This document presents a developmental psychopathology model for understanding childhood traumatic stress and its intersection with anxiety disorders over the lifespan. The model incorporates a tripartite etiology of post-trauma distress involving child-intrinsic factors, developmental experiences, and environmental influences. It recognizes the complex interplay between trauma exposure, reminders, secondary stresses, and developmental stages in shaping proximal and long-term outcomes. A key aspect is how appraisal and response to danger evolves throughout childhood, which impacts trauma responses. The model provides a framework for investigating interactions between trauma, psychopathology, and disturbances in acquiring competencies over the life course.

1. A Developmental Psychopathology Model
of Childhood Traumatic Stress and Intersection with
Anxiety Disorders
Robert S. Pynoos, Alan M. Steinberg, and John C. Piacentini
Empirical findings regarding childhood traumatic stress
are placed within a developmental life-trajectory model
that incorporates a tripartite etiology of posttrauma dis-
tress. This approach recognizes an intricate matrix of
child-intrinsic factors, developmental maturation and ex-
perience, life events, and evolving family and social
ecologies. Of central developmental importance in the
field of traumatic stress is the ontogenesis of appraisal,
emotional response, emotional and physiological regula-
tion, and consideration of protective action with regard to
danger. The complexity of traumatic situations and their
aftermath suggests the relevance of multiple stress diathe-
ses in understanding individual variability in proximal
and distal effects. Neurobiological systems that subserve
danger mature over childhood and adolescence. Neuro-
physiological and neurohormonal studies among trauma-
tized children and adolescents suggest potential neurode-
velopmental stage-related vulnerabilities within these
systems. Advances in child development and traumatic
stress provide tools for investigating proximal and distal
interplay of psychopathology, disturbances in the acqui-
sition and maintenance of developmental competencies,
and life-trajectory outcomes. A developmental psychopa-
thology model suggests different avenues by which dan-
gerous circumstances, childhood traumatic experiences,
and posttraumatic stress disorder (PTSD) can intersect
with other anxiety disorders over the life span. Biol
Psychiatry 1999;46:1542–1554 © 1999 Society of Biolog-
ical Psychiatry
Key Words: Developmental psychopathology, PTSD,
child trauma, anxiety
Introduction
Danger, trauma, fear and anxiety are embedded in the
human condition. There is a wide spectrum of ap-
praisal, response, and adaptation to danger within the
lifecycle of the individual, family, group, and society. A
developmental psychopathology approach recognizes the
intricate matrix of intrinsic factors, developmental matu-
ration and experience, life events, and evolving familial
and social ecologies that contribute to proximal and distal
outcomes. A developmental psychopathology framework
recognizes the intimate theoretical relationship between
adaptive and maladaptive outcomes and between pathol-
ogy and normality (Cicchetti and Cohen 1995). Figure 1
presents an updated developmental life-trajectory schema
(Pynoos et al 1995; Steinberg and Ritzmann 1990), orga-
nizing selected current clinical and research knowledge
about childhood traumatic stress.
This schema indicates that there are multiple sources of
acute posttrauma distress, falling into three major categories.
Whereas the contribution of traumatic experience(s) has been
well recognized, both associated proximal secondary adver-
sities and proximal trauma and loss reminders introduce
additional stress diathesis. Aspects of the appraisal and
response to danger and resistance and vulnerability mediate
acute distress. Resilience refers to early effective efforts at
adjustment and recovery. A developmental psychopathology
model places equal importance on proximal development,
proximal psychopathology, and their interactions as out-
comes of early adjustment. Ongoing adjustment takes place
in an interactive matrix encompassing distal trauma remind-
ers, distal secondary stresses, distal development and distal
pathology. Child-intrinsic factors and the ecology of the child
operate throughout the schema. This model suggests a revi-
sion of the acute-chronic typology to a more developmentally
sound approach. Repeated or sequential traumatic experi-
ences should be analyzed in regard to emerging developmen-
tal contexts. These contexts generate new sources of trau-
matic distress, situation-specific reminders, secondary
stresses, and new efforts at adjustment, which carry addi-
tional implications at each occurrence for acquisition of
developmental competencies and prolongation or new onset
of psychopathology.
