Continuing Education Activity

Psychological or mental health trauma refers to a stressor experienced either directly or indirectly, resulting in significant and severe subjective distress. Mental health trauma is ubiquitous and frequently experienced throughout the lifespan. A frequent sequela of traumatic experiences is functional impairment, which can result in decreased quality of life, morbidity, and poorer health outcomes. One categorization for trauma experiences is distinguishing between acute and chronic traumas. This activity describes similarities and differences between acute and chronic mental health traumas and outlines the role of interprofessional teams in evaluating and managing patients who experience trauma-associated symptoms.

Objectives:

• Compare and contrast acute and chronic mental health traumas.
• Describe the prevalence and associated risk factors of various types of mental health trauma.
• Evaluate patients for the physical and mental health sequelae of mental health trauma exposure.
• Develop and employ effective interprofessional team strategies to prevent and manage mental health trauma-associated symptoms.

Introduction

The word "trauma" derives from the Greek word for "wound" or "hurt." Mental health or psychological trauma has since become more broadly defined as an experience that is subjectively perceived as painful or distressing and results in acute or chronic mental and physical impairment or dysfunction.[1][2] The Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), defines a traumatic event as the exposure to "death, threatened death, actual or threatened serious injury, or actual or threatened sexual violence." Trauma may be experienced either through direct involvement or by witnessing or learning of such an event happening to others and is often accompanied by a sense of shock, helplessness, or loss of control.

Trauma can be categorized and described across myriad factors, and one such categorization is acute versus chronic forms of trauma. These can include the sudden loss of a loved one, physical abuse, sexual predation, natural disasters, or exposure to war and violence, among many others. Causes of trauma are thus ubiquitous and a nearly universal human experience. Traumas can occur throughout the lifespan; current data suggest that childhood trauma leads to worse outcomes than trauma experienced in adulthood.[3][4]

Trauma is typically described as either an acute or chronic process. The acute trauma response or acute stress reaction is characterized by a short-lived sympathetic response to a real or perceived threat that typically results in a "fight or flight" response. If this response does not resolve or the perceived threats remain ongoing, this initial acute response can progress to a chronic trauma response. This chronic response is often associated with significant impairment and comorbidity.[5]

Like acute stress reactions, chronic stress reactions can occur in response to a single traumatic event or following multiple stressors. Chronic trauma usually presents with aberrant behavioral and physiological processes, outlined in the DSM-5 as the following symptom clusters: (1) hyperarousal states, (2) avoidance behaviors, (3) intrusive trauma-associated memories, and (4) altered cognitions and moods.[6] These symptoms can occur in both Acute Stress Disorder (ASD) and Posttraumatic Stress Disorder (PTSD), which are further distinguished by the duration of the symptoms following a traumatic event, where ASD lasts less than a month, and PTSD lasts greater than a month, respectively.[7][5]

In addition to acute and chronic trauma, complex trauma includes repeated trauma exposure that can be severe and prolonged, resulting from the perversion or loss of a significant relationship.[8][9] While repeated trauma exposures may occur in adulthood, this typically occurs in childhood or adolescence and is often perpetrated by adult caregivers or other authority figures who were previously perceived as trustworthy or protective. Such trauma tends to be characterized by the real or perceived impossibility of escape; this sense of feeling trapped and a loss of safety leads to trauma responses such as hypervigilance and persistent negative mood.[8] Complex posttraumatic stress disorder (CPTSD) includes the symptoms of PTSD accompanied by dysfunction in self-concept, affect regulation, and relationships.[9]

Etiology

The causes of trauma are manifold and can include:

• Natural disasters such as tornados, hurricanes, earthquakes, fires, etc.
• Accidents such as motor vehicle accidents, chemical spills, etc.
• Physical violence, such as being attacked, mugged, etc.
• Physical abuse, such as excessive physical discipline, intimate partner violence, etc.
• Physical trauma such as accidents, illness with sudden onset, etc.
• Sexual violence such as rape, sexual assault, etc.
• Sexual abuse, such as the sexual grooming of minors, prolonged threat of sexual violence or manipulation, stalking, human trafficking, etc.
• Verbal and emotional abuse
• Sudden loss of a loved one
• Emotional or interpersonal abuse, such as yelling, emotional manipulation, controlling behaviors, etc.
• Homelessness or housing instability[10]
• Extreme financial distress
• Manufactured conflicts such as armed conflict, civilian exposure to war, relief work, refugeeism, terrorism, and torture.
• Chronic illness
• Experiencing bullying
• Real or perceived neglect or abandonment
• Witnessing others experiencing any of the above

Other factors influence the impact of trauma on an individual’s well-being by either predisposing or precipitating trauma responses. Such factors include:

• Gender[11]
• Age[12]
• Socioeconomic factors[13]
• Race, ethnicity, and culture[14]
• Sexual orientation and gender identity[15]
• Time to adequately process the trauma experience[16]
• Losses secondary to trauma, such as losing an important relationship, job, stable housing, etc.
• Anticipation of trauma exposure[17][18]
• Relationship to the person or entity responsible for trauma exposure[19]
• Perceived individual or cultural meaning of trauma[20]
• Disruption of core assumptions and beliefs[21]
• Prior trauma history[22]
• History of resilience[23]
• History of mental illness[24]

Epidemiology

According to multiple worldwide surveys of exposure to traumatic events, including findings from the World Mental Health Survey Consortium, which derived survey data from 24 countries, approximately 70% of respondents reported experiencing lifetime traumas.[25][26][27] A more recent international study from 2022 surveyed over 50,000 individuals and confirmed the same finding, with an average of 3.2 traumatic experiences per capita.[4]

The incidence and types of trauma sustained varied across age and socioeconomic factors. Violent trauma and accidents were more likely to occur during adolescence to early adulthood and inversely associated with socioeconomic status. Additionally, women were far more likely than men to report intimate partner sexual violence; men were more likely to experience physical violence and accidents than women.[4]

Police officers, first responders, and soldiers in active combat situations report a lower prevalence of trauma-associated symptoms.[4] This finding is secondary to selection bias or prior experiences that contributed to greater resilience in the first-responder and police officer population. Additional research suggested the possibility of resilience as the primary mechanism of decreased PTSD risk in this population; it remains unclear whether prior trauma experiences may increase vulnerability to trauma rather than promote resilience.[28][29]

In the United States, recent research finds that nearly 90% of adults report exposure to at least one potentially traumatic event (PTE) during their lifetime.[11] Approximately 5% to 6% of men and 10% to 12% of women suffer from PTSD, making it one of the most common psychiatric disorders encountered in clinical practice.[5] Approximately 8% of trauma-exposed individuals develop symptoms consistent with PTSD, with most recovering after initial exposure.[30] Recent research finds that the prevalence of trauma in the United States is equivalent across urban and rural regions; there appears to be more exposure to wartime trauma in rural settings and substance abuse in urban settings.[31] Most individuals exposed to trauma do not go on to develop PTSD or other psychiatric disorders associated with trauma, such as depression, anxiety, or substance abuse.[5][32][5]

The most commonly reported individual traumatic event from the 2016 World Mental Health Survey Consortium data was the sudden loss of a loved one, especially if the loss was violent and unexpected.[4][25] Many individuals in this study experienced multiple traumatic events in their lifetime. As such, the data was reported as the percentage of respondents reporting a specific traumatic event and the proportion that the traumatic event represented within all traumatic events.

