Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

ppc_235 26..36

Donna Scott-Tilley, PhD, RN, CNE, Abigail Tilton, PhD, and Mark Sandel, MSW

The purpose of this article is to discuss the current literature about the risk of
PURPOSE.

post-traumatic stress disorder (PTSD) in victims of intimate partner violence (IPV). PTSD is a complex and serious syndrome with emotional symptoms, psychiatric
CONCLUSIONS.

Donna Scott-Tilley, PhD, RN, CNE, is Associate Professor, Department of Nursing; Abigail Tilton, PhD, is Social Work Program Director and Assistant Professor; and Mark Sandel, MSW, is Associate Professor, Department of Social Work, Texas Womans University, Denton, TX, USA.

symptoms, and physical consequences. PTSD is associated with impaired immune function, obesity, increased risk of diabetes, increased severity of premenstrual syndrome symptoms, depression, suicide, and increased likelihood of re-abuse. Female victims of IPV develop PTSD and related consequences at a rate of 7492%, compared to 613% in non-abused women.
PRACTICE IMPLICATIONS.

Advanced practice nurses (APNs) are likely to see one or both of these problems in their practices. The vague, nonspecic symptoms can present challenges to APNs. Biologic correlates are identied to help the APNs identify those most at risk of developing PTSD. Treatment options are discussed.

Search terms: IPV, PTSD, screening

First Received October 30, 2008; Final Revision received June 25, 2009; Accepted for publication June 28, 2009.
26

his review examines the biologic factors that are correlated with the development of post-traumatic stress disorder (PTSD) in women who have experienced intimate partner violence (IPV). PTSD is a complex and serious syndrome in which a trauma victim is negatively affected by pervasive thoughts of a traumatic event (Yehuda, 2002). In addition to the troubling emotional and psychiatric symptoms of PTSD, the victim often experiences serious physical consequences that can include impaired immune function, difculty falling or staying asleep, increased insulin resistance, increased central obesity, and increased risk for type II diabetes (Gill, Szanton, & Page, 2005). Early interest in PTSD centered on combat experiences. It is now clear that female victims of IPV develop PTSD and subsequent consequences at an alarming rate. IPV, the most common form of violence against women, takes various forms, such as physical violence, assaults with weapons, homicide, and sexual abuse (Watts & Zimmerman, 2002). These physical acts are often accompanied by psychological or emotional abuse, which can include social isolation, belittlement and humiliation, intimidation, economic restriction, and other forms of control (Watts & Zimmerman, 2002). Given the prevalence of IPV, it is important that advanced nurse practitioners (APNs) be well informed about the serious potential of PTSD with IPV. This article seeks to increase knowledge of biologic factors that predispose female victims of IPV to development of PTSD. The term biologic correlates was chosen
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

because it indicates that there is a relationship between biologic functions, such as immune function and hormone function, with IPV and PTSD. A review of the literature regarding prevalence, diagnostic criteria, predispositions, associated neuroendocrine changes, and structural changes is presented, followed by a discussion of practice and treatment implications. The psychosocial factors regarding PTSD, including family history, previous traumas, and stress, have been well documented in the literature. It is important to note that these psychosocial factors often intersect with biologic factors. APNs caring for victims of IPV need to have a solid understanding of biologic correlates as they provide preventive and supportive care for both physical and psychological problems associated with PTSD. These conditions may serve as indicators to help the practitioner identify patients most at risk for development of PTSD. Prevalence Lifetime exposure to traumatic events is estimated to be between 40 and 90% for the general population, while the PTSD prevalence is much lower at an estimated 712% (Astur et al., 2006). Said another way, many of us experience trauma, but not all of us develop PTSD. Estimates vary, but as many as 13% of women worldwide and 6% of women in the United States experience PTSD. Researchers have reported that PTSD is signicantly more prevalent in abused women than in women who experience trauma that is not IPV (Campbell, 2002; Campbell et al., 2002). Estimated prevalence for PTSD among female victims of IPV is 7492% (Campbell, 2002; Watson et al., 1997). This is approximately three times the rate of PTSD in women who experience trauma that is not IPV (Watson et al., 1997). Standard Diagnostic Criteria PTSD was established as a diagnosis by the American Psychiatric Association (APA) in 1980 (APA, 2000). In
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

