023 - Pediatric Trauma and Stress - Part 2 - Developmental Perspectives

This is the second of a three-part series on pediatric trauma, delveing into the epidemiology and underlying mechanisms of trauma-related disorders in children and adolescents. Dr. O'Leary discusses what might increase risk of developing PTSD after trauma. The discussion also explores the neurobiological impact of trauma, detailing how it can dysregulate the hypothalamic-pituitary axis, alter neurotransmitter systems, and affect crucial brain regions like the amygdala, hippocampus, and prefrontal cortex. The episode highlights the profound effects of early deprivation on attachment disorders and outlines the diverse manifestations of trauma across various developmental stages, from infancy through adolescence, underscoring the importance of considering age-specific presentations and potential regressions when assessing affected youth.

Referenced resources can be found within the show transcripts at https://psydactic_caps.buzzsprout.com

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This is not medical advice. Please see a licensed physician for any personal questions regarding your own or your child's health.

Transcript

The following is a script and outline used to create this episode.  The audio episode may or may not contain all of this content or additional content not listed here.

Welcome to PsyDactic Child and Adolescent Psychiatry Edition.  I am your host Dr. O’Leary, a fellow in Child and Adolescent Psychiatry in the National Capital region.  I started this podcast feed to help me study for my board exams and I hope it helps you as well, but anyone interested in human development or mental health may enjoy this content.  I need to let you know that everything that I say here should be considered to be my own opinion even if I am quoting or referencing someone or some institution.  Additionally, I have been learning how to use A.I. to assist me with the content creation and research.  Specifically, for this episode I used Gemini’s Deep Research tool to produce a detailed overview of Pediatric Trauma and Stressor Related Disorders and then consolidated that information into a podcast script that includes my own content merged with the A.I. content.  I use my own background knowledge as well as spot checking of the facts to make sure that the A.I. isn’t just making stuff up.  Like humans, A.I. makes mistakes, but I have found it more and more to be at least or even more reliable than human produced content.

This is part 2 of a 3 part series on Trauma and Stressor related disorders in the pediatric population.  Part one was focused on the diagnosis of things like PTSD, Acute Stress Disorder, Reactive Attachment Disorder, and Disinhibited Social Engagement disorders.  I also briefly discussed Adjustment Disorder.  In this episode, I’m going to touch briefly on the epidemiology of these disorders with particular attention on PTSD in children, and then I am going to discuss the kinds of things that might cause, or predispose or perpetuate these disorders.  In the next episode, I will talk about treatment.

Let’s get started with some epidemiology…

III. Epidemiology of Pediatric Trauma- and Stressor-Related Disorders

The epidemiology of pediatric TSRDs is shaped by the prevalence of trauma exposure and a complex interplay of risk and protective factors that influence a child's response to such adversities.

A. Prevalence and Incidence of Child Trauma Exposure

A significant portion of children, 26% in the U.S., witness or experience a traumatic event before reaching the age of 4.5 More broadly, it's estimated that two-thirds of children report experiencing at least one traumatic event by the time they turn 16 6, and some data suggest that 71% of children have been exposed to one or more victimization incidents in the past year alone.34  Exposure to multiple types of traumatic events is also a significant concern, with 40% of children and youth in the National Child Traumatic Stress Network (NCTSN) having experienced four or more distinct types of traumatic events.5 This high rate of polyvictimization underscores the complex traumatic histories many children carry.

B. Epidemiology of PTSD in Children

While a large number of children are exposed to trauma, a smaller but substantial percentage go on to develop PTSD. Overall, about 16% of trauma-exposed youth may develop PTSD, with higher rates following interpersonal traumas (approximately 25%) compared to non-interpersonal traumatic events (almost 10%).12 This significantly higher risk following interpersonal trauma, such as assault or abuse, suggests that the human element of betrayal, violation, or intentional harm may be a particularly potent factor in the development of PTSD. This could be due to its profound impact on core beliefs about safety, trust, and the nature of relationships, and treatment approaches for these children should address these.

Consistent with findings for adults, girls are more likely than boys to develop PTSD following trauma exposure.33 Comorbidity is exceptionally high in pediatric PTSD; approximately 80% of children and adolescents with PTSD meet criteria for at least one other mental disorder, most commonly depressive disorders, other anxiety disorders, bipolar disorders, or substance use disorders.3 This high level of comorbidity complicates diagnostic assessment, requiring comprehensive evaluation beyond the presenting trauma symptoms, and necessitates integrated treatment planning that can address multiple conditions, either sequentially or concurrently. It also implies shared underlying vulnerabilities or suggests that the presence of one disorder may create a fertile ground for the development of another.

C-D. I am not going to deeply discuss the epidemiology of acute stress disorder or adjustment disorder because I don’t think these numbers are very reliable or helpful for a clinician to know.  Statistically, the current population prevalence of acute stress disorder is likely much lower than that of PTSD because PTSD is chronic and Acute Stress Disorder converts to PTSD after 1 month.  The lifetime incidence, though, of acute stress disorder is likely much higher than PTSD because AcStDr generally precedes PTSD, except in those with a delayed onset, and it doesn’t necessarily develop into PTSD.