Approximately 31% of the respondents experienced losing a loved one, and this traumatic event accounted for approximately one-sixth of all traumatic event exposures. Witnessing death or serious bodily harm to someone else was the second most commonly experienced traumatic event, reported by approximately 23% of respondents, accounting for another one-sixth of all traumatic event exposures.[25] The third and fourth most commonly experienced traumatic events were muggings and severe motor vehicle collisions, reported by 14.5% and 14.0% of respondents and represented 7% and 6.1% of traumatic events, respectively. The fifth most commonly experienced trauma was life-threatening injury or illness, reported by 11.8% of respondents and represented an additional 5% of traumatic events. All 5 exposures to traumatic events accounted for approximately 50%. The risk of developing PTSD follows a bimodal pattern, with the highest risks during childhood, adolescence, and after age 65.[3]

Current evidence suggests that the type of trauma carries different risks of developing trauma-associated pathology. Recurrent physical violence, including combat, carries the highest risk of developing PTSD, along with sexual violence ranging from 13% to 14% in one study.[3][27][33] The unexpected death of a loved one and direct exposure to death or grave injury carry intermediate risks of developing PTSD, approximately 5% to 8% in the same study; these exposures are common occurrences in the general population.[27]

Pathophysiology

The pathophysiology of stress responses can be divided into acute and chronic processes. The two primary physiological responses to acute stressors involve the direct stimulation of catecholamine release by activation of the sympathetic nervous system and the activation of the hypothalamic-pituitary-adrenal (HPA) axis resulting in increased systemic cortisol levels.[34]

Physiologic responses to chronic trauma include several additional processes. Research has consistently demonstrated alterations in brain structure, neuroendocrine dysregulation, and cognitive or affective changes because of exposure to trauma.[5][35] Despite a wide variety of neuroanatomical findings, the exact psychobiological mechanisms underlying the development of PTSD and other psychiatric conditions are not fully understood.[35]

The Hypothalamic-Pituitary-Adrenal (HPA) Axis

Current hypotheses regarding aberrant trauma responses typically recognize the role of the HPA axis; this system is essential in mediating responses to stress via homeostatic mechanisms.[34] Initial research into this system and its relation to PTSD measured basal cortisol levels. Several studies of patients diagnosed with PTSD and depression demonstrated low basal cortisol levels with blunted endogenous cortisol release in response to new stressors. However, subsequent studies of basal cortisol levels later demonstrated equivocal levels in PTSD compared to control groups. As a result of these findings, the pathophysiological focus consequently moved toward the HPA axis and glucocorticoid-receptor sensitivity to cortisol, as opposed to blood cortisol levels.[36]

The dexamethasone suppression test was used further to study the sensitivity of the HPA axis and glucocorticoid-receptor. The dexamethasone suppression test involves administering the exogenous corticosteroid dexamethasone via the bloodstream and measuring endogenous cortisol before and after the administration. Exaggerated cortisol suppression with dexamethasone administration in individuals with PTSD was demonstrated in multiple studies.[37] This exaggerated cortisol suppression has also been associated with reduced fear response in those with PTSD.[5][35][37][35]

The Brain

Multiple brain structures involved in acute and chronic trauma responses have been identified and include the hypothalamus, hippocampus, amygdala, medial prefrontal cortex (MPFC), and dorsolateral prefrontal cortex (DLPFC).

The hypothalamus synthesizes and releases corticotropin-releasing hormone (CRH), which stimulates adrenocorticotropic hormone (ACTH) release from the anterior pituitary resulting in systemic cortisol release from the adrenal glands.[35] Early stress in rat models, akin to adverse childhood events in humans, resulted in increased hypothalamic CRH mRNA expression and increased CRH within the median eminence of the hypothalamus. Adverse experiences early in the postnatal period in nonhuman primates also resulted in elevated levels of CRH in the cerebrospinal fluid.

The hippocampus is involved in forming declarative memory, all associated learning, and possibly fear extinction.[38] The hippocampus is considered very sensitive to stress; specifically, studies of the cornu ammonis (CA3) region of the hippocampus in animals have demonstrated neuronal damage and inhibition of neurogenesis after stress. The mediating factors for these changes include decreased brain-derived neurotrophic factor (BDNF), elevated blood cortisol, and elevated glutamate levels.[35] These changes have also been associated with learning inhibition. In addition, research has shown that pretraumatic low hippocampal volume predisposes individuals to develop trauma-associated symptoms.[39] 

The amygdala is responsible for processing emotional valence and fear responses, with extensive connectivity to the hippocampus and prefrontal cortex. Amygdalar development is thought to be complete during adolescence, prior to the development of the prefrontal cortex. Increased dendritic growth and synaptic development within the amygdala have been associated with emotional stressors and contribute to behaviors seen in anxiety, phobias, and trauma-related disorders.[40]

The MPFC and DLPFC are hypothesized hubs for working memory, and both continue to mature through early adulthood.[40] Chronic stress has been shown to affect prefrontal cortex (PFC) development negatively. The differential rate of development between the PFC and amygdala is hypothesized to contribute to the development of increased reactivity from stress occurring in adolescence and early adulthood.[41][42] The MPFC and DLPFC are thought to be inhibitory in managing amygdala function in fear and anxiety responses.[34] Reduced MPFC parenchymal volume has been demonstrated in patients diagnosed with PTSD.[43] Fear acquisition studies in human subjects have shown a negative correlation in blood flow between the amygdala and MPFC, as amygdalar blood flow increased in response to stress while MPFC blood flow decreased.

Neurotransmitters

Several neurotransmitters and hormones have been shown to influence the development or extinction of trauma-associated symptoms.[44]

• Norepinephrine (NE): moderate levels of NE engage α2 receptors in the PFC to facilitate working memory and inhibit amygdala function in response to an acute threat, whereas high levels of NE and its metabolites disrupt these same functions.[35]
• Corticotropin-releasing hormone (CRH) stimulates the release of adrenocorticotropic hormone and has a direct anxiogenic effect in the amygdala and stria terminalis. CRH has also been elevated in the CSF of men with PTSD.
• Adrenocorticotropic hormone (ACTH) is released from the pituitary after stimulation from CRH, and ACTH acts on the adrenal glands, producing and systemically releasing corticosteroids. Release of ACTH from CRH stimulation is generally increased in women diagnosed with PTSD, whereas ACTH release is generally decreased in men; these findings may vary.
• Neuropeptide Y (NPY) is co-localized with several neurotransmitters, and the specific neurotransmitters can vary depending on the location within the nervous system. Depending on the intensity of the presynaptic signal, NPY can either reduce the release of the co-localized neurotransmitters or facilitate the effects of these neurotransmitters on the postsynaptic neuron. The facilitator effect occurs in response to intense presynaptic stimulation. In sympathetic neurons, NPY is co-localized with NE. In male veterans with chronic PTSD, plasma resting levels of NPY were significantly lower than in healthy men without combat trauma exposure. NPY has also decreased CRH-induced symptoms, including sleep disturbances, in individuals diagnosed with PTSD.
• Gamma-amino-butyric acid (GABA) is an inhibitory neurotransmitter connected to the allopregnanolone system. Decreased basal plasma levels of GABA have been demonstrated in individuals with PTSD, along with decreased GABA concentration in the cortex. A decreased plasma GABA level is hypothesized to be a risk factor for developing PTSD.
• Allopregnanolone is a neuroactive peptide that modulates GABA activity; lower levels of allopregnanolone are associated with increased anxiety, aggression, fear conditioning, and inhibition of fear extinction.
• Glucocorticoids are systemic hormones that typically increase in response to stress but appear to be at a lower basal plasma level with concomitant increased glucocorticoid-receptor sensitivity in patients diagnosed with PTSD.
• Dehydroepiandrosterone (DHEA) inhibits GABA_A receptors through antagonism and induces increased metabolism of the glucocorticoid cortisol into cortisone, which is an inactive metabolite. DHEAS is the sulfated form of DHEA and is a significantly more potent modulator of GABA_A receptors. Higher DHEA/DHEAS levels have been associated with stress resilience and are a protective factor against PTSD and depression, whereas a lower DHEA to cortisol ratio is found in individuals with a history of childhood trauma.
• 17β-estradiol is synthesized in the adrenal glands, brain, and ovaries. 17β-estradiol exerts antidepressant effects via an intracellular G-protein-coupled estrogen receptor. 17β-estradiol also demonstrates activity at both the estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) receptors. ERα-receptor activation in the amygdala is anxiogenic, whereas ERβ-receptor activation is anxiolytic. The ERβ-receptor also enhances the long-term retention of fear extinction, and ERβ-receptors are found in the amygdala, hippocampus, and PFC. The differential effects of estradiol are thought to be dependent on the activity levels at these receptors, which are modulated in conjunction with allopregnanolone. 17β-estradiol has also been found to be low in women with PTSD.
• Serotonin (5-HT) receptors are the primary treatment target of antidepressants that are FDA-approved for treating PTSD. Selective serotonin reuptake inhibitors (SSRI) increase 5-HT within the synapse. Allopregnanolone levels in rodents increased at low SSRI doses, suggesting that clinically dosed SSRI treatments may increase allopregnanolone synthesis. Stress has been associated with the depletion of tryptophan, a precursor of 5-HT; stress-induced tryptophan depletion has been demonstrated to be greater in women than men.

