REVIEW

Psychopharmacological treatment for military posttraumatic stress disorder: An integrative review Jennifer Tawa, APRN (Psychiatric Nurse Practitioner)1 & Susan Murphy, PhD, APRN, RN-BS/MS (Program Director)2 1 2

Nursing Master’s Program, Rivier College, Nashua, New Hampshire Division of Nursing, Rivier College, Nashua, New Hampshire

Keywords Posttraumatic stress disorder (PTSD); veterans; pharmacotherapy; treatment; selective serotonin reuptake inhibitors (SSRI). Correspondence Jennifer Tawa, APRN, Center for Life Management, 10 Tsienneto Road, Derry, NH 03038. Tel: 603-434-1577; Fax: 603-930-4746; E-mail: [email protected] Received: June 2011; accepted: August 2011 doi: 10.1111/1745-7599.12016 Disclosure Jennifer Tawa was not employed by or affiliated with any United States Veterans Administration or the U.S. government during the composition period of this manuscript. The views reflected within this manuscript are not those of the USVA or military.

Abstract Purpose: Posttraumatic stress disorder (PTSD) is a serious mental health disorder. The current first-line psychopharmacologic treatment for PTSD is selective serotonin reuptake inhibitors (SSRIs). Recently, the efficacy of SSRIs has been challenged in favor of propranolol use. This article reviews the origins of PTSD, its impact within the veteran population, psychopharmacological treatment of PTSD, and current literature on the use of propranolol for PTSD treatment. Data sources: The search strategies used included ProQuest, Medline, CINAHL, and Psychiatry Online and were searched using the key terms: PTSD, psychopharmacological treatment, SSRIs, propranolol, military, and veterans in multiple combinations. Conclusions: Studies to date indicate that (a) SSRIs are only moderately effective as a first-line treatment for PTSD and less so for military personnel, (b) propranolol has the ability to attenuate traumatic memory in primary and tertiary use, and (c) ethical and moral consideration as well as further research and testing is needed for substantiating propranolol as a first-line PTSD psychopharmacological treatment. Implications for practice: Current research has shown propranolol to be an effective treatment option for PTSD.

Introduction The history of posttraumatic stress disorder (PTSD) is directly correlated with the rise of humankind. Birbaum (2007) and Marmar (2009) examined PTSD’s history noting early accounts have been recorded in biblical texts through the story of Jacob and Joseph, and described by Homer with the Trojan warriors. Terminology such as “soldier’s heart,” “shellshock,” “battle fatigue,” and “Vietnam Syndrome” have been used with service men and women in the Civil War, World Wars I and II, and the Vietnam War, respectively. Despite PTSD’s obvious presence throughout human development, it was not until 1980 that the illness was formally designated an official anxiety disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM; Birbaum, 2007; Mirkes, 2010; Roman, 2010). The DSM-IV diagnostic criteria for PTSD is as follows: . . . development of characteristic symptoms following exposure to a traumatic stressor involving direct expe-

rience of an event that involves actual or threatened death or serious injury . . . or witnessing an event that involves death, injury, or a threat . . . of another person. The person’s response must involve intense fear, helplessness, or horror . . . symptoms resulting from the exposure to the trauma include persistent reexperiencing of the traumatic event, avoidance of stimuli associated with the trauma and numbing of general responsiveness, and persistent symptoms of increased arousal. The full symptom picture must be present for more than 1 month, and the disturbance must cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (American Psychiatric Association [APA], 2010, p. 2).

According to the National Institutes of Health (NIH, 2009), 7.7 million American adults are affected by PTSD. Of late, psychopharmacology for PTSD treatment has experienced rapid growth. While psychotherapy is the premier treatment for PTSD, a combination of psychotherapy and medication offers greater benefits and a better treatment prognosis. The current first-line

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psychopharmacologic treatment for PTSD is selective serotonin reuptake inhibitors (SSRIs), although the efficacy of SSRIs has recently been challenged in favor of propranolol use (Cukor, Spitalnick, Difede, Rizzo, & Rothbaum 2009; Fletcher, Creamer, & Forbes, 2010). This review examines whether propranolol use is a more effective treatment option in comparison to firstline sertraline for PTSD in military personnel. The search strategies used for this review included ProQuest, Medline, CINAHL, and Psychiatry Online using the key terms: PTSD, psychopharmacological treatment, SSRIs, propranolol, military, and veterans in multiple combinations. All journal articles and research papers obtained from these databases were peer reviewed, limited to the English language, and published between 2001 and 2011. Additional references were sourced from the reference lists of key papers obtained from the databases searches and were published between 2001 and 2011. Five datadriven papers (randomized controlled trials) and 27 nondata-driven papers (review, conceptual, or ethical debate) were examined.

