inhibit reconsolidation of conditioned fear and/or to produce psychological states that facilitate emotional closeness, existential insight, and feelings of well-being—all of which may assist in the psychotherapeutic treatment of trauma-related symptoms. We first describe these potential medications and the evidence for their application to posttraumatic stress, and then outline, in several cases, their potential use in medication-assisted psychotherapy. Notably, the use of medications to block reconsolidation of the implicit, fear-related components of trauma memories is a different approach to reconsolidation than what was described in Chapter 9 for psychotherapy. In psychotherapy, reconsolidation takes advantage of the temporary destabilization and pliability of activated memory to “add” new insights and emotional counterconditioning, so when memories of traumatic events are reconsolidated, they no longer contain as much of their original conditioned emotional distress and painful schema, and may include more positive associations. In pharmacological interventions, the goal is to (a) biologically facilitate the extinction of the fearful component of trauma memory, whether through the endocannabinoid system (Hill et al., 2018) or via some other mechanism; and/or (b) prevent reconsolidation of the previously conditioned distress back into neural tissue, so that it is no longer triggerable. In other words, psychotherapy may harness reconsolidation to update traumatic memories so they are less distressing, whereas these medications seek to both

extinguish fear conditioning and keep it from reappearing by blocking subsequent reconsolidation. Propranolol Revisited As noted earlier, propranolol is a noradrenergic beta-blocker. Research suggests that when it is administered prior to memory activation in psychotherapy it can block reconsolidation of fear- conditioning and thereby reduce the ability of triggered trauma memories to generate fearful responses (e.g., Brunet et al., 2018), perhaps especially when it is given over multiple sessions (Roullet et al., 2021). This effect, in turn, may lead to reduced PTSD severity, hyperreactivity, and PTSD-related cognitive difficulties (Young & Butcher, 2020). Cannabinoids: Tetrahydrocannabinol (THC) and Cannabidiol (CBD) Given that many chronic PTSD survivors, including veterans, appear to gravitate to extra-legal cannabis use (Hill et al., 2021), it is perhaps not surprising that exogenous cannabinoids have been found helpful in reducing PTSD symptoms in several studies (Krediet et al., 2020). As noted earlier, cannabinoids act on the endocannabinoid (eCB) system which, in turn, has downstream effects on the amygdala and the HPA axis. Dysregulated eCB signaling, including downregulated cannabinoid type 1 receptors, has been linked to posttraumatic hyperarousal, sleep disturbance, and intrusive memories (Hill et al., 2018; Morena et al., 2016). In theory, taking exogenous cannabinoids might reregulate this process. Of the many different cannabinoids, THC and CBD have been most studied for their possible effects on PTSD. Several lines of research indicate that cannabinoid administration increases fear extinction (e.g., Rabinak et al., 2013), prevents the reconsolidation of hippocampally mediated fear conditioning (Stern et al., 2017), and reduces amygdaloid responses to threatening stimuli (Phan et al., 2008). These findings support a limited literature that suggests THC and a related synthetic (nabilone) may reduce PTSD symptoms, sleep disturbance, and nightmares (e.g., Jetly et al., 2015; Roitman et al., 2014). Recently, a prospective non-RTC study of 150 PTSD sufferers found that over the course of a year those using dispensary-obtained cannabis reported decreased PTSD symptom severity and were 2.5 times more likely to no longer meet DSM-5 criteria for PTSD as compared to those with PTSD who did not use cannabis (Bonn-Miller et al., 2022). Lasty, a double-blind crossover RTC of 80 veterans found no statistically significant difference in PTSD symptom reduction in the first phase of the study, but significant reductions in PTSD symptoms associated with combined THC and CBD in the crossover phase (Bonn-Miller et al., 2021). Ketamine Ketamine is a noncompetitive N-methyl-D-aspartate-receptor antagonist, initially developed as a surgical anesthetic and later used as a recreational psychedelic. Its primary psychiatric use is as a rapid antidepressant that acts on glutamatergic and other related signaling pathways. The glutamate system is known to, among other functions, support fear extinction and block its reconsolidation (Krediet et al., 2020). Its short-term effectiveness in reducing depressive

