The Diagnostic and Statistical Manual of Mental Disorders estimated 9-11 % of the general population experience traumatic distress and about half of the people who experienced trauma continue to develop Posttraumatic stress disorder (PTSD). PTSD is an anxiety disorder for which cognitive-behavioural therapy (CBT) is employed to treat or prevent maladaptive behaviour, beliefs and thought processes. According to the diagnostic criteria for PTSD, individuals exposed to trauma experience three distinct types of persistent post-trauma symptoms. The arousal symptom clusters describe re-experiencing traumatic moments, nightmares, flashbacks and sleep-disturbances. The second clusters of symptoms describe physiological responses such as helplessness, anger outbursts, concentration problems, hyper vigilance and exaggerated startle responses. The third cluster of symptoms describes avoidance and emotional numbing symptoms that leads to avoidance of people, trauma reminders, emotional dissociation and trouble recalling trauma events.
The persistent PTSD symptoms detrimentally affect mental health, social behaviour and occupational functioning. The issue whether PTSD symptoms own their existence to biological and learning or whether they are entirely cognitively determined has been the subject of much debate. Each approach provides evidence supporting fear activation and problems in emotion regulation leading to various symptoms of PTSD but these findings do not settle the issue for the maintenance of persistent symptoms of PTSD. In fact, it is posited that individual differences in the appraisal of trauma events and emotion regulation strategies determine the maintenance of the PTSD symptoms. Hence, the existing cognitive-behaviour therapy for PTSD was conceptualised to provide clinicians and therapists with an evidence-based framework that addresses individualised case formulation and treatment needs. The purpose of this essay is to discuss and evaluate the theoretical findings and treatment models, which contributed to the understanding of persistent symptoms of PTSD.
The Diagnostic and Statistical Manual of Mental Disorders ([DSM IV-TR], APA, 2015) estimated 9-11 % of general population experience traumatic distress and about half of people who experienced trauma continue to develop Posttraumatic stress disorder (PTSD). PTSD is an anxiety disorder for which cognitive - behavioural therapy (CBT) is employed to treat or prevent maladaptive behaviour, beliefs and thought process. According to the diagnostic criteria for PTSD (DSM-IV –TR, 2015, p.467-468), individuals exposed to trauma, experience three distinct types of persistent post-trauma symptoms. The arousal symptom clusters describe re-experiencing traumatic moments, nightmares, flashbacks and sleep-disturbances (DSM-IV-TR, 2015,p467-468). The second clusters of symptoms describe physiological response such as helplessness, anger outbursts, concentration problems, hyper vigilance and exaggerated startle responses. The third cluster of symptoms describes avoidance and emotional numbing symptoms that leads to avoidance of people, trauma reminders, emotional dissociation and trouble recalling trauma events (DSM-IV-TR, 2015,p.467-468). The persistent PTST symptoms detrimentally affect mental health, social behaviour and occupational functioning. The issue whether PTSD symptoms is something that owns its existence to biological and learning or whether it is entirely cognitively determined has been the subject of much debate (Dalgleish, 2004). Each approach provides evidence supporting fear activation and problems in emotion regulation leading to various symptoms of PTSD but these findings do not settle the issue for the maintenance of persistent symptoms of PTSD (Brewn & Holmes, 2003; Dalgleish, 2004). In fact, it is posited that individual differences in the appraisal of trauma events and emotion regulation strategies determine the maintenance of the PTSD symptoms (Ehler & Clark, 2000). Hence, the existing cognitive behaviour therapy for PTSD (Ehler & Clark, 2000) was conceptualised to provide clinicians and therapists evidence based framework that address individualised case formulation and treatment needs. The purpose of this essay is to discuss and evaluate the theoretical findings and treatment model, which contributed to the understanding of persistent symptoms of PTSD.
Witnessing, direct experiencing, learning about a trauma that happened to someone close and repeated exposure to critical incidences contributes to the risk of developing PTSD (DSM-IV-TR, 2015, p271). Epidemiological studies indicate PTSD affects direct victims of disaster such as war veterans (Dohrenwend et al., 2008; Sareen et al., 2007; Hoge et al., 2004), war refugees (Marshall et al., 2005), civilian chemical warfare (Hashemian et al., 2006), exposure to natural disasters (Vetter et al., 2008). In the general population, the risk of developing PTSD is found greater among victims of sexual assault, vehicle accidents, learning of trauma to close friend and learning about unexpected death (Breslau et al., 2004). According to the World Health Organization (WHO, 2011), work functioning impairment due to absenteeism among PTSD sufferers is as high as 4.9 days per month. PTSD also contributes to high lifetime psychiatric co-morbidity such as anxiety disorder, major depression disorder, alcohol abuse and obsessive-compulsive disorder (Brown et al., 2001). The economic and the social burden of PTSD can be reduced significantly with an accurate assessment of PTSD vulnerability factors, early symptoms identification and followed with appropriate cognitive and behaviour intervention (WHO, 2011).