With regard to Adjustment disorder, in my experience it is vastly under-diagnosed because, even though it can have a profound impact on someones life, insurance complanies generally won’t pay to treat it.  Therefore, instead of adjustment disorder with depressed mood or adjustment disorder with anxiety, etc, patients are more likely to get a major depressive disorder or generalized anxiety disorder diagnosis, because this is something the clinician or inpatient unit can use to justify billing for services that the person needs.

E. Epidemiology of Reactive Attachment Disorder (RAD) in Children

RAD is considered a rare disorder in the general pediatric population, with prevalence estimates typically <2%.37 However, its prevalence is higher in specific high-risk populations. For example, among children in foster care or those raised in institutional settings, rates are substantially elevated.25 One report indicated that 42% of children removed from their homes and placed in alternative care settings met DSM-IV criteria for some form of behavioral health disorder, and this population at high risk for any number of unnamed attachment disturbances.38

The core etiological factor for RAD is a history of pathogenic care, including persistent social neglect, lack of basic emotional needs being met, repeated changes of primary caregivers that prevent stable attachments, or rearing in unusual settings like institutions with high child-to-caregiver ratios.23 

While gender, race and ethnicity are not considered direct risk factors for RAD in themselves, socioeconomic factors that disproportionately affect on racial, ethnic, or gender are associated with RAD. Concordance rates for RAD among siblings raised in the same neglectful home environment are reported to be high, around ⅔ to ¾.38 The age of children experiencing severe neglect is also a factor; a high percentage of children who die due to abuse or neglect are younger than 4 years old, and many children entering the foster care system are under the age of 5 38, a critical period for attachment formation. The profound impact of neglect is underscored by its position as the most commonly reported form of child maltreatment 33, forming the specific etiological basis for RAD. This emphasizes that the absence of essential caregiving inputs can be profoundly damaging to socio-emotional development… and the same is true for RAD’s sibling diagnosis: DSED.

F. Epidemiology of Disinhibited Social Engagement Disorder (DSED) in Children

Similar to RAD, the exact prevalence of DSED in the general population is unknown but is thought to be low. One UK population-based study estimated a prevalence of just under 1% (0.72%).41 However, in high-risk populations, such as children with histories of institutional rearing or multiple foster care placements, prevalence is significantly higher, with estimates around 20%.42 DSED is consistently linked to early experiences of severe social neglect or deprivation, including insufficient caregiving that limits opportunities for children to form selective attachments.28 Signs of DSED are consistently identified in children currently or formerly in foster care and those raised in institutions.45

G. Risk and Protective Factors (General for TSRDs)

The development of TSRDs in children is influenced by a complex interplay of risk and protective factors spanning pre-traumatic, peri-traumatic, and post-traumatic periods.47

• Risk Factors:
• Pre-traumatic factors include child characteristics such as female gender (associated with higher risk for PTSD and ASD) 19, younger age at the time of trauma 30, a history of prior trauma exposure 19, and pre-existing mental health conditions like anxiety or depression.3 Cognitive factors like intellectual disability 19, and familial/environmental factors such as family dysfunction or stress 35, low socioeconomic status 46, minority status or experiences of discrimination 30, and a genetic predisposition or family history of mental illness also increase vulnerability.8
• Peri-traumatic factors relate to the nature of the traumatic event itself, including its severity and intensity.33 Interpersonal violence (e.g., assault, abuse) carries a particularly high risk.12 The child's subjective perception of life threat during the event is also a significant predictor, though this can be challenging to assess accurately in very young children.51
• Post-traumatic factors include the psychosocial environment following the trauma. A lack of parental or social support 33, negative or unsupportive parental reactions to the child's trauma 33, the child's use of unhealthy coping strategies (e.g., thought suppression, distraction, blaming others) 46, negative appraisals of the trauma or its consequences 46, and the development of Acute Stress Disorder (which is a strong predictor of later PTSD) 46 all increase the risk of persistent TSRDs.
• Protective Factors:
• Conversely, several factors can buffer the impact of trauma and promote resilience. Strong parental and family support, coupled with positive family functioning, are crucial protective elements.33 Secure attachment relationships with caregivers provide a foundation of safety and support.47 Individual child characteristics such as a positive self-image, good self-control, and social competence can enhance coping.47 A strong sense of agency or internal locus of control are also beneficial.47 Furthermore, access to supportive learning environments, positive peer relationships, and timely access to appropriate care and support services can mitigate the long-term negative effects of trauma.47

A social-ecological framework, as described by Urie Bronfenbrenner and others, is useful for conceptualizing these interacting influences, highlighting how factors at the individual, family, school, community, and societal levels collectively shape a child's risk and resilience in the face of trauma.47 I don’t have the time to get into that today, but it is broadly relevant to child pathology and I encourage you to Google Bronfenbrenner.

