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Chapter11.docxAnouk L. Grubaugh
The Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5; American Psychiatric Association [APA], 2013) includes a chapter titled “Trauma and Stress-Related Disorders,” which contains post-traumatic stress disorder (PTSD), acute stress disorder (ASD), and the adjustment disorders. Both PTSD and ASD were previously classified under the “Anxiety Disorders” chapter of the DSM-IV, whereas adjustment disorders were classified separately as a residual diagnostic category (APA, 1994). PTSD is characterized as a psychiatric disorder resulting from a life-threatening event and requires a history of exposure to a traumatic event (criterion A) that results in a minimum threshold of symptoms across four symptom clusters: intrusion, avoidance, negative alterations in cognitions and mood, and alterations in arousal and reactivity (criteria B–E). Additional criteria concern duration of symptoms (criterion F), functioning (criterion G), and differential diagnosis due to a substance or other co-occurring condition (criterion H).
For criterion A, an event associated with PTSD must include actual or threatened death, serious injury, or sexual violation resulting from one or more of the following scenarios:
· Directly experiencing the traumatic event.
· Witnessing the traumatic event in person.
· Experiencing the actual or threatened death of a close family member or friend that is either violent or accidental.
· Directly experiencing repeated and extreme exposure to aversive details of the event (i.e., the types of exposure frequently encountered by police officers and first responders).
With regard to criteria B–E, an individual must report symptoms from each of the four symptom clusters. Intrusion symptoms (criterion B) include repetitive, involuntary, and intrusive memories of the event; traumatic nightmares; dissociative reactions (i.e., flashbacks) along a broad continuum; intense prolonged distress after exposure to reminders of the trauma; and heightened physiological reactivity to reminders of the trauma. Avoidance symptoms (criterion C) include avoidance of trauma-related thoughts or feelings; and avoidance of people, places, activities, and so forth that cue distressing thoughts or feelings about the traumatic event. Negative alterations in cognitions and mood symptoms (criterion D) include a persistent and distorted sense of self or the world; blame of self or others; persistent trauma-related emotions such as anger, guilt, shame; feeling estranged or detached from others; marked lack of interest in pre-trauma activities; restricted range of affect; and difficulty or inability remembering important parts of the traumatic event. Finally, alterations in arousal and reactivity symptoms (criterion E) include irritability and aggressiveness, self-destructive or reckless behaviors, sleep difficulties, hypervigilance, marked startle response, concentration difficulties, and sleep disturbance.
For a diagnosis of PTSD, an individual must exhibit at least one symptom from criterion B, one symptom from criterion C, two symptoms from criterion D, and two symptoms from criterion E, and the symptoms endorsed in categories B through E must be present for 1 month or longer (criterion F). The symptoms must also be accompanied by significant distress or impairment in social, occupational, or other important life domains (criterion G), and symptoms cannot be better explained by another medical or psychiatric illness (criterion H).
The DSM-5 includes two additional specifiers or associated features that can be added to a PTSD diagnosis: “with dissociated symptoms” and “with delayed expression.” The dissociated symptoms specifier includes either depersonalization (i.e., experience of being an outside observer to one's experience or feeling detached from oneself) or derealization (i.e., experience of unreality or distortion) in response to trauma-related cues. The delayed onset specifier includes an onset of symptoms that can occur immediately after the trauma, but that may not meet full criteria for PTSD until at least 6 months after the trauma.
Some notable changes were made to the diagnostic criteria for PTSD from DSM-IV (APA, 1994) to DSM-5. In addition to the inclusion of specifiers for depersonalization and derealization, the DSM-5 provides greater specification regarding what events constitute a traumatic event (i.e., what events constitute a criterion A event); and excludes the need for an individual to have experienced intense fear, helplessness, or horror at the time of the trauma due to its lack of predictive utility. Additionally, the avoidance/numbing symptom cluster found in the DSM-IV is divided into two distinct clusters in the DSM-5: avoidance and negative alterations in cognitions and mood. The second of these clusters retain most of the DSM-IV numbing symptoms while also including a broader range of emotional reactions. Last, criterion E, alterations in arousal and reactivity, retains the majority of DSM-IV arousal symptoms but also includes additional symptoms regarding aggressive or reckless behavior.
A diagnosis of ASD requires an antecedent event (criterion A event) in which the person:
· experienced an event or events that involved a threat of death, actual or threatened serious injury, or actual or threatened physical or sexual violation;
· witnessed an event or events that involved the actual or threatened death, serious injury, or physical or sexual violation of others;
· learned of such harm coming to a close relative or friend;
· experienced repeated or extreme exposure to aversive details of unnatural death, serious injury, or serious assault or sexual violation of others that were not limited to electronic media, television, video games, and so forth.