Advances in the developmental epidemiology of traumatic
stress support the adoption of such a complex developmental
perspective. This literature points to several important con-
From the Trauma Psychiatry Service and Child and Adolescent OCD and Anxiety
Disorders Program, Department of Psychiatry and Biobehavioral Sciences,
University of California at Los Angeles.
Address reprint requests to Robert S. Pynoos, UCLA, Ste. 2235, 300 Medical Plaza,
Department of Psychiatry, Los Angeles, CA 90024.
Received March 31, 1999; revised August 30, 1999; accepted September 24, 1999.
© 1999 Society of Biological Psychiatry 0006-3223/99/$20.00
PII S0006-3223(99)00262-0

2. siderations. First, by using refined typologies of exposure,
there is evidence of differential exposure rates through the
course of childhood and adolescence. Age, sex, and child-
intrinsic factors interact with evolving ecologies of the
family, school, peer group, community, and society. Second,
careful review of rates of exposure across age groups sug-
gests that children or adolescents may experience a highly
variable series of exposures occurring at different develop-
mental periods (Boney-McCoy and Finkelhor 1995). Third,
studies of the impact of different forms of exposure are
becoming more interdependent as we document, for exam-
ple, the interaction of extrafamilial and intrafamilial violence,
and their respective environments of chronic danger and
pathogenic family disturbance (Foy et al 1996; Lynch and
Cicchetti 1998).
Traumatic Stress
Empirical studies among acutely traumatized school-age
children and adolescents have found that their traumatic
experiences involve complex sensory, physiological, emo-
tional, and cognitive experiences of multiple moments
with different vantage points of concern (Pynoos et al
1997a).
There may be different moments and types of phys-
iological alarm and serial or simultaneous onset of
extreme negative emotions, as well as frightening ac-
celerations in physiological and emotional reactions.
Emotional reactions can range from terror over the
external danger, to extreme helplessness over failure of
protective action, to extreme shame over loss of bodily
function. Cognitions can include sudden shifts in alert-
ness and attention; radical challenges to expectancy
sets; extreme uncertainty about event parameters, in-
cluding confusions and misappraisals; attributions of
intent, responsibility, and efficacy of actions by self or
others; and catastrophic intraevent cognitions regarding
personal consequence. Witnessing of threat to signifi-
cant others may be accompanied by suppression of
one’s fear for self and unalleviated empathic distress,
whereas immediate threat or injury to a child may
engender moments of estrangement. Radical shifts in
attention may occur after injury or sexual violation,
away from vigilance to external threat toward concern
for the extent and personal consequences of injury or
violation.
Children often experience the alarm and fear expres-
sions, agitated behavior, cries of distress, and ineffective
or potentially endangering behavior of adult caretakers.
They may witness mutilating injuries and grotesque death
of family members and friends, experiencing horror and
acute grief reactions, even while the threat to the child
continues. There may also be intense worry about the
well-being of a significant other whose whereabouts or
safety are unknown. After the cessation of threat, addi-
tional traumatic moments can include efforts to assist the
injured, emergency medical procedures and surgery,
abrupt separations from family members, and reunion with
agitated or terrified parents or school personnel.
Appraisal and Response to Danger
This theoretical framework assigns a prominent role to the
ontogenesis of human appraisal, reaction, and response to
danger. A modern approach to the theory of anxiety must
recognize three interrelated mental operations: 1) estima-
tion of the nature and magnitude of external and internal
dangers, 2) emotional and physiological reaction and their
regulation, and 3) estimation of the type, degree, and
efficacy of protective intervention. These operations are
strongly rooted in neurobiological development, experien-
tial history, and, for children in particular, availability of
and reliance on adults as auxiliary agents with regard to
danger and tolerance of anxiety. Over time, these basic
processes become modified or rigidified, related to sec-
ondary reappraisals, secondary efforts at regulating re-
newed or new emotional and physiological reactions, and
reconsideration, planning, and enactment of preventive
and protective intervention for the future.