IV. Pathophysiology and Neurobiology of Pediatric Trauma- and Stressor-Related Disorders

The pathophysiological mechanisms underlying pediatric TSRDs have been hypothesized to result from a complex interplay of neuroendocrine, neurochemical, and neuroanatomical factors, particularly in response to overwhelming stress or severe early environmental deprivation. The timing of such adverse exposures is, over course, critical, because sensitive periods in brain development can render a child more vulnerable to lasting neurobiological changes.8

A. PTSD

PTSD is characterized by enduring changes in stress-response systems and brain circuits involved in threat processing, memory, and emotion regulation.8

• Hypothalamic-Pituitary-Adrenal (HPA) Axis Dysregulation: The initial physiological response to trauma includes a surge of catecholamines (e.g., adrenaline aka epinephrine) via sympathetic nervous system activation and the release of cortisol from the HPA axis.15 Chronic or repeated trauma can lead to persistent HPA axis dysregulation.8 In children, this often manifests as HPA axis upregulation, characterized by elevated baseline cortisol levels and greater cortisol reactivity to subsequent stressors.8 Conversely, a pattern of HPA axis downregulation, with lower baseline cortisol and blunted stress reactivity, can emerge, typically during adolescence. This shift may represent some kind of compensatory mechanism or possibly an "exhaustion" of the stress response system after prolonged upregulation.8 In either case, the system is not in allostatis, which means it is not predicting well the needs of the individual given cues in the environment.  Persistently elevated corticotropin-releasing hormone (CRH), a key HPA axis regulator, can also overstimulate the sympathetic nervous system, contributing to hyperarousal symptoms.51
• Neurotransmitter Alterations: Several neurotransmitter systems are implicated. Re-experiencing symptoms, such as intrusive memories, may be linked to dysregulation in the serotonin system, potentially through a classical conditioning model where trauma-related cues trigger memories.51 Disturbances in norepinephrine, dopamine, and GABA have been associated with nightmares.51 Avoidance and numbing symptoms, including anhedonia, might relate to dopamine deficiency or overactivation of the endogenous opioid system.51 The brain's catecholamine systems (norepinephrine, dopamine, epinephrine), crucial for the "fight, flight, or freeze" response, are acutely activated during trauma; prolonged or repeated activation can alter central nervous system development and contribute to a "dysregulated" or poorly regulated brainstem, leading to symptoms like emotional lability, impulsivity, anxiety, excessive risk taking, heightened startle response, and sleep abnormalities.9
• Brain Structure and Function: Key brain regions consistently implicated in PTSD include the hippocampus, prefrontal cortex (PFC), and amygdala.8
• The amygdala, among many other jobs, is a center of threat detection and fear processing, often exhibits hyper-responsivity to threat-related cues in individuals with PTSD.8
• The hippocampus, crucial for memory formation, consolidation, and contextualizing fear memories, can be adversely affected by chronic stress and elevated glucocorticoids. This leads to reduced neurogenesis and impaired neuroplasticity.8 While hippocampal atrophy is a common finding in adult PTSD, this is less consistently observed in children. Instead, children with trauma exposure may exhibit smaller overall brain volumes.55
• The PFC is vital for executive functions, emotion regulation, and the top-down inhibition of fear responses. Trauma can impair PFC development and function, weakening its connectivity with and ability to modify activity in the amygdala and hippocampus, thereby diminishing its capacity to regulate fear and emotional reactivity.8 Functional imaging studies in adults with PTSD often show hypoactivity in the frontal cortex.19
• Other general neurodevelopmental consequences of trauma can include reduced brain growth factors, delayed myelination, abnormalities in synaptic pruning, inhibited neurogenesis, and increased apoptosis (programmed cell death).51 Maltreated youth have been found to have smaller cerebral and cerebellar volumes compared to non-maltreated peers.51
• Genetic and Epigenetic Factors: There is growing evidence for gene-environment interactions in PTSD. Polymorphisms in genes such as FKBP5 (which regulates glucocorticoid receptor sensitivity) have been shown to interact with early life maltreatment to predict the likelihood of developing PTSD symptoms in adulthood.8 Furthermore, trauma exposure can induce epigenetic modifications, such as DNA methylation, in stress-related genes like FKBP5. These epigenetic changes can lead to long-term alterations in the body's stress response systems and neuronal circuits, thereby increasing vulnerability to PTSD.8 Epigenetic changes can even be passed from generation to generation, change gene expression without changing the DNA sequence.

