Abstract
Recently, there has been extensive research from various psychological and biological perspectives on the co-occurrence of Post-Traumatic Stress Disorder (PTSD) and chronic pain. However, Complex PTSD (CPTSD) has not received as much attention despite its potential prevalence. This paper aims to fill this gap by examining the connection between somatic complaints, chronic pain, and physical health parameters in patients with CPTSD. The review emphasizes the disabling impact of CPTSD, the necessity of integrated treatment approaches, and provides a detailed explanation of the neurobiological basis of complex PTSD and concurrent chronic pain conditions. The paper also delves into theoretical models for this comorbidity, backed by relevant statistics that underscore the effect of CPTSD on physical well-being.
I, METHODOLOGY
The research employed a systematic literature review, using databases such as PubMed, PsycINFO, and Google Scholar to identify studies on the co-occurrence of somatic complaints, chronic pain, and physical health parameters in Complex PTSD (CPTSD) patients. Inclusion criteria prioritized peer-reviewed articles in English, while exclusion criteria removed irrelevant and low-quality studies. Data collection involved screening titles and abstracts, followed by a thorough evaluation of full-text articles meeting the inclusion criteria. The selected articles were critically appraised for methodological quality, and their findings were synthesized to explore the relationship between the variables. Ethical considerations focused on proper citation and avoidance of plagiarism. The review's limitations included potential constraints in the availability and diversity of relevant literature. Overall, this methodology aimed to provide a rigorous and systematic approach to synthesizing existing literature on the topic.
II. INTRODUCTION
In the past two decades, PTSD and chronic pain have just recently been studied through a limited amount of perspectives. The biological and physiological mechanisms underlying trauma have been extensively studied since, but more questions arise. Some studies include childhood abuse and trauma, PTSD, or complex PTSD, with more research on PTSD and chronic pain and trauma and chronic pain. It is therefore important to understand the difference in results between trauma symptoms, PTSD, and complex PTSD when assessing studies and their relevance to the question: How do somatic complaints and chronic pain present in patients with complex PTSD (CPTSD), and what are the associated phenotypical changes in physical health parameters?
Existing literature on the subject starts with Sharp and Harvey who found that the presence of chronic pain was in 20–80% of trauma cases, and PTSD in 10–50% of chronic pain cases [1]. They postulated seven processes that could explain the mutual maintenance of the two conditions. The first of these is attentional biases, saying that pain sensations can serve as trauma reminders. The second is anxiety sensitivity or the belief that those sensations are harmful, fueling the anxious interpretation of pain. The third is the persistent reminders of the trauma given the link between a traumatic event and pain-producing injuries, fourth an avoidant coping style, which can lead to an abstinence from physical activity that emphasizes the chronic pain, fifth the depression and reduced levels of behavioral activity, sixth is pain perception, as heightened by anxiety, and lastly, cognitive resources, where the demands of both PTSD and chronic pain limit one's capacity to manage distress. They proposed operant and cognitive behavioral theories and used tasks like the Stroop task to measure attentional bias in pain patients. Avoidant coping was found to maintain chronic pain and PTSD. Thus, chronic pain and PTSD may be mutually maintaining conditions, with seven processes explaining this relationship.
In 2011 Beck and Clapp expanded on this, mentioning that the comorbidity of chronic pain and PTSD has been well studied among the Western population, with differences ranging from 7.7% of people with PTSD having fibromyalgia, and up to 46% having chronic back pain [2], [3]. They also mention a study that explains that instead of the theorized increase in pain perception due to anxiety sensitivity, PTSD patients have a decrease in pain perception, called stress-induced analgesia, compared to the control group [2]. In the same year, Lanius added that social cognitive and affective neuroscience (SCAN) can be helpful in complex PTSD and understanding the underlying mechanisms of biological functions[4] . Because CPTSD comes from interpersonal, chronic trauma at significant developmental phases, emotional awareness tends to be a key problem in its manifestation. Previous studies suggest that a history of a secure attachment with one's primary caregivers plays a key role in the development of emotional awareness (Lane & Schwartz, 1987; WINNICOTT, 1960).
Conceptual emotional awareness uses logic at more than just the present moment and is thought to be mediated partially by the dorsomedial prefrontal cortex, which controls emotional regulation and self-control, while embodied emotional awareness, which is based on feeling at the present moment, is mediated by the ventromedial prefrontal cortex, which helps make decisions in an emotional state [7]. Being trapped in an abusive situation with a caregiver might force the understanding that the impulse to escape does not mean escape is possible, creating a feeling of learned helplessness [4]. These individuals learn that emotional responses to trauma don't mean anything, creating a disconnect to inner emotional life. Studies have shown that these individuals have lower scores on the Levels of Emotional Awareness Scale [5], [8] and that they consistently exhibit higher levels of alexithymia (difficulties identifying and labeling emotional states; Frewen et al., 2008, 2012). In a study checking the neural responses to positive praise and negative criticism to patients with PTSD related to childhood abuse and healthy women, a higher activation of the dorsomedial prefrontal cortex was seen in healthy women when identifying their feelings, compared to a lower activation of the same area for women with PTSD who struggled to identify their feelings, suggesting that the dorsomedial prefrontal cortex plays a key role in alexithymia [4]. When recalling traumatic events, alexithymia was associated with reduced activity of the ventromedial prefrontal cortex (related to embodied emotional awareness) and the anterior insula (related to introspectiveness). Emotional dysregulation was divided into pathways of fear conditioning and the inaccurate development of neural pathways due to childhood abuse. Social emotional processing was split into feelings derived solely from social interactions and non-social emotions. The default mode network (DMN) of chronic PTSD patients was shown to be similar to that of a healthy 7-9 year-old, indicating interference with the maturation process. For treatment, exposure-based therapy with teaching emotional awareness skills beforehand may be effective.
Numerous studies have expanded on Complex PTSD and its somatic effects, ranging from refugee populations, abuse survivors, sexual abuse survivors, and more. Studies have also examined specific symptoms of C-PTSD and how they correspond to neural activity. In this paper, I will expand on how C-PTSD manifests somatically, what mechanisms support the development of C-PTSD, how chronic pain is interlinked to complex PTSD, and what treatment can help.
IV. LITERATURE REVIEW
What are CPTSD and PTSD?
CPTSD is defined by the ICD-11 as including all the symptoms of PTSD, with the addition of symptoms in the Disturbances in Self Organization category. This includes symptoms of warped self-perception and a negative perspective on the world [10], amongst others. PTSD would then be defined as a narrowly fear-based disorder, usually stemming from a single traumatic event. Complex PTSD forms from repeated, interpersonal trauma at significant developmental phases during childhood. This specific set of qualities makes complex PTSD more disabling than PTSD, which only requires one traumatic event at any developmental phase. While complex PTSD is not a universally recognized diagnosis, it has been shown that the addition of complex PTSD can help a wider variety of people [11]. Besides the psychological variations of PTSD and CPTSD, there are also many biological differences. For the purpose of this paper, any study including PTSD with regards to chronic pain, somatic complaints, and underlying biological mechanisms was included, as complex PTSD is an extension of that.
