PSY404 Unit 1 Assessment: Aetiology and Treatment of Post-Traumatic Stress Disorder (PTSD)
A wide range of both common events, such as traffic accidents, and extraordinary events, e.g. rape, can be traumatic (Nolen-Hoeksema, 2011). Although processing of traumatic events differs between individuals, it is very likely to be exposed to extreme stressors at some point in life which can lead to PTSD (54-64% in Europe and Japan, see Atwoli et al., 2015) making PTSD a common disorder (Bennett, 2006).
This essay will give an overview of the history of the term PTSD, PTSD-prevalence, and the DSM-V diagnosis for individuals older than 6 years. Moreover, aetiology (particularly social, environmental, psychological, and biological vulnerability-factors); and current treatments: Trauma-Focussed Cognitive-Behavioural-Therapy, Eye-Movement-Desensitization-and-Reprocessing, pharmacological/drug-assisted and alternative treatments will be discussed, considering recent psychological theories on PTSD by Foa and Kozak’s (1986) Emotional-Processing-Theory and Ehlers and Clark’s (2000) Cognitive Model of PTSD.
In early psychiatric diagnostics, PTSD was labelled as idiotism. Later, post-WW1, the large scale phenomenon of PTSD-affected soldiers led to coining the terms battle hypnosis, shellshock, war neurosis – which was explained by individuals’ weakness and insanity (Crocq & Crocq, 2000). Particularly the need of psychological treatment in circa 700,000 – nearly a quarter of all – US Vietnam veterans lead the American Psychiatric Association (APA) to coin the term PTSD and listing it firstly as a mental disorder caused by an external event in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) in 1980 (Crocq & Crocq, 2000).
According to the current DSM-V (APA, 2013), PTSD is a trauma-related disorder, characterised by one or more direct or indirect exposures to a traumatic event/stressor, such as “actual or threatened death, serious injury, or sexual violence” (APA, 2013, p.271) followed by, first, persistent re-experiencing of the event(s) through unwanted memories, nightmares, flashbacks, emotional distress and/or physical reactivity; and second, by avoidance of internal and/or external cues associated with traumatic events. Third, individuals show at least two of the following negative alterations of cognition and mood associated to traumatic events: inability to remember important aspects of the traumatic event(s), exaggerated negative beliefs about oneself and the world, persistent distorted cognitions in causes or consequences of the traumatic event(s) and self-blame, persistent negative emotional state, disengagement and loss of interest, feeling of detachment of others, and persistent inability to experience positive emotions. Fourth, individuals also show two or more of the following alterations in arousal/reactivity: irritability and angry outbursts, risky/destructive behaviour, hypervigilance, heightened startle reaction, concentration-problems, and/or sleep-problems. Moreover, the symptoms must last for more than 1 month, create clinically significant distress or functional impairment (e.g. socially, occupationally) and are not due to medication, substance use, or other illness. Additionally, individuals might show dissociative symptoms of depersonalisation (outside-observing/self-detached) or derealisation (unreality, distance, and distortion).
Atwoli and colleagues (2015) estimated international random and worst event lifetime-prevalence of 9.2% and 13.6%, respectively. According to APA (2013), among countries at peace, the highest 12-months prevalence could be found among U.S. adults (3.5%); and most South American, European, Asian and African countries’ prevalence was 0.5%-1.0%. Highest PTSD rates (33-50%) can be found among individuals who experienced rape, military combat and captivity, internment and genocide (APA, 2013); and accordingly in countries at war (Nolen-Hoeksema, 2011). Of 799 observed Afghans by Cardozo and colleagues (2004), 42% were found to have PTSD. Kazour and colleagues (2017) found PTSD lifetime-prevalence and point-prevalence among Syrian refugees of 35.4% and 27.2%, respectively. However, many cases might stay undiagnosed or misdiagnosed due to overlapping symptoms and comorbidity with, for example, depression, general anxiety and substance abuse disorder (NICE, 2005).