B. Reactive Attachment Disorder (RAD)

The pathophysiology of RAD is generally understood through the lens of attachment theory and the profound impact of severe early environmental deprivation on the development of the attachment behavioral system.23 The core etiological factor is pathogenic care, characterized by social neglect or a consistent lack of opportunity to form stable, selective attachments with caregivers during critical early developmental periods.23 This absence of consistent, responsive, and nurturing caregiving deprives the infant of the expected environmental input necessary for the expected development of the attachment system. As a consequence, affected infants may cease attempts to engage with caregivers for comfort or support and exhibit a pattern of emotional withdrawal and avoidance of physical or emotional closeness.38

Pioneering observational studies, such as those by René Spitz in the mid-20th century, documented the devastating effects of severe maternal deprivation in institutionalized infants, including profound developmental regression, failure to thrive, emotional blunting, and even increased mortality.38 Spitz coined the term "hospitalism" to describe the severe developmental delays and high mortality rates observed in infants raised in institutions lacking adequate social interaction and nurturing, despite receiving basic care. Spitz also identified "anaclitic depression" as a syndrome of grief, apathy, and developmental decline in infants experiencing partial emotional deprivation, particularly separation from a primary caregiver.

These findings highlighted the critical need for consistent emotional interaction and mental stimulation for healthy development. While specific neurobiological markers uniquely linked to RAD are still under investigation, research on children exposed to early institutional deprivation (a primary risk factor for RAD) has shown alterations such as reductions in overall brain volume, including both gray and white matter.28 These findings suggest that severe early neglect can have tangible impacts on brain structure, which likely contribute to the observed attachment disturbances.

C. Disinhibited Social Engagement Disorder (DSED)

Like RAD, DSED arises from a background of severe early social neglect or deprivation that limits a child's opportunities to form selective attachments.25 However, instead of the emotional withdrawal characteristic of RAD, DSED manifests as a pattern of indiscriminate sociability and a lack of appropriate reticence with unfamiliar adults.25 This divergence in behavioral presentation, despite a shared etiology of pathogenic care, suggests that early neglect does not have a monolithic neurobiological outcome. It may be that different children, perhaps due to subtle genetic predispositions (some research suggests genetic factors, including polymorphisms in the Williams syndrome critical region, may interact with care quality to influence DSED likelihood 51) or variations in the nature or timing of the neglectful environment, develop different maladaptive coping strategies that become ingrained as distinct neurobehavioral patterns.

Neurobiological research in children exposed to early deprivation (the population at highest risk for DSED) has identified findings such as reductions in gray and white matter volumes 28 and potential disruptions in connectivity between the amygdala and prefrontal cortex.28 Such alterations could contribute to impaired social judgment, difficulties in regulating social behavior, and a diminished ability to differentiate between familiar caregivers and strangers, which are hallmarks of DSED.

D. Common Neurobiological Pathways and Alterations

Despite the distinct clinical presentations of the various TSRDs, many share common underlying neurobiological vulnerabilities related to how the developing brain responds to severe stress and adversity. These common pathways often involve 8:

• HPA Axis Dysregulation: As discussed, chronic stress from trauma or neglect frequently leads to dysregulation of cortisol and CRH secretion, impacting multiple bodily systems and brain development.8
• Amygdala Hyper-reactivity: The amygdala is often hyper-responsive to threat cues in trauma-exposed individuals, contributing to heightened fear, anxiety, and vigilance.8
• Hippocampal Impairment: The hippocampus, crucial for memory consolidation and contextualizing experiences, can have its development and function impaired by chronic stress and elevated glucocorticoids. This affects the processing of fear memories and the ability to discriminate safe from unsafe contexts.8
• Prefrontal Cortex (PFC) Dysfunction: The PFC, involved in executive functions and top-down regulation of emotion and fear, can also be adversely affected by early trauma. This may result in weakened PFC ability to modulate amygdala activity and regulate emotional responses.8
• Neurotransmitter Imbalances: Key neurotransmitter systems, including serotonin, norepinephrine, and dopamine, are consistently implicated in the stress response and the regulation of mood and anxiety. Dysregulation in these systems is common across various TSRDs.9
• Structural Brain Changes: Early adversity can lead to more global structural changes, such as reduced overall brain volume, altered white and gray matter development, and impaired connectivity between key brain regions involved in emotion processing and regulation.8

These shared neurobiological alterations underscore that while the specific manifestation of a TSRD may vary, the underlying impact of severe stress on core brain systems for threat processing, memory, and emotional regulation is a common theme.

V. Impact of Trauma, Stress, Abuse, and Neglect on Child Development

Exposure to trauma, stress, abuse, and neglect during childhood can have pervasive and detrimental effects on a child's developmental trajectory, impacting physical, cognitive, emotional, and social domains. The nature and severity of these impacts often vary depending on the child's developmental stage at the time of exposure, the type and chronicity of the trauma, and the availability of protective factors.10 It is crucial to recognize that trauma's effects are not merely psychological "symptoms" but can fundamentally alter the course of development itself.