Early life corresponds to a period when contextual
estimation of danger and protective intervention rests with
parent(s) or caretakers. The infant is equipped with alarm
reactions, relatively uninhibited defensive mechanisms,
and evolved care-eliciting behaviors. Ontogenesis of am-
bulatory exploratory behavior in toddlers coincides with
increasing maturation of the hippocampus and orbitofron-
tal cortex that relates to spatial mapping and contextual
discrimination. The early stages of appraisal of danger rely
on social referencing to attachment figures (Klinnert et al
1983) and an amygdala-related capacity for recognizing
facial expression of emotion. The preschool child responds
to limited natural clues that elicit fearful responses, relies
on a protective shield provided by others, and utilizes
emerging catastrophic emotions that enable him or her to
act more self-protectively against threats of bodily injury.
Preschool children begin to consciously include safety of
parents in their schemas of danger and their own self-
protection. School age children develop an increasing
appreciation of dangerous circumstances, envision more
self-efficacy (with conscious themes of courage and cow-
ardliness), are engaged in skill and safety training, and
experience a sense of culpability and ineffectualness when
protective action fails. By midadolescence, there is pre-
dominant reliance on self and peer appraisal of threat,
motivation, consequence, and protection, with accompa-
nying struggles over decisions to directly intervene and
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3. themes of hero and antihero. Throughout these stages of
development, false alarms, under-estimations of danger,
and narrow escapes are mediated by child-parent interac-
tions. Major parent-child transitions that occur over these
periods include renegotiations of risk parameters and
authority over decision making.
Emotional and physiological responses not only serve to
warn of external danger or initiate protective action, but also
may constitute a perceived internal threat. Children often
report becoming frightened by the intensity, acceleration, and
duration of alarm reactions, physiological arousal, somatic
sensations, and extreme negative emotions, for example, a
7-year-old child who says, “My heart was beating so fast I
thought it was going to break.” Disturbing bodily sensations
associated with traumatic experiences can lead to enduring
responses to trauma reminders due to interoceptive condi-
tioning (Craske 1997), for example, a 10-year-old boy’s
renewed nausea at olfactory reminders of witnessing his
mother’s rape. The metacognition of emotions, the
emergence of self-conscious negative emotions, and an
increased motivational understanding add new dimen-
sions to the appraisal of threat over childhood and
adolescence (Saarni and Harris 1991).
Secondary appraisals, emotional and physiological reg-
ulation, and considerations of prevention and protective
intervention extend over years and are typically highly
interactional social processes in childhood (Fivush 1991).
They rely on co-construction and assistance from parents,
siblings, school personnel, and peers; new information;
and subsequent experience. Appropriate assistance can
facilitate recovery from failed developmental expectan-
cies, readdressing issues of accountability and integrating
the complex experience into veridical memory represen-
tations for use in future appraisals and response to danger.
In humans, there is a long developmental delay in
achieving inhibitory modulation of some basic defensive
mechanisms. For example, it takes approximately 8 years
for children to reach mature prepulse inhibition of the
startle reflex, passing through a preschool period during
which there is instead an exaggerated prepulse facilitation
Figure 1. Developmental psychopathology model of childhood traumatic stress.
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4. (Pynoos et al 1997b). At this age, we have found that
children begin to actively entertain thoughts of personally
addressing, disarming, or directly harming the source of
danger. This is in contrast to the preschool child’s inter-
vention thoughts of escaping from danger and searching
for external protection.