2000, the diagnostic criteria were revised for the fourth edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR). Diagnostic criteria for PTSD include a history of exposure to a traumatic event meeting two criteria and symptoms from each of three symptom clusters: intrusive recollections, avoidant/ numbing symptoms, and hyperarousal symptoms. The fth criterion addresses duration of symptoms. A sixth criterion addresses functioning (National Center for PTSD. United States Department of Veterans Affairs. 2009; see Table 1). PTSD and acute stress disorder (ASD) are similar in many ways, and can be distinguished from one another by onset of symptoms. Symptoms of ASD occur immediately following a traumatic event, while PTSD symptoms typically manifest 3 months to years after the traumatic event (APA, 2000). Although PTSD differs from major depression, it often occurs along with depression (Pico-Alfonso et al., 2006). The type of abusephysical, sexual, or psychologicalmay impact the co-occurrence of PTSD and depression. Pico-Alfonso et al. (2006) found that the incidence of PTSD without depression was rare; depressive symptoms were found in 90.3% of physically/psychologically abused women with PTSD, and 89.3% of psychologically abused women with PTSD. Physical and Mental Health Consequences of PTSD The complex interplay between stress, neuroendocrine function, and the immune system is part of an array of physical and psychological symptoms of PTSD. Immune function, when measured on a large number of variables, was impaired in women with PTSD who were victims of IPV (Woods et al., 2005). Specically, abused women with PTSD, when compared with women experiencing trauma that was not IPV, were found to have signicant higher mean total white blood cell counts, higher median absolute counts for total T cells, and lower salivary IgA levels (Woods et al., 2005). Because of the effect on the endocrine system, women with PTSD originating with
27

Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

Table 1. DSM Diagnostic Criteria for PTSD

Diagnostic criteria for PTSD include a history of exposure to a traumatic event meeting two criteria and symptoms from each of three symptom clusters: intrusive recollections, avoidant/numbing symptoms, and hyperarousal symptoms. The fth criterion addresses duration of symptoms. A sixth criterion addresses functioning. Criterion A: Stressor The person has been exposed to a traumatic event in which both of the following have been present: 1. The person has experienced, witnessed, or been confronted with an event or events that involve actual or threatened death or serious injury, or a threat to the physical integrity of oneself or others. 2. The persons response involved intense fear, helplessness, or horror. In children, it may be expressed instead by disorganized or agitated behavior. Criterion B: Intrusive recollection The traumatic event is persistently re-experienced in at least one of the following ways: 1. Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. In young children, repetitive play may occur in which themes or aspects of the trauma are expressed. 2. Recurrent distressing dreams of the event. In children, there may be frightening dreams without recognizable content. 3. Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative ashback episodes, including those that occur upon awakening or when intoxicated). In children, trauma-specic reenactment may occur. 4. Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event. 5. Physiologic reactivity upon exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event. Criterion C: Avoidant/numbing Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by at least three of the following: 1. Efforts to avoid thoughts, feelings, or conversations associated with the trauma 2. Efforts to avoid activities, places, or people that arouse recollections of the trauma 3. Inability to recall an important aspect of the trauma 4. Markedly diminished interest or participation in signicant activities 5. Feeling of detachment or estrangement from others 6. Restricted range of affect (e.g., unable to have loving feelings) 7. Sense of foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span) Criterion D: Hyperarousal Persistent symptoms of increasing arousal (not present before the trauma), indicated by at least two of the following: 1. Difculty falling or staying asleep 2. Irritability or outbursts of anger 3. Difculty concentrating 4. Hypervigilance 5. Exaggerated startle response Criterion E: Duration Duration of the disturbance (symptoms in BD) is more than 1 month. Criterion F: Functional signicance The disturbance causes clinically signicant distress or impairment in social, occupational, or other important areas of functioning. Specify if: Acute: if duration of symptoms is less than 3 months Chronic: if duration of symptoms is 3 months or more Specify if: With or without delay onset: onset of symptoms at least 6 months after the stressor
Source: American Psychiatric Association, 2000. PTSD, post-traumatic stress disorder.