The ICD-11 varies from the DSM-5 in several ways, specifically regarding PTSD and complex PTSD. This distinction made in the ICD-11 is more beneficial in regards to symptomatology and treatment compared to the DSM-5 combining it under PTSD. The logical question that follows asks whether one should be more highly regarded, and why. While some may argue that Complex PTSD is too similar to PTSD to warrant a separate diagnosis, this distinction might be beneficial to numerous populations around the world and may be more universally applicable. Silva, Glover, and Katona explore this by looking into a refugee population. Unlike many other research papers that constitute CPTSD as derived solely from childhood abuse, these authors also put forth the fact that many refugees, war prisoners, and more suffer from complex trauma due to developmental time, an organized system of oppression, and interpersonal trauma [11]. Their findings suggest that refugees and the asylum-seeking population have higher rates of CPTSD, more selective needs than patients with just PTSD, and that CPTSD develops from childhood adversity, with a greater tendency to develop with complex trauma. Refugee samples from around the world had a wide range of people who met the criteria for CPTSD, from 16 to 50.9% of their respective population. CPTSD usually comes with some sort of personality change after the event as there is a change in belief system [11]. In a diagram, CPTSD is shown to generally include the somatization of the disorder, enduring personality changes, a hostile attitude towards the world, and more that come with Disturbances in Self Organization. While this study was mainly to understand the rates of CPTSD in refugee populations, it was noticed that many had general physical complaints too, with a higher frequency and severity of pain from the Yazidi women population as they endured severe sexual abuse and torture.
Six out of thirteen studies indicated that CPTSD is more common than PTSD in refugee populations, suggesting that the addition of CPTSD as a formal diagnosis can help aid complex trauma [11]. The other studies showed an almost equal amount of CPTSD versus PTSD, with minimal studies showing lower rates of CPTSD compared to PTSD. Since 6/13 studies showed that CPTSD was more prevalent than PTSD among refugees, about half or more of the refugee population would benefit from increased research in complex trauma, the recognition of chronic pain in CPTSD, a better support system for refugees, as well as the addition of CPTSD as a formal diagnosis in America (the DSM-5). In a majority of trauma-exposed individuals, childhood trauma is co-occurring, often chronic, including types of victimization and other troubling experiences [12], [13], [14]. The differences regarding complex PTSD, the DSM-5, and the ICD-11 are highlighted, where the ICD-11 is used globally (excluding America) and mainly in Europe, and the DSM-5 is used in America for mental illnesses. While there may be differences, he noted that current research can support conclusions made by either version of the disorder [15]. In another study, cumulative adulthood trauma was associated with both PTSD and CPTSD; however, cumulative childhood trauma was more strongly associated with CPTSD than PTSD. Adverse childhood events were associated with both PTSD and CPTSD and equally so. Individuals with CPTSD reported substantially higher psychiatric burdens and lower levels of psychological well-being compared to those with PTSD and those with neither diagnosis [16]. Accordingly, complex PTSD and chronic pain must receive more attention.
Chronic Pain in Complex PTSD
As mentioned earlier, Sharp and Harvey were the starting point of researching comorbid chronic pain and PTSD. In their study, the presence of chronic pain was in 20–80% of trauma cases, and PTSD in 10–50% of chronic pain cases [1]. They put forth 7 processes that could explain the mutual maintenance of the two conditions. The first of these is attentional biases, saying that pain sensations can serve as trauma reminders. The second is anxiety sensitivity, or the belief that those sensations are harmful, fueling the anxious interpretation of pain. The third is the persistent reminders of the trauma given the link between a traumatic event and pain-producing injuries, fourth an avoidant coping style, which can lead to an abstinence from physical activity that emphasizes the chronic pain, fifth the depression and reduced levels of behavioral activity, sixth is pain perception, as heightened by anxiety, and lastly, cognitive resources, where the demands of both PTSD and chronic pain limit one's capacity to manage distress. Sharp and Harvey also propose multiple theories on the mutual maintenance of chronic pain and PTSD, one being the operant theory. In this theory, it is stated that regardless of sensory activity, pain behavior can persist indefinitely if it occurs within the context of certain reinforcement. Cognitive Behavioral Theory is the theory that thoughts create actions, actions create behaviors and behaviors reinforce thoughts, so in the context of PTSD and chronic pain, a patient's interpretation of pain is key to understanding a patient's response to pain. In laboratory investigations, the Stroop task has been used as a measure of attentional bias in pain patients. This task requires that subjects color-name different groups of words while trying to ignore their meaning. Longer naming reaction times are said to reflect an attentional bias as the meaning of the word has grabbed attention and interfered with the simple task of naming the color of the word. Avoidant coping led to the maintenance of chronic pain and PTSD, but avoidance was not directly related to pain. For example, someone with PTSD (relating to people) could avoid crowds and experience chronic migraines. Thus, chronic pain and PTSD may be mutually maintaining conditions, with seven processes explaining this relationship.
Otis argues that PTSD and trauma are some of the most frequent psychological issues after depression and substance abuse, with PTSD in the US accounting for 6 percent in males and 12 percent in females [17], [18]. However, exposure to traumatic events has been estimated to be as high as 70 percent of the adult population [19], [20]. Furthermore, hospitalized burn patients have been found to have high rates of PTSD (45%) at 12 months post-injury [21]. The two-factor learning theory explains how fear is learned and maintained through avoidance behaviors, and highlights the role of cognitive and information-processing models in understanding PTSD [17]. Several models were mentioned explaining the comorbidity between chronic pain and PTSD, the first of which is the mutual maintenance model with seven processes maintaining both chronic pain and PTSD [1]. The second model is the shared vulnerability model, which states that anxiety sensitivity makes individuals more likely to develop PTSD or chronic pain due to their heightened fear response to physical sensations, as well as the exacerbation of symptoms of both chronic pain and PTSD [22]. The third mentioned was the fear-avoidance model, which states that physiological symptoms can reinforce fears and negative beliefs about pain, leading to increased avoidance behaviors [23]. These avoidance behaviors can then lead individuals to refrain from doing tasks that cause pain, worsening their fear of physiological symptoms and their physical state. Lastly, the triple vulnerability model specifies three risk factors: generalized psychological vulnerability based on early experiences regarding control, generalized biological vulnerability (i.e. genetic predisposition), and specific psychological vulnerability where one learns to anxiously fixate on certain situations [24]. These four models have been proposed but not adequately tested, though it seems to be the main focus of this topic.
Studies have found that nearly 50% of veterans report that they experience pain regularly [17]. Studies of veteran and non-veteran patients reporting for the treatment of pain have indicated that between 34% to 50% of patients have PTSD or significant PTSD symptomatology [25], [26]. However, studies of patients reporting for treatment of PTSD have found that between 45% to 80% report the presence of a chronic pain condition [27], [28]. Consistently the rates of chronic pain in PTSD have been higher than PTSD in chronic pain. This could be for a variety of reasons, including 1) PTSD is narrowly defined so studies including PTSD, CPTSD, and childhood trauma may be more accurate, 2) there are many types of chronic pain and chronic pain disorders, 3) PTSD and CPTSD consistently raise cortisol levels and cause many neuroendocrine dysfunctions, which can lead to chronic pain and more. While these are only a few reasons, PTSD and CPTSD tend to have a greater disabling effect than chronic pain, particularly because of an extremely high comorbidity. Additionally, when assessing veterans receiving care at Level 2 Polytrauma Network Sites in the VA, one study found that in a sample of 62 patients, 97% complained of pain and 71% met the criteria for PTSD [29]. Across the majority of studies, there is a huge overlap in chronic pain and PTSD, suggesting that an integrated approach is necessary. Otis argues that the sequential approach for treating dual disorders does more harm than good as one disorder can worsen the other, and there are many abuses among clinicians through this approach [30]. An integrated approach with highly individualized support is essential. Rather than following any set of rules, any clinician should be educated on basic therapy and physical therapy, while focusing on an individual's specific needs.