Individuals must then exhibit a minimum of nine out of 14 symptoms across a broad spectrum of post-traumatic reactions (criterion B). This spectrum includes symptoms related to negative mood, intrusive thoughts, dissociation, avoidance, and anxiety. Aside from a greater emphasis on dissociative symptoms, the other criterion B symptoms for ASD largely mirror the criteria B–E symptoms for PTSD. Additional criteria for ASD concern duration of symptoms (criterion C), functioning (criterion D), and differential diagnosis due to a substance or other co-occurring condition (criterion E).
Changes to the diagnostic criteria of ASD from DSM-IV to DSM-5 include less emphasis on dissociative criteria (i.e., feeling detached from one's body, emotions, or the world). Rather than being required for a diagnosis, as was the case in the DSM-IV, dissociative symptoms in DSM-5 are viewed as one of several possible post-traumatic reactions that an individual may experience. Comparable to changes to the diagnostic criteria for PTSD, the DSM-5 provides more specification regarding the qualifying traumatic event for ASD; and the criterion requiring a subjective reaction to the trauma (i.e., fear, helplessness, horror) was eliminated.
Adjustment disorders are classified in the DSM-5 as a range of stress response syndromes. This differs from the DSM-IV in which adjustment disorders were part of a residual category for individuals experiencing clinically significant distress that did not fit diagnostic criteria for other psychiatric disorders. Specific DSM-5 criteria for an adjustment disorder include: (a) the development of emotional or behavioral problems in response to an identifiable stressor occurring within 3 months of exposure to the stressor (this feature is considered the core feature of adjustment disorders; (b) symptoms or behaviors are clinically significant and out of proportion to the severity of the stressor once cultural and contextual factors are taken into account. Additionally, the stress response (a) cannot be better accounted for by another disorder and is not an exacerbation of a pre-existing condition; (b) is not indicative of normal bereavement (if this is the precipitating event); and (c) once the stressor is removed, the symptoms do not persist for more than an additional 6 months. Diagnostic specifiers for the adjustment disorders include depressed mood, anxiety, mixed anxiety and depressed mood, disturbance of conduct, mixed disturbance of emotions and conduct, and unspecified.
Whereas PTSD and ASD emphasize fear and anxiety responses, adjustment disorders can accommodate a broader range of stress reactions. Second, although there is an explicit potential for ASD to predict subsequent impairment (i.e., to predict the development of PTSD), an adjustment disorder is typically viewed as a discrete disorder that has a fairly immediate onset and is relatively short in duration. A third distinction between PTSD, ASD, and adjustment disorders regards the timing of diagnosis. Adjustment disorders can be diagnosed immediately after the event, ASD can be diagnosed from 2 days up to 1 month after the event, and PTSD can be diagnosed from 1 month to several years after the trauma.
Clinical Features
The clinical expression of PTSD can vary significantly in terms of severity. Although the diagnosis is categorical, there is evidence of a dimensional structure to PTSD (Broman-Fulks et al., 2006; Forbes, Haslam, Williams, & Creamer, 2005). An implication of this dimensional structure is that milder symptoms of PTSD may cause significant distress and impairment. A recent meta-analytic review found that individuals with subthreshold PTSD experienced worse psychological and behavioral impairment than did individuals without PTSD, but less impairment relative to those with full PTSD (Brancu et al., 2016). Several of the studies cited also reported an increased risk of suicidality and hopelessness as well as higher health care utilization among those with subthreshold PTSD relative to those without PTSD.
Suicidality is elevated among individuals with PTSD (Bentley et al., 2016; McKinney et al., 2017), and particular types of trauma, such as childhood abuse, military sexual trauma, and combat, may be more strongly associated with suicidality than others (Kimerling et al., 2016; McLean et al., 2017). Additionally, increased risk of suicidality is uniquely associated with PTSD (McKinney et al., 2017). That is, this association is not solely accounted for by the presence of other psychiatric conditions commonly found with PTSD. Of course, an increased risk of suicidality is present in a number of other psychiatric conditions to a comparable or greater degree than that found in PTSD (Nock, Hwang, Sampson, & Kessler, 2010).
The clinical picture of ASD is similar to that of PTSD. Additionally, a review on the topic found that at least half of trauma survivors with ASD subsequently met criteria for PTSD (Bryant, Friedman, Spiegel, Ursano, & Starin, 2011). A more recent evaluation using DSM-V criteria found that 43% of individuals with ASD developed PTSD at 3 months and 42% of individuals with ASD developed PTSD at 12 months (Bryant et al., 2015). This study also found that DSM-V criteria for ASD were better than DSM-IV criteria for predicting PTSD. These findings suggest that individuals with ASD are, in fact, at higher risk of subsequently developing PTSD, and that DSM-V may yield more predictive validity for PTSD than earlier versions of the DSM.