A. Effects on Infant Development (0-2 years)

Infancy is a period of profound vulnerability due to rapid brain development and complete dependence on caregivers for survival and regulation.10 Trauma during this stage can disrupt the very foundations of development.10

• Brain Development: Traumatic experiences can lead to measurable changes in brain architecture, including potentially smaller brain size, a reduction in neural connections, decreased myelination (which is crucial for efficient neural communication), and altered patterns of brain activity.61 Early relational experiences, or their absence, shape neural pathways far into the future.61 Therefore trauma and neglect disrupt the development of foundational neural capacities for self-regulation and secure attachment.10
• Physical Development: Infants exposed to trauma or severe neglect may exhibit failure to thrive, digestive problems, sleep disturbances (frequent nightmares, difficulty falling asleep), feeding difficulties, and low weight, and even death.58
• Cognitive and Language Development: Progress in cognitive and language milestones may be slowed, and in some cases, there can be a loss of previously acquired developmental achievements, such as early vocalizations or simple words.62
• Emotional Development: Traumatized infants are often irritable, fussy, and easily startled. They may be difficult to soothe and show an inability to self-soothe.62
• Behavioral Manifestations: Common behaviors include persistent and inconsolable crying or tantrums, a reluctance to explore their environment, and sometimes aggression directed towards themselves or others.62
• Social and Attachment: A profound impact in infancy is the development of attachment. Traumatized infants may exhibit fear of separation from caregivers (excessive clinginess) or, conversely, disengagement from previously trusted adults. They may avoid eye contact or physical touch and fail to seek comfort when hurt or frightened, hindering the formation of secure attachment bonds.10

B. Effects on Early Childhood Development (3-5 years)

During the preschool years, children continue to develop rapidly in cognitive, emotional, and social domains. Trauma can significantly impede this progress.55

• Brain Development: The adverse effects on brain structure and function initiated in infancy can continue or become more pronounced.55
• Physical Health: Sleep disturbances, frequent nightmares, and fluctuations in appetite and weight are common.62 Somatic complaints without clear medical cause may also emerge.
• Cognitive and Language Development: Preschoolers may experience difficulties with concentration, focus, and learning new skills. There can be a loss of previously mastered skills, such as potty training or more complex speech. A pervasive difficulty in trusting others may also develop.62
• Emotional Development: Trauma can lead to a lack of self-confidence, persistent fear, anxiety, sadness, and irritability. Children at this age may struggle to verbalize their emotions or regulate their emotional states effectively.62
• Behavioral Manifestations: Temper tantrums may be frequent and intense. Aggressive behaviors such as hitting, kicking, or biting can occur. Children might scream or cry excessively. A notable sign is the reenactment of traumatic events through play, which may be repetitive and involve violent or sexual themes if those were part of the trauma.59 They may also exhibit hypervigilance, being constantly on guard, and show regressive behaviors like bedwetting or thumb-sucking. Clinginess or, conversely, withdrawal from caregivers can be observed.59
• Social and Attachment: Making friends can become difficult, and children may withdraw from social interactions or exhibit overly bossy or controlling behavior with peers. An extreme fear of punishment, leading to excessive compliance or attempts to run away, can also be a sign.62

C. Effects on Middle Childhood Development (6-12 years)

School-aged children have more developed cognitive and verbal skills, but trauma can still profoundly affect their functioning, particularly in academic and social spheres.62

• Physical Health: Frequent unexplained physical symptoms such as headaches and stomachaches are common.62 Children may overreact to minor injuries or show significant changes in eating habits.
• Cognitive Functioning: Difficulties with attention, concentration, and memory are prevalent, often leading to academic problems and declining grades.62 Executive functioning skills, such as planning and organization, may be diminished.11 An inability to trust others can persist or worsen.
• Emotional Experience: Children may exhibit increased anger, social withdrawal, feelings of loneliness, and a preoccupation with fears that something bad will happen or with themes of death and dying.55 Symptoms of anxiety and depression are common.
• Behavioral Problems: Difficulty transitioning between activities, increased fighting with peers or adults, and a general increase in activity level can be observed. Early experimentation with drugs or alcohol may begin in later middle childhood. A notable lack of enjoyment in previously pleasurable activities is common. Some children may display sexual knowledge or behaviors beyond their age, or engage in self-injurious behaviors like picking scabs or pulling hair or more recently, cutting has been increasing. Regression to behaviors seen in younger children (e.g., thumb-sucking, bedwetting, fear of the dark) is a significant indicator of distress.62
• Social and Attachment: Difficulties with social boundaries, making and keeping friends, and problems with authority figures at school or home are frequent.62 Some may show a persistent fear of separation from parents, while others may fail to seek help from adults when needed.

A common theme across developmental stages, including middle childhood, is the potential for regression to behaviors characteristic of earlier developmental phases.59 This reversion, such as a school-aged child resuming thumb-sucking or experiencing enuresis, can be understood as a coping mechanism where the child retreats to a period perceived as safer or less demanding under the weight of overwhelming stress.

D. Effects on Adolescent Development (13-18 years)

Adolescence is a critical period for identity formation, increasing independence, and significant brain maturation, particularly in the prefrontal cortex which governs executive functions. Trauma during these years can disrupt these processes, often leading to high-risk behaviors and other mental health disorders, including dissociative disorders and psychosis.62 This stage represents a second crucial window of brain development where the impact of trauma can be particularly complex and severe.