The comorbidity of chronic pain and PTSD is also highlighted by Beck and Clapp, as the comorbidity between these two disorders is found to be extremely high [2]. The prevalence of chronic pain within trauma samples ranges from 20-80% and the prevalence of PTSD within chronic pain samples ranges from 10-50% [1] . Sharp and Harvey postulated seven processes that could explain the mutual maintenance of the two conditions, and the comorbidity of chronic pain and PTSD since then has been well-studied among the Western population. Differences of such ranged from 7.7% of people with PTSD having fibromyalgia, and up to 46% having chronic back pain [3]. Recovery from PTSD is also closely linked with recovery from chronic pain and vice versa [2] . Depression, PTSD, and chronic pain tend to show high comorbidities, and pain perception tends to impact chronic pain levels [2]. Pitman argues that instead of the theorized increase in pain perception due to anxiety sensitivity, PTSD patients have a decrease in pain perception, called stress-induced analgesia, compared to the control group [31].
Brennstuhl emphasizes a link between chronic pain and PTSD and particularly notes that the recovery is worth attention [32]. She mentions that the link between chronic pain and PTSD could be a comorbidity relation or a cause-and-effect, with one aggravating the other. The focus on persistent pain called “chronic,” without a direct link to physical deterioration, suggests the need to seek a psychological understanding of the problem. The onset of PTSD is a strong indicator of a patient developing chronic pain [32]. Out of a sample of patients who had a serious injury, 44% of them developed chronic pain, and they had more PTSD symptoms, medical leave from work, depression, and anxiety than those who fully recovered from their injury [33]. Van Loey's longitudinal study on 301 patients indicated that peritraumatic dissociation, pain-related anxiety, injury severity, and gender were significant predictors of PTSD severity 1 year later [34] . In another study, PTSD patients experienced more chronic pain, more severe pain, and pain in more areas of the body than did persons with a secondary anxiety disorder [35]. A different study by Lee found that childhood physical and sexual abuse increases the chances of a fibromyalgia diagnosis in adulthood because of abnormal neuroendocrinal development [36]. With studies involving childhood abuse and the onset of chronic pain in adulthood, PTSD seems to be the mediator of childhood abuse and chronic pain later on. PTSD can also be characterized as a reactive disorder and chronic pain may be as well [32].
Chronic pain can affect every aspect of a person’s life and is generally associated with high rates of emotional disorders. Kind and Otis argue that this is not surprising given evidence suggesting that pain and emotional disorders share common neurobiological pathways [37]. In the USA, it is estimated that 3.5 to 4.7% of people experience PTSD each year [38]. However, this rate is much higher within the chronic pain population - between 9 and 10%, though rates of PTSD can vary depending on the type of pain reported or the pain setting [39], [40]. Two groups of vulnerable people, veterans, and children, are also studied regarding PTSD and chronic pain. Veterans with chronic pain suffer from a rate of PTSD as high as 50.1% [39]. Comorbidity between pain and symptoms of PTSD also has been found among children and adolescents, with 32% of youth with chronic pain showing symptoms of PTSD compared to 8% of youth without chronic pain [41]. These examples present a high comorbidity between chronic pain and trauma. With PTSD and chronic pain, three vulnerabilities are specifically mentioned: biological, generalized psychological, and specific psychological vulnerabilities [17], [42]. Biological vulnerabilities include a genetic predisposition to PTSD or chronic pain, while generalized psychological vulnerabilities include childhood learning and beliefs. Specific psychological vulnerability is when one learns to focus anxious thoughts on specific situations perceiving the event as unpredictable and uncontrollable. Without this, a person cannot develop PTSD or chronic pain [37]. Catastrophizing does not only worsen psychological distress but can make acute pain chronic [38], consequently mitigating the effects of physical therapy.
One of the heaviest burdens on healthcare systems worldwide has been somatic problems and cardiovascular diseases, with both consistently being linked to early childhood trauma [10]. Existing evidence indicates that CPTSD is more likely to result following exposure to childhood trauma than PTSD [16], that it is a more impairing disorder [43]; and is more strongly correlated with other mental health problems such as depression, generalized anxiety, dissociation [16] and comorbid borderline personality and somatoform disorders [44]. Ho explores the relationship between particularly Complex PTSD and chronic pain in adulthood, with a sample of Irish and British people who went through childhood physical or sexual abuse, and childhood emotional abuse or neglect [10]. Her goal was to see if PTSD and Disturbances in Self Organization symptoms (DSO) mediate the link between childhood abuse and cardiovascular and somatic problems in adulthood. Her findings consist of an indirect link between childhood abuse to CPTSD to cardiovascular disease and a direct association between PTSD and DSO (the two variables of CPTSD) with somatic problems, specifically cardiovascular disease. The link between PTSD and DSO to cardiovascular disease is very clear, but the indirectness arises when considering that not all people who went through childhood physical, sexual, or emotional abuse developed PTSD or DSO symptoms [10]. Ho also mentions that the inclusion of DSO symptoms in CPTSD does not mitigate previous research studies that connect PTSD symptoms to cardiovascular disease load. Instead, the addition of DSO symptoms is positively correlated with physical health problems and CVD load. Even in the past, somatization of the disorder PTSD was prevalent. During the aftermath of the Civil War, a condition nicknamed "soldier's heart" coined by DaCosta in 1871 described the autonomic cardiac symptoms of soldiers and felt that this syndrome was a disorder involving the cardiovascular system that was caused by extreme stress; this positively correlates with the history of the connection between the psyche and soma, as emphasized in Asian, African, and Indigenous cultures from the beginning of time.
Gupta conducts a thorough analysis and review of PTSD and the overlap of chronic pain issues of every category, including neurological, neuroendocrine, cardiovascular, gastrointestinal, musculoskeletal, and more categories [45]. She finds out that with PTSD, it is also common to have fibromyalgia [46], complex regional pain syndrome [47], autoimmune disorders [48], endometriosis [49], hypertension, coronary artery disease [50], chronic fatigue syndrome [51], PNES [52], [53], Parkinson’s and more [54], [55], establishing a clear link between psychological and all aspects of physical health. PTSD is associated with possibly the highest frequency of ill-defined medical symptoms of all psychiatric disorders [56]. Gupta argues that “in the review of the somatic symptoms of PTSD, it is also considerable to note the extensive earlier literature on somatoform disorders [57], especially conversion disorder or hysteria and pain disorder” [45]. Over the years, terms such as ‘conversion’, ‘hysteria’, ‘dissociation’, and 'somatization’ have sometimes been used interchangeably to essentially describe the somatic symptoms of psychological trauma and PTSD [45].