Additional Considerations

An individual's response to trauma also appears to be mediated by genetic predisposition and the developmental stage during which trauma occurs.[34] Additional factors include the security of attachment to important figures, personality, prior history of stressors, psychosocial supports, and a litany of other factors.[5]

History and Physical

Practitioners should obtain a comprehensive history to fully assess for behavioral, emotional, and cognitive disturbances that patients may experience due to trauma exposure.[4] In acute trauma, patients may initially complain of sleep abnormalities, difficulty concentrating, and mood changes, among other trauma-associated symptoms. Traumatized individuals frequently report behavioral disturbances, including greater impulsivity, self-isolation, psychomotor agitation, and self-injurious behaviors. Mood disturbances may include depressed mood, emotional numbing, irritability, and rage.

Patients may also report cognitive impairments such as difficulties with sustaining attention, dissociation, disorganized thinking, and memory impairments. Complaints of autonomic arousal may also be reported as sensory sensitivity to sound and touch, exaggerated startle reflexes, anxiety, and fear. Identifying trauma exposures is essential in ruling out trauma-associated diagnoses, including ASD and PTSD. ASD and PTSD are primarily distinguished based on the duration of the symptoms, where the former resolves within 1 month following trauma exposure, and the latter carries a more chronic symptom burden. Additionally, practitioners should assess suicide risk, as trauma exposure is associated with an increased risk of suicidal ideation and suicide attempts.[30]

In inpatient clinical settings, obtaining a detailed history of traumatic exposures is often inappropriate or unnecessary. The detailed recounting of traumatic experiences can result in trauma responses and activate the autonomic nervous system, which risks emotion dysregulation and the potential for re-traumatization in the clinical setting.[45] Exceptions to this include history gathering to report the abuse of elders, children, and those with intellectual disabilities or if a trauma-specific treatment is being delivered in agreement with the patient.

Practitioners should carefully seek an understanding of the reported symptoms, aligning self-descriptions of trauma with accepted terminology to ensure an accurate diagnosis. For example, a patient may report feeling “paranoid,” which is clarified on evaluation as hypervigilance, or they may report experiencing “amnesia,” which is instead a dissociative episode.

Evaluation

Physicians and clinicians should complete a full evaluation and assessment to rule out organic pathology that may exacerbate or complicate treatment, such as liver disease and other conditions that may influence drug metabolism or drug-drug interactions.[46] Currently, cortisol levels, dexamethasone suppression testing, and other neuroendocrine tests are not routinely performed. Substance use disorders, including alcohol and tobacco, often coexist with trauma and should be screened for during the initial evaluation.

Although no recommended guidelines exist, screening for trauma history consistently is advisable. This is especially true for patients presenting with psychiatric complaints consistent with depression and anxiety or with a history that increases the risk of trauma exposure, such as military service.[46] Determining the level of impairment in various aspects of a patient’s life is essential in determining the presence of ASD or PTSD.

Practitioners may utilize several screening and diagnostic tools to aid in assessing trauma-associated pathology. Several psychometrically sound assessments and tools are available, many of which are self-report or short structured interviews. The following tools are available in the public domain:

• Screen for Posttraumatic Stress Symptoms (SPTSS)[47]
• Clinician-administered PTSD Scale (CAPS-5)[48]
• Impact of Event Scale - Revised (IES-R)[49]
• PTSD Symptom Scale: Self-report Version (PSS-SR)[50]
• Trauma History Questionnaire (THQ)[51]

SPTSS, IES-R, and PSS-SR are self-report assessments that patients can quickly complete. SPTSS is frequently used to assess if patients meet criteria for PTSD that do not depend upon identifying a particular stressor, whereas IES-R is used as a screener only. The PSS-SR is also a screener that focuses on the level of dysfunction across core trauma-associated symptoms. The THQ is specially designed to facilitate the description of multiple traumatic events across the lifespan and elucidate complicated trauma histories. CAPS-5 is a structured interview and is considered the gold standard for diagnosing PTSD, given its in-depth exploration of various aspects of trauma-associated symptoms, including duration, severity, and timing.

In general, research finds that using structured clinical interviews yields more accurate diagnoses of trauma-associated disorders but at the cost of additional time burden and training to perform appropriately.[52] Screening and assessment tools are helpful adjuncts in screening at-risk individuals but do not replace a thorough medical and mental health evaluation.

Treatment / Management

Therapy is the mainstay treatment for trauma-associated symptoms and pathologies like ASD and PTSD. Multiple randomized controlled studies completed with child, adolescent, and adult populations have found that most psychotherapeutic modalities show efficacy compared to control groups.[53] Current evidence suggests that cognitive behavioral therapy (CBT) can reduce symptoms of PTSD and comorbid anxiety and depression in children and adolescents regardless of trauma type.[53]

Additional treatment modalities such as cognitive processing therapy (CPT) and exposure therapy are equally effective in treating general PTSD and PTSD specifically related to interpersonal physical and sexual violence.[54] Stress inoculation training appears to have some efficacy in reducing the severity of PTSD symptoms compared to waitlist control, with the maintenance of benefits up to a year after discontinuation.[55] Eye movement desensitization and reprocessing (EMDR) is a commonly used therapeutic modality effective in addressing trauma and PTSD.[56] Psychodynamic psychotherapy has also demonstrated effectiveness in the treatment of PTSD.[57][58]

The goal of therapy is to assist patients in identifying and managing maladaptive cognitions, affect, and behaviors to reduce avoidance behaviors, extinguish autonomic psychological responses, and develop greater overall function. Each psychotherapy technique approaches this treatment goal using differing theoretical formulations.