28

Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

childhood sexual abuse are at increased risk for obesity and development of diabetes (Lemieux & Coe, 1995; Noll, Zeller, Trickett, & Putnam, 2007). Pico-Alfonso et al. (2006) reported that women exposed to physical/psychological and psychological IPV had higher incidence and severity of depression and anxiety symptoms. When compared with nonabused counterparts, women in the study were found to have more severe premenstrual syndrome symptoms, greater severity of depression, increased disruptions in home life, impaired work productivity, and higher suicide risk (Pico-Alfonso et al., 2006). In addition to the physical and mental health symptoms that accompanied PTSD, there was a higher risk of reabuse among women with PTSD (Krause, Kaltman, Goodman, & Dutton, 2008). Neuroendocrine Changes Associated with PTSD It has long been known that the impact of stress has a strong biologic component (Cannon, 1914). Most people have experienced the ght or ight response at some time. While a certain level of stress can heighten awareness and increase reexes, there is a threshold at which stress hormones, epinephrine and norepinephrine, can begin to impair learning and memory. These biologic stress responses may severely affect life functioning for patients with a diagnosis of PTSD. The theory of sensitization postulates that initial trauma triggers the rst set of PTSD symptoms, but repeated stressful life events may result in diminished resistance to further symptoms (McFarlane & Yehuda, 1996). This is similar to the idea of kindling, in which an emotional response is linked with a fear-inducing stimulus. When the stimulus or other fear-inducing stimuli are experienced again, the patient experiences a heightened emotional response. This cycle can spiral into a condition in which arousing conditions can induce the conditioned response (Kolb, 1987). The theory of sensitization, which accounts for physical and emotional responses, also assumes that repeated
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

exposure to stress hormones stimulates release of higher levels of stress hormones at lower stress levels, that is, the IPV can lead to changes in hormone levels (McFarlane & Yehuda, 1996). These assumptions are consistent with the ndings of a cross-sectional study designed to determine the relationship of previous life stressors with current traumatic stress symptoms. Researchers found that traumatic stress symptoms were exacerbated by other life stressors in women who had current PTSD arising from childhood abuse (Classen et al., 2002). Prolonged abuse may result in higher and higher levels of stress hormone levels. However, it is yet unclear whether these hormonal changes indicate increased risk for development of PTSD or are a long lasting change occurring as a result of PTSD. The hypothalamicpituitaryadrenal (HPA) axis is a complex union between the hypothalamus (which controls hormone secretion), the pituitary gland (which secretes hormones to maintain homeostasis), and the adrenal glands (which are responsible for cortisol secretion). The HPA axis controls the bodys response to stress and regulates body processes such as digestion, immunity, mood and emotions, and sexuality. Alterations in HPA axis function are proposed as one causative factor in the development of PTSD; specically, altered levels of cortisol and alteration in circadian rhythms of cortisol (Gill et al., 2005). Cortisol, produced in the adrenal glands, is the hormone released during stress. Typically, people have diurnal variations in cortisol levels, with highest levels generally occurring in the morning and lowest levels occurring around midnight. Among the rst studies to explore the neuroendocrine effects of PTSD in women, Lemieux and Coe (1995) found that when compared with men with PTSD, women with PTSD had signicantly elevated daily levels of norepinephrine, dopamine, and cortisol. Later studies reported diverse patterns of cortisol levels in PTSD (Heim et al., 2000; Inslicht et al., 2006). The neuroendocrine function of female victims of IPV was found to be signicantly altered in women with
29

Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

PTSD as opposed to those without PTSD (Inslicht et al., 2006). Women with lifetime PTSD had signicantly higher cortisol levels across the day. Similar results were reported by Heim et al. (2000), who studied women with histories of abuse but no documented PTSD. Heim et al.s study presented the additional nding that abused women with concurrent depression demonstrated the highest cortisol levels. Norepinephrine is a major catecholamine activated in a normal stress response. Geracioti et al. (2001) reported that norepinephrine levels in cerebrospinal uid samples were higher in men with PTSD than those without PTSD. Levels of norepinephrine were positively correlated with severity of PTSD symptoms. While women were not the focus of the study, it is important to be aware of the potential for alterations in norepinephrine levels in women with a possible PTSD diagnosis. Another study reported that PTSD patients demonstrated elevated norepinephrine, but low levels of urinary-free cortisol. The higher catecholamine levels and low cortisol levels, expressed as the norepinephrine-to-cortisol (NE/C) ratio, appeared to be signicantly higher in PTSD patients than those in other psychiatric groups (Lemieux & Coe, 1995). This disturbance in the NE/C ratio persisted long after the initial trauma (Heim et al., 2000). Predispositions to PTSD The DSM-IV states that there is a heritable component to the transmission of PTSD (APA, 2000). Previous depression in a rst-degree relative is related to increased vulnerability to developing PTSD (American Psychiatric Association, 2000). The idea that familial contributions can increase the likelihood of developing PTSD was supported by Yehuda et al. in their study of the adult offspring of Holocaust survivors (Yehuda, Bell, Bierer, & Schmeidler, 2008). Parental PTSD was found to be associated with low cortisol levels in offspring of Holocaust survivors (Yehuda et al., 2008). These ndings suggest that the
30