Due to the conceptualization of adjustment disorders as fairly time-limited, as well as their history as a nebulous catch-all diagnostic category they have not been well studied in the psychiatric literature. The findings that do exist consist largely of non-US samples, focus on children or adolescents, and/or were published in the 1980s and early 1990s. Some commonly agreed-upon emotional signs of adjustment disorder are sadness, hopelessness, lack of enjoyment, crying spells, nervousness, anxiety, worry, trouble sleeping, difficulty concentrating, feeling overwhelmed, and thoughts of suicide. Some behavioral signs of disorders include fighting, reckless behaviors, neglecting important tasks or responsibilities, and avoiding family or friends. Although the presence of an adjustment disorder has been linked to increased suicidal ideation and risk of suicide in a review of the topic (e.g., Appart et al., 2017), they are often considered less severe than other psychiatric disorders. Supporting this view, one study found that adjustment disorders range in severity between no psychiatric disorder and the presence of a mood or anxiety disorder (Fernandez et al., 2012).
Diagnostic Considerations
Comorbidity is common with PTSD. Large, nationally representative samples have found that PTSD is significantly correlated with the majority of mood and anxiety disorders, as well as alcohol use disorders (National Comorbidity Survey Replication [NCS-R]; Kessler, Chiu, Demler, & Walters, 2005; National Comorbidity Survey [NCS]; Kessler, Sonnega, Bromet, Hughes, & Nelson, 1995). Data from the NCS-R found that approximately half of those who met criteria for PTSD also met criteria for at least three additional psychiatric diagnoses (Kessler et al., 1995). Although there is some degree of symptom overlap between PTSD and other psychiatric diagnoses (e.g., sleep and concentration difficulties and diminished interest in activities are common to both depression and PTSD), this overlap does not account for the high rate of comorbidity (Elhai, Grubaugh, Kashdan, & Frueh, 2008). When comorbid with mood disorders, PTSD is more likely to be primary, whereas it is more likely to be secondary when comorbid with anxiety disorders (Kessler et al., 1995). Importantly, PTSD and comorbid diagnoses may change over time within a given individual. A study of trauma survivors found that half of those who reported PTSD only at 3-month follow-up reported depression only at 12-month follow-up; likewise, half of those with depression only at 3-month follow-up reported PTSD only at 12-month follow-up (O'Donnell, Creamer, & Pattison, 2004).
Due to the lack of epidemiological studies specific to ASD or the adjustment disorders, there are few reliable data on the clinical comorbidity associated with these disorders. Given the conceptual overlap between ASD and PTSD, it is likely that individuals with ASD experience high rates of mood, anxiety, and substance disorders relative to the general population, as well as an increased risk of suicidality. As noted elsewhere, adjustment disorders in the DSM-IV served as a residual “catch-all” diagnostic category once other psychiatric conditions were ruled out. As such, they are seldom diagnosed with other psychiatric conditions. With this restriction in mind and the lack of studies using DSM-V criteria, adjustment disorders have most often been linked in adult samples to a comorbid diagnosis of a personality disorder or certain personality profiles and increased suicidality (Appart et al., 2017).
Epidemiology
In the general population, the 12-month and lifetime prevalence rates of PTSD are 3.5% and 6.8%, respectively (Kessler, Burglund, Demler, et al., 2005; Kessler et al., 2005). Point prevalence of PTSD among US combat veterans is estimated to be between 2% and 17%, depending on the characteristics of the sample and the measurement strategies that were used (Richardson, Frueh, & Acierno, 2010). There are different conditional probabilities of developing PTSD by trauma type. For example, combat exposure and physical and sexual abuse are more often associated with PTSD than are other types of trauma. Despite this variability, the symptom expression of PTSD remains fairly consistent regardless of the type of trauma experienced.
Little is known about the prevalence of ASD and the adjustment disorders in the general population. Large-scale epidemiological studies, such as the World Health Organization (WHO) Mental Health Epidemiologic Survey, the Epidemiologic Catchment Area study, and the National Comorbidity Survey Replication, did not report on these disorders. Rates of ASD in community and clinical samples range from 7% to as high as 28%, with a mean rate of 13% (Bryant et al., 2011), and rates of ASD are typically higher among victims of violent versus nonviolent traumas. When subsyndromal cases of ASD are included, estimates of the disorder increase from 10% to 32% with a mean rate of 23% (Bryant et al., 2011).
There are few reliable findings on the prevalence of adjustment disorders. This gap in our knowledge is likely influenced by the poor delineation between adjustment disorders and normal or adaptive stress responses, as well as the use of adjustment disorders as a residual “last resort” diagnostic category in the DSM-IV. One epidemiological study, the European Outcome of Depression International Network, found a 1% prevalence of adjustment disorder with depressed mood (ODIN; Ayuso-Mateos et al., 2001). More circumscribed samples of adults suggest that adjustment disorders are more common in hospital psychiatric consultation settings (12%; Strain et al., 1998; 18.5%; Foster & Oxman, 1994) and among psychiatric inpatient admissions (Koran et al., 2002). A recent meta-analysis found prevalence rates of 15.4% and 19.4% in palliative care and oncology settings, respectively (Mitchell et al., 2011).