The mainstay of pharmacological treatment for trauma-related conditions includes selective serotonin reuptake inhibitors (SSRI) and selective norepinephrine reuptake inhibitors (SNRI). Currently, the only FDA-approved medications for PTSD treatment are the SSRIs paroxetine and sertraline. However, the SSRI fluoxetine and the SNRI venlafaxine are also frequently prescribed; both are recommended by the Veteran Affairs/Department of Defense (VA/DoD) Clinical Practice Guidelines.[59][60] Other non-SSRI antidepressants, such as trazodone and mirtazapine, have also shown benefits for the treatment of PTSD, along with several monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs).[61]

Studies of antidepressants in animals have demonstrated hippocampal neurogenesis, a hypothesized mechanism of action in PTSD.[35] Antipsychotics such as quetiapine, risperidone, and aripiprazole and mood-stabilizing agents such as topiramate have shown clinical benefits.[62][63] However, the increased burden of adverse effects can limit the utility of these medications.[3][59] Multiple clinical investigations have indicated that a combination of trauma-informed psychotherapeutic and pharmacologic interventions has beneficial and possibly synergistic effects; this remains unclear and will require additional study.[3][64]

Research has been undertaken to determine psychopharmacological and therapeutic approaches to preventing the development of trauma-associated symptoms and diagnoses. A recent literature review by Qi et al suggests that brief psychotherapeutic interventions are likely unnecessary or inappropriate for most symptomatic trauma survivors.[65] Additionally, hydrocortisone has shown some efficacy as a preventative treatment, especially for those who are corticosteroid naive, but no efficacy has been demonstrated for escitalopram, gabapentin, propranolol, or temazepam.[66] New treatment avenues utilizing hallucinogenic substances have shown some promise in clinical trials but will require further investigation to establish safety and efficacy profiles in clinical practice.[67] 

Differential Diagnosis

Trauma-associated symptoms appear transdiagnostically and must be carefully assessed; the final diagnosis can significantly alter the treatment course. For example, persistent negative mood, social isolation, and disturbed sleep are common in PTSD and depressive disorders.[68] Dissociative symptoms, hyperarousal states, and intrusive memories appear in neurodevelopmental disorders such as attention deficit and hyperactive disorder (ADHD).[69][70] Anxiety disorders and trauma-related pathologies share arousal states and avoidant behaviors and cognitions.[71] Symptoms typically associated with active psychosis, like auditory and visual hallucinations, are frequently experienced by individuals with trauma histories.[72] Moreover, paranoid ideation and hypervigilance are frequently difficult for patients to accurately describe. Negative psychotic symptoms mimic self-isolation and distrust found in PTSD.[73]

Complex posttraumatic stress disorder (CPTSD) is a newly recognized diagnostic category within the mental health field.[9] As described earlier, CPTSD has been conceptualized as similar to PTSD with the added component of disturbances in self-organization. These disturbances include impaired affect regulation, decreased functioning in relationships, perceived emotional numbing, distortions in the sense of self, and persistent worthlessness.[74][21] Many of these symptoms are present with borderline personality disorder (BPD); as such, debate has ensued regarding whether CPTSD and BPD refer to the same pathological picture. However, current literature suggests that CPTSD and BPD are distinct conditions.[74]

Due to recurrent and distinct clinical pictures that emerge from prominent or prolonged exposure to childhood traumas, researchers have proposed criteria for a new trauma diagnosis of Developmental Trauma Disorder (DTD) designed to capture more chronic forms of trauma.[3] The disorder comprises a constellation of pervasive disruptions in typical cognitive, emotional, and behavioral functioning. Such dysfunction may present heterogeneously with recurrent nonsuicidal self-injurious behaviors, suicidal behaviors, antisocial traits, and inability to cope with reality.[75] The hope of utilizing a diagnosis encompassing a broad spectrum of symptoms is to decrease inappropriate over-pathologizing of individuals and promote an interdisciplinary approach to treating individuals who have suffered severe and recurrent childhood traumas.[3]

Prognosis

Investigations of the duration of trauma-associated symptoms find that nearly half of PTSD cases remit within 6 months post-exposure and do not vary significantly across different types of trauma exposure.[4] Why some individuals do not recover from a traumatic event while the majority do remains unclear.[7] For the other half of PTSD cases, the mean duration of trauma-associated symptoms can vary greatly. For example, the average duration of traumatic symptoms following a natural disaster is 1 year, while symptoms associated with combat experience endure an average of 13 years. It is important to note that recurrent traumas, especially same-type physical or sexual violence, substantially increase the risk of developing pathology and are associated with poor mental health.[4]

A prospective study involving participants who recently sustained physically traumatic injuries requiring treatment in an acute care setting found that patients who experienced mild symptoms shortly after a traumatic event were unlikely to develop symptoms of ASD or PTSD.[76] Alternatively, the development of significantly elevated symptoms in the acute posttrauma period was associated with much higher risks of mental illness that were unlikely to resolve spontaneously. Additionally, patients who developed moderate symptoms would differ markedly in rates of symptom trajectories during recovery.[76] This finding is consistent with the current understanding that most individuals exposed to potentially traumatic events (PTE) do not develop clinically significant mental illness.

In addition, ASD is commonly referred to as a precursor for PTSD, which can suggest that ASD naturally develops into PTSD. However, research finds this is not necessarily the case. A recent meta-analysis identified that approximately half of the individuals who meet the criteria for PTSD did not meet the criteria for ASD within the first 30 days following trauma.[7] Of the remaining half of individuals, symptom development immediately after trauma did not consistently predict the development of PTSD.

Complications

Research has shown that individuals who experience acute or chronic trauma are at risk of developing poor health outcomes. A recent extensive literature review of various health outcomes showed that acute stress responses are associated with increased risks of all-cause mortality, healthcare service utilization, pain, and poor physical health.[32] Additionally, other risks show increased rates of injury, cardiovascular disease through a wide variety of secondary risk factors, and greater use of medical and mental health services.[77] 

A diagnosis of PTSD is associated with myriad poor health outcomes, including poor physical health, a greater number of medical diagnoses, and functional impairment that can develop years after an initial trauma complicated by prolonged trauma responses.[78] Cumulative victimization traumas are associated with a worsened subjective sense of well-being and life satisfaction positively correlated to the severity of traumas sustained.[79] This was brought to the forefront of trauma research with the landmark study by Felittie et al in which a survey of more than 16,000 adults showed a positive correlation between the number of traumatic events across the lifespan and significant adverse health outcomes.[80]

Adverse childhood experiences include potentially traumatic events such as abuse, neglect, and loss of a caregiver that occur during developmentally vital periods like childhood and adolescence.[3][80][75] Current evidence suggests that repeated childhood trauma exposures have significant implications for coping skills, attachment styles, personality development, and increased risk for further trauma and the development of psychiatric illness. Severe acute emotional reactions or distress experienced following trauma exposure accompanied by significant autonomic activation appears to predict the development of PTSD.[5]

This initial response and subsequent avoidant coping behaviors are associated with increased PTSD symptom burden. This finding was the basis for establishing acute debrief protocols that were eventually not found beneficial and, in some instances, appeared to exacerbate peritraumatic symptoms.[35] Current medical literature makes a strong case that chronic childhood stress is associated with disrupted early attachments, poor acquisition of adaptive coping skills, heightened HPA axis response, and a markedly elevated risk of developing psychiatric illness in adulthood.[5] Moreover, chronic childhood trauma is associated with worsened academic performance mediated by mental illness that is pronounced by barriers to appropriate mental health care; this is associated with an increased risk of reduced employment and educational opportunities.[81]

The literature describing the association of sexual and physical violence with various poor health outcomes is extensive. In general, sexual trauma and nonsexual physical violence are associated with the more symptomatic presentation of PTSD and lifetime trauma types compared to other trauma types.[82] Nonsexual physical violence is associated with comorbid substance use disorder in approximately 25% to 45% of PTSD cases.[83] The unexpected death of a loved one was associated with comorbid depression. In all cases, developing depressive symptoms with and without PTSD is common, especially following high acute stress responses.[32]

Trauma exposure is strongly associated with suicidal ideation and suicide attempts across the lifespan.[30] This finding is true of childhood trauma exposure, which increases the risk of later developing suicidal ideation in children and adults, especially with sexual trauma. Trauma responses appear to be influenced by gender. For example, male military members with a history of any childhood trauma, especially sexual abuse, significantly increased the likelihood of presenting to the hospital for attempting suicide instead of suicidal ideation; females are more likely to take their own life if exposed to childhood neglect, particularly emotional neglect.[30]

Current research indicates a strong association between trauma exposure and the risk of later developing psychotic symptoms, including chronic auditory and visual hallucinations. One study by Medjkane found that the number of hallucinatory modalities that patients experienced was a statistically significant predictor of childhood trauma after controlling for suicidal ideation and comorbid diagnoses.[84] Additionally, exposure to at least 1 traumatic event led to a 2.5 increased risk of developing paranoid ideations and a nearly five-fold increase in developing verbal hallucinations.[85]

These risks were associated with severe childhood sexual abuse and non-victimization or witnessed events; only sustaining a physical attack as an adult was not associated with an increased risk of developing these symptoms. A recent meta-analysis of hallucinations and delusions associated with trauma also found that hallucination severity is associated with specific trauma types, which included childhood sexual abuse and neglect; the severity of delusions is associated with childhood sexual abuse and total trauma sustained.[72] Negative symptoms of psychosis, such as alogia, limited social interactions, and flat affect, were found to be associated with childhood neglect.