low cortisol levels associated with parental PTSD may constitute a vulnerability marker for offspring. There are signicant changes in brain functioning, specically the hippocampus, in persons with PTSD. While correlations between structural and functional changes in the hippocampus are well established (Astur et al., 2006; Bremner et al., 2003), it is yet unclear whether the hippocampal abnormalities are a consequence of chronic stress or are a preexisting risk factor. The hippocampus is critical for memory functioning. The size of the hippocampus is altered in persons with PTSD, possibly as a result of early stress (Bremner et al., 2003). The volume of the hippocampus was 16% lower in abused women with PTSD than in abused women without PTSD, and 19% lower than those without abuse or PTSD (Bremner et al., 2003). This same study found that dissociation symptoms were correlated with smaller left hippocampal volume, while PTSD symptoms were correlated with smaller right hippocampal volume. In addition to alterations in hippocampal volume, hippocampal function is altered in patients with PTSD. When completing the virtual Morris water task, a spatial memory test that activates hippocampal function, persons with PTSD did not differ in task performance from non-PTSD controls, but hippocampal activation did vary. Persons without PTSD demonstrated right hippocampal activity while completing the task, but subjects with PTSD demonstrated no hippocampal activity during task completion (Astur et al., 2006). Alterations in cerebral blood ow have also been associated with PTSD (Liberzon, Britton, & Phan, 2003; Mirzaie et al., 2001). Cerebral blood ow to the medial prefrontal and anterior cingulate cortex, the area of the brain that is responsible for emotional processing and regulation, was studied in combat veterans without PTSD and combat veterans with PTSD (Liberzon et al., 2003). Subjects with PTSD demonstrated increased blood ow to the rostral anterior cingulate, which is consistent with an exaggerated autonomic response, as well as poor emotional regulation. The non-PTSD
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

Table 2. PTSD Symptoms

Symptoms of PTSD Sleeplessness Hypersensitivity Nightmares Avoidance of trauma-related stimuli Intrusive thoughts about the event Feelings of re-experiencing the event Depression Disruptions in home life Increased risk for suicide Impaired work production Increased severity of premenstrual symptoms

Detection of PTSD The biologic predispositions and responses to PTSD are complex and do not lend themselves to a simple series of lab tests. However, if medical histories are available, practitioners should be alerted to any indications of HPA axis anomalies, most signicantly, elevated catecholamine levels in combination with low cortisol levels. Although symptoms of PTSD may be similar to those of other psychiatric disorders, urinary cortisol and urinary catecholamine levels may distinguish PTSD from major depressive disorders, bipolar disorder, and schizophrenia. Hippocampal functioning might also indicate who is at risk for PTSD; hippocampal abnormalities, typically manifested as diminished memory, may prove to be a preexisting correlate to PTSD vulnerability. The practitioner should be alert to an exaggerated autonomic response, which may also indicate PTSD. The autonomic nervous system is responsible for maintaining homeostasis in the body via heart rate, respiratory rate, perspiration, pupil dilation, micturition, and salivation. Patients experiencing autonomic hyperresponsiveness may report increased motion sickness and sweating, and demonstrate elevated blood pressure (Finley et al., 2004). A thorough psychosocial interview may yield important information to enhance clinical ndings. The practitioner observing signs of dissociation and/or changes in memory should be alert to the possibility of PTSD in the patient. Dissociation, often associated with the experience of trauma, is characterized by depersonalization, disengagement, or amnesia regarding the traumatic event (APA, 2000). Patients with repeated traumatic events, ongoing abuse, or multiple forms of abuse should be closely observed for development of PTSD. The neuroendocrine changes from ongoing or severe abuse may lead to diminished resilience to symptom development. Patient reports of parental PTSD and depressive symptoms might also indicate heightened risk.
31

Sources: Krause et al., 2008; Lemieux and Coe, 1995; Pico-Alfonso et al., 2006; Woods et al., 2005. PTSD, post-traumatic stress disorder.

control group demonstrated deactivation of the amygdala and prefrontal cortex, which suggests adaptation or even resilience to the effects of trauma. While we understand more about the biologic components of PTSD than in previous years, many questions remain. What we do know is that patients with PTSD can present with a wide array of alterations in neuroendocrine and physical manifestations (see Table 2). It requires an astute and alert practitioner to recognize more subtle presentations of PTSD in victims of IPV. Implications for Practice Although not all abused women develop PTSD, abused women seen in medical settings should be considered at risk for the disorder. A thorough medical and psychosocial history may reveal clues about the propensity of a victim of IPV to develop later PTSD. Clinical observations may also yield helpful information about a patients risk of developing PTSD. The practitioner should consider possible symptoms not as diagnostic tools, but as markers to indicate elevated risk.
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