PTSD and the military War is a rich breeding ground for a host of combatrelated mental health disorders. Since 9/11, the U.S. military has deployed 1.64 million serving members in Operation Iraqi Freedom and Operation Enduring Freedom. The RAND Corporation and the U.S. Army’s Mental Health Advisory Team summarized that one third of all U.S. deployed troops will develop PTSD, major depressive disorder, traumatic brain injury, or a combination of any of the three conditions (Callahan, 2010). Donovan (2010) examined the role of PTSD in the United States Army noting that recent studies have shown that 17%– 25% of soldiers serving in Iraq return with PTSD and 20%–42% of all active soldiers require mental health services of some form. One misconception concerning “battle scars” is that they are physical, a visual reminder of the horrors of war. In truth, with many veterans “not all wounds are visible” and scars of the mind are equally, if not more, debilitating than those observable on the body. The numbers alone of service men and women who return affected by PTSD are reason enough for the U.S. military to take notice of this looming mental health epidemic. Presently, PTSD has numerous treatment challenges, ranging from stigma to ethical considerations to understanding neurotransmitters and their pathways. One of the greatest issues facing PTSD sufferers, particularly those in the military, is the stigma of being labeled weak and cowardly (Yarvis, 2011). In addition, Yarvis (2011) explained how fear of PTSD documentation and its negative effect on military career advancement and 420

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other employment opportunities, such as law enforcement, deters those suffering from obtaining treatment.

The neurobiology of PTSD Recent medical technology and the advent of neuroimaging has identified multiple neurotransmitters and pathways that seem to play an integral role in PTSD formation but also raises the question as to which of these is the key to successful treatment. Through neuroimaging, the processes of memory formation and retrieval, both critical in PTSD formation, are being examined and provide insight into formulating successful PTSD treatment. Multiple researchers, including Chamberlain, Ulrich, Blackwell, Robbins, and Sahakian (2006), Donovan (2010), Evers (2007), Mirkes (2010), and Pitman and Delahanty (2005), have studied the role of emotional stress and its triggering of neurohormones, which affect memory consolidation. Donovan (2010) explained that, simultaneously, the sympathetic nervous system is stimulated to elicit production from the adrenal medulla and further produces an exorbitant amount of epinephrine and norepinephrine. These two hormones stimulate α-adrenergic and β-adrenergic receptors, and trigger a cascade of neurohormones, to include corticotropin-releasing hormone, adrenocorticotropin, arginine vasopressin, and cortisol (Pitman & Delahanty, 2005). In studying the neurohormonal involvement in fear-memory formation, researchers concluded that all of these hormones create a state of hyperemotional arousal that reinforces the stressful event in the amygdala (Donovan, 2010; Pitman & Delahanty, 2005). Chamberlain et al. (2006), Mirkes (2010), and Pitman and Delahanty (2005) specified that because memory itself is associated with the amygdala, it is in this organ, specifically the basolateral nucleus of the amygdala, where fear conditioning occurs. Roman (2010) and Corchs, Nutt, Hood, and Bernik (2009) found that the neurotransmitter serotonin is heavily involved in regulating the processing of information in the amygdala, specifically inhibiting formal output. Pitman and Delahanty (2005) and Mirkes (2010) examined neurotransmission pathways and surmised that β-adrenergic neurotransmission is the main route by which the majority of other stress hormones reach the basolateral amygdala (BLA), encoding the fear response to the stressful event/encounter. Several studies, particularly those by Strawn and Geracioti (2008) and Pitman and Delahanty (2005), have postulated that PTSD is a condition stemming from excessive norepinephrine and stress hormone secretion in response to a physiologic stressor making PTSD

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an “endocrinologically atypical response” (Pitman & Delahanty, 2005, p. 101). Evers (2007), Antai-Otong (2007), Garfinkel and Liberzon (2009), Mirkes (2010), and Robinson and Shergill (2011) examined the differences between people who experienced similar traumatic events and found that individuals who are vulnerable to PTSD have structural abnormalities of the brain, specifically decreased hippocampal volume and size, low cortisol levels, and a decreased anterior cingulate cortex (ACC). These predisposing structural factors directly affect the processing of fear in the amygdala, particularly the ACC, which appears to have an inverse reaction of fear ascription with the amygdala. This gives rise to the notion that two people can be exposed to the same traumatic stimuli and one will be afflicted with PTSD following the event and the other will not.

