Table of Contents
The biological hypotheses of PTSD
Animal model of PTSD
Issues and Debates on Diagnostics and Medication of Posttraumatic Stress Disorder (PTSD)
Whether it is war-traumatized soldiers, refugees, victims of sexual assault or victims of catastrophic life events, the psychiatric consequence of the posttraumatic stress leading to a mental disorder if left untreated can be debilitating. The prevalence of posttraumatic stress disorder (PTSD) in countries that have suffered war and political conflicts such as Northern Ireland (Muldoon et.al.2007, p.146), Uganda (Mugisha et.al, 2015,p.2) and Palestine (Canetti et.al.2010, p.219) ranged between twenty to seventy percent. Analysis of epidemiological surveys by the World Mental Health, between 2012 until 2015 for non-war related traumatic event reported 54% of lifetime prevalence in Europe, 56.1% in Italy and 60.6% in Northern Ireland (Atwoli et al., 2015, p.302). Given the potential economic and psychosocial impact of PTSD, efforts to identify biomarkers of risk, disease and treatment of PTSD is of significant public health importance (McCrone et al., 2003,p.519). The psychiatric codification of PTSD has made possible for patients to access medical care and treatment. Likewise, mental health professionals were able to predict reliably, distinguish and diagnose trauma-associated disorder from other major mental illness (APA, 2013). However, the issue of whether PTSD owes its existence to environmental context, individual differences and learning or whether it is entirely neurobiological determined has been debated fiercely (Charney et. al., 2002, p.32). Findings from the neuroimaging and translational research provide evidence that supports the neurobiological theories of etiology but yet to find a specific biomarker for PTSD (Zoladz & Diamond, 2013,p. 890). In fact, research outcome strongly suggest PTSD is a result of interaction between biological, individual predisposition and environmental context.
According to Birmes and colleagues (2003,p.18) history of trauma symptoms experienced by people existed in different names long before the formal diagnostic classification status as PTSD in DSM-III in 1980 (APA, 1980). During the 19th century, soldiers returning from the American Civil war were believed to develop traumatic neurotic caused by adverse emotional volatility, nostalgia and homesickness (Birmes et al., 2003, p 18). Analysis of historical war medical files between 1916 until 1918 revealed two hundred cases known as disordered action of the heart and two hundred cases of shell shock disorder, which clinicians during that time believed those conditions rose due to tight chest constricting combat gears, adjustment problems and irrational expectations of war (Jones et al., 2003, p 159). However, it was the impact of Vietnam War on mental health long after the war ended highlighted the need for formal categorization of PTSD. The first health survey on combat fatigue by the National Vietnam Veterans Readjustment Survey revealed that the risk of developing PTSD among the Vietnam War veterans was as high as 30.9% (Kulka et al., 1990a). The findings helped recognize PTSD as a distinct psychological disorder that develop after a traumatic experience such as war. Analysis of Pension file records from the First, Second, Malaya, Korean and the Persian Gulf War revealed clusters of symptoms similar to PTSD, persistent avoidance, hyperarousal and mood alterations with diagnostic labels, for example, shell shock disorder, psychoneurosis, battle hysteria and cardiac neurosis (Jones et al., 2003, p159).
Other than combat experiences, evidence of PTSD symptoms among civilian population led to the recognition that PTSD symptoms could be reliably diagnosed and received the formal classification as a psychobiological mental disorder in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders in 1980 [DSM-III], (NIH, 2010, p1). The International Classification of Diseases, Tenth Revision (ICD-10) by the World Health Organizations (WHO) is another classification system recognizes PTSD as a diagnosable mental disorder since its inception in 1992. Both classification systems of PTSD share similar diagnostic features and also, the current DSM-5 (APA, 2013) has been revised to be compatible with the ICD-10 (WHO, 1992).