Listening to patients is an important element of any good practice, but a thoughtful, probing interview is especially important for recognizing poor emotional control in a patient, particularly with patients who are less open and social. Wirtz et al. (2006) reported a clear link between poor emotional regulation and its relationship to increased stress hormone. They describe emotional control as a persons ability to regulate emotions in a self-preserving way, that is, the ability to intensify or maintain positive affect and practice mood repair when facing negative events (Wirtz et al., 2006). Practitioners should be alert to some of the symptoms of poor emotional regulation described by Wirtz et al. (2006): ruminating negative affect, little eye contact, few positive assertive statements, lack of assertiveness, and lack of social support. Many women who have experienced IPV may exhibit some of these symptoms in the absence of PTSD. However, the practitioner who suspects PTSD or risk for PTSD based on these predispositions and symptoms should intervene early and intensively. While some symptoms can be managed in a clinical setting, immediate referral to a mental health specialist is crucial for comprehensive care. Treatment of PTSD Treatment of PTSD should begin as soon as it is identied. Treatment options can include nonpharmacologic, as well as pharmacologic, interventions. Immediate referral for non-pharmacologic therapies is also an important component of comprehensive care. Psychotherapy is a primary therapy that should be instituted immediately. Psychotherapy is essential to effective use of pharmacologic and other nonpharmacologic interventions (Bisson & Andrew, 2008; Parslow, Purcell, Garner, & Hetrick, 2008). Referral to a mental health specialist is essential for non-pharmacologic interventions. Common nonpharmacologic interventions for PTSD include cogni32

tive behavioral therapy (CBT), stress management, group CBT, and eye movement desensitization and reprocessing (EMDR). Bisson and Andrew (2008) reported that patients undergoing CBT and EMDR demonstrated fewer stress-related symptoms than patients receiving other psychological therapies. CBT, based on learning and cognitive therapies, addresses distorted beliefs and attributions about the trauma while focusing on provision of a supportive environment. Generally, CBT involves a psychotherapist and patient engaging in discussion and abuse education, typical emotional and behavioral reactions to abuse, relaxation methods, affective expression and regulation, cognitive coping and processing, trauma narrative, and in vivo exposure (U.S. Department of Health and Human Services, 2007). EMDR is an information processing therapy that integrates elements of several psychotherapies in a structured protocol. In EMDR, psychodynamic, cognitive behavioral, interpersonal, experiential, and bodycentered therapies are combined by a therapist to reduce the patients emotional distress related to recurring memories (EMDR Institute, n.d.). The goals of pharmacotherapy for PTSD are to: (a) reduce core symptoms; (b) improve quality of life; (c) improve functioning in work, social, and family settings; (d) improve resilience to stress; (e) reduce comorbidity; and (f) prevent relapse (Brunello et al., 2001). An additional goal for pharmacotherapy for some might be treatment of associated depression (Stein, Ipser, & Seedat, 2006). Selective serotonin reuptake inhibitors (SSRIs) are reported to be the rst-line agent in pharmacologic treatment of PTSD (Stein et al., 2006). The SSRI uoxetine has been found to be effective in female trauma victims (Stein et al., 2006). There is a question about the possible effectiveness of anticonvulsants in the treatment of PTSD, but little has been published to support their use. Advanced practice nurses (APNs) who treat patients with PTSD should stay abreast of current research on pharmacologic interventions, as several promising therapeutic agents are currently being
Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