Psychopharmacological treatment SSRIs Serotonin was one of the first neurotransmitters to be associated with reduced amygdala output and hence SSRIs have become the main psychopharmacological choice of treatment for PTSD. Sertraline and paroxetine, in particular, have been effective in treating PTSD and are the only SSRIs to be approved by the Food and Drug Administration specifically for PTSD treatment (Antai-Otong, 2007; Dowben, Grant, & Keltner, 2007; Roman, 2010; Sullivan & Neria, 2009). One of the premier and largest studies concerning sertraline and PTSD was performed by Londborg et al. (2001), who conducted a 24-week double-blind placebocontrolled study on subjects who had been treated with sertraline for a 12-week open-label period. It was found that 92% of all subjects who responded positively during the first testing period continued to do so the next 12 weeks. Additionally, 42% of subjects who had not converted during the initial 12-week testing period had positive outcomes during the second half of the testing. Most SSRIs trials, such as in the Davis, Frazier, Williford, and Newell (2006) study, showed that those who responded in the initial 12 weeks, or in short-term treatment, and continued on the SSRI, maintained a positive response. A third of the subjects who did not respond during the short-term treatment phase converted on long-term SSRI management. Further research by Antai-Otong (2007), Corchs et al. (2009), Davis et al. (2006), and Marmar (2009) has shown that SSRIs treat comorbid depression, and their broad spectrum targets PTSD’s three cluster symptoms: re-experiencing, avoidance, and hyperarousal. SSRIs also have high tolerability and relatively low side effects. Yet, while SSRIs offer a foundation upon which to build fur-

ther psychopharmacological treatments, Berger et al.’s (2009) findings indicate that SSRIs’ efficacy rates “rarely exceed 60% and less than 20–30% of the patients achieve full remission” (p. 170).

Propranolol The minimally effective results of SSRIs have urged researchers to examine the neurotransmission pathways associated with memory formation and consolidation. There is evidence that the primary transmission of stress hormones to the BLA for event encoding occurs via the β-adrenergic neurotransmission route (Mirkes, 2010; Pitman & Delahanty, 2005). This makes propranolol, a β-adrenergic inhibitor, a prime candidate for blocking or severely diminishing transmission of stress hormones to the amygdala, limiting traumatic memory. Chamberlain et al. (2006), as well as Pitman et al. (2002), along with other researchers have recognized that what separates propranolol from other beta blockers, such as nadolol, is its high lipophilic nature that allows propranolol to cross the blood–brain barrier. In multiple studies, propranolol has been shown to offer “secondary prevention” through inhibition of the overconsolidation of fear-based memories in the direct wake of a traumatic event (Bell, 2008). Vaiva et al. (2003) explained that “traumatic events are hypothesized to be followed by a critical period of increased brain plasticity, during which long lasting neuronal changes may occur in those who develop traumatic stress disorders” (p. 949). Pitman et al. (2002) and Vaiva et al. (2003) performed studies producing evidence supporting the hypothesis that the administration of propranolol soon after a traumatic event would block the flooding of the β-adrenergic receptors and prevent formation of PTSD symptoms and further mitigate emotional trauma.

Propranolol research General population Pitman et al. (2002) and Vaiva et al. (2003) used Emergency Department patients as their subjects and administered oral propranolol to subjects within 6 h of the traumatic event and continued treatment for 7–10 days. Pitman et al.’s (2002) 3-month study found that during the first month, the percentage of placebo subjects with PTSD symptoms was 30% (p = .03) versus 18% in the test group (p = .15). At the 3-month follow-up however, both the test and placebo group were equal in symptom scores as the “patient’s symptoms settle to nonclinical levels” (p. 192) with the increase in time (Pitman et al., 2002). Vaiva et al.’s (2003) 2-month study indicated that propranolol was effective in “mitigating PTSD 421