The main cause of PTSD is a traumatic event (NICE, 2005). Longer-lasting, more severe and directly affecting traumas are more likely to lead to PTSD (Nolen-Hoeksema, 2011) and influence individuals’ experience. In Ozer and colleagues’ (2003) meta-analysis peri-traumatic dissociation was found to be the most influential factor in predicting PTSD (weighted r=.35), followed by perceived threat (weighted r=.26). As in classical conditioning theory, Foa and Kozak (1986) argue in Emotional-Processing-Theory that complex fear structures in the memory can become pathological in traumatic situations as non-dangerous stimuli become associated with danger, arousal as well as behavioural reaction, and beliefs about the world and ‘self’ change negatively. Ehlers and Clark’s (2000) Cognitive Model (CM) explains that events’ negative appraisals lead to misinterpretations of situations, biased recalls of memories and associations of (often unconscious) negative triggers to situations.
A variety of social and environmental, psychological, genetic and biological pre-traumatic, peri-traumatic and post-traumatic factors can interact over time influencing individual’ vulnerability to develop PTSD (also epigenetically: Meaney & Yehuda, 2018).
Examples of social and environmental factors are lower socioeconomic status (in motorcycle accidents; Bhatt et al., 2017), income (Kung et al., 2018), education (Kung et al., 2018), being part of a minority (such as discriminated African Americans; Brooks Holliday et al., 2018), different cultural characteristics (such as cultural-dependent developments of the self Hobfoll, Gaffey, & Wagner, 2018), prior trauma, childhood adversity (Meaney & Yehuda, 2018), and younger age (APA, 2013). Several researchers argue that PTSD is a socially constructed pathologizing and over-diagnosing of culturally shaped emotions to traumatic events (Bisson, 2009). For example, intentions behind traumatic events moderate the disorder’s course: Santiago and colleague’s (2013) literature-review shows that PTSD-symptoms caused by non-intentional events tend to decrease over the first 12 months but increase for intentional events. Another explanation are moderating effects of social factors, such as community and family function and support, living-condition, loss of material or role, on individuals’ cognitive and emotional ability to be exposed to desensitization-enhancing processes (Bisson, 2009). Individuals receiving emotional support from their peers recover quicker (Nolen-Hoeksema, 2011) and perceived support is one of the best predictors for PTSD-development (Ozer et al., 2003).
Several psychological vulnerability-factors may increase individuals’ PTSD-risk; for example, a family-history of psychopathology (FHP) and pre-traumatic adjustment problems pre-trauma mental health treatment, emotional problems, anxiety or affective disorders, and pre-military-service antisocial personality disorder (Ozer et al., 2003). However, Ozer and colleagues’ meta-analysis could only show small correlations (weighted r=.17) of pre-traumatic adjustment-problems and PTSD; and only few studies could reveal prior depression as a further predictor. Furthermore, the relation of FHP and PTSD was moderated by the experienced traumatic event and strongest for noncombat interpersonal violence (weighted r=.31), then combat exposure (weighted r=.12) and accidents (weighted r=.08) (Ozer et al., 2003). Findings support Ehlers and Clark’s (2000) CM stating that appraisal and coping influence individuals’ post-traumatic vulnerability: self-destructive and avoiding coping, such as drug-abuse and self-isolation (Nolen-Hoeksema, 2011), as well as negative appraisal of PTSD-symptoms (Su & Chen, 2018) were found to increase PTSD-vulnerability (e.g. in avoidance-coping firefighters: Witt, Stelcer, & Czarnecka-Iwańczuk, 2018).