• Brain Development: Ongoing development of the prefrontal cortex can be adversely affected by trauma, leading to impairments in decision-making, impulse control, and emotion regulation.64 The brain may adapt by strengthening neural pathways associated with fear and anxiety while relatively weakening those involved in logic or critical thinking.65
• Physical Health: Eating disorders or disordered eating patterns, significant sleep disturbances (insomnia or hypersomnia), recurrent nightmares, and dissociative experiences ("spacing out") are reported.62 Some adolescents may make drastic and sudden changes to their physical appearance (e.g., hair, piercings, tattoos, or gender expression).62
• Cognitive Functioning: Symptoms can include hyperactivity, distractibility, and inattention, sometimes mimicking ADHD. Feelings of helplessness, poor self-esteem, negative self-talk, and an overly self-reliant or conversely overly-dependent stance may develop.62 Trauma can lead to a pervasive distrust of others and significant alterations in how the adolescent views the world, themselves, and their future, often shattering previously held belief systems.62
• Emotional Experience: Intense emotions such as shame, embarrassment, depression, and anxiety are common.62 Feelings of alienation, loneliness, and hopelessness can be profound. Flashbacks and panic attacks may occur. Hormonal changes during adolescence can interact with trauma-induced alterations in neurochemistry (e.g., serotonin production), potentially increasing irritability and low moods.65
• Behavioral Problems: A wide range of problematic behaviors can emerge, including food hoarding, substance abuse (alcohol and drugs), suicidal ideation and attempts, and non-suicidal self-injury (e.g., cutting, burning).62 Adolescents may run away from home, engage in unsafe sexual behaviors, exhibit aggression, or become involved in the juvenile justice system. School absenteeism, declining academic performance, and dropping out of school are also significant concerns.62
• Social and Attachment: Trauma can lead to significant difficulties in relating to peers and forming healthy romantic relationships. Adolescents may be more susceptible to negative peer influences or develop unhealthy relationship patterns. Maintaining relationships can be challenging, and some may exhibit problematic sexual behaviors.62

E. Differential Impact of Abuse vs. Neglect

While all forms of child maltreatment are harmful and can cause trauma, the specific nature of the maltreatment—whether it involves acts of commission (abuse) or acts of omission (neglect)—may lead to somewhat different, though often overlapping, developmental sequelae and risk profiles for specific disorders.11 It is increasingly recognized that the absence of essential developmental inputs (neglect) can be as profoundly damaging as the presence of harmful experiences (abuse).51

• Neglect: This is the most commonly reported form of child maltreatment.6 It involves the failure to provide for a child's basic needs, including physical (food, shelter, hygiene), emotional (affection, comfort, support), medical, or educational needs. Research has linked neglect to an increased risk for medical conditions such as diabetes, poorer lung functioning, and vision and oral health problems in the long term.11 
• Abuse: This involves acts that cause or risk serious harm to a child.
• Physical abuse has been linked to an increased risk for diabetes and malnutrition.11
• Emotional abuse (e.g., verbal assaults, terrorizing, isolating) is associated with an increased risk for personality disorders and schizophrenia.67
• Sexual abuse has been linked to a higher likelihood of experiencing hallucinations, among other severe mental health outcomes.67

This distinction is important because it suggests that different types of adverse experiences may differentially impact developing brain systems and psychological functions, requiring tailored prevention and intervention efforts.

F. Clinical Presentation Variations by Developmental Stage

The way children manifest symptoms of trauma- and stressor-related disorders varies significantly with their age and developmental level.60 Clinicians must be adept at recognizing these age-specific presentations to avoid misdiagnosis, such as confusing trauma symptoms with ADHD or oppositional defiant disorder.68

• Infants and Toddlers (0-3 years): Trauma is often expressed through non-verbal cues, changes in physiological regulation (feeding, sleeping), developmental regressions (loss of acquired skills), and disruptions in attachment behaviors (e.g., excessive clinginess, withdrawal, or failure to seek comfort).62
• Preschoolers (3-5 years): May exhibit trauma through play reenactment (often repetitive and literal), behavioral regressions (e.g., enuresis, thumb-sucking), heightened fears, aggression, irritability, and difficulty verbalizing their experiences or emotions.59 For PTSD specifically, preschoolers often show constricted play, social withdrawal, and restricted positive affect, with less emphasis on verbalized cognitive distortions or elaborate avoidance strategies seen in older children.51
• School-Age Children (6-12 years): Somatic complaints (headaches, stomachaches) are common. Academic difficulties, peer relationship problems, and a mix of internalizing (anxiety, depression, withdrawal) and externalizing (aggression, defiance) behaviors may be evident.62 PTSD symptoms may include more clearly defined intrusive thoughts or images, more deliberate avoidance, and cognitive distortions such as distorted blame or loss of interest in activities.51
• Adolescents (13-18 years): Manifestations can be more complex, often involving risk-taking behaviors (substance use, unsafe sex), self-harm, prominent mood swings, identity issues, and more elaborate cognitive appraisals of the trauma and its meaning.62 They may exhibit symptoms similar to adult presentations of PTSD but within the context of ongoing developmental challenges related to autonomy, peer relationships, and future orientation.