Specifically, psychogenic nonepileptic seizures (PNES) have been associated with a higher prevalence of dissociative symptoms, general trauma (44 – 100%), physical and/or sexual abuse (23 – 77%), and PTSD than controls [52], [53]. It was also found that in Chronic Fatigue Syndrome (CFS), one study reported that 25% of people with CFS meet the criteria for PTSD [58]. Some studies show that patients with PTSD are more at risk of cardiomyopathy, severe reversible left ventricular dysfunction, coronary artery disease, and more [59]. For respiratory diseases, a study at an asthma clinic concluded that 25% met the DSM-IV criteria of PTSD, and 74% had at least one traumatic event [60]. PTSD was directly correlated with increased severity in several respiratory diseases [61]. PTSD has also been associated with type-2 diabetes [62], hyperthyroidism [63], and a 4-fold increased risk of autoimmune diseases [48]. Childhood neglect and physical and sexual abuse have been associated with a higher risk of arthritis and regional pain syndromes [48]. PTSD was also found to be associated with functional dyspepsia, gastroesophageal reflux symptoms [64], chronic pelvic pain [65], endometriosis [49], psoriasis [66], and more. A group of traumatized refugees were studied and 60% of patients in CBT and a physical activity group improved in at least one pain subscale versus 30% of patients improving under CBT alone [67]. Essentially, Gupta goes into every category to see where and how PTSD manifests biologically, and her reputable work is cited many times.
Approximately half to over three-quarters of patients who present for PTSD treatment have significant chronic pain (CP) condition [22], [28], [68], [69] while 20% to 37% with chronic pain have PTSD [70]. This prevalence has been extensively studied since 2001, with several different models explaining this comorbidity. Recently, research has gone more in-depth to include generally excluded populations and to characterize collective experiences, which has led to the topic of complex trauma. Although somatic symptoms in PTSD have been well-documented, somatic symptoms in CPTSD can be further elaborated upon.
Somatic (physical) Symptoms of Complex PTSD
Firstly, to understand the somatic symptoms of Complex PTSD, the somatic symptoms of PTSD must be discussed. To do so, Pacella conducted a meta-analysis study and found that people with PTSD or high post-traumatic stress symptoms (PTSS) had greater general health symptoms, general medical conditions, poorer quality of life, higher severity of pain, and higher cardio-respiratory and gastrointestinal complaints [71]. Pacella looked at general health and quality of life separately as those two encompassed the broader view of health compared to specific categories like cardio-respiratory and gastrointestinal complaints. In physiological terms, she cited a study that characterized PTSD as the long-term activation of stress pathways, like the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis, in a way that influences immune activity and places individuals at a greater risk of developing or exacerbating medical conditions. PTSD has been associated with general medical conditions, including but not limited to asthma, irritable bowel syndrome, heart disease, and fibromyalgia [72], [73]. Pain complaints are very common in trauma patients, one study estimated that 80% of combat veterans with PTSD also reported comorbid chronic pain [28]. PTSD patients also report greater severity of pain, more specifically complaints included fibromyalgia, [74], back pain and headaches [75], [76], and arthritis pain [77]. In another study relating to gastrointestinal health, it was found that approximately 36% of patients seeking help for irritable bowel syndrome meet the criteria for PTSD [78], with studies showing that a failure to medically treat gastrointestinal problems causes persistence in psychological disturbance [79]. Pacella’s findings are consistent with previous research, further cementing the connection of PTSD and PTSS to cardio-respiratory and gastrointestinal health problems. She also suggests that research in other specific health categories (i.e. diabetes, infectious diseases, neurologic, etc.) should occur, given that HPA axis alterations and autonomic dysfunction are related to thyroid disorders, diabetes, and endocrine/metabolic disorders. Pacella finds a clear link between PTSD/PTSS and physical impairments, especially in the general health, quality of life, cardiovascular, and gastrointestinal sections.
With both PTSD and complex trauma, after stressful situations, NPY promotes the release of growth hormone, as well as fat accumulation to help replenish energy stores burned during stress [80]. Although NPY levels were not measured in women, increased dissociation at peak military survival training stress was associated with increased somatic symptoms, including pain, during the aftermath [81]. As dissociation is a key symptom of CPTSD, it can be concluded that somatic symptoms and painful sensations are associated with dissociation from trauma, and thus, a disassociation from the body. The brain is involved in the somatization of CPTSD and PTSD as well, with the medial prefrontal cortex, the anterior cingulate cortex, the hippocampus, the amygdala, and the anterior insula playing a significant role in the somatoform symptoms regarding PTSD [45].
It is critical to note that complex trauma is highly prevalent not just in the Western world, but the non-Western world as well. In fact, due to higher rates of violence and more complex forms of trauma, CPTSD tends to be even higher in underrepresented populations. To examine this, Wilson studied 106 Palestinian refugees aged 11-17 in the West Bank with all showing either post-traumatic stress symptoms (PTSS), full-blown PTSD, or CPTSD after exposure to systematic genocide [82]. They used interviews, the Strengths and Difficulties Questionnaire, the Patient Health Questionnaire-15, and the Child and Youth Resilience Measure to gather their data. Their findings included having a greater risk of mental health issues and psychosomatic complaints, while also finding that some risk factors included poverty, marginalization, and violence. Previous studies have extensively researched the levels of trauma and concluded that in conflict-driven zones, PTSD rates among children are estimated to be around 90%, maybe even higher [83], [84], [85]. This is especially significant given that PTSD is a narrowly defined fear-based disorder, so if CPTSD was included in that particular study, PTSD/CPTSD rates could be higher than 90%. They found that girls tended to have more psychosomatic complaints among the Palestinian refugee population. Out of all 106 people, 41% of them scored medium to high levels of psychosomatic complaints [82]. Compared to a non-refugee population of the same cultural background, this group scored lower on resilience factors (i.e. supportive friends, strong family bonds, etc) and higher on psychosomatic complaints and mental health disorders. The study suggests that there should be more research done on PTSS/PTSD/CPTSD and psychosomatic complaints regarding gender, or at least to take gender into account. Some common psychosomatic complaints among refugees in the West Bank include recurrent abdominal and musculoskeletal pain, along with headaches, dizziness, and fatigue. He notes that PTSD is not a universally applicable diagnosis because the concept was developed by only studying Western populations. Wilson’s findings also suggest a deeper dive is needed to explain some medically unexplained psychosomatic issues in a refugee population, and that resilience should be more deeply studied in these populations.
Current research has intensively explained the coexistence of PTSD, somatic symptoms, and chronic pain, however, research is still limited to including diverse populations. As such, it should be noted that the future of research (in general, and specific to complex trauma and chronic pain) is reliant on developing a better understanding by including non-Western populations.