According to Jewell and colleagues (2009, p.37) the diagnostic systems adopted a universally understood medical language to facilitate reliable clinical practice among the health professionals without them getting mired in hypothetical disputes about the etiology of the mental disorder. However, critiques argued that the biological model of PTSD has remained descriptive in nature and have not been reliable in actual clinical application (Charney, et al., 2002, p 33). Others concerned that the ‘medical’ model approach assumes neurobiological basis rather than looking at how environmental and psychosocial factors influence the onset of PTSD symptoms (Suvak & Barrett, 2011, p6). Contractor and colleagues (2014, p146) argued that most PTSD symptom dimensions co-morbid with other major psychiatric disorder, which consequently increases the risk of co-morbid diagnosis. The experts in the mental health field are also concerned the classification spectrums of ‘abnormal’ experiences risk labeling typical stress responses as a mental disorder (Brewin et al., 2009,p364). According to Charney and colleagues (2002, p. 33) for classification to be valid, the diagnostic criteria should meaningfully classify findings from real underlying etiological assumptions rather than based on clusters of symptoms, which could consequently inform an appropriate treatment and accurate prognosis. These arguments as will be explored impelled researchers to venture into new directions using testable conceptual models to develop valid and functional diagnostic criteria.
The biological hypotheses of PTSD
The biological theory proposes the etiology of PTSD is linked to maladaptive stress responses and neurobiological processes that influence susceptibility and resilience to PTSD symptoms (Depperman et al., p168). According to Koenen and colleagues (2008, p.53), stress responses inherently activate hypothalamic-pituitary-adrenal (HPA) axis by releasing the corticotrophin-releasing hormone from the hypothalamus and adrenocorticotropic hormone from the pituitary and glucocorticoids from the adrenal cortex. The HPA pathway and the sympathetic nervous system together they bind to two types of receptors, the mineral corticoid and glucocorticoid receptors that mediate the fear conditioning in the amygdala, memory consolidation in the hippocampus and fear extinction in the prefrontal cortex (Depperman et. al., 2014, p 170). Persistent pathological conditions of PTSD occur when the limbic structures fail to restore its homeostasis functioning even after ‘flight or fight’ state no longer exist suggesting the brain’s inability to extinguish the conditioned fear response (Jones & Moller, 2011,p.394).
Animal model of PTSD
Fortunately, the development of animal models of predator exposure, Pavlovian fear conditioning, and extinction have allowed translational findings of brain regions responsible for PTSD symptoms, fear circuit functions, the neural plasticity of fear memory and fear extinguishing processes (Daskalakis, Yehuda & Diamond, 2013,p.2) Laboratory simulated stressors such as predator threat; psychosocial behavior and psychogenic probes are used to examine the effects of trauma. Cellular and molecular functions in laboratory simulated freezing and avoidance behaviors observed in the animal models are consistent with neural circuits underlying fear processing in human, with correlational evidence of HPA axis dysregulation, prefrontal cortex, amygdala and hippocampus functioning (Daskalakis, Yehuda & Diamond, 2013,p.3).
However, PTSD research using animal models do not capture all of the PTSD causal attributes and critics argue they are too simplified to account human pathology. For instance, patients receive a diagnosis of PTSD based on their verbal recount of experiences, cognition and understanding skill compared with behavioral assessment of animal models of PTSD. According to Cohen and Richter-Levin (2009, p. 30) differences in stress level and the type of stress between laboratories simulated trauma stimuli such as restraining and foot shock methods may not emulate the same degree or type of traumatic events experienced by traumatized humans. The animal models have a short lifespan and, therefore, evidence of delayed onset of PTSD symptoms that is common in war veterans cannot be studied. Although, the animal models have its limitations, they have provided an abundance of valuable information for the shared benefits of education and potential translational evidence for the development of trials and studies in humans with implications for treatment and therapies (Rasmusson et. al., 1997, p332).