Proximal Trauma and Loss Reminders
Trauma reminders derive from trauma-specific features of
the child’s experience. They are ubiquitous in the after-
math of trauma. Because of the complexity of a traumatic
experience and its occurrence in a natural setting, there
may be a large number of cues, whose previous more
neutral or even positive associations are now superseded
by associations with the traumatic experience(s). There
may be widely different patterns of frequency among
types of reminders, ranging from relatively infrequent to
daily, with diminished or increased recurrence over the life
span, depending on alterations in family circumstances
and social ecology, and future developmental transitions.
The media may serve as an unrecognized source of trauma
reminders (Nader et al 1993). Compounding posttrauma
distress, there may be an additional set of loss reminders
that evoke a different range of negative emotions, includ-
ing extreme sadness, anger over the loss, separation
anxieties, and worries about the future.
Psychological and physiological reactivity to reminders
contributes to the periodic or phasic nature of renewed
traumatic anxiety and avoidant behavior and, perhaps, to a
transition from phasic to tonic physiological arousal. The
unexpected nature and often-unrecognized occurrence of
reminders may reevoke a sense of unpreparedness and
lack of control. Features of one-trial aversive learning
(Garcia et al 1986), fear-conditioning (Armony and Le-
Doux 1997), and context-related anxiety (Davis et al 1997)
have been proposed to explain different mechanisms
underlying the longevity, fear, and anxiety-provoking
Figure 1. Continued.
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5. nature of reminders. These paradigms point to different
aspects of the response, corresponding to extreme cata-
strophic expectancies (in regard to naturalistic dangers and
noxious physical states), bouts of fear, and chronic appre-
hensions over recurrence and associated dangers. Our
report demonstrating time-dependent sensitization of the
acoustic startle reflex, bidirectional abnormal behavior in
a fear-provoking environment, and dysregulation of ag-
gression in mice after weekly exposures to a situational
reminder (Pynoos et al 1996) indicates the powerful
multidimensional impact of reminders.
Proximal Secondary Stresses
There is a striking increase in risk of psychiatric disorder
among children associated with accumulation of adverse
life events (Tiet et al 1998). Traumatic events are com-
monly associated with a cascade of secondary stresses.
They constitute additional sources of distress and increase
the risk of comorbidity of posttraumatic stress reactions
with other adverse reactions. They complicate efforts at
adjustment and may interfere with normal opportunities
for developmental maturation, or initiate maladaptive
coping responses that, over time, may be associated with
chronic psychopathology other than posttraumatic stress
disorder (PTSD). Secondary adversities or stresses may
substantially interfere with the availability of support to
the child from parents, family, school, and community.
Parental loss is associated with risk of impaired care-
taking, disruption of the school community is associated
with lost educational opportunities, and community disor-
ganization and unemployment are associated with in-
creases in intrafamilial violence, parental substance abuse,
and juvenile delinquency (Pynoos et al 1998).
Distress
Distress is the acute subjective registration of the effects of a
traumatic experience or reactivity to reminders and chal-
lenges of secondary stresses. There is compelling evidence
that by school age, children experience the full range of acute
posttraumatic stress and grief reactions (for review see
Pfefferbaum 1997). In addition, posttrauma distress may
include fears of recurrence, guilt and shame, ongoing worries
about a significant other, and reactivation of posttraumatic
reactions associated with previous adverse life experiences.
Distress encompasses 1) the registration of personal conse-
quences, 2) causal attributions to self and other (including
introduction of fear into a primary attachment relationship),
and 3) failure of developmental expectancies arising from
physical helplessness at moments of irreversible harm, of
social referencing of catastrophic emotions to prevent injury,
and of beliefs in a socially modulated world.
Resistance, Vulnerability, Resilience,
and Adjustment
This schema discriminates between resistance and resilience,
concepts that are often confused in the child stress literature.