Turning now to the early research evidence-investigating symptoms related to PTSD. The behaviourists suggested that behaviour is learned from the environment and thus investigated the learning outcome. Behavioural processes are investigated by exposing animal and human subjects to conditioning and unconditional stimulus in a controlled laboratory experiments (Bouton, 2007). Research outcome examines the conditioning responses, reinforcement, interference paradigms, etc. (Bouton, 2007). With regards to PTSD, the learning theory posited that individuals with PTSD must have endured a strong form of classical conditioning causing the pathological disorder (Brewn & Holmes, 2003). Mowrer (1960) suggested a two-factor theory of fear, involving classical and operant conditioning. According to Mowrer, (1960) aversive emotions are activated when neutral stimuli become exposed to unconditioned trauma stimuli. Consequently, the fear of traumatic stressor primes the avoidance coping behaviour. (Brewn & Holmes, 2003). Repeated avoidance of fear cues reinforces the avoidance maintenance (Brewn & Holmes, 2003). Mowrer’s (1960) findings highlighted the avoidance conditioning as a way to escape from the source of fear. The outcome of the animal experiment was generalised to explain many human psychopathologies, including the avoidance symptoms of PTSD. However, the behaviourists approach ignores cognitive processes and other mental experiences involved in learning (Brewn & Holmes, 2003; Buck, 2010).
The following are the theoretical understanding relating to cognitive processes and models of PTSD. Horowitz’s (1986 as cited in Brewin, Dalgleish & Joseph, 1996) stress response syndrome proposed that intrusive re-experiencing symptoms of PTSD occur when threatened with trauma reminder. The theory suggested cognitive processing of traumatic information is exposed to completion tendency by which meaning; the psychological tendency for assimilating newly acquired information with existing cognitive schemas (Brewin et al., 1996). However, because trauma memory is incompatible with the existing world model, emotional defence mechanisms are activated instead. The defence mechanism keeps the trauma memory alive in the form of intrusive thoughts interrupted by periods of denial. Stress related symptoms negative thoughts, flashbacks, nightmares, and emotional numbing occur as one try to assimilate the trauma information into the existing world model, (Brewin et al., 1996). Following the findings, Horowitz, Wilner and Alvarez (1979) developed the Impact of Event Scale (IES) to measure the two symptoms, the intrusion of involuntary re-experiencing and the avoidance of trauma reminders. Although Horowitz and colleagues (1979) has developed a decisive tool to measure the two prominent symptoms of PTSD, the tool is not without its limitations. Mc.Gorry and colleagues (1991) found an insignificant correlation between the subscales measuring intrusive symptoms and avoidance. In addition, Horowitz’s formulation doesn’t explain how elements of social support, individual differences and meaning interpretations affect emotion processing (Dalgleish, 2004).
Jaoff-Bulman’s (1992) model of shattered assumptions addresses the issues with regards to social cognition and stimuli interpretations in PTSD. According to the model, trauma- related information is incongruent in nature and causes disruption when the incongruent information is unable to readily assimilate into the existing schemas. Hence, the friction between pre-existing assumptions and trauma related reality causes oscillating phases between intrusive thoughts, difficulty in accepting the reality and emotional numbing. Jaoff-Bulman’s (1992) theory is significant in understanding the role of worldview in the interpretation of traumatic events. Due to the weakened worldviews, individuals with PTSD tend to either exaggerate or minimise their existence and about the world. While, schemas based theory is instinctively convincing, the theory doesn’t explain how the model is represented (Drescher & Foy, 1995). Evaluation of the theory has mainly relied using The World Assumptions Scale ([WAS], Janoff-Bulman, 1989), which has been reported for psychometric issues (Kaler et al., 2008). Most of the findings are from the self-administered retrospective reporting and lacks prospective studies to support the arguments (Drescher & Foy, 1995). The theory also fails to explain how shattered worldview affects PTSD suffers from comorbid disorders (Drescher & Foy, 1995).