In human participants, functional Magnetic resonance imaging (fMRI) of patients with PTSD has demonstrated similar decreased hippocampal volume as evidenced in the animal model (Bremner et al., 1995, p. 973). Neuroimaging findings suggest trauma-eliciting stimuli activated anterior cingulate, dorsal anterior cingulate, left amygdala and posterior parietal networks that are responsible for generalized hypervigilance (Garfinkel & Liberzon, 2009, p.371). Bremner and colleagues (1999, p.806) reported decreased blood flow in the frontal gyrus in PTSD patients exposed to trauma reminders than healthy controls. Enhanced amygdala activity and decreased prefrontal cortex activity was observed in patients with PTSD than fear exposed healthy participants (Bryant et al., 2007, p. 517).
Although type and severity of trauma exposure are implicated with the risk of PTSD development but the effect of individual differences in stress, coping and adaptation coupled with ecological and environmental characteristics equally contribute to the risk of developing PTSD (Jeremy et. al., 2009,p 44). Jeremy and colleagues (2009) suggested those factors might hold significant indicators to why and what causes some people to be resilient to and others susceptible to developing PTSD symptoms.
Evidence from animal model and fMRI studies of human brain suggest men and women react to stress and emotion differently. Goldstein and colleagues (2010, p.435) found significant physiological differences in the stress response circuitry, especially the amygdala, hypothalamus, hippocampus, brainstem, orbitofrontal cortex and the cingulate gyrus (Goldstein et al., 2010). The researchers concluded that females have greater fear processing capacity due to naturally endowed high estrogen state than men (Goldstein et al., 2010, p 435).
The formation, consolidation, and retrieval of emotional memories vary developmentally. Kim and Richardson (2010, p 177) revealed very young rats learned to extinguish fear without the activation of the NMDA receptors, but the adult rats took more fear extinction trials for the NMDA receptors to deactivate (Kim & Richardson, 2010, p.177). Thus, the researchers concluded that fear extinguishing training at an early age significantly erases fear associations in the amygdala. The research identified a critical marker for fear resilience with potential development of effective treatment.
Deary and Batty (2007, p.379) found children who had an intelligence quotient (IQ) >115 during developmental years are more resilient to PTSD in adulthood and suggested the role of cognitive ability in the risk of PTSD. In another study, Hoffman and Mathew (2008,p.249) argued that cognitive reserve play a significant role in extinguishing fear memories and that people who are with lower cognitive reserve may not respond well to cognitive and exposure therapies.
Twin studies comparing monozygotic and dizygotic twins raised in a shared environment showed that PTSD may be heritable, but possible co-morbid with another mental disorder has not been ruled out (Afifi et. al.,2010, p.101). Krishnan and colleagues (2007, p 396) showed molecular adaptations underlying the resilience and vulnerability to a stress-induced environment. The study found differential gene expression, whereby, susceptible mice demonstrated sucrose preference, BDNF signaling, increased anxiety, weight-loss, a sensitized corticosterone and exaggerated response compared with unsusceptible mice. The researchers then compared the findings with human brain specimen and identified an epigenetic adaptation signature in the brain region within the mesolimbic dopamine circuit associated with susceptibility and resistance to symptoms of avoidance in PTSD.
Sleep deprivation has been implicated in mediating memory consolidation and restoration of physiological functions (Mohammed et al., 2011, p.39). Mohammed and colleagues (2011, p39) demonstrated neurochemical and electrophysiological changes induced by REM-sleep deprivations affect brain functionality in rats. Numerous findings reveal that sleep; especially the rapid-eye-movement (REM) sleep type facilitates extinction of conditioned fear following exposure therapy (Mohammed et al., 2011, p 41).
Biological, social learning, individual differences and environmental context have been suggested to contribute to the development of PTSD. But, because human brain, mind, and body are interrelated, it is challenging to single out which particular factor influences the development of PTSD. Hence, validating the severity of the illness based on one characteristic of the disorder does not provide sufficient information for clinical decisions. Instead, integrated approach provides multiple scales of diagnostic dimensions that are essential for early detection and treatment intervention in patients with PTSD (Jakovljevic et al., 2012, p253).
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