Biological and Physiological Mechanisms Underlying Complex PTSD and Chronic Pain
Researchers have spent decades attempting to understand the neurobiology of PTSD, just recently learning more about the intertwined neurobiology and the underlying mechanisms of PTSD or CPTSD and chronic pain. In 2011, Lanius wrote a review focusing on the field of social cognitive and affective neuroscience, or SCAN, concerning the brain mechanisms of CPTSD and how they mediate social and emotional functions [4]. He primarily explains the psychological reasoning behind emotional awareness in PTSD and how that activates different parts of the pain. The use of the SCAN paradigm is because of the interconnectedness of biology, neuroscience, and psychology to biological systems. This paradigm can help understand complex PTSD in a physiological, developmental, environmental, and social way, and this study aims to understand how CPTSD affects emotional awareness, emotional regulation, social-emotional processing, and self-referential processing. Because CPTSD comes from interpersonal, chronic trauma at significant developmental phases, emotional awareness tends to be a key problem in the manifestation of CPTSD. Previous studies suggest that a history of a secure attachment with one's primary caregivers plays a key role in the development of emotional awareness [5], [6]. This suggests that people with Complex PTSD struggle more with emotional awareness than patients with just PTSD. The current theory marks a difference in conceptual emotional awareness, which uses logic and is more than just at the present moment, to embodied emotional awareness, which is based on feeling at the present moment and tends to be spontaneous [7]. Lanius and Bluhm also analyze the impact of early trauma, stating that being trapped in an abusive situation with a caregiver might force the understanding that the impulse to escape does not mean escape is possible, creating a feeling of learned helplessness [4]. These individuals learn that emotional responses to trauma don't mean anything - creating a disconnect to inner emotional life. Studies have shown that these people have lower scores on the Levels of Emotional Awareness Scale [4], [8] and that they consistently exhibit higher levels of alexithymia (difficulties identifying and labeling emotional states; Frewen et al., 2008, 2012). Therefore, his study focuses on a) how types of emotional awareness trigger different parts of the brain, b) the impact of alexithymia developed from PTSD on brain activity, and c) the effect of emotional dysregulation on neural pathways using SCAN.
As mentioned earlier, conceptual emotional awareness is thought to be mediated partially by the dorsomedial prefrontal cortex, which controls emotional regulation and self-control, while embodied emotional awareness is mediated by the ventromedial prefrontal cortex, which helps make decisions in an emotional state. In a study done checking the brain responses to positive praise and negative criticism to patients with PTSD related to childhood abuse and healthy women, a higher activation of the dorsomedial prefrontal cortex was seen in healthy women when identifying their feelings, compared to a lower activation of the same area for women with PTSD who struggled to identify their feelings, suggesting that the dorsomedial prefrontal cortex plays a key role in alexithymia [4]. When recalling traumatic events, alexithymia was associated with reduced activity of the ventromedial prefrontal cortex (related to embodied emotional awareness) and the anterior insula (related to introspectiveness). As alexithymia can be considered a disassociation from internal emotions, this behavior would be more prevalent in CPTSD, or under the DSM-5, the dissociative subtype of PTSD. Emotional dysregulation was divided into pathways of fear conditioning and the inaccurate development of neural pathways due to childhood abuse [4], illustrating that childhood abuse, a cause of CPTSD, can directly change neural pathways. Social emotional processing was split into feelings derived solely from social interactions and non-social emotions. The default mode network (DMN) of chronic PTSD patients was shown to be similar to that of a healthy 7-9 year-old, indicating interference with the maturation process.
In 2012, some researchers started focusing on the genetics and molecular studies of PTSD. Biologically, it was found that gene-environment interactions involving polymorphisms in two key genes, CRHR1 and FKBP5, play a role in PTSD by regulating hypothalamic–pituitary–adrenal (HPA) axis function in conjunction with exposure to child maltreatment or abuse [15]. In a diagram, Vermetten indicates that early life stress and genetic predisposition lead to hypothalamic-pituitary-adrenal (HPA) axis/corticotropin-releasing factor (CRF) system hyperactivity, norepinephrine (NE) system hyperactivity, impaired neurogenesis in the hippocampus, neurotoxicity in the hippocampus, and altered glucocorticoid receptors. The most brain activity was found to be in the hippocampus and the amygdala, with the prefrontal cortex following after [15] - this is relevant because it shows the nature of the PTSD brain working overtime and perceiving the world through a fear-based lens.
Physical and emotional pain exists on the same continuum [86], [87], [88] with common brain networks involved [89]. Brain regions consistently implicated in chronic pain include the primary and secondary somatosensory cortex, spinal cord, thalamus, insula, anterior cingulate cortex, prefrontal cortex [90], [91], [92]; midbrain areas including the periaqueductal gray [93] and cerebellum [94], and the hippocampus, basal ganglia, and amygdala [95], [96], [97], [98] . Two ideas were proposed: (1) experiencing pain can trigger a cascade of neurological (initially sensory) events leading to an altered psychological state, and (2) prior psychological states can confer a heightened risk for chronicity due to cross-sensitization, where exposure to stress in the past results in greater sensitivity to other seemingly unrelated stimuli (e.g., childhood trauma, loss of a parent, and addiction) [99], [100], [101]. The brain reacts to stressors by adjusting physiology, which in turn results in chemical and structural brain changes [102], [103], sequentially leading to chronic pain conditions.
Centralization of pain may be used to capture the process where the initial stimulus (e.g., surgical trauma) progresses to a chronic pain state (neuropathic pain) but also alters cognition, memory, and executive function [104], potential for suicide [99], and may diminish pain processes [105], [106]. Cognitive changes and neurodegenerative changes have been reported in chronic pancreatitis [107], complex regional pain syndrome [108], and fibromyalgia [109] amongst others [110]. Simons discusses the phenomenon of hemineglect, where patients with chronic pain exhibit deficits in processing sensory stimuli, leading to a disconnection from their affected body parts [98] . This altered perception is linked to diminished awareness of both external and internal environments [98]. Chronic pain can lead to alterations in reward circuitry, resulting in mood and cognitive changes [98], and social pain may have the same neurobiological underpinnings as physical pain [111]. Brain areas that are activated by social distress parallel those activated by acute experimental pain [112], [113]. Fear learning is described as a protective mechanism that can become maladaptive in chronic pain, leading to hypervigilance and avoidance behaviors [98]. Overall, chronic pain can lead to allostatic failure, or systemic failures at both physiological and psychological levels.
Shortly after in 2015, Scioli-Salter found that the amygdala is activated by peripheral pain signals from the spinal cord to activate a coordinated response (i.e. increased heart rate, behavioral changes, etc) for immediate survival and reminders of threats [80]. While low plasma Neuropeptide Y (NPY) levels have been associated with increased noradrenergic system reactivity, PTSD symptoms, and systolic blood pressure responses during the activation of the sympathetic system [114], higher plasma NPY has been associated with greater improvement in PTSD symptoms [115]. In addition, sex hormones seem to affect NPY and allopregnanolone (ALLO) levels, with testosterone promoting NPY synthesis and estrogen decreasing it; however, ALLO comes from the base hormone progesterone, complicating any broad gender interpretations of PTSD risk regarding sex (although women have a higher risk of PTSD). In premenopausal women with PTSD, cerebrospinal fluid (CSF) levels of ALLO were ~40% of healthy subject levels and lowest among those with comorbid depression. ALLO levels are also inversely correlated with PTSD reexperiencing symptoms and negative mood [116].