Psychological and Biological Assessment
There are a number of diagnostic measures for assessing PTSD. The Clinician-Administered PTSD Scale (CAPS; Weathers, Keane, & Davidson, 2001) is the most common interviewer-based instrument for PTSD and has robust psychometric properties (Weathers et al., 2001). The CAPS was revised for DSM-V and includes a detailed assessment of each traumatic event, a combined frequency and severity rating for each symptom, and overall distress and impairment ratings. Other interview measures include the PTSD Symptom Scale–Interview (PSS-I for DSM-V; Foa et al., 2016), the Structured Clinical Interview for PTSD (SCID; First et al., 2015), and the Anxiety Disorders Interview Schedule for DSM-V (ADIS-V; Brown & Barlow, 2014).
Self-report questionnaires may also be used to assess PTSD. Commonly used measures include the PTSD Checklist for DSM-V (Weathers et al., 2013b), the Posttraumatic Diagnostic Scale for DSM-V (PDS; Foa, 2016), and the Life Events Checklist for DSM-V (LEC-5; Weathers et al., 2013a). A more extensive list of measures used to assess PTSD is available from the National Center for PTSD ( www.ptsd.va.gov ). Not all of these measures have been updated to reflect changes in PTSD criteria from DSM-IV to DSM-V.
Aside from interview and self-report measures of PTSD, several physiological variables have been found to distinguish current PTSD from lifetime PTSD and the absence of PTSD. These include an increased resting heart rate, an increased response to non-trauma-related stressors, and increased heart rate, skin conductance, and diastolic blood pressure in response to trauma cues (Shvil et al., 2013). However, the diagnostic utility of these physiological variables is limited in that they tend to be less accurate than interview-based and self-report assessments in predicting PTSD.
There are few empirically validated diagnostic measures for ASD or adjustment disorders. Measures designed specifically for ASD include the Acute Stress Disorder Interview (ASDI) and the Acute Stress Disorder Scale (ASDS), both developed by the same group of investigators (Bryant, Harvey, Dang, Sackville, & Basten, 1998). The SCID-V contains an optional module for ASD, as well as a section on adjustment disorders that specifies that the diagnosis should not be made if the criteria for any other psychiatric disorders are met (First et al., 2015). With regard to physiological measures, there are some data indicating that individuals who subsequently develop PTSD have higher heart and respiration rates immediately post-trauma as compared with those who do not (Bryant et al., 2011). However, these data are not limited to individuals with ASD, and are likely hampered by the same classification precision of these measures for PTSD.
Etiological Considerations
A number of causal mechanisms have been implicated in the development of PTSD. These include genetic factors, brain structure and neurochemical abnormalities, pre- and post-trauma life events, cognitive appraisals and attentional biases, and sociodemographic variables such as gender.
Behavioral and Molecular Genetics
Increasing data support the role of gene–environment interactions in PTSD (Mehta & Binder 2012). Among Vietnam era veterans, the risk of developing PTSD has been explained by (a) a genetic factor common to alcohol use and PTSD, (b) a genetic factor associated with PTSD but not with alcohol use, and (c) unique environmental effects (Xian et al., 2000). Yet another twin study of Vietnam-era veterans found that the genetic factors that accounted for the relationship between combat exposure and PTSD also accounted for the relationship between combat exposure and alcohol use (McLeod et al., 2001). Genetic factors contributed more to the relationship between combat exposure and PTSD as compared with environmental factors, whereas genetic and environmental factors contributed equally to the relationship between combat exposure and alcohol use. Interestingly, the genetic factors that account for the presence of PTSD may also influence exposure to certain types of traumatic events. Concordance of both interpersonal violence and PTSD is higher among monozygotic twins than among dizygotic twins, whereas other types of trauma (i.e., natural disasters, motor vehicle accidents) are not accounted for by genetic factors (Stein, Jang, Taylor, Vernon, & Livesley, 2002).
In terms of specific genetic markers, the 5-HTTLPR polymorphism has been associated with an increased risk of developing PTSD in specific groups of trauma survivors, including hurricane survivors with a high degree of exposure (Kilpatrick et al., 2007) and individuals reporting a traumatic event in childhood as well as adulthood (Xie et al., 2009). A similar interaction has been reported for variants of polymorphisms in the FK506 binding protein 5 (FKBP5) gene, which is involved in regulating the intracellular effects of cortisol. Individuals with these variants, who reported severe child abuse, were found to be at increased risk for developing PTSD after experiencing a traumatic event in adulthood (Binder et al., 2008; Xie et al., 2009). This gene was under-expressed among survivors of the September 11, 2001 attacks on the World Trade Center who developed PTSD compared with those who did not (Yehuda et al., 2009). There is evidence for candidate genes in other systems (e.g., the dopamine system), but findings have been limited or inconsistent (Broekman, Olff, & Boer, 2007; Koenen, 2007; Nugent, Amstadter, & Koenen, 2008). Genetic research on the trauma and stress-related disorders of the DSM-5 are limited to PTSD.