symptoms is so substantial that in 2019 the FDA approved esketamine (the “S” enantiomer of ketamine, brand name Spravato), in conjunction with an oral antidepressant, for major depression accompanied by suicidal ideation or behavior (FDA, 2019). Most recently, it also has been studied as a potential rapid treatment for PTSD. The few studies of ketamine and PTSD are encouraging, although they point to a problem also found in ketamine treatment for depression: its effects often do not persist for long. An RCT involving a single ketamine infusion as compared to an infusion of midazolam (Feder et al., 2014) revealed a rapid reduction in PTSD symptoms, albeit an effect that faded by 7 days. In an effort to extend and enhance this outcome, Albott and colleagues (2018) administered six ketamine infusions over 12 days to 15 people diagnosed with PTSD and treatment-resistant depression. This open-label trial resulted in a PTSD remission rate of 80 percent, and 93 percent of participants reported decreased depression. Repeated infusions were associated with transient dissociative symptoms, but no participants reported worsening of PTSD symptoms. As has been found for depression (Murrough et al., 2013), repeated administrations resulted in a longer period of effectiveness, with a median PTSD remission duration of 41 days. A final RTC examined the effects of a single infusion of ketamine in the context of a mindfulness-based cognitive therapy that includes traumatic memory activation (Mindfulness Based Extinction and Reconsolidation) as a treatment for refractory PTSD (Pradhan et al., 2017). Notably, this drug-assisted psychotherapy resulted in an extended recovery duration of 34 days. Although this extended remission period was still relatively short-lived, it involved only a single administration, as per the Feder et al. study. With multiple infusions, it is possible that remission might have been longer. Psilocybin Psilocybin is a 5-HT2A agonist. Originally a recreational hallucinogen derived from several genera of mushrooms, a number of studies have been conducted regarding psilocybin’s efficacy for depression, anxiety, addictions, and obsessive-compulsive disorder. Most significantly, psilocybin was recently named a “breakthrough therapy” for depression by the FDA (Norring & Spigarelli, 2024), a designation designed to expedite research. Psilocybin has been shown to promote fear extinction, neurogenesis, and reduced amygdaloid reactivity (Krediet et al., 2020). Relevant to its possible use in drug-assisted psychotherapy for traumatic stress, psilocybin administered during therapy also appears to heighten empathy and interpersonal trust, increase mindfulness and acceptance, and promote openness to experience. However, no RCT-level research to date has investigated the specific effectiveness of this drug in the treatment of PTSD. Given the successes associated with MDMA (see below), it is possible that psilocybin, too, might be a candidate for drug-assisted psychotherapy. Mdma MDMA (3,4-methylenedioxymethamphetamine), referred to as ecstasy or molly when used as a recreational drug, is an indirect serotonergic agonist, promoting serotonin (and to a lesser extent, noradrenaline) release and inhibiting reuptake (e.g., Rothman & Baumann 2002). It also triggers