Further, the ratio of ALLO to its immediate predecessor, 5a-dihydroprogesterone (5a-DHP) also decreased, supporting the idea of a block in ALLO synthesis. This could also affect chronic pain as ALLO is in the pathophysiology of chronic pain. Another study shows that fibromyalgia tends to occur in individuals with a history of lifetime sexual, physical, and emotional abuse who also experience PTSD [117], [118]. This is important to note as C-PTSD tends to follow this description of repeated trauma, making this set of data the equivalent to C-PTSD as defined by the ICD-11. A particular FKBP gene risk allele interacts with childhood trauma to produce glucocorticoid receptor resistance and increased cortisol reactivity due to developmental trauma-related demethylation of the glucocorticoid response elements [119]. This impacts immune cell function, brain structure, and PTSD risk. A decrease in glucocorticoid receptor sensitivity could also impact the transcription of genes in the NPY and ALLO synthesis pathways [120], [121] thus contributing to chronic pain.
FIGURE 1 SHOWS THE STRESS RESPONSE IN PTSD AND CPTSD WHILE EXPLAINING WHAT THE NORMAL BIOLOGICAL FUNCTIONS WOULD BE. THE IMPACT ON CHRONIC PAIN IS LATER DISCUSSED.
In 2018, Rasmusson reviewed and expanded on the idea of molecular abnormalities by mentioning that PTSD has molecular abnormalities and that there isn't one common abnormality with neurotransmitters or molecules that defines all PTSD [122]. With targeted therapies, a problem also arises that PTSD can be comorbid with depression and other disorders, changing the endophenotype. Norepinephrine (NE) is released in stressful situations and neuropeptide, or NPY, generally stops the excessive release of NE. NPY also acts as a storage space for bioenergy reserved for high-stress situations [123]. In one study, cerebrospinal fluid (CSF) NPY levels were lower in male veterans with PTSD compared to healthy trauma-exposed controls [124], and veterans without PTSD but with comparable levels of combat trauma exposure [125], indicating that PTSD lowers NPY levels even through the blood-brain barrier. For studies done on humans, baseline plasma NPY levels generally predicted PTSD improvement over time [115]. Corticotropin-releasing Releasing Hormone/Factor, or CRH, is also released from the hypothalamus during times of stress and is found in high levels for patients with PTSD and depression. NPY with CRH has been shown to decrease CRH-induced symptoms of PTSD [126]. Gamma-amino-butyric acid (GABA), GABAergic neurosteroids, and excitatory amino acids also play a significant role in PTSD symptoms, as GABA helps calm the brain by reducing the effects of other neurotransmitters, GABAergic neurosteroids enhance GABA, and excitatory amino acids increase alertness and excitement [122], [127]. Allopregnanolone, or ALLO, is a neurosteroid that helps regulate brain activity and enhance GABA [122]. Lower levels of ALLO contribute to flashbacks and depressive symptoms, and the synthesis of ALLO is shown to be affected by stress and trauma [128] - a mini cycle that maintains PTSD. Adrenocorticotropic Hormone (ACTH) is released after CRF stimulates the adrenal glands to produce neurosteroids, and plays a pivotal role in the stress response system [122]. However, studies examining ACTH's role in PTSD differ greatly by sex, with women with PTSD showing increased levels and men with PTSD showing decreased levels [129]. Glucocorticoids play a significant role in PTSD by regulating cortisol and having distinct endophenotypes associated with PTSD, with studies suggesting that glucocorticoid system plasticity is essential for effective stress adaptation [130]. When considering smoking, tobacco usage may relieve hyperactivity in PTSD but also risks the development of comorbid disorders. There is a potential biological link between smoking, ALLO levels, and PTSD symptoms [122].
Hawkins describes the neurobiology of trauma, explaining the sympathetic nervous system (SNS), the parasympathetic nervous system (PNS), and the brain structures activated due to trauma [131]. While the amygdala perceives and processes emotional, somatic, and attachment experiences, the hippocampus mediates between the cerebral cortex and the amygdala, making sense of experiences, applying context, and sometimes tempering emotions in response to inhibitory messages from the cerebral cortex (Cozolino et al., 2010, pp. 60, 83-84) . The hippocampus is affected by hyperactivation of the amygdala which signals that an experience is important and should be remembered but also impedes hippocampal down-regulation and memory (Cozolino et al., 2010, pp. 81-85, 228-231). The vagal complex is then responsible for the "freeze" response as the emergency backup system if all else fails. The dorsal components of the vagal complex (DVC) which are responsible for immobilization develop first, followed by the SNS fight/flight responses. Lastly, and only in humans, the ventral vagal complex (VVC) develops ; (Kolacz & Porges, 2018, p. 3; Ogden et al., 2006, loc. 1077), which engages the socialization circuitry that mediates facial and vocal expression (Levine, 2010, pp. 97-99). Although it develops last, infants activate the VVC as their first response to distress or fear - an instinctive defense for crossed boundaries. This freeze response is necessary as a last resort, often mimicking the "playing dead" instinct when a predator is near, speeding up the healing process by preserving energy, and disassociating to make a traumatic event more tolerable.
Adrenaline and cortisol direct energy to critical action systems like the brain, muscles, heart, and lungs, while also producing an analgesic effect that minimizes pain perception for immediate protection. Once activated, these survival responses must find release or deactivation in order for the body to return to homeostasis (Butler & Moseley, 2014, pp. 85-88). In early development, the amygdala is particularly sensitive to stress, with early trauma causing high levels of CRH and glucocorticoids and lowering individual response to other emotional threats [137]. Complex trauma can include violence in the home or community, oppression based on gender, ethnicity, sexual orientation, religion, and experiences of terrorism, war, and displacement [138]. Hawkins mentions that complex trauma is so prevalent that van der Kolk estimates that “for every U.S. soldier who serves in a war zone abroad, there are 10 children endangered in their own homes” (~ 3 million/year) (Hawkins, 2019; van der Kolk, 2014, p. 20). In Canada, 1 in 3 adults report experiencing some form of child abuse before age 16 (Afifi et al., 2014, E324-E332). In 2010, the Public Health Agency of Canada categorized child abuse as: exposure to intimate partner violence (34%), neglect (34%), physical abuse (20%), emotional abuse (9%), and sexual abuse (3%). These statistics are likely to rise when taking into account non-Western populations who tend to experience more violence in their home countries.
Major chronic pain conditions with no discernible medical cause are generally connected to psychological causes and are referred to as Functional Somatic Disorders, including fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular pain syndrome, chronic pelvic pain, and multiple chemical sensitivity. Research supports this, with 90% of women with fibromyalgia reporting either childhood or adult trauma [136] . Central sensitivity theory holds that the impact of this unrelenting SNS activation (specifically excess adrenaline, cortisol, and immune response suppression) is linked to chronic inflammation, nerve damage, and increased adrenaline receptors which magnify danger signals. The mind can no longer accurately discern between pain or no pain, and normally soothing touch can be felt as painful (Butler & Moseley, 2014, p. 42). Persistent and unexplained chronic pain is found to be rooted in the “changes in brain circuitry associated with unresolved trauma” [140]. Van der Kolk asserts that our organs maintain the effects of the over-activation of stress hormones until they no longer can stay silent and scream for our attention via illness (van der Kolk, 2014, p. 46). Hawkins argues that complex trauma is more difficult to treat, as working directly with trauma can activate the same immobilization response and a person must have a wide window of tolerance first [131].