Deterrence and Patient Education

Primary prevention of exposure to avoidable traumatic experiences is a vital but elusive goal, given the ubiquitous nature of trauma.[2] Practitioners frequently engage in secondary and tertiary prevention in response to trauma exposures in which a minority of individuals progress to impaired functioning. Establishing safety is paramount in assisting patients with preventing or managing trauma-associated symptoms. Factors to assist individuals in preventing and managing trauma and its various effects have been identified.[86] These factors include:

• Establish physical and psychological safety where possible
• Prevent iatrogenic retraumatization[45][87]
• Provide trauma-informed education to help patients recognize their symptoms, normalize trauma-associated symptoms, and foster hope for recovery from trauma through understanding the effectiveness of treatments
• Encourage patients to learn about trauma
• Address disturbances in sleep
• Acknowledge loss or grief resulting from trauma

An important concept that has recently gained prominence in trauma research is resilience, defined as an ability to adapt to significant change or stressors that are overwhelming, life-threatening, or disruptive.[23] While frequently thought of as a trait that one either possesses or does not, resilience may be better conceptualized as the process of developing and utilizing adaptive cognitions and behaviors that promote adaptation or recovery from a psychological insult. Aspects of resilience include bolstering positive relational attachments, emotion regulation strategies, and identifying and developing personal strengths. Multiple school-based and community programs have been designed and implemented to improve resilience in children and adults with positive results.

Pearls and Other Issues

• Practitioners should screen for trauma which can be described as anything that the patient has experienced or witnessed that has significantly impacted the patient. Many events or occurrences may be stressful but not traumatic.[88]
• Consider implementing screening tools to assess a history of traumatic events and ongoing trauma.
• Diagnosis and treatment of a single discrete traumatic event are often more easily managed than chronic recurrent traumas; this is especially true if the trauma is experienced in adulthood compared to childhood.
• A history of trauma, especially sexual violence or abuse, significantly increases the risk of suicidal ideation and behaviors in patients. Patients with a trauma history should be screened for suicide risk.
• A history of trauma increases the risk of developing ASD and PTSD. PTSD is often comorbid with depression, anxiety, substance use, psychotic symptoms, and personality disorders.
• Psychotic symptoms such as hallucinations and paranoia can be present in individuals with a history of trauma but do not typically constitute a primary psychotic disorder.

Enhancing Healthcare Team Outcomes

The sequelae of acute and chronic trauma impact physical and mental health. In cases where the trauma leads to functional impairment, utilizing an interprofessional team of healthcare practitioners to manage symptoms is recommended. Such professionals include a psychiatrist, primary care practitioner, psychologist, social worker, and other behavioral health specialists of different backgrounds depending upon the needs and comorbidities of the patient. Resources to educate and train members of multidisciplinary teams are becoming increasingly common and developed.[89] [Level V]

Patients across the lifespan benefit from trauma-informed therapeutic interventions coordinated between primary care practitioners and mental health specialists. An example is the implementation of collaborative care models in both outpatient and acute care settings designed to reduce the effects of trauma [Level I] and comorbid symptoms, including depression and substance abuse.[90] [Level III]

In cases of suicidal ideation or comorbid substance use, additional consultation with a mental health specialist for psychopharmacological and therapeutic interventions may be required. In the case of active suicidal ideation, inpatient psychiatric hospitalization for stabilization and safety is often necessary. Medical management with SSRIs or SNRIs is the first-line pharmacological treatment for symptoms of ASD or PTSD.[53][59] [Level I] Similarly, cognitive behavioral therapy is a first-line treatment with comparatively effective treatments available, such as CPT, PE, EMDR, and narrative therapy.[53][59] [Level I]

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Kleber RJ. Trauma and Public Mental Health: A Focused Review. Front Psychiatry. 2019;10:451. [PMC free article: PMC6603306] [PubMed: 31293461]

2.

Friedberg A, Malefakis D. Resilience, Trauma, and Coping. Psychodyn Psychiatry. 2022 Summer;50(2):382-409. [PubMed: 35653526]

3.

Cruz D, Lichten M, Berg K, George P. Developmental trauma: Conceptual framework, associated risks and comorbidities, and evaluation and treatment. Front Psychiatry. 2022;13:800687. [PMC free article: PMC9352895] [PubMed: 35935425]

4.

Kessler RC, Aguilar-Gaxiola S, Alonso J, Benjet C, Bromet EJ, Cardoso G, Degenhardt L, de Girolamo G, Dinolova RV, Ferry F, Florescu S, Gureje O, Haro JM, Huang Y, Karam EG, Kawakami N, Lee S, Lepine JP, Levinson D, Navarro-Mateu F, Pennell BE, Piazza M, Posada-Villa J, Scott KM, Stein DJ, Ten Have M, Torres Y, Viana MC, Petukhova MV, Sampson NA, Zaslavsky AM, Koenen KC. Trauma and PTSD in the WHO World Mental Health Surveys. Eur J Psychotraumatol. 2017;8(sup5):1353383. [PMC free article: PMC5632781] [PubMed: 29075426]

5.

Olff M, Langeland W, Gersons BP. The psychobiology of PTSD: coping with trauma. Psychoneuroendocrinology. 2005 Nov;30(10):974-82. [PubMed: 15964146]

6.

Bisson JI, Cosgrove S, Lewis C, Robert NP. Post-traumatic stress disorder. BMJ. 2015 Nov 26;351:h6161. [PMC free article: PMC4663500] [PubMed: 26611143]

7.

Bryant RA. Acute stress disorder as a predictor of posttraumatic stress disorder: a systematic review. J Clin Psychiatry. 2011 Feb;72(2):233-9. [PubMed: 21208593]

8.

Ford JD, Courtois CA. Complex PTSD and borderline personality disorder. Borderline Personal Disord Emot Dysregul. 2021 May 06;8(1):16. [PMC free article: PMC8103648] [PubMed: 33958001]

9.

Ross SL, Sharma-Patel K, Brown EJ, Huntt JS, Chaplin WF. Complex trauma and Trauma-Focused Cognitive-Behavioral Therapy: How do trauma chronicity and PTSD presentation affect treatment outcome? Child Abuse Negl. 2021 Jan;111:104734. [PubMed: 33162104]

10.

Gradus JL, Galea S. Reconsidering the definition of trauma. Lancet Psychiatry. 2022 Aug;9(8):608-609. [PubMed: 35843252]

11.

Kilpatrick DG, Resnick HS, Milanak ME, Miller MW, Keyes KM, Friedman MJ. National estimates of exposure to traumatic events and PTSD prevalence using DSM-IV and DSM-5 criteria. J Trauma Stress. 2013 Oct;26(5):537-47. [PMC free article: PMC4096796] [PubMed: 24151000]

12.