Adopting Lang’s (1968, as cited in Foa & Kozak, 1986) proposition of fear network, Foa and colleagues (Foa & Kozak, 1986) proposed an emotional processing network for escaping danger. According to Foa and Kozak (1986) memory processing of trauma is influenced by emotion experienced during the traumatic event and during retrieval of emotional events. The fear network consists of information about the feared stimuli, meanings that attached to the fear stimuli, behaviour responses and coping elements (Foa & Kozak, 1986). Pathological fears in PTSD are the consequence of unrealistic meaning about the feared stimuli, excessive avoidance strategies and resistance to modification. The framework suggested activation and habituation through repeated exposure to feared stimuli modifies information structure in memory enabling greater emotional processing leading to lasting fear reduction (Foa & Kozak, 1986).
Many randomized controlled trials indicated the effectiveness of prolonged exposure and exposure-based psycho-education (Foa et al., 2005). When compared with other therapies such as EMDR and relaxation training, exposure therapy indicated greater efficacy and treatment outcome (Taylor et al., 2001). Prolonged exposure is also a recommended worldwide treatment choice for PTSD (NICE, 2005; Forbes et al., 2007). Despite the efficacy, exposure therapy is not widely suggested within the clinical practice. The main reason is a view that the therapy contraindicated for patients with pre-existing psychiatric conditions and in individuals who are predisposed with PTSD vulnerability (Becker et al., 2004). Secondly, emotional numbing and dissociation are indicated to hamper fear activation and invoking matching stimuli for accessing fear structure can be challenging (van Minnen, Harned, Zoellner & Mills, 2012).
According to Brewin, Dalgleish and Joseph (1996) two parallel brain systems handles emotional processing of the trauma. Encoding problems in these two processors contributes to the complexity of PTSD. One verbally accessible memory (VAMs) and another format situation ally accessible memory (SAMs) (Brewin et al., 1996). The theory describes three types of encoding occur in the emotional processing of trauma, which is, successful completion, chronic processing and premature inhibition (Brewin et.al.1996). The SAMs is a primitive system that processes non-verbal sensory information such as sounds and images obtained from the environment (Brewin, Gregory, Lipton & Burgess, 2010). The visual information that passes through the subcortical pathways reaches the amygdala and activates the sensory receptors for the fear response (Brewin, et.al. 2010). The insufficient attention processing at the onset of the stimulus warrants the trauma messages crudely processed. The fragmented sensory information is unable to discriminate between the past and current threats. Hence, activating past trauma images in present tense resulting PTSD symptoms of flashbacks and nightmares (Brewin et. al., 2010).
On the contrast, the VAMs are a slower processing system and the same captured information is processed in much detail than SAMs (Brewin, 2001). The attended information is kept in the working memory temporarily in the hippocampus region prior to transfer to the long-term autobiographical memory storage (Brewin, 2001). Sufficient simulated attention on the spatial and temporal images allow successful re-encoding of information into the VAMs system. The attended images enable the brain to register trauma as past events absent from current threats (Brewin, 2001). However, avoidance coping strategies to block out flashbacks of intrusive trauma memories causes weak inhibition, and the fragmented information remains in the SAM without being transferred to the VAM. Thus, in the presence of weak stimuli or trauma reminders, the fragmented memories activate the SAMs emotional response (Brewin, 2001; Brewin et.al, 2010). Fear motivated by possible future threat leads to secondary emotion generation such as anger outbursts, guilt, remorse, and helplessness (Brewin, Andrews & Rose, 2000).
According to Brewin and Lennard (1999) psychotherapy treatments that promote emotional narratives of trauma events and trauma reminders allow assimilation of information into the VAM. Secondly, adding contextual meanings, elaboration of worst periods of trauma and recalling extra details during flashback occurrences aid to identify maladaptive beliefs. The defined beliefs are challenged, and new evidence that is in support of positive views are highlighted and systematically incorporated to replace the negative beliefs (Brewin & Lennard, 1999). Techniques such as repeated exposure to stimulus reminders are indicated to habituate intrusive memories (Foa & Kozak, 1986). The re-evaluation of past traumas consequently reduces negative affect and increase relaxation (Foa & Kozak, 1986).
The main limitation of the dual processing theory, however, is the theory lacks compelling evidence to support the argument about the fragmented VAMs (Dalgleish, 2004). Another criticism of much of the researchers is that there is no significant evidence to show the exact location of SAMs (Dalgleish, 2004; Berntsen et al., 2008). Also, the theory places hefty emphasis on flashbacks and not much detail on other symptoms of PTSD is another potential concern. However, The dual processing theory contributed two significant clinical implications in the treatment of PTSD symptoms, the resolution for maladaptive thoughts and handling flashbacks (Brewin & Lennard; Foa & Kozak, 1986).
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