Neuroanatomy and Neurobiology
Several brain structures have been implicated in PTSD, including the amygdala, the medial prefrontal cortex, and the hippocampus. First, PTSD is associated with increased activation in the amygdala in response to trauma-related stimuli (Francati, Vermetten, & Bremner, 2007). This increased activity likely represents the neural substrates of exaggerated fear acquisition and expression and may explain the salience of trauma memories in PTSD (Rauch, Shin, & Phelps, 2006). Importantly, hyperactivity in the amygdala is not unique to PTSD; increased activity in response to disorder-related stimuli has also been noted in specific phobia and social anxiety disorder (Etkin & Wagner, 2007; Shin & Liberzon, 2010). Second, PTSD is associated with deficient functioning in the medial prefrontal cortex (Francati et al., 2007; Shin & Liberzon, 2010). This deficiency is thought to underlie inadequate top-down modulation of the amygdala (Rauch et al., 2006). Moreover, the medial prefrontal cortex is thought to regulate processes that are important for habituation and extinction of fear responses, including emotional appraisal (Liberzon & Sripada, 2008). Third, PTSD is associated with abnormalities in the hippocampus. These abnormalities may underlie difficulties contextualizing memories (e.g., recognizing that certain contexts are safe; Liberzon & Spirada, 2008; Rauch et al., 2006). A meta-analysis concluded that increased PTSD severity is associated with decreased volume of the hippocampus, as well as decreased volume in the amygdala and the anterior cingulate, a structure in the medial prefrontal cortex (Karl et al., 2006).
Decreased hippocampal volume likely represents a risk factor for developing PTSD, as opposed to a neurobiological effect of trauma (McNally, 2003). Consistent with this, hippocampal volume does not change over time following trauma exposure (Bonne et al., 2001). Moreover, a study of veteran twin pairs discordant for combat exposure and PTSD found that PTSD severity among affected twins was negatively correlated with not only their own hippocampal volume but also that of their nonexposed twin (Gilbertson et al., 2002).
The neurochemical underpinnings of PTSD likely involve catecholamines (epinephrine, norepinephrine, and dopamine) and cortisol, a hormone involved in the neuroendocrine response to stress, as well as a variety of other neurotransmitters (Yehuda, 2006). PTSD may also be characterized by disturbance of the hypothalamic–pituitary–adrenal axis, arising primarily from hypersensitivity of glucocorticoid (i.e., cortisol) receptors (Yehuda et al., 2009). This may represent a risk factor, although the research findings are not yet clearly integrated into a cohesive model.
There are few data specifically reporting on neurobiological models of ASD or adjustment disorders. When viewed as a stress reaction conceptually related to PTSD, ASD in particular may also involve a dysregulation of the neurotransmitter and neuroendocrine systems implicated in PTSD. In addition, ASD may quite possibly involve deficits in certain brain regions such as the hippocampus, which are implicated as a risk factor for PTSD.
Learning, Modeling, and Life Events
Clearly, traumatic life events contribute to PTSD. Less clear is whether trauma exposure and PTSD share a dose–response relationship in which frequency and/or intensity of trauma correspond with symptom severity. Rates of PTSD vary based on the type of traumatic event, with assaultive violence and sexual assault being associated with the highest rates (Breslau et al., 1998; Norris, 1992). Furthermore, rates of PTSD among veterans roughly correspond to degree of combat exposure (Dohrenwend et al., 2006). However, PTSD severity has not been found to correspond to severity of exposure in other trauma samples such as motor vehicle accident survivors and political prisoners (Başoğlu et al., 1994; Schnyder, Moergeli, Klaghofer, & Buddeberg, 2001). Importantly, a dose–response relationship between trauma exposure and PTSD may be nonlinear. That is, after a certain degree of trauma exposure, symptom exacerbation may reach a plateau (McNally, 2003).
Post-traumatic stress disorder may also be related to degree of trauma exposure prior to the traumatic event. Exposure to childhood physical or sexual abuse is associated with an increased risk of future trauma exposure, as well as the development of PTSD in response to those subsequent traumas (Koenen, Moffitt, Poulton, Martin, & Caspi, 2007). In addition to previous childhood abuse or neglect, meta-analyses on the topic have identified other pre-trauma risk factors for PTSD, such as level of prior psychological adjustment and/or the presence of a previous personal or family history of psychiatric illness. Post-trauma risk factors include a lack of social support and additional life stressors (Brewin, Andrews, & Valentine, 2000; Keane, Marshall, & Taft, 2006; Ozer, Best, Lipsey, & Weiss, 2008).