G. Table: Impact of Trauma on Child Development Across Stages

 | Developmental Stage | Physical Development | Cognitive Development | Emotional Development | Social Development
| Infants (0-2 years)62 | Failure to thrive, sleep/feeding issues, digestive problems, low weight. | Delays in milestones, loss of acquired skills (e.g., speech), impaired early brain architecture. 61 | Irritability, easily startled, difficulty being soothed, limited positive affect, fearfulness. | Impaired attachment, fear of separation or withdrawal, avoidance of eye contact/touch, disinterest in social interaction.
| Early Childhood (3-5 years)59 | Sleep disturbances (nightmares), appetite changes, regression (e.g., enuresis). | Difficulty concentrating/learning, loss of mastered skills (speech, potty training), developmental delays, distrust. | Lack of self-confidence, fear, anxiety, sadness, irritability, difficulty verbalizing/managing emotions, emotional numbing. | Difficulty with peers, withdrawal or aggression, overly bossy/controlling, clinginess, play reenactment of trauma.
| Middle Childhood (6-12 years)62 | Headaches, stomachaches, somatic complaints, appetite/sleep changes, overreaction to pain. | Attention/memory problems, academic decline, learning difficulties, impaired executive function. 11 | Anger, withdrawal, loneliness, anxiety, depression, fear of recurrence, preoccupation with death, guilt, shame. | Difficulty with friendships/authority, poor boundaries, social withdrawal, acting out, regression to younger behaviors.
| Adolescence (13-18 years)62 | Eating disorders, sleep problems (insomnia/hypersomnia), nightmares, dissociation, fatigue, risk-taking leading to injury. | Inattention, distractibility, poor self-esteem, negative cognitions (self/world), altered beliefs, memory problems. | Shame, guilt, depression, anxiety, panic attacks, flashbacks, emotional lability, irritability, hopelessness, alienation. | Impaired peer/romantic relationships, social withdrawal, substance use, delinquency, unsafe sexual behavior, defiance.

VI. Etiological Theories and Longitudinal Evolution of Pediatric Trauma- and Stressor-Related Disorders

I want to discuss some of the etiological perspectives that have been used to understand trauma.  Few of these are mutually exclusive of the others.  Instead, they provide us with narratives, metaphors, and possible ways we can intervene in order to reduce the burden of trauma and adverse experiences on youth.

A. Neurobiological Models of Trauma Development

I previously discussed neurobiological perspectives, so I won’t repeat that here.

B. Attachment Theory and its Role in RAD and DSED

I have also already mentioned attachment.  Attachment theory, pioneered by John Bowlby and Mary Ainsworth, and posits that a secure attachment bond, formed through consistent, sensitive, and responsive interactions with a primary caregiver, is foundational for a child's healthy emotional, social, and cognitive development.9 This bond provides a "secure base" from which the child can explore the world and a "safe haven" to return to in times of distress.

C. Learning Theories and Conditioned Responses in PTSD and ASD

Learning theories, particularly principles of classical and operant conditioning, provide a valuable framework for understanding the acquisition and maintenance of certain symptoms in PTSD and ASD.15

• Classical Conditioning: Mowrer's two-factor theory, for example, suggests that fear is acquired through classical conditioning. The traumatic event (an unconditioned stimulus, UCS) which naturally elicits intense fear (an unconditioned response, UCR) becomes paired with neutral environmental cues or internal sensations (conditioned stimuli, CS) present during the trauma. Subsequently, these CSs alone can trigger the fear response (now a conditioned response, CR), leading to intrusive memories, flashbacks, and physiological reactivity when encountering trauma reminders.15
• Operant Conditioning: Avoidance behaviors, a core feature of PTSD and ASD, are thought to be maintained through operant conditioning, specifically negative reinforcement. When an individual avoids trauma-related thoughts, feelings, or external reminders, they experience a temporary reduction in anxiety or distress. This relief reinforces the avoidance behavior, making it more likely to occur in the future, even if it is maladaptive in the long term by preventing emotional processing and extinction of the fear response.

These learning mechanisms help explain why symptoms like intrusive recollections and avoidance can persist long after the traumatic event has ended.

D. Social-Ecological Models

Social-ecological models, such as Bronfenbrenner's ecological systems theory, emphasize that child development and responses to trauma occur within a complex, nested set of interacting environmental systems.47 These systems range from the most proximal to the most distal:

• Individual: Includes the child's genetic predispositions, temperament, age, gender, and existing coping skills.
• Microsystem: The immediate environments where the child directly interacts, such as family, school, peers, and childcare settings.
• Mesosystem: The interconnections between different microsystems (e.g., the relationship between home and school).
• Exosystem: Social settings that indirectly affect the child, such as the parents' workplace, community resources, and social services.
• Macrosystem: The broader cultural values, societal norms, laws, and political and economic systems.
• Chronosystem: The dimension of time, reflecting how these systems and their interactions change over the child's life course and in response to historical events.