Table 3. Summary of Selected Literature

Reference Astur et al. (2006) Sample size 24 patients (12 patients with PTSD and 12 control) Study design Non-probability convenience design with controls using structured interviews and laboratory testing Case-control study Major ndings While performing the virtual Morris water task, people with PTSD and age-matched controls do not differ in task performance. PTSD group did not show signicant hippocampal activation during the task, suggesting damage to the hippocampus from chronic stress. Abused women have 5070% increase in gynecological, central nervous system, and stress-related problems, with women sexually and physically abused most likely to report problems. Women with lifetime PTSD had signicantly higher cortisol levels across the day compared to abuseexposed participants without PTSD, after controlling for age. Avoidant coping was associated with PTSD symptoms at 1 year. Revictimization had long-term consequences. Reducing avoidant coping and increasing safety may improve coping. Both groups of abused women had clinical indications of polyuria; however, the women with PTSD also had a signicantly higher rate of obesity, as well as elevated levels of norepinephrine, epinephrine, dopamine, and cortisol. However, the norepinephrine-to-cortisol ratio was not signicantly higher in women with PTSD as is found in men with PTSD. This may be due to gender differences or differences in the onset of age of traumatic event, or an interaction between the two. Psychological and physical abuse seems to be of equal importance in the development of PTSD. Abused women have more PTSD symptoms (avoidance, arousal, depression) than non-abused controls. Only psychologically abused women were found to have lower suicidal ideation and attempts. Abused women experienced signicantly more childhood maltreatment, IPV and PTSD symptoms than comparison. The abused women had statistically signicant higher white blood cell counts, also had higher median absolute counts for total T cells, CD4, CD8, and CD19-+B cells. Mean pm salivary IgA level was lower in abused than non-abused women.

Campbell et al. (2002) Inslicht et al. (2006) Krause et al. (2008)

2,535 women (ages 2155)

49 women (29 women with IPV and PTSD, and 20 women with IPV only) 262 women

Cross-sectional design

Longitudinal

Lemieux and Coe (1995)

28 women (11 with PTSD and childhood sexual abuse, 8 with childhood sexual abuse and no PTSD, 9 non-abused controls)

Non-probability convenience design with controls using structured interviews and laboratory testing

Pico-Alfonso et al. (2006)

Woods et al. (2005)

182 women (75 physically and psychologically abused, 55 psychologically abused, 52 non-abused controls) 126 abused; 12 non-abused women

Non-probability convenience design with controls using structured interviews

Predictive exploratory

IgA, immunoglobulin A; IPV, intimate partner violence; PTSD, post-traumatic stress disorder.

Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

33

Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

Table 4. PTSD Assessment Guide

Biologic change or predisposition Neuroendocrine effects on immune system Neuroendocrine changes Assessment nding or area of increased risk Higher mean total white blood cell counts Higher median absolute counts for total T cells Repeated exposure to trauma can diminish resistance to symptoms Increased risk for obesity Increased risk for type II diabetes Alterations in diurnal cortisol levels Depression PTSD Alterations in memory Dissociation symptoms Exaggerated autonomic response Poor emotional regulation

Familial history of depression Familial history of PTSD Altered structure and function of hippocampus Altered cerebral blood ow

Sources: American Psychiatric Association, 2000; Astur et al., 2006; Classen et al., 2002; Finley et al., 2004; Gill et al., 2005; Inslicht et al., 2006; McFarlane & Yehuda, 1996; Wirtz et al., 2006; Woods et al., 2005. PTSD, post-traumatic stress disorder.

studied, including inositol, propranolol, clonidine, and mirtazepine (Brunello et al., 2001; Stein et al., 2006). A case study (see Appendix) is presented in this article to illustrate some of the concepts with implications for practice. Practitioners may be intimidated by the idea of identifying and treating a patient with PTSD, but should recognize that good assessment and some effective teamwork with other healthcare professionals make the process fairly straightforward. PTSD is far more than psychological weakness; rather it is a complex, biologically based syndrome that requires thoughtful and informed intervention (see Table 3). It is incumbent upon the APN to be alert to the possibility of PTSD in patients who experience IPV, particularly those with concurrent depression and a family history of PTSD or depression, and treat appropriately (See Table 4). Conclusion PTSD is a complex, distressing, and serious disorder that affects a large number of women who experience IPV. Left untreated, PTSD can have serious and long34

term health consequences. PTSD is not necessarily an inevitable outcome of IPV, so careful assessment is needed. While it is clear that PTSD has a biologic and heritable basis, biologic correlates to the development of PTSD may prove helpful in mitigating or perhaps even preventing development of this serious and debilitating condition. Practitioners must be aware of not only the symptoms of PTSD but possible risk factors related to vulnerability to the disorder and the treatment options.
Author contact: DTilley@TWU.edu, with a copy to the Editor: gpearson@uchc.edu References
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th ed., text revision). Washington, DC: Author. Astur, R., St Germain, S., Tolin, K. D., Ford, J., Russell, D., & Stevens, M. (2006). Hippocampus function predicts severity of post traumatic stress disorder. Cyber Psychology & Behavior, 9(2), 234240. doi:10.1089/cpb.2006.9.234 Bisson, J., & Andrew, M. (2008). Psychological treatment of post traumatic stress disorder (PTSD). Cochrane Database of Systematic Reviews 3 (CD003388).

Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

Bremner, J., Vythilingham, M., Vermetten, E., Southwick, S., McGlashan, T., Nazeer, A., et al. (2003). MRI and PET study of decits in hippocampal structure and function in women with childhood sexual abuse and posttraumatic stress disorder. American Journal of Psychiatry, 160(5), 924932. Brunello, N., Davidson, J., Deahl, M., Kessler, R., Mendlewicz, J., Racagni, G., et al. (2001). Posttraumatic stress disorder: Diagnosis and epidemiology, comorbidity and social consequences, biology and treatment. Neuropsychobiology, 43, 150162. doi: 10.1159/ 000054884 Campbell, J. (2002). Health consequences of intimate partner violence. Lancet, 359(9314), 13311337. Campbell, J., Jones, A., Dienemann, J., Kub, J., Schollenberger, J., OCampo, P., et al. (2002). Intimate partner violence and health consequences. Archives of Internal Medicine, 162(10), 11571163. Cannon, Walter B. (1914). The emergency function of the adrenal medulla in pain and the major emotions. American Journal of Physiology, 33, 356372. Classen, C., Nevo, R., Koopman, C., Neville-Manning, K., GoreFelton, C., Rose, D., et al. (2002). Recent stressful life events, sexual revictimization, and their relationship with traumatic stress symptoms among women sexually abused in childhood. Journal of Interpersonal Violence, 17(12), 12741290. doi: 10.1177/ 088626002237856 EMDR Institute. (n.d.). A brief description of EMDR. Retrieved from http://www.emdr.com/briefdes.htm. Finley, J.C., OLeary, M., Wester, D., MacKenzie, S., Shepard, N., Farrow, S., et al. (2004). A genetic polymorphism of the alpha2 adrenergic receptor increases autonomic responses to stress. Journal of Applied Physiology, 96, 22312239. Geracioti, T., Baker, D., Ekhator, N., West, S., Hill, K., Bruce, A., et al. (2001). CSF norepinephrine concentrations in post traumatic stress disorder. American Journal of Psychiatry, 158, 1227 1230. Gill, J., Szanton, S., & Page, G. (2005). Biological underpinnings of health alterations in women with PTSD: A sex disparity. Biological Research for Nursing, 7(1), 4454. doi: 10.1177/1099800405276709 Heim, C., Newport, J., Heit, S., Graham, Y., Wilcox, M., Bonsall, R., et al. (2000). Pituitary adrenal and autonomic responses to stress in women after physical and sexual abuse in childhood. Journal of the American Medical Association, 284(5), 592597. Inslicht, S., Marmar, C., Neylan, T., Metzler, T., Hart, S., Otte, C., et al. (2006). Increased cortisol in women with intimate partner violence related post traumatic stress disorder. Psychoneuroendocrinology, 31, 825838. doi: 10.1196/annals.1364.035 Kolb, L. (1987). A neuropsychological hypothesis explaining posttraumatic stress disorder. American Journal of Psychiatry, 144, 989995. Krause, E. D., Kaltman, S., Goodman, L. A., & Dutton, M. A. (2008). Avoidant coping and PTSD symptoms related to domestic violence exposure: A longitudinal study. Journal of Traumatic Stress, 21(1), 8390. doi: 10.1002/jts.20288 Lemieux, A., & Coe, C. (1995). Abuse related post traumatic stress disorder: Evidence for chronic neuroendocrine activation in women. Psychosomatic Medicine, 57(2), 105115.