Few studies have examined risk factors specifically in relation to the development of ASD or adjustment disorders. However, given the conceptual overlap between PTSD and ASD, they likely share similar pre- and post-trauma risk factors. Supporting this line of reasoning, one study found that individuals with a previous history of trauma exposure or PTSD and those with more psychiatric dysfunction were at greater risk for developing ASD when experiencing a new trauma (Barton, Blanchard, & Hickling, 1996).
Cognitive Influences
Cognitive influences of PTSD include maladaptive beliefs that one holds about the meaning of the traumatic event that is experienced (e.g., self-blame, guilt). Consistent with this view, cognitive processing therapy (CPT) emphasizes the importance of identifying and revising maladaptive beliefs about the trauma and promoting a more balanced integration of the traumatic event (Resick & Schnicke, 1993). Other possible cognitive mechanisms of PTSD include attentional or memory related biases toward threat-related stimuli or trauma-related material, which may specifically reflect a cognitive vulnerability to developing PTSD (Brewin & Homes, 2003; Fani et al., 2012; Weber, 2008). PTSD may also be influenced by perceived seriousness of threat, which in turn may be influenced by cognitive variables such as poor contextualization of autobiographical memory (Ehlers & Clark, 2000). Although not specific to ASD, a number of studies have found that maladaptive or negative appraisals and beliefs predict the subsequent development of PTSD (Bryant, Salmon, Sinclair, & Davidson, 2007; Mayou, Bryant, & Ehlers, 2001).
Sex and Racial-Ethnic Considerations
Epidemiological surveys suggest that women are more likely to report sexual assault or child molestation and men are more likely to report physical assault, combat exposure, or being threatened or attacked with a weapon (Norris, 1992). Prevalence studies of PTSD further indicate that women are more likely to develop PTSD relative to men (at a 2:1 ratio) given exposure to a traumatic event (Norris et al., 1992). That is, women have a higher conditional risk of developing PTSD relative to men. Traumas associated with ASD are similar to those for PTSD. However, systematic efforts are needed to confirm whether gender differences in rates of ASD are comparable to those associated with PTSD.
Findings regarding the interplay among trauma exposure, PTSD, and race/ethnicity are often mixed (Pole, Gone, & Kulkarni, 2008). Overall, however, most studies have found comparable rates of PTSD between African Americans and Caucasians. The few studies that have found significant racial/ethnic differences report higher base rates of PTSD among African Americans relative to Caucasians that largely disappear once severity of trauma exposure is controlled for. The most consistent findings regarding PTSD and race/ethnicity pertain to Hispanics. Relative to non-Hispanic Caucasians, Hispanics often have higher rates of PTSD in both community and clinical samples (Pole et al., 2008). Cultural context may influence some aspects of PTSD, but the disorder generally presents as a coherent group of symptoms across cultures. Parallel efforts to study the relationship between race/ethnicity and both ASD and adjustment disorders are lacking.
Course, Prognosis, and Treatment
According to the DSM-5, symptoms consistent with a diagnosis of PTSD may begin immediately following or long after a traumatic event, and there is sufficient evidence that PTSD can persist for several years after the index trauma. The diagnostic specifier “with delayed expression” allows for a diagnosis of PTSD when all of the criteria for the disorder are not met for 6 months or longer after the traumatic event. A review on the occurrence of delayed-onset PTSD revealed an average prevalence of 5.6% (Utzon-Frank et al., 2014). The proportion of delayed-onset PTSD cases relative to all PTSD cases was 24.5%, with significant variation in rates across studies. It was further noted that delayed-onset PTSD was almost always preceded by subthreshold PTSD symptoms. Data show that delayed-onset PTSD in the absence of prior symptoms is exceedingly rare (Andrews, Brewin, Philpott, & Stewart, 2007; Frueh, Grubaugh, Yeager, & Magruder, 2009). These and other findings suggest that delayed-onset PTSD is likely due to an exacerbation of prior symptoms over time.
Post-traumatic stress disorder symptoms can persist over time. Findings from the National Vietnam Veterans Longitudinal Study found that 4.5% of male veterans met criteria for DSM-V PTSD 40 years after the Vietnam War (Marmar et al., 2015). In a national sample of Vietnam-era male twins, 3.65% of theatre veterans retained their PTSD diagnosis 20 years later (Magruder et al., 2016). Studies using civilian samples likewise suggest that PTSD can be a chronic condition but report much shorter time frames from the baseline to follow-up.
Parallel with its theoretical underpinnings, clinical practice guidelines generally recommend cognitive behavioral interventions as the most effective treatment approach for PTSD (DVA, 2010; Foa, Keane, & Friedman, 2009; IOM, 2007; NICE, 2005). Treatments that fall under this umbrella typically include elements of psychoeducation, stress reduction, exposure to trauma-related cues and memories, and cognitive restructuring, with the latter two components being considered the “active ingredients” for PTSD symptom reduction.
