Acute and Chronic Mental Health Trauma

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](A1)

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](A1)

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](A1)

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] (A1)

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.