Tolin DF, Foa EB. Sex differences in trauma and posttraumatic stress disorder: a quantitative review of 25 years of research. Psychol Bull. 2006 Nov;132(6):959-92. [PubMed: 17073529]

13.

Assari S. Family Socioeconomic Status and Exposure to Childhood Trauma: Racial Differences. Children (Basel). 2020 Jun 03;7(6) [PMC free article: PMC7346200] [PubMed: 32503310]

14.

Asnaani A, Hall-Clark B. Recent developments in understanding ethnocultural and race differences in trauma exposure and PTSD. Curr Opin Psychol. 2017 Apr;14:96-101. [PubMed: 28813327]

15.

Smidt AM, Platt MG. Sexuality and trauma: Intersections between sexual orientation, sexual functioning, and sexual health and traumatic events. J Trauma Dissociation. 2018 Jul-Sep;19(4):399-402. [PubMed: 29601289]

16.

Brewin CR, Andrews B, Valentine JD. Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol. 2000 Oct;68(5):748-66. [PubMed: 11068961]

17.

Brinkmann L, Buff C, Neumeister P, Tupak SV, Becker MP, Herrmann MJ, Straube T. Dissociation between amygdala and bed nucleus of the stria terminalis during threat anticipation in female post-traumatic stress disorder patients. Hum Brain Mapp. 2017 Apr;38(4):2190-2205. [PMC free article: PMC6866898] [PubMed: 28070973]

18.

Paetzold I, Gugel J, Schick A, Kirtley OJ, Achterhof R, Hagemann N, Hermans KSFM, Hiekkaranta AP, Lecei A, Myin-Germeys I, Reininghaus U. The role of threat anticipation in the development of psychopathology in adolescence: findings from the SIGMA Study. Eur Child Adolesc Psychiatry. 2023 Nov;32(11):2119-2127. [PMC free article: PMC10576675] [PubMed: 35906425]

19.

Pierce ME, Fortier C, Fonda JR, Milberg W, McGlinchey R. Intimate Partner Violence Predicts Posttraumatic Stress Disorder Severity Independent of Early Life and Deployment-Related Trauma in Deployed Men and Women Veterans. J Interpers Violence. 2022 Mar;37(5-6):2659-2680. [PubMed: 32659158]

20.

Oakley LD, Kuo WC, Kowalkowski JA, Park W. Meta-Analysis of Cultural Influences in Trauma Exposure and PTSD Prevalence Rates. J Transcult Nurs. 2021 Jul;32(4):412-424. [PubMed: 33593236]

21.

Sripada RK, Rauch SA, Liberzon I. Psychological Mechanisms of PTSD and Its Treatment. Curr Psychiatry Rep. 2016 Nov;18(11):99. [PubMed: 27671916]

22.

Young J, Schweber A, Sumner JA, Chang BP, Cornelius T, Kronish IM. Impact of prior trauma exposure on the development of PTSD symptoms after suspected acute coronary syndrome. Gen Hosp Psychiatry. 2021 Jan-Feb;68:7-11. [PMC free article: PMC7855440] [PubMed: 33232851]

23.

Horn SR, Feder A. Understanding Resilience and Preventing and Treating PTSD. Harv Rev Psychiatry. 2018 May/Jun;26(3):158-174. [PubMed: 29734229]

24.

Mueser KT, Goodman LB, Trumbetta SL, Rosenberg SD, Osher fC, Vidaver R, Auciello P, Foy DW. Trauma and posttraumatic stress disorder in severe mental illness. J Consult Clin Psychol. 1998 Jun;66(3):493-9. [PubMed: 9642887]

25.

Benjet C, Bromet E, Karam EG, Kessler RC, McLaughlin KA, Ruscio AM, Shahly V, Stein DJ, Petukhova M, Hill E, Alonso J, Atwoli L, Bunting B, Bruffaerts R, Caldas-de-Almeida JM, de Girolamo G, Florescu S, Gureje O, Huang Y, Lepine JP, Kawakami N, Kovess-Masfety V, Medina-Mora ME, Navarro-Mateu F, Piazza M, Posada-Villa J, Scott KM, Shalev A, Slade T, ten Have M, Torres Y, Viana MC, Zarkov Z, Koenen KC. The epidemiology of traumatic event exposure worldwide: results from the World Mental Health Survey Consortium. Psychol Med. 2016 Jan;46(2):327-43. [PMC free article: PMC4869975] [PubMed: 26511595]

26.

Storr CL, Schaeffer CM, Petras H, Ialongo NS, Breslau N. Early childhood behavior trajectories and the likelihood of experiencing a traumatic event and PTSD by young adulthood. Soc Psychiatry Psychiatr Epidemiol. 2009 May;44(5):398-406. [PMC free article: PMC4342112] [PubMed: 19139797]

27.

Norris FH. Epidemiology of trauma: frequency and impact of different potentially traumatic events on different demographic groups. J Consult Clin Psychol. 1992 Jun;60(3):409-18. [PubMed: 1619095]

28.

Wilson J, Jones M, Fear NT, Hull L, Hotopf M, Wessely S, Rona RJ. Is previous psychological health associated with the likelihood of Iraq War deployment? An investigation of the "healthy warrior effect". Am J Epidemiol. 2009 Jun 01;169(11):1362-9. [PubMed: 19363099]

29.

Sayed S, Iacoviello BM, Charney DS. Risk factors for the development of psychopathology following trauma. Curr Psychiatry Rep. 2015 Aug;17(8):612. [PubMed: 26206108]

30.

Ryan AT, Daruwala SE, Perera KU, Lee-Tauler SY, Tucker J, Grammer G, Weaver J, Ghahramanlou-Holloway M. The Relationship between Trauma Exposure and Psychiatric Hospitalization for Suicide Ideation or Suicide Attempt among Patients Admitted to a Military Treatment Setting. Int J Environ Res Public Health. 2020 Apr 15;17(8) [PMC free article: PMC7215778] [PubMed: 32326534]

31.

McCall-Hosenfeld JS, Mukherjee S, Lehman EB. The prevalence and correlates of lifetime psychiatric disorders and trauma exposures in urban and rural settings: results from the national comorbidity survey replication (NCS-R). PLoS One. 2014;9(11):e112416. [PMC free article: PMC4224442] [PubMed: 25380277]

32.

Garfin DR, Thompson RR, Holman EA. Acute stress and subsequent health outcomes: A systematic review. J Psychosom Res. 2018 Sep;112:107-113. [PubMed: 30097129]

33.

Guina J, Nahhas RW, Sutton P, Farnsworth S. The Influence of Trauma Type and Timing on PTSD Symptoms. J Nerv Ment Dis. 2018 Jan;206(1):72-76. [PubMed: 29271827]

34.

Solomon EP, Heide KM. The biology of trauma: implications for treatment. J Interpers Violence. 2005 Jan;20(1):51-60. [PubMed: 15618561]

35.

Bremner JD. Traumatic stress: effects on the brain. Dialogues Clin Neurosci. 2006;8(4):445-61. [PMC free article: PMC3181836] [PubMed: 17290802]

36.

Michopoulos V, Norrholm SD, Stevens JS, Glover EM, Rothbaum BO, Gillespie CF, Schwartz AC, Ressler KJ, Jovanovic T. Dexamethasone facilitates fear extinction and safety discrimination in PTSD: A placebo-controlled, double-blind study. Psychoneuroendocrinology. 2017 Sep;83:65-71. [PMC free article: PMC5524593] [PubMed: 28595089]

37.