Although there are a number of interventions that emphasize exposure and/or cognitive restructuring, the empirical data weigh heavily in support of two specific manualized treatments for adults with PTSD: prolonged exposure (PE—an exposure-based intervention; Foa, Hembree, & Rothbaum, 2007) and CPT (predominantly a cognitive restructuring intervention that includes elements of exposure; Resick & Schnicke, 1993). The focus in PE is on habituation to graded fear exposures, whereas the focus in CPT is on modification of maladaptive trauma-related beliefs (e.g., denial or self-blame). However, CPT often includes exposure exercises, and PE often includes elements of cognitive restructuring. Adding cognitive restructuring to PE does not appear to increase its efficacy (Foa et al., 2005), nor does adding writing exposure exercises to CPT (Resick et al., 2008), indicating that the therapies are efficacious in both their combined and component forms.
Reviews on the topic suggest the average patient receiving PE or CPT fares better than 86–90% of patients who are assigned to a control group (i.e., do not receive what is considered an active treatment) (Bradley, Greene, Russ, Dutra, & Westen, 2005; Powers, Halpern, Ferenschak, Gillihan, & Foa, 2010). Despite the overall efficacy of PTSD interventions, 18–35% of individuals who complete treatment retain the diagnosis at follow-up, with civilians showing dramatically greater improvement than military veterans (Bradley et al., 2005). Disability incentives to remain ill have been posited as one possible reason why veterans evidence less clinical improvement than civilians (Frueh, Grubaugh, Elhai, & Buckley, 2007), as have other characteristics unique to veteran populations (e.g., nature of combat trauma). Additionally, treatment dropout rates hover around 30% across clinical populations (Cloitre, 2009). Recently, multicomponent interventions combining exposure therapy and other cognitive-behavioral interventions (e.g., behavioral activation, anger management, social skills) have been demonstrated to be effective in treating the range of symptoms associated with the PTSD syndrome (e.g., Acierno et al., 2016; Beidel, Frueh, Uhde, Wong, & Mentrikoski, 2011). Multicomponent interventions have also been shown to have special promise when delivered in an intensive outpatient program format (Beidel, Frueh, Neer, & Lejuez, 2017).
Reflecting neurobiological models of the disorder, pharmacological treatments for PTSD act primarily on the neurotransmitters associated with fear and anxiety, which include serotonin, norepinephrine, GABA, and dopamine. Selective serotonin reuptake inhibitors (SSRIs) are generally considered the pharmacological treatment of choice for PTSD (DVA, 2010; Hoskins et al., 2015; Stein, Ipser, & McAnda, 2009), and this class of drugs include the only two medications that are currently FDA-approved for the treatment of PTSD—sertraline (Zoloft) and paroxetine (Paxil). Although there is some support for the efficacy of psychotropic medications for the treatment of PTSD, not all practice guidelines support their use. For example, after a review of 37 PTSD pharmacotherapy trials, the Institute of Medicine determined that there was insufficient evidence in support of any psychotropic medications for PTSD including SSRIs (IOM, 2007). A more recent review found that SSRIs were superior to placebo in reducing PTSD symptoms but the effect size was small (Hoskins et al., 2015). Additionally, psychotropic medications do not typically alleviate all the symptoms associated with this disorder and it is generally recommended that patients take medications in conjunction with a psychotherapy specifically developed to treat PTSD, particularly with more complex symptom presentations.
Brief cognitive behavioral interventions immediately post-trauma have yielded promising results in terms of preventing the subsequent development of PTSD among those with ASD (Bryant, Moulds, Nixon, & Basten, 2003; Echeburua, deCorral, Sarasua, & Zubizarreta, 1996; Gidron et al., 2001). These interventions generally consist of education about symptoms, relaxation training, exposure exercises, and cognitive therapy. In contrast, psychological debriefing interventions, which were sometimes used in the aftermath of traumatic events like natural disasters, have failed to demonstrate sufficient efficacy and are generally contraindicated with more severe traumas or post-traumatic reactions (Forneris et al., 2013; North & Pfefferbaum, 2013).
Due to the acute nature of most adjustment disorders, they often do not require treatment, or require limited treatment. Additionally, however, the high degree of variability in the symptom expression of adjustment disorders has likely complicated the development of standardized treatment approaches. Consistent with this, systematic investigations on the efficacy of specific interventions for adjustment disorders are limited to two randomized controlled trials, one targeting adjustment disorder with depressed mood secondary to myocardial infarction (Gonzales-Jaimes & Turnbull-Plaza, 2003) and another targeting adjustment disorder resulting in occupational dysfunction (van der Klink, Blonk, Schene, & van Dijk, 2003). Both of these interventions were tailored for a specific target population and anticipated deficits, with the first demonstrating efficacy of the intervention in terms of symptom reduction and the latter in terms of decreasing absenteeism but not symptom reduction. Pharmacotherapy trials for the treatment of adjustment disorders are likewise few in number and have not established the superiority of antidepressants versus placebo for symptom reduction (Casey, 2009; Casey et al., 2013). Less systematic efforts and clinical wisdom would suggest that psychosocial treatments for adjustment disorders should be relatively brief in duration, and focus on decreasing or removing the stressor as well as improving the patient's adaptation and coping skills.