the release of oxytocin, a peptide involved in social bonding (Vizeli & Liechti, 2018). Research indicates that MDMA attenuates amygdaloid activity, enhances fear extinction, blocks fear reconsolidation, and promotes empathy, introspection, openness, and feelings of closeness to others (Feduccia et al., 2018; Krystal et al., 2021). These outcomes are all consistent with what is thought to be helpful in remediating PTSD and contributing to the efficacy of psychotherapy. Recent research, especially a study published in Nature Medicine (Mitchell et al., 2021) indicates that MDMA may be the most promising medication thus far for treating PTSD within the context of a specific psychotherapy. Apropos of this, the FDA (2019) established Expanded Access research permission for MDMA-assisted therapy for PTSD, a program designed to address urgent and life-threatening conditions in patients who do not currently have promising treatment options. There have been several RCTs examining the effects of MDMA-assisted psychotherapy for PTSD. In the first of these, 12 patients with treatment-resistant PTSD had an 83 percent remission rate after just two memory activation and MDMA doses, as compared to a 25 percent rate for eight control patients (Mithoefer et al., 2011). A follow-up study found that these effects were sustained for over three years (Mithoefer et al., 2013). Mithoefer and colleagues (2018) then conducted a double-blind, dose-response, phase 2 RCT on a sample of veterans, firefighters, and police officers, and found equivalent results with large effect sizes for two separate dosages and sustained outcomes at 12-month follow-up. In another double-blind RTC, Ot’alora et al. (2018) essentially replicated these results, finding a 76 percent PTSD remission rate at 12 months for the MDMA group. In 2020, Jerome and colleagues conducted a long-term pooled analysis of six phase 2 RTCs of MDMA and PTSD (N = 105) reported by Mithoefer et al. (2019) and found an overall remission rate of 54.2 percent, versus 22.6 percent for the placebo group, after only two sessions of MDMA administration followed by memory activation. The Jerome et al. (2020) and Mithoefer et al. (2019) papers ultimately were retracted in August, 2024 for protocol violations. Therefore, it is not clear whether the data reported are valid, and these papers should be interpreted with caution. As significant as these studies are, a comprehensive multicenter double-blind phase 3 RCT by Mitchell and colleagues (2021) is one of the most tightly controlled studies on MDMA for PTSD thus far. Following psychiatric medication wash-out, 90 participants carrying a DSM-5 diagnosis of PTSD were either given three doses of MDMA or a placebo, and both groups received three preparatory and nine integrative therapy sessions. At the study endpoint (18 weeks after baseline), 67 percent of the participants in the MDMA group no longer met the diagnostic criteria for PTSD, compared with 32 percent of those in the placebo group. MDMA was found to be safe and well tolerated. Notably, the effect size for MDMA on PTSD symptom reduction was quite large—per the authors, greater than any other previously identified PTSD pharmacotherapy reported in the literature. These findings were generally replicated in a later study using a more diverse participant pool (Mitchell et al., 2023). Although research on the use of MDMA in trauma-related symptomatology has yielded very promising results, at the time of this writing an FDA panel concluded that the effectiveness of this drug was “unproven,” and that “the risks of MDMA treatment for post-traumatic stress disorder outweigh the benefits” (Reardon, 2024). This decision was surprising for many,

including the authors, and may be partially due to the FDA’s response to the informal structure of the psychotherapy module accompanying the MDMA protocol. As a result, though likely an eventual outcome, MDMA is not currently approved by the FDA for the treatment of PTSD. Drug-Assisted Psychotherapy As noted in this chapter, there are two separate ways in which psychoactive medications may improve outcomes of trauma-focused psychotherapy. The first of these employs pretreatment propranolol to encourage extinction and block reconsolidation of therapy-activated trauma memories. The second involves the combined use of MDMA and a specific form of psychotherapy. Method 1: Memory extinction and reconsolidation. This approach involves pretreatment administration of propranolol, followed by emotional activation of trauma memories, with an end goal of deconsolidating fear-laden memories into their unstable, labile form and then preventing them from reconsolidating. The signature example of this approach was conducted by Brunet et al (2018) although it was not replicated for severe PTSD survivors in another RCT by Roullet et al., (2021). In the Brunet study, 60 participants with PTSD were pretreated on six occasions with either propranolol or a placebo, followed 90 minutes later by a brief memory-activating protocol. Those receiving propranolol demonstrated significant reductions in PTSD following treatment as compared to placebo. Although the memory activation protocol did not involve psychotherapy, per se, it is likely analogous to the exposure-based treatment as outlined in Chapter 9. Apropos of this, a previous study of extinction learning in transcutaneously shocked participants found that a single dose of propranolol administered before an extinction trial caused a loss of conditioned fear responses and prevented a subsequent return of fear (Kroes et al., 2016). Taken together, research to date suggests that, as noted by Brunet et al. (2018), “pre-reactivation propranolol, a treatment protocol suggested by reconsolidation theory, appears to be a novel and efficacious treatment for PTSD” (p. 1). Method 2: Facilitation of the psychotherapy process. In contrast to drug-assisted interventions that rely solely on fear extinction and reconsolidation blocking, there has been considerable and growing interest in using psychedelics to “catalyze” the psychotherapy process (Mithoefer et al., 2019). In addition to altering fear conditioning, psychedelics have been used to (a) reduce the client’s distress while allowing them to remain fully engaged in the recall of trauma memories, while, at the same time (b) increasing their relational trust, empathy, and sense of emotional connection with the therapist; and (c) deepening their introspection and openness to internal experience (Krediet et al., 2020). Although various drugs have been suggested as agents for drug-assisted therapy, including ketamine, psilocybin, LSD, cannabis, and ayahuasca, by far the most research has been conducted on MDMA. In the usual MDMA-assisted therapy protocol, the client attends one or more preparatory sessions and then, in a series of sessions, is administered a dose of MDMA (followed by a booster 1 to 2 hours later) and engaged in a manualized but nondirective psychotherapy, often in the context of music designed to encourage internal awareness and introspection. The treatment manual used for MDMA-assisted psychotherapy was developed by Mithoefer and colleagues (2017), version 8.1 of which can be found at http://www.maps.org/research/mdma/mdma-