Liberzon, I., Britton, J., & Phan, K. (2003). Neural correlates of traumatic recall in posttraumatic stress disorder. Stress, 6(3), 151156. McFarlane, A., & Yehuda, R. (1996). Resilience, vulnerability, and the course of posttraumatic reactions. In B. A. van der Kolk, A. C. McFarlane, & L. Weisaeth (Eds.), Traumatic stress: The effects of overwhelming experience on the mind, body, and society (pp. 155181). New York: Guildford. Mirzaie, S., Knoll, P., Keck, A., Preitler, B., Gutierrez, E., Umek, H., et al. (2001). Regional cerebral blood ow in patients suffering from posttraumatic stress disorder. Neuropsychobiology, 43, 260 264. doi: 10.1159/000054900 Noll, J., Zeller, M., Trickett, P., & Putnam, F. (2007). Obesity risk for female victims of childhood sexual abuse: A prospective study. Pediatrics, 129(1), e61e67. doi: 10.1542/peds.2006-3058 Parslow, R., Purcell, R., Garner, B., & Hetrick, S. E. (2008). Combined pharmacotherapy and psychological therapies for posttraumatic stress disorder. Cochrane Database of Systematic Reviews, 2008, Issue 3, Art. No: CD007316. doi: 10.1002/14651858.CD007316 Pico-Alfonso, M., Garcia-Linares, I., Celda-Navarro, N., Blasco-Ros, C., Echeburua, E., & Martinez, M. (2006). The impact of physical, psychological, and sexual intimate partner violence on womens mental health: Depressive symptoms, posttraumatic stress disorder, state anxiety, and suicide. Journal of Womens Health, 15(5), 599611. Stein, D. J., Ipser, J. C., & Seedat, S. (2006). Pharmacotherapy for post traumatic stress disorder (PTSD). Cochrane Database of Systematic Reviews 1 (CD002795). doi:10.1002/14651858.CD002795.pub2 U.S. Department of Health and Human Services. Child Welfare Information Gateway. (2007). Trauma focused cognitive behavioral therapy: Addressing the mental health of sexually abused children. Retrieved from http://www.childwelfare.gov/pubs/trauma/ trauma.pdf. Watson, C., Barnett, M., Nikunen, L., Schultz, C., Randolph-Elgin, T., & Mendez, C. (1997). Lifetime prevalence of nine common psychiatric/personality disorders in female domestic abuse survivors. Journal of Nervous and Mental Disease, 185(10), 645647. Watts, C., & Zimmerman, C. (2002). Violence against women: Global scope and magnitude. The Lancet, 359, 12321336. Wirtz, P., von Kanel, R., Mohiyeddini, C., Emini, L., Ruedisueli, K., Groessbauer, S., et al. (2006). Low social support and poor emotional regulation are associated with increased stress hormone reactivity to mental stress in systemic hypertension. Journal of Clinical Endocrinology & Metabolism, 91(10), 38573865. doi: 10.1210/jc.2005-2586 Woods, S., Wineman, M., Page, G., Hall, R., Alexander, T., & Campbell, J. (2005). Predicting immune status in women from PTSD and childhood and adult violence. Advances in Nursing Science, 28(4), 306319. Yehuda, R. (2002). Clinical relevance of biologic ndings in PTSD. Psychiatric Quarterly, 73(2), 123133. doi: 10.1023/ A:1015055711424 Yehuda, R., Bell, A., Bierer, L. M., & Schmeidler, J. (2008). Maternal, not paternal, PTSD is related to increased risk for PTSD in offspring of Holocaust survivors. Journal of Psychiatric Research, 42(13), 11041111. doi: 10.1016/j.jpsychires.2008.01.002

Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

35

Biologic Correlates to the Development of Post-traumatic Stress Disorder in Female Victims of Intimate Partner Violence: Implications for Practice

Appendix Case Study Angela is a 36-year-old elementary school teacher who complained of insomnia. She was concerned about her ability to work effectively in her class because of chronic sleep deprivation and fatigue. She reported a lack of ability to concentrate and irritability. She stated that she previously never got a cold, but she has become constantly sick and that she catches everything the students bring to school. Physical assessment ndings include mid-abdominal obesity and a weight gain of 20 lbs since her last visit. She does not make eye contact and appears to be anxious. Otherwise, physical assessment is unremarkable. Alerted by the changes in immune status, sleep patterns, weight, and affect, the practitioner questioned Angela further. Angela reported that she has been recently separated from her husband of 9 years. She

and her two children are still living in their home and are nancially stable. The practitioner asked Angela whether she has been a victim of intimate partner violence and if she is afraid of her estranged husband. At this point, Angela began to cry, almost uncontrollably. After giving her some time to express her emotions, the practitioner discovered that Angela was psychologically abused for the 9 years of her marriage, and occasionally physically abused with increasing frequency and severity in the past 2 years. Angela left the relationship 5 months ago when she began to fear for the safety of her children. Based on Angelas history and physical condition, the practitioner suspected possible PTSD. In addition to making an immediate psychiatry referral, the APN discussed pharmacologic treatments with Angela and prescribed uoxetine. The APN encouraged Angela to return to the clinic after 2 weeks to evaluate the effectiveness of the uoxetine and to verify that she has met with a psychiatrist.

36

Perspectives in Psychiatric Care Vol. 46, No. 1, January 2010

Copyright of Perspectives in Psychiatric Care is the property of Blackwell Publishing Limited and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.