Yehuda R, Southwick SM, Krystal JH, Bremner D, Charney DS, Mason JW. Enhanced suppression of cortisol following dexamethasone administration in posttraumatic stress disorder. Am J Psychiatry. 1993 Jan;150(1):83-6. [PubMed: 8417586]

38.

Al Abed AS, Ducourneau EG, Bouarab C, Sellami A, Marighetto A, Desmedt A. Preventing and treating PTSD-like memory by trauma contextualization. Nat Commun. 2020 Aug 24;11(1):4220. [PMC free article: PMC7445258] [PubMed: 32839437]

39.

Gilbertson MW, Shenton ME, Ciszewski A, Kasai K, Lasko NB, Orr SP, Pitman RK. Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nat Neurosci. 2002 Nov;5(11):1242-7. [PMC free article: PMC2819093] [PubMed: 12379862]

40.

Giotakos O. Neurobiology of emotional trauma. Psychiatriki. 2020 Apr-Jun;31(2):162-171. [PubMed: 32840220]

41.

de Araújo Costa Folha OA, Bahia CP, de Aguiar GPS, Herculano AM, Coelho NLG, de Sousa MBC, Shiramizu VKM, de Menezes Galvão AC, de Carvalho WA, Pereira A. Effect of chronic stress during adolescence in prefrontal cortex structure and function. Behav Brain Res. 2017 May 30;326:44-51. [PubMed: 28238824]

42.

Eiland L, Romeo RD. Stress and the developing adolescent brain. Neuroscience. 2013 Sep 26;249:162-71. [PMC free article: PMC3601560] [PubMed: 23123920]

43.

Antonelli-Salgado T, Ramos-Lima LF, Machado CDS, Cassidy RM, Cardoso TA, Kapczinski F, Passos IC. Neuroprogression in post-traumatic stress disorder: a systematic review. Trends Psychiatry Psychother. 2021 Jul-Sep;43(3):167-176. [PMC free article: PMC8638708] [PubMed: 33872477]

44.

Rasmusson AM, Pineles SL. Neurotransmitter, Peptide, and Steroid Hormone Abnormalities in PTSD: Biological Endophenotypes Relevant to Treatment. Curr Psychiatry Rep. 2018 Jul 17;20(7):52. [PubMed: 30019147]

45.

Frueh BC, Knapp RG, Cusack KJ, Grubaugh AL, Sauvageot JA, Cousins VC, Yim E, Robins CS, Monnier J, Hiers TG. Patients' reports of traumatic or harmful experiences within the psychiatric setting. Psychiatr Serv. 2005 Sep;56(9):1123-33. [PubMed: 16148328]

46.

Sartor Z, Kelley L, Laschober R. Posttraumatic Stress Disorder: Evaluation and Treatment. Am Fam Physician. 2023 Mar;107(3):273-281. [PubMed: 36920821]

47.

Carlson EB. Psychometric study of a brief screen for PTSD: assessing the impact of multiple traumatic events. Assessment. 2001 Dec;8(4):431-41. [PubMed: 11785587]

48.

Weathers FW, Bovin MJ, Lee DJ, Sloan DM, Schnurr PP, Kaloupek DG, Keane TM, Marx BP. The Clinician-Administered PTSD Scale for DSM-5 (CAPS-5): Development and initial psychometric evaluation in military veterans. Psychol Assess. 2018 Mar;30(3):383-395. [PMC free article: PMC5805662] [PubMed: 28493729]

49.

Beck JG, Grant DM, Read JP, Clapp JD, Coffey SF, Miller LM, Palyo SA. The impact of event scale-revised: psychometric properties in a sample of motor vehicle accident survivors. J Anxiety Disord. 2008;22(2):187-98. [PMC free article: PMC2259224] [PubMed: 17369016]

50.

Stramrood CA, Huis In 't Veld EM, Van Pampus MG, Berger LW, Vingerhoets AJ, Schultz WC, Van den Berg PP, Van Sonderen EL, Paarlberg KM. Measuring posttraumatic stress following childbirth: a critical evaluation of instruments. J Psychosom Obstet Gynaecol. 2010 Mar;31(1):40-9. [PubMed: 20146642]

51.

Mueser KT, Salyers MP, Rosenberg SD, Ford JD, Fox L, Carty P. Psychometric evaluation of trauma and posttraumatic stress disorder assessments in persons with severe mental illness. Psychol Assess. 2001 Mar;13(1):110-7. [PubMed: 11281032]

52.

Steel JL, Dunlavy AC, Stillman J, Pape HC. Measuring depression and PTSD after trauma: common scales and checklists. Injury. 2011 Mar;42(3):288-300. [PMC free article: PMC3295610] [PubMed: 21216400]

53.

Gillies D, Taylor F, Gray C, O'Brien L, D'Abrew N. Psychological therapies for the treatment of post-traumatic stress disorder in children and adolescents (Review). Evid Based Child Health. 2013 May;8(3):1004-116. [PubMed: 23877914]

54.

Resick PA, Nishith P, Weaver TL, Astin MC, Feuer CA. A comparison of cognitive-processing therapy with prolonged exposure and a waiting condition for the treatment of chronic posttraumatic stress disorder in female rape victims. J Consult Clin Psychol. 2002 Aug;70(4):867-79. [PMC free article: PMC2977927] [PubMed: 12182270]

55.

Foa EB, Dancu CV, Hembree EA, Jaycox LH, Meadows EA, Street GP. A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. J Consult Clin Psychol. 1999 Apr;67(2):194-200. [PubMed: 10224729]

56.

Seidler GH, Wagner FE. Comparing the efficacy of EMDR and trauma-focused cognitive-behavioral therapy in the treatment of PTSD: a meta-analytic study. Psychol Med. 2006 Nov;36(11):1515-22. [PubMed: 16740177]

57.

Levi O, Bar-Haim Y, Kreiss Y, Fruchter E. Cognitive-Behavioural Therapy and Psychodynamic Psychotherapy in the Treatment of Combat-Related Post-Traumatic Stress Disorder: A Comparative Effectiveness Study. Clin Psychol Psychother. 2016 Jul;23(4):298-307. [PubMed: 26189337]

58.

Hendin H. An innovative approach to treating combat veterans with PTSD at risk for suicide. Suicide Life Threat Behav. 2014 Oct;44(5):582-90. [PubMed: 25306917]

59.

Watts BV, Schnurr PP, Mayo L, Young-Xu Y, Weeks WB, Friedman MJ. Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. J Clin Psychiatry. 2013 Jun;74(6):e541-50. [PubMed: 23842024]

60.

Reisman M. PTSD Treatment for Veterans: What's Working, What's New, and What's Next. P T. 2016 Oct;41(10):623-634. [PMC free article: PMC5047000] [PubMed: 27757001]

61.

Asnis GM, Kohn SR, Henderson M, Brown NL. SSRIs versus non-SSRIs in post-traumatic stress disorder: an update with recommendations. Drugs. 2004;64(4):383-404. [PubMed: 14969574]

62.

Ahearn EP, Juergens T, Cordes T, Becker T, Krahn D. A review of atypical antipsychotic medications for posttraumatic stress disorder. Int Clin Psychopharmacol. 2011 Jul;26(4):193-200. [PubMed: 21597381]

63.

Berlant J. Topiramate as a therapy for chronic posttraumatic stress disorder. Psychiatry (Edgmont). 2006 Mar;3(3):40-5. [PMC free article: PMC2990556] [PubMed: 21103163]

64.

Schneier FR, Neria Y, Pavlicova M, Hembree E, Suh EJ, Amsel L, Marshall RD. Combined prolonged exposure therapy and paroxetine for PTSD related to the World Trade Center attack: a randomized controlled trial. Am J Psychiatry. 2012 Jan;169(1):80-8. [PMC free article: PMC3606709] [PubMed: 21908494]

65.