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symptoms and perhaps in preventing PTSD” (p. 949) as the PTSD score of the test group was 6.18 in comparison to the placebo group’s PTSD score of 11.75 (U = 85, p = .037). The previous studies reviewed dealt with secondary prevention of PTSD symptoms, and possibly the disorder itself, by administrating propranolol very soon after the traumatic event. However, according to the DSM-IV (APA, 2010), a PTSD diagnosis cannot be formally made until after a month of symptom development, requiring the need for tertiary treatment. Brunet et al. (2008) addressed the use of propranolol as a tertiary PTSD treatment based upon the work of Debiec and Ledoux (2004), Pitman et al. (2002), and Vaiva et al. (2003). Vaiva et al. (2003) evaluated the concept of “increased brain plasticity” (p. 949) during and directly after the occurrence of a traumatic event as a platform for the next level of research into propranolol efficacy and usage. Brunet et al. (2008) tested the retrieval of a past traumatic event and a window of vulnerable plasticity, where a β-adrenergic inhibitor would block the neurotransmission of the trauma encoding stress hormones associated with PTSD and reduce the memory’s emotional and physiologic impact despite prior formation. In this double-blind placebo study, subjects were asked to describe the traumatic event that caused their PTSD and the researchers recorded the description. Then 40 mg of short acting propranolol was promptly administered, followed by 60 mg of long acting propranolol 2 h after the initial dose. A week later the recordings were replayed and physiologic responses, such as heart rate, skin conductance, and left corrugator electromyogram, were assessed. The results verified the hypothesis, with the post trauma propranolol group showing significantly lower physiologic reactions and scores than those treated with placebo. The researchers concluded that “ . . . the PTSD subjects who received post-retrieval propranolol showed physiologic responses typical of trauma victims without PTSD” (p. 505).

Military population Currently, the National Institute of Mental Health is funding and recruiting for multiple studies testing propranolol’s overall efficacy in PTSD prevention (Bell, 2008). In addition, the U.S. Veterans Association (USVA) is moving forward with recruitment for several PTSD and propranolol clinical trials, some in which tertiary, or “reactivated trauma” (USNIH, 2011, p. 1), will be the source of PTSD testing. The U.S. military’s interest in alternative psychopharmalogical treatment for PTSD continues to spur research into treatment, as well as further investigation into the disease itself. PTSD treatment has been 422

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found to be much more resistant in war veterans versus civilian populations, although the reasons for this remain unclear (Cukor et al., 2009). Research from Sullivan and Neria (2009), who worked with both civilian and veteran PTSD populations using standard SSRI psychopharmacology, reported findings indicating that “ . . . veteran populations with chronic PTSD may be less responsive to SSRIs” (p. 343). Thus, propranolol, which blocks the reuptake of norepinephrine versus serotonin and reduces the reconsolidation of fear in the amygdala, has emerged at the forefront of PTSD psychopharmacology treatment agents.

Ethical considerations of propranolol use The advantage of propranolol is the ability of the drug to block fear memories through reduction in catecholamines that induce fearful memory consolidation (Callahan, 2010). The President’s Council on Bioethics has voiced opposition to new psychopharmacological agents, like propranolol, stating that such regimens are dangerous in that they “disrupt the sense of self” (Bell, 2008). This altering of the mind raises an ethical concern with propranolol use. The “attenuation of memory” (p. 225) with propranolol use provoked the Bioethical Council to take a stance against the use of the drug on the basis that it would “separate the subjective experience of memory from the truth of the experience that is remembered” (President’s Council on Bioethics, 2003, p. 225). While this may be a legitimate concern, the validity of this argument remains debatable because of multiple factors. Evidence supports that propranolol use does not cause deletion of the event or memory, but disassociates the paralyzing emotional reaction to the memories (Donovan, 2010). In fact, sense of self has the potential to be gained with PTSD sufferers using propranolol as “ . . . Propranolol attenuation of a traumatic memory . . . constitutes a change enabling PTSD patients to integrate the life threatening experience into their pursuit of happiness, and has the potential to improve rather than detract from the health maturation of their personality” (Mirkes, 2010, p. 184).

Implications for practice In light of convincing research findings, propranolol use for PTSD treatment for both prevention and management of PTSD is compelling. The efficacy of propranolol for PTSD has proven to be significant enough to be included in the Veterans Administration/Department of Defense Clinical Practical Guidelines for PTSD and its treatment (Callahan, 2010). The cost of pharmacological treatment is crucial in any treatment regimen.

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Expense may lead to insurance companies denying the drug or mandating heavy paperwork for authorization, which may deter mental healthcare providers from prescribing the treatment. However, because propranolol is not patented and is available in generic form at a lower cost, like generic SSRIs, the overall cost can be reduced. Therefore, financially, propranolol could prove to be an economical treatment option or adjunct therapy (Bell, 2008).

Conclusion In conclusion, future studies with propranolol and PTSD treatment are reasonable, not only focusing on efficacy in comparison to SSRIs, but in other areas, such as in determining suitable duration of dosing to attain positive results, as well as its use in conjunction with psychotherapy. Propranolol does have limitations, particularly for patients who have cardiac, pulmonary, or vascular comorbidities (Davis Drug Guide, 2010). Further study is warranted, as a new use for this pharmacological agent, together with other therapies, may well hold the key to unraveling the human experience of fear and trauma and the management of its aftermath.

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