Benedikt and Kolb reported that 10 percent of a sample of 225 patients referred to a Veterans Administration pain clinic met criteria for PTSD [141], while Muse reported that 9.5 percent of a sample of patients attending a multidisciplinary chronic pain center met criteria for “post-traumatic pain syndrome” [142]. Meanwhile, up to 80% of veterans with PTSD had a chronic pain condition [28]. Interestingly, 90% of the vagal nerves (from the vagal complex; responsible for “freeze” response) are sensory and travel from the gut to the brain (i.e., bottom-up, somatic), and only 10% travel top-down (Levine, 2010, p. 121). This could explain the high prevalence of chronic pain among PTSD patients and a lower prevalence of PTSD in chronic pain patients, as the high cortisol during a traumatic situation impacts the gut the most (i.e. repressed immune system, lack of blood supplying the gastrointestinal system, etc), signaling to the brain that a high level of pain or a lack of bodily functioning should be associated with the traumatic event. It is also entirely possible that reductions in NPY influence the high comorbidity between PTSD and chronic pain [80]. NPY can be released to synaptic vessels or mitochondria, and in mitochondria, NPY can reduce cellular functions like oxidative metabolism and thermogenesis to protect neurons, but with chronic stress, it causes more damage to neural function. This can also account for the development of metabolic syndrome with PTSD [121].
Scolio-Salter defines stress conditioning as forming learned associations between unconditioned stimuli and previously neutral stimuli, resulting in hyperarousal and avoidance behaviors associated with PTSD. Management of chronic pain will help PTSD symptoms, and restraining the amygdala's reaction may help chronic pain symptoms as demonstrated with rodents for visceral pain [30], [143], [144]. Molecular studies indicate that specific receptor blockades in the amygdala can decrease pain reactions and inflammation-induced hypersensitivity, supporting the idea of targeted treatments for pain and PTSD symptoms [143], [144], [145]. Pain signals are transmitted to the brain through numerous pathways, including direct ones to the amygdala that may contribute to chronic pain through structural and sensory gating changes [80]. Certain neurotransmitters and hormones like Neuropeptide Y and allopregnanolone (ALLO) have a huge role in the pathophysiology of both chronic pain and PTSD, suggesting that these may underlie this comorbidity.
Chronic pain → CPTSD | CPTSD → Chronic pain |
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TABLE 1 IS A GENERAL SUMMARY OF THE BIOLOGICAL MECHANISMS IN BOTH DIRECTIONS<, FIRST FROM CHRONIC PAIN TO CPTSD, THEN CPTSD TO CHRONIC PAIN. ALL INFORMATION REGARDING PTSD IS ALSO APPLICABLE TO CPTSD.
Furthermore, people in poverty or of a lower socioeconomic status tend to have worse medical morbidities and mortalities [152], [153]. Children growing up in poor communities also developed more behavioral problems, were at a greater risk of crime, and developed poorer neurodevelopmental outcomes (e.g., psychopathology and brain changes) [154], [155]. Educational level was also a protective factor against frequent knee pain in a cohort of Swedish patients examined for knee osteoarthritis [156]. In fMRI's, there seemed to be a big overlap between stress and pain responses, specifically in the amygdala, hippocampus, striatum, insula, and anterior cingulate cortex [157], [158]. PTSD and chronic pain can be considered conditions where the brain fails to extinguish the negative memory (i.e. of trauma or pain) [159], [160]. This theory that the brain can't let go in both PTSD and chronic pain is consistent with PTSD and chronic pain patients show a deficiency in extinction learning [161], [162]. Acute stress also activates the autonomic nervous system which is controlled by the brain-stem, [163] leading to increased blood pressure and redirection of blood from the gastrointestinal tract to the brain and muscles [164]. This could lead to the prevalence of gastrointestinal issues among PTSD patients with the frequent redirection of blood and thus a lack of blood supplying the gastrointestinal tract. In humans, chronic pain and stress-related psychiatric disorders have been associated with shrinkage of the hippocampal volume [165], [166], [167], [168] . Smaller hippocampal volume predicts the risk of persistence of back pain after three years of a new episode of subacute back pain (SBP; pain duration 6–16 weeks) [166]. This goes to show that the pathophysiological pathways of stress and pain are interconnected, and can contribute to the comorbidity of chronic pain and PTSD or complex PTSD. The relationship between neurogenesis and acute stress or pain is much more complex, with conflicting studies on rodents showing impaired contextual fear extinction [165] or enhanced fear extinction two weeks after an acute stressor [169]. In animal models, chronic stress and chronic pain are both associated with dendritic growth in the amygdala [170], [171], [172] suggesting enhanced synaptic activity, possibly in response to increased glucocorticoid levels [173]. Patients with either depression, PTSD, or chronic pain generally had a smaller amygdala, however with depressed patients on medication, there was an increase in amygdala size [166], [174], [175], [176], [177]. The ventromedial prefrontal cortex is brought up again, with a deduction in size among PTSD patients [178]. There seems to be a wide variance among studies, particularly because stress can be defined so broadly and different types of stress can use different pathways, along with the brain having many different endophenotypes [179].
Most recently, a study from 2024 aims to show the genetic overlap between cardiovascular diseases and some neuropsychiatric conditions, including ADHD, ASD, depression, PTSD, Anorexia Nervosa, Alzheimer’s, Schizophrenia, Bipolar, and more [180]. Using a multi-phenotypical analysis which included genome-wide association studies (GWAS), linkage-disequilibrium-score-regression (LDSC), Mendelian randomization (MR), and functional mapping and annotation (FUMA) to determine what genomes and genes from certain neuropsychiatric disorders are common with cardiovascular diseases. The cardiovascular diseases that were looked at include but are not limited to, atrial fibrillation, CAD, cardiomyopathy, heart failure, hypertension, and myocardial infarction. Their results found 18 pairwise traits, significant genetic overlaps, and many casual relationships, particularly for ADHD, major depressive disorder, and PTSD. They also found that all neuropsychiatric disorders meant a higher risk of cardiac MRI changes in heart structure and function.
Chen mentions that coronary artery disease and heart failure were significantly associated with PTSD, even after accounting for lifestyle and drug effects. The goal was to highlight the genetic etiology of the brain-heart axis, which proved to be successful. ADHD, Depression, and PTSD showed a stronger genetic association to cardiovascular diseases compared to other mental disorders. Their analysis showed that PTSD was associated with a heightened risk of myocardial infarction, and in general, displayed a higher risk of cardiovascular diseases genetically. A backward MR analysis proved no significant relationship between cardiovascular diseases to PTSD, compared to a high association from the forward MR analysis proving a strong association between PTSD to cardiovascular diseases. Some diseases like dyslipidemia were also reported as risk factors for many other psychiatric disorders, such as PTSD and schizophrenia. Chen goes into the possible biological reasons for certain disorders and connections, for example, she mentions that in her analysis, APOC4 and the lipoprotein of very low-density lipoprotein and triglyceride were found to participate in the interactions between neuropsychiatric and CVD [180]. Chen's work to find common genes was the first multi-phenotypical study that found what genes were in common with many mental disorders, including PTSD, to certain cardiovascular diseases, showing a higher association with specifically heart failure, atrial fibrillation, hypertension, and myocardial infarction, and some correlation with coronary artery disease.