Qi W, Gevonden M, Shalev A. Prevention of Post-Traumatic Stress Disorder After Trauma: Current Evidence and Future Directions. Curr Psychiatry Rep. 2016 Feb;18(2):20. [PMC free article: PMC4723637] [PubMed: 26800995]

66.

Amos T, Stein DJ, Ipser JC. Pharmacological interventions for preventing post-traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2014 Jul 08;2014(7):CD006239. [PMC free article: PMC11064759] [PubMed: 25001071]

67.

Reiff CM, Richman EE, Nemeroff CB, Carpenter LL, Widge AS, Rodriguez CI, Kalin NH, McDonald WM., the Work Group on Biomarkers and Novel Treatments, a Division of the American Psychiatric Association Council of Research. Psychedelics and Psychedelic-Assisted Psychotherapy. Am J Psychiatry. 2020 May 01;177(5):391-410. [PubMed: 32098487]

68.

Barbano AC, van der Mei WF, deRoon-Cassini TA, Grauer E, Lowe SR, Matsuoka YJ, O'Donnell M, Olff M, Qi W, Ratanatharathorn A, Schnyder U, Seedat S, Kessler RC, Koenen KC, Shalev AY., International Consortium to Prevent PTSD. Differentiating PTSD from anxiety and depression: Lessons from the ICD-11 PTSD diagnostic criteria. Depress Anxiety. 2019 Jun;36(6):490-498. [PMC free article: PMC6548615] [PubMed: 30681235]

69.

Biederman J, Petty CR, Spencer TJ, Woodworth KY, Bhide P, Zhu J, Faraone SV. Examining the nature of the comorbidity between pediatric attention deficit/hyperactivity disorder and post-traumatic stress disorder. Acta Psychiatr Scand. 2013 Jul;128(1):78-87. [PMC free article: PMC3527641] [PubMed: 22985097]

70.

Malhi P, Bharti B. Traumatic Stress or ADHD? Making a Case for Trauma Informed Care in Pediatric Practice. Indian J Pediatr. 2021 Mar;88(3):287. [PubMed: 33095396]

71.

Williamson JB, Jaffee MS, Jorge RE. Posttraumatic Stress Disorder and Anxiety-Related Conditions. Continuum (Minneap Minn). 2021 Dec 01;27(6):1738-1763. [PubMed: 34881734]

72.

Bailey T, Alvarez-Jimenez M, Garcia-Sanchez AM, Hulbert C, Barlow E, Bendall S. Childhood Trauma Is Associated With Severity of Hallucinations and Delusions in Psychotic Disorders: A Systematic Review and Meta-Analysis. Schizophr Bull. 2018 Aug 20;44(5):1111-1122. [PMC free article: PMC6101549] [PubMed: 29301025]

73.

Berry K, Ford S, Jellicoe-Jones L, Haddock G. PTSD symptoms associated with the experiences of psychosis and hospitalisation: a review of the literature. Clin Psychol Rev. 2013 Jun;33(4):526-38. [PubMed: 23500156]

74.

Cyr G, Godbout N, Cloitre M, Bélanger C. Distinguishing Among Symptoms of Posttraumatic Stress Disorder, Complex Posttraumatic Stress Disorder, and Borderline Personality Disorder in a Community Sample of Women. J Trauma Stress. 2022 Feb;35(1):186-196. [PubMed: 34374135]

75.

Lawson DM, Quinn J. Complex trauma in children and adolescents: evidence-based practice in clinical settings. J Clin Psychol. 2013 May;69(5):497-509. [PubMed: 23564579]

76.

Brier ZMF, Connor J, Legrand AC, Price M. Different trajectories of PTSD symptoms during the acute post-trauma period. J Psychiatr Res. 2020 Dec;131:127-131. [PMC free article: PMC7676876] [PubMed: 32961502]

77.

Bedi US, Arora R. Cardiovascular manifestations of posttraumatic stress disorder. J Natl Med Assoc. 2007 Jun;99(6):642-9. [PMC free article: PMC2574374] [PubMed: 17595933]

78.

D'Andrea W, Sharma R, Zelechoski AD, Spinazzola J. Physical health problems after single trauma exposure: when stress takes root in the body. J Am Psychiatr Nurses Assoc. 2011 Nov-Dec;17(6):378-92. [PubMed: 22142975]

79.

Sacchi L, Merzhvynska M, Augsburger M. Effects of cumulative trauma load on long-term trajectories of life satisfaction and health in a population-based study. BMC Public Health. 2020 Oct 27;20(1):1612. [PMC free article: PMC7590721] [PubMed: 33109171]

80.

Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edwards V, Koss MP, Marks JS. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. Am J Prev Med. 1998 May;14(4):245-58. [PubMed: 9635069]

81.

Larson S, Chapman S, Spetz J, Brindis CD. Chronic Childhood Trauma, Mental Health, Academic Achievement, and School-Based Health Center Mental Health Services. J Sch Health. 2017 Sep;87(9):675-686. [PubMed: 28766317]

82.

Davydow DS, Katon WJ, Zatzick DF. Psychiatric morbidity and functional impairments in survivors of burns, traumatic injuries, and ICU stays for other critical illnesses: a review of the literature. Int Rev Psychiatry. 2009 Dec;21(6):531-8. [PMC free article: PMC2857565] [PubMed: 19919206]

83.

Jacobsen LK, Southwick SM, Kosten TR. Substance use disorders in patients with posttraumatic stress disorder: a review of the literature. Am J Psychiatry. 2001 Aug;158(8):1184-90. [PubMed: 11481147]

84.

Medjkane F, Notredame CE, Sharkey L, D'Hondt F, Vaiva G, Jardri R. Association between childhood trauma and multimodal early-onset hallucinations. Br J Psychiatry. 2020 Mar;216(3):156-158. [PMC free article: PMC7557870] [PubMed: 31902385]

85.

Freeman D, Fowler D. Routes to psychotic symptoms: trauma, anxiety and psychosis-like experiences. Psychiatry Res. 2009 Sep 30;169(2):107-12. [PMC free article: PMC2748122] [PubMed: 19700201]

86.

Varghese L, Emerson A. Trauma-informed care in the primary care setting: An evolutionary analysis. J Am Assoc Nurse Pract. 2022 Mar 01;34(3):465-473. [PubMed: 34618717]

87.

Bryan CJ, Clemans TA, Hernandez AM, Mintz J, Peterson AL, Yarvis JS, Resick PA., STRONG STAR Consortium. EVALUATING POTENTIAL IATROGENIC SUICIDE RISK IN TRAUMA-FOCUSED GROUP COGNITIVE BEHAVIORAL THERAPY FOR THE TREATMENT OF PTSD IN ACTIVE DUTY MILITARY PERSONNEL. Depress Anxiety. 2016 Jun;33(6):549-57. [PubMed: 26636426]

88.

Richter-Levin G, Sandi C. Title: "Labels Matter: Is it stress or is it Trauma?". Transl Psychiatry. 2021 Jul 10;11(1):385. [PMC free article: PMC8272714] [PubMed: 34247187]

89.

Fiske E, Reed Ashcraft K, Hege A, Harmon K. An Interprofessional Course on Trauma-Informed Care. 2021 Jul-Aug 01Nurse Educ. 46(4):E50-E54. [PubMed: 33234832]

90.

Petrie M, Zatzick D. Collaborative care interventions in general trauma patients. Oral Maxillofac Surg Clin North Am. 2010 May;22(2):261-7. [PMC free article: PMC2858047] [PubMed: 20403558]

Disclosure: Joshua Feriante declares no relevant financial relationships with ineligible companies.

Disclosure: Naveen Sharma declares no relevant financial relationships with ineligible companies.