research-timeline/4887-a-manualfor-mdma-assisted-psychotherapy-in-the-treatment-of-ptsd. Note, however, that this is an experimental manual and was not developed for regular clinical practice. Further, the lack of a formal evidence-base for the psychotherapy component may have been instrumental in the FDA’s nonapproval (to date) of the MDMA protocol. We would note, however, that the specific elements of this guided approach are similar to what is recommended in this book:

A focus on safety and wellbeing Prebriefing before treatment begins The development of a positive therapeutic relationship, alliance, and support Nondirective interventions that foster self-exploration, self-healing, and “empathic presence,” and, critically The opportunity to process traumatic memories in the context of (in our terminology) the therapeutic window. As the manual directs, “therapists seek to maximize the benefits of the inner experience catalyzed by MDMA, while at the same time ensuring that the participant is safe and is not re-traumatized by internal conflicts that may arise” (p. 8)

As described earlier, this combination of MDMA pretreatment and psychotherapy has been associated with significant reductions, and in some cases full remission of PTSD, generally at a level not found for traditional psychiatric medications or psychological treatments. CONCLUSION This chapter has reviewed the wide range of medications that appear to be helpful in the treatment of posttraumatic stress. Two points should be reemphasized, however:

There is little reason to believe, based on the extant clinical literature, that psychiatric medication can by itself resolve most cases of PTSD or other forms of posttraumatic disturbance. Such medication is often helpful, but it tends to be palliative rather than curative. In many cases medication will yield some level of symptom reduction but will not completely remove all symptomatology and may only be effective for certain posttraumatic symptom clusters. In addition, among those clients who experience significant symptom remission, a significant proportion will relapse when medication is discontinued. Finally, some clients are unable or unwilling to tolerate the side effects of psychotropic medication, regardless of whether or not the drug might technically be effective. Although psychiatric medication will rarely permanently resolve all posttraumatic symptoms in a given client, it is often helpful. In our experience, the effective use of medication can provide initial symptom relief—sometimes before initial psychotherapy effects. This initial response may increase compliance, discourage dropout, and reduce the sleep deprivation and/or autonomic hyperarousal that contributes significantly to

many clients’ distress. In this way, psychiatric medication may provide benefits that allow the client to participate in psychotherapy long enough for the more substantial and enduring effects of psychological intervention to emerge.

Finally, new developments in drug-assisted psychotherapy have the potential to dramatically change how trauma treatment is conducted in the future. Importantly, research to date indicates that administering the relevant drugs (e.g., propranolol and MDMA) without concomitant psychotherapy is unlikely to be especially useful. Instead, these drugs are most effective when used synergistically with psychotherapy.