Case Studies
Post-Traumatic Stress Disorder
Paul is a 26-year-old African American Iraq War veteran who presented to his local VA primary care clinic due to feelings of anxiety. Paul served two tours of duty in Iraq and witnessed multiple roadside bombings in which members of his unit were injured and killed. His final tour ended 2 years ago. He reports symptoms that began shortly after the first roadside bombing he witnessed while overseas, and an increase in the severity and frequency of these symptoms since his return to the US. He experiences frequent nightmares and intrusive memories about Iraq, including nightmares and unwanted thoughts related to a bombing in which he witnessed the death of two of his comrades with whom he was particularly close. Paul questions in his mind why he lived while his comrades died and feels certain that he should have been able to prevent what happened. He avoids internal and external reminders of the event, which include thinking about the bombings and other graphic scenes from his service, as well as driving. Last, he is experiencing marked irritability, anger, and hypervigilance, especially while driving. Paul often catches himself gripping the steering wheel of his car, anticipating an improvised explosive device. Because of his symptoms, Paul's relationships have suffered, most notably his relationship with his girlfriend of several years, who has made a number of comments to him about him having changed since coming back from Iraq and not being the same “easygoing” guy she met. Paul is enrolled in college under the GI Bill and is having difficulty studying due to problems concentrating and a persistent lack of sleep. He fears he may have to withdraw from the semester.
Paul's experiences in Iraq are consistent with the definition of a traumatic event, and his symptoms reflect chronic PTSD with acute onset.
Adjustment Disorder
Susan is a 42-year-old Caucasian woman who presented to her primary care physician for her annual appointment. During the course of the appointment, Susan admits to her physician that she has been struggling emotionally since the end of her marriage (2 months prior) and the loss of her job (9 months prior). After both of these events, but to a much greater extent since her son moved out of the home, Susan describes feeling a mixture of depression and sadness about her failed marriage and lack of new job prospects, as well as general feelings of anxiety and fear about her future. She reports feeling at a loss as to how to manage her time and feels overwhelming sadness at being 45 and alone, with few friends or family to rely on. She acknowledges calling in sick from work a few times a month for the past few months and then ruminating about the potential consequences of having not gone in to work. She reports watching television several hours a day followed by periods of anxious and somewhat obsessive housecleaning. She also reports having crying spells “over just about anything” and is tearful while discussing her symptoms during her primary care appointment.
Susan's clinical presentation is consistent with a diagnosis of adjustment disorder with mixed anxiety and depressed mood.
Summary
Post-traumatic stress disorder, ASD, and adjustment disorders are classified in the DSM-5 as trauma- and stress-related disorders that were precipitated by a stressful or traumatic event. The value of classifying these disorders together will enable clinicians to better differentiate normal and mild stress reactions from more severe and pathological stress reactions. It also more clearly highlights the temporal and symptom requirement distinctions between PTSD, ASD, and adjustment disorders. Whereas PTSD and ASD emphasize fear and anxiety responses, adjustment disorder symptoms can accommodate a broader range of stress reactions. Second, although there is an explicit potential for ASD to predict subsequent impairment (i.e., to predict PTSD), an adjustment disorder is typically viewed as a discrete disorder that has a fairly immediate and time-limited symptom duration. A third distinction between PTSD, ASD, and adjustment disorders regards the timing of diagnosis. Adjustment disorders can be diagnosed immediately after the event, ASD can be diagnosed from 2 days up to 1 month after the event, and PTSD can be diagnosed from 1 month to several years after the trauma.
In conclusion, based on being linked to a clear precipitating stressful or traumatic event, PTSD, ASD, and adjustment disorders are viewed as stress reactions along a continuum that are differentiated by the severity of the initial stressor, an anxiety-focused or broader set of symptoms in reaction to the event, and the onset and duration of the symptoms. PTSD and ASD share many of the same symptoms, with ASD being limited in duration to 1 month, and in some but not all cases predicting the subsequent development of PTSD. The relationship among adjustment disorders, PTSD, and ASD is poorly understood as there has been little systematic study on the topic. The placement of adjustment disorders in the same chapter as PTSD and ASD in the DSM-5 will likely prompt a better understanding of the unique and overlapping features of this disorder in relation to PTSD and ASD. Future studies will likely shed light on the similarities and differences between these three disorders with regard to prevalence, diagnosis, clinical presentation, correlates, and treatment.
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