In summary, glucocorticoids play a significant role in PTSD and chronic pain by regulating cortisol, low NPY, and ALLO is associated with increased PTSD and chronic pain symptoms, the brain regions involved in both CPTSD and chronic pain include the thalamus, insula, anterior cingulate cortex, prefrontal cortex, ventromedial and dorsomedial prefrontal cortex, hippocampus, cerebellum, and the amygdala; low ACTH in PTSD also leads to weakness and fatigue in chronic pain, high CRH sensitizes nerves, and increased cortisol affects autoimmune disorders. Along with this, there are chemical and neural changes associated with both CPTSD and chronic pain that affect each other, demonstrating a complicated, biological network maintaining the two conditions.
Concerns
In a majority of these studies, PTSD was taken from veterans from the war and not childhood abuse, sexual assault, or violence and systematic oppression. While there are minimal studies including underrepresented populations, there is a clear limitation when only considering Western populations. For example, Vermetten describes PTSD as mainly derived from wartime experiences and how the diagnosis is crucial in a time of many wars, naming Afghanistan and Iran [15]. Immediately there seems to be a bias by overemphasizing soldiers and not the majority of people with PTSD. In 2012, he recounts that PTSD in diverse populations has just recently been studied, owing to the lack of representation in PTSD research for minorities. Still, to this day there is a lack of representation which is greatly affecting research on CPTSD. In more stable, first-world countries, a majority of traumatic experiences are singular or if they are repeated, there is better access to care to minimize symptoms and the development of PTSD or CPTSD. Third-world countries do not get that added benefit, and that is where there is a higher prevalence of mental disorders, especially regarding PTSD and CPTSD. Thus, the biggest concern would be a lack of representation for the majority of those with PTSD or CPTSD and an overrepresentation of veterans. Additionally, some of the longitudinal studies included in this paper had a very small sample size, so they may not be representative of everyone.
Treatment
For treatment, several researchers had different ideas of treatment. Lanius suggests exposure-based therapy by teaching emotional awareness skills beforehand [4]. Beck and Clapp link chronic pain and PTSD and suggest an integrative treatment approach for the two disorders, placing an emphasis on CBT, neutral writing, and a new integrative approach for comorbid chronic pain and PTSD [2]. Kind and Otis also mention various types of therapies, including CBT, ACT, PE (prolonged exposure), and CPT (cognitive processing therapy), which all help PTSD [37]. There haven't been many treatments involving chronic pain and PTSD besides one program, Pain and Trauma Intensive Outpatient Treatment (PATRIOT), which has proved effective.
In one longitudinal study over 10 years, the psychotherapist said, “I used cognitive reframing and hypnotherapeutic interventions to teach her to establish an effectively regulated baseline to which she could return when triggered by a flashback or a present-day situation. I use a toolbox of integrative approaches (including exposure therapy, ego strengthening, cognitive restructuring through reality testing and self-statements, Emotional Freedom Technique (EFT), Eye Movement Desensitization and Reprocessing (EMDR) and other approaches) and shift directions according to the client’s responsiveness to each intervention rather than adhering to one treatment modality” [181]. This was proven effective for the patient. Specifically, the patient regarded self-hypnosis as the most helpful protocol [182]; EMDR [183] assisted with recovery from flashbacks, and EFT, tapping acupressure points [184], was the most useful technique when waiting for medical appointments [181].
The occurrence of PTSD is significantly higher in females, with an incidence as high as 32% for females who are sexually assaulted [185]. In military veterans, the incidence may be as high as 39% [186]. This goes to show that while veterans have a high chance of developing PTSD, sexual assault survivors do as well. Interestingly, much of the literature regarding PTSD has always come from male veterans, when most studies show that sexual assault is one of the biggest indicators for PTSD. Of 10 events varying in importance, tragic death occurred the most often, and sexual assault yielded the highest rate of PTSD [15]. This goes to show that more research must be done on all minorities. Weisfeld and Dunleavy follow a patient with PTSD (from sexual assault) and chronic pain over 10 years to gather more reliable information on treatment [181]. This patient suffered from delayed onset complex PTSD involving sexual assault (rape) by a physician when seeking medical attention for a kidney infection and associated back pain. The patient avoided doctors until experiencing heart palpitations in her 50s, and only at 60 did she meet a psychotherapist. Her psychotherapist notes, "As I contemplated the contrast between the term ‘episode’ and my undisclosed counter feelings, I realized that she was not angry at this doctor; I was. It helped me fully grasp the level of wounding and the psychological protections put into place to paradoxically keep her functioning at the cost of a free integrated self" [181]. At some points like in phase 2, the patient’s processing of traumatic memory appears to be delayed until back pain is brought down to manageable levels, emphasizing the need for an integrative approach. There is also room for integrating movement in therapy, as yoga relieves PTSD symptoms [139], [187]; exercise reduces depression [188]; Qi Gong and yoga reduce anxiety [189], [190]; and progressive muscle relaxation training can relieve many pain conditions [191].
Personally, with my own experience and the studies I’ve mentioned, exposure therapy, an integrative approach, yoga, pilates, other types of physical exercise, EMDR, CBT, and more individualized approaches to treatment are the most effective. An individualized and integrative approach is necessary for sufficient healing, but how one goes about that can vary. Many traumatized individuals do not like regular CBT unless the therapist or clinician has a good therapeutic connection. With complex trauma, oftentimes talking is not enough. While there is not enough evidence to fully support this, Internal Family Systems Therapy (IFS) is very effective for CPTSD, BPD, and dissociative disorders. EMDR, any therapy integrating the body and the bodily sensations in therapy or trauma work, and a good, individualized therapeutic approach seems to work the best. Regardless of whether a CPTSD or PTSD patient has a comorbid chronic pain disorder, being aware of how one physically feels at heightened states gives insightful feedback for long-term usage. Chronic pain patients should also seek therapy or have a clinician who is generally understanding. With every approach, the key to healing relies on the therapeutic relationship, trust, and education.
Conclusions
The mind and body remain interconnected in various ways. There are many approaches to this, but some areas should remain of significant importance: 1) including diversity and accurately representing all people with CPTSD, PTSD, and chronic pain in research, to better help underrepresented populations, 2) understanding the neurobiological underpinnings of comorbid CPTSD and chronic pain to find holistic treatment options, develop technology that can correct biological functions, and to make patients’ lives better considering the financial burden of medication and various types of therapy, and 3) developing a better understanding on complex PTSD and chronic pain at the root causes. The main focus should always be to help patients and others to better understand them. Future researchers should go more into the neurobiological factors causing this comorbidity and look into how our brain changes due to this, while including diverse populations.
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