Moreover, genetic and biological vulnerability-factors include certain gene expressions (e.g. miR-1299: Wingo et al., 2018), lower intelligence (Buckley, Blanchard, & Neill, 2000) age and (female) gender (e.g. following traffic accidents; Kobayashi, Sledjeski, & Delahanty, 2018). However, reasons of higher PTSD rates in females are likely to be due to gender role socialisations and learned trauma-response, not genetic (Street & Dardis, 2018). Pathologically activated fear structures (see Emotional-Processing-Theory) and negative appraisal (see CM) lead to increased physical activation. Accordingly, PTSD sufferers showed prolonged high cortisol-levels and increased activity in brain areas regulating emotions, fight-flight-and-freeze response, and memory: amygdala, hippocampus and prefrontal cortex (Nolen-Hoeksema, 2011). Different neuroendocrine systems, such as the hypothalamic–pituitary–adrenal axis, change in the course of PTSD (Heim et al., 2018) and some studies reported hippocampus shrinkage (Nolen-Hoeksema, 2011).
In conclusion, traumatic events’ characteristics, fear conditioning, trauma-memories, coping/appraising, pre-traumatic psychopathology and trauma, social support, neurochemical and neurophysical abnormalities, and a variety of other vulnerability-factors are associated with developing PTSD. Vulnerability-factors moderate the illness’s course and responsiveness to treatments. Therefore, different kinds of psychological, pharmacological and physical treatments are applied.
Most commonly, psychological treatments (with a cognitive focus) are being used to treat PTSD relatively successfully. Erford and colleagues’ (2016) meta-analysis shows effectiveness (small to large effects) of psychotherapeutic PTSD-treatment and a longevity of treatment-gains of more than 2 years after treatment-termination. Similar effects could be measured in an earlier meta-analysis by Sherman (1998). Pharmacological and physical treatments are used as secondary option alongside psychotherapy when other approaches do not work, for example, in cases of complex and multiple trauma (NICE, 2005).
Psychological theories as Emotional-Processing-Theory (Foa & Kozak, 1986) and Cognitive Model (Ehlers & Clark, 2000) argue that re-conditioning and re-learning about traumatic events is helped by exposing clients to traumatic memories and trauma-associations. The re-exposure of traumatic memories allows clients’ trauma-accessing, trauma-processing and then trauma-resolving (cognitive approach) and connected emotional responses to become habituated over time (conditioning approach)(Bennett, 2006). Meta-analytical research suggests exposure-based therapy as superior to other approaches (Cusack et al., 2016), specifically individual exposure-treatments (Ehring et al., 2014).
Current, efficacious and exposure-based treatments are Trauma-Focussed Cognitive-Behavioural-Therapy (TF-CBT) and Eye-Movement-Desensitization-and-Reprocessing (EMDR) (Bisson et al., 2013). TF-CBT focusses on systematic desensitization, using clients’ rankings of anxiety-giving thoughts and situations (Nolen-Hoeksema, 2011). Clients’ following gradual exposed to the ranking is supported by relaxation techniques to avoid drop-outs (Nolen-Hoeksema, 2011). When clients do not respond with stress-responses, the therapy can focus on more distressing details (Bennett, 2006). If the exposure is intolerable, stress-management-interventions can also help reduce general life-stress (Nolen-Hoeksema, 2011). Research widely supports TF-CBT to be an efficacious and safe treatment for PTSD (Bisson et al., 2007), for example in adults (Bisson et al., 2013), children and adolescents (Phillips & Schrom, 2018) or asylum-seekers (Thompson, Vidgen, & Roberts, 2018). However, the treatment can produce high non-responsiveness of up to 50% across cultures (Kar, 2011).
In EMDR, clients are asked to recall memories as visual images and to pair each with a negative cognition and rate evoked emotions. Then, clients follow the therapist’s increasingly fast-moving finger with their eyes. After 24 finger-movements, clients are asked to ‘let it go’. The emotional state is re-assessed and the procedure repeated until only minimal distress is experienced (Bennett, 2006). Mechanisms behind EMDR remain unclear, nevertheless, different meta-analysis could show EMDR’s success in reducing PTSD-symptoms and its superiority to no treatment/placebo (Chen et al., 2014; Wilson et al., 2018), also in children and adolescents (Moreno-Alcázar et al., 2017). However, further research is needed due to studies’ small sample sizes and limited follow-up data (Wilson et al., 2018).