This kind of thinking really helps to inform things like public policy, the design of our educational systems, even the design of our infrastructure to promote community engagement.  Within this framework, risk factors (e.g., poverty, community violence, parental psychopathology) and protective factors (e.g., supportive family relationships, access to quality education, positive peer groups) exist at each level and interact to influence a child's vulnerability and resilience following trauma.47 For example, strong family support (microsystem) can buffer the negative effects of community violence (exosystem). Disruptions or stressors in one system can have cascading effects on others.48 These models encourage a holistic understanding of trauma, moving beyond individual psychopathology to consider the broader environmental and societal contexts that shape a child's experience and recovery.

E. Developmental Psychopathology Perspective

The developmental psychopathology perspective integrates principles from developmental science and clinical psychology to understand the origins and course of maladaptive behavior and psychopathology across the lifespan.10 It views trauma not as a static event but as a significant risk factor that can divert a child's developmental trajectory, particularly when it occurs during sensitive periods of brain and psychological development.10

This perspective emphasizes the dynamic interplay between risk factors (like trauma exposure) and protective factors (like supportive relationships or strong coping skills) over time.71 It recognizes that psychopathology is often an initially adaptive response to an adverse or atypical environment that becomes maladaptive when it persists beyond the context of the adversity or is generalized to new, non-threatening situations.51 For example, hypervigilance might be adaptive in an abusive home but becomes problematic in a safe school environment. Developmental psychopathology also highlights equifinality (multiple pathways can lead to the same outcome - this can also be called degeneracy of causation); and then there is multifinality (a single risk factor can lead to multiple different outcomes), underscoring the heterogeneity in children's responses to trauma.

G. Longitudinal Trajectories and Evolution of Disorders Over Time

Longitudinal research is crucial for understanding the natural course of pediatric TSRDs, identifying different developmental pathways following trauma, and informing the timing and targets of interventions. Such studies reveal considerable heterogeneity in how these disorders evolve.12

• PTSD: While many children and adolescents show a reduction in PTSD symptoms within the first 1 to 6 months post-trauma, a significant subset experiences persistent symptoms, and some researchers express doubt about substantial further natural recovery after 6 months without targeted treatment.12 Longitudinal studies have identified several distinct PTSD trajectories. For example, a four-year study of children following the Wenchuan earthquake identified three primary trajectories: a resilient trajectory (74.9% of the sample), characterized by consistently low and stable PTSD symptoms over time; a recovery trajectory (7.5%), marked by high initial symptom levels that gradually decreased to a normal range; and a relapsing trajectory (17.7%), where children showed initial improvement followed by a later recurrence or worsening of symptoms.74 Other studies have also identified chronic (persistently high symptoms) and delayed-onset trajectories. Factors such as initial PTSD severity, exposure to subsequent major life stressors, and the level of ongoing support can influence which trajectory a child follows.74 The identification of these varied pathways challenges a "one-size-fits-all" prognostic view and highlights the need for ongoing monitoring and tailored interventions.
• DSED: Signs of DSED can be remarkably persistent, often continuing from early childhood into adolescence and, for some, into early adulthood, particularly for children who experienced prolonged institutional care or were placed into family environments at older ages.41 The Bucharest Early Intervention Project (BEIP) demonstrated that children placed in high-quality foster care showed a sharper decline in DSED signs compared to those who remained in institutional care ("care as usual").43 Person-centered analyses from BEIP identified four DSED profiles over time: elevated (persistently high signs), persistent modest (moderate, stable signs), early decreasing (initial signs that diminished), and minimal (consistently low signs). Histories of more adverse care (e.g., longer institutionalization, more placement disruptions) were associated with the elevated and persistent modest profiles.43
• RAD: Compared to DSED, RAD symptoms often show a more favorable response to placement in an adequate and stable caregiving environment. The provision of a sensitive and responsive attachment figure can lead to significant improvement or resolution of RAD symptoms.25 Findings from the BEIP also indicated that foster care placement was effective in reducing signs of RAD.75
• General Evolution: Without effective treatment, PTSD can become a chronic condition with substantial negative impacts on long-term psychosocial development and functioning into adulthood.12 Similarly, Adjustment Disorders in youth, if unaddressed, can sometimes evolve into more severe or persistent psychiatric illnesses.36 This underscores the importance of early identification and intervention for all pediatric TSRDs to alter potentially negative long-term trajectories.

The integration of these varied etiological perspectives—from molecular GxE interactions to broad social-ecological contexts, viewed through a developmental lens and informed by longitudinal data—provides a progressively more nuanced understanding of how pediatric TSRDs develop and evolve.

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