While Bisson and colleagues (2013) argue that both TF-CBT and EMDR are equally effective in treating chronic PTSD in adults, Chen and colleagues’ (2015) data suggests EMDR to be more suitable, and Cusack and colleagues’ (2016) state that the data was insufficient to determine comparative effectiveness. In children and adolescents, TF-CBD could be found to be more effective (Lewey et al., 2018; Morina, Koerssen, & Pollet, 2016). Conversely, Rodenburg and colleagues (2009) made opposing findings. Moreover, particular groups require specific treatments: EMDR was more efficacious than TF-CBT in treating refugees and asylum seekers (Thompson et al., 2018). Group-therapy seems more successful in encouraging veterans’ treatment-continuation and treatment-participation than individual treatments (Sripada et al., 2016). Accordingly, initially combined treatments should be considered for certain groups. One of the latest developments is the use of technology in therapy. A growing body of evidence of treatment-efficaciousness supports online-based therapy (Simblett et al., 2017). Furthermore, VR-supported exposure-therapy seems to be non-deleterious (Fernández-Álvarez et al., 2018). While Carl et al. (2018) found VR-treatment outcomes to be indifferent from in-vivo exposure-therapy, van't Wout-Frank and colleagues’ (2018) promising results suggest more research on combining transcranial magnetic stimulation (TMS) with VR.
Furthermore, variety of drugs (e.g. serotonin reuptake inhibitors(SSRI), monoamine oxidase inhibitors, tricyclics) has been used to treat PTSD (Bennett, 2006). Stein and colleagues’ (2006) meta-analysis could show the superiority of a variety of medications in treating PTSD over placebo, with SSRI reported to be most efficient (Stein et al., 2006). Generally, Drug-treatments’ efficaciousness is lower and drop-out rates higher than in psychotherapy, but most effective drug-treatments’ and psychotherapies’ efficaciousness is similar (Van Etten & Taylor, 1998). A more recent, promising, safe and efficacious approach is micro-dosing methylenedioxymethamphetamine in inpatients along psychotherapy to reduce neurobiological fear reactions when conventional treatments cannot help (Amoroso & Workman, 2016; Thal & Lommen, 2018).
More research is needed on alternative treatments. While some research shows weak or inconclusive support – e.g. for needle acupuncture (Grant et al., 2018), meditation (Hedman-Lagerlöf, Hedman-Lagerlöf, & Öst, 2018; Jayatunge & Pokorski, 2018) – other sources report promising evidence. For example, Wahbeh and colleagues’ (2018) meta-analytical evidence for benefits was strong for repetitive TMS, and good for acupuncture, hypnotherapy (for PTSD-insomnia, see: Szigethy & Vermetten, 2018), meditation, and visualization.
In conclusion, PTSD has a relatively high life-time prevalence and counts to the more common mental disorders. The disorder has a large range of symptoms differing in their expression due to differences in traumas, experiencing them and individual predispositions. Further research is needed to support the most common explanations of PTSD and knowledge on group-specific aetiology. A variety of different psychotherapies are being used, all using exposure techniques with relative success. Research suggests exposure-based therapies TF-CBT and EMDR to be most efficacious. EMDR and different pharmacological interventions can be used to treat multiple and complex trauma. However, most patients experience posttreatment residual symptoms (Bradley et al., 2005). Problematically, most findings on treatment-efficaciousness include only psychological symptom-measures, whereas including biological measures could help explaining mechanisms underlaying effective treatment (Schumacher et al., 2018). Some alternative approaches seem promising and offer new treatment-opportunities, such as TMS, hypnotherapy and online treatment, but still require scientific validation.
- Quote paper
- Max Korbmacher (Author), 2018, Aetiology and Treatment of Post-Traumatic Stress Disorder (PTSD), Munich, GRIN Verlag, https://www.grin.com/document/490267