Resistance may entail positive or negative mental health
attributes that check the production of acute posttrauma
reactions. For example, a lack of empathy related to conduct
disorder when witnessing the distress of others may be
protective. Resilience, on the other hand, refers to the
capacity to respond to different levels of distress with
effective efforts at recovery. Resistance and vulnerability
factors mediate or moderate the impact of trauma, proximal
reminders, and proximal secondary stresses on the type and
severity of acute posttrauma distress. Different aspects of
child-intrinsic factors may mediate the impact of these three
components. The strength and reliance on affiliative attach-
ment represent a critical developmental vulnerability in
childhood to witnessing threat or harm to a parent or family
member, to being without parental protection, or to being the
victim of a violent betrayal of affiliative expectancies when
the parent is the agent of the trauma. In young children, there
is also vulnerability to fear acquisition by witnessing parental
response during the event or upon reunion. Temperament and
anxiety sensitivity may be especially relevant with regard to
trauma reminders, including reactivity, attributions of con-
trollability, catastrophizing of bodily sensations, cognitive
discrimination, ability to calm down, or capacity to be
comforted by efforts at safety improvements or parental
reassurances. Intrinsic factors that mediate childhood stress in
general are particularly relevant with regard to secondary
adversities (Rutter 1985). These include a positive relation-
ship with a competent adult, skill at learning and problem
solving, engaging personality, competence and perceived
efficacy by self or society, high IQ score, positive school
experience, mastery motivation, and previous successful
coping experiences (Masten et al 1990).
With regard to child-extrinsic factors, different aspects of
parent behavior and family, school, and social ecology may
moderate each of the three components (Pynoos et al, in
press). In situations of imminent danger, parental overreac-
tion, uncertainty, or conflict may exacerbate children’s anx-
iety over appropriate protective action. Adult or parental
decisions that result in separation of children from parents
can measurably increase children’s posttrauma distress. Re-
sponding to the distress of a traumatized child requires
parental skills, for example, to address reactivity to reminders
and behavioral regressions. Parental responsiveness can be
mediated by parent-intrinsic factors, especially anxiety sen-
sitivity, prior trauma and loss experiences, and reactivity to
reminders. Maternal trauma-related avoidance and overt
parental anxious responses to trauma reminders and fears of
recurrence increase young children’s posttrauma distress.
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6. Variations in parental proactive interventions, such as secur-
ing a bookcase that fell in the child’s room during an
earthquake, can be critical to alleviate a child’s ongoing
apprehensions and sleep disturbance.
Adjustment refers to the child’s ability to tolerate, manage,
or alleviate ongoing psychological, physiological, behavioral,
and developmental disturbances. Effective adjustment in-
cludes the achievement of adequate understanding of the
experience and subsequent reactions and, as two outcome
measures, resumption of age-related developmental progres-
sion and acquisition of developmental competencies, as well
as recovery from traumatic-stress-related symptoms. We
would emphasize the importance to adjustment of veridical
reappraisals of danger, renewed efforts at emotional and
physiological regulation, and evolving thoughts and plans of
future protective intervention.
Several elements of these adjustment processes rely on the
maturation of key neurobiological mechanisms. Animal stud-
ies suggest that decreased conditioned-fear responses rely on
active new learning to achieve conditioned inhibition and
modulation of contextual reactivity. Such new learning is, in
part, governed by evolving functions of the prefrontal cortex
that permit more complex stimulus representation and greater
capacity for stimulus analysis (Armory and LeDoux 1997). A
recent report suggests that fear conditioning and escape
behavior may operate through different anatomical pathways
within the amygdala (Amorapanth et al 1999), introducing
considerations of the role of maturing capacities for protec-
tive intervention in mediating ongoing emotional regulation
and reactivity to reminders. Considerations of protective
intervention rely on maturing capacities for information
processing and motor behavior. As pointed out by Korn and
Faber (1996), escape behaviors have short latencies, which
leave minimal time for complex treatment of sensory infor-
mation and analysis of environmental parameters, paralleling
the preschool child’s limited use of appraisal and consider-
ation of intervention other than escape.
Parents can play a critical role in facilitating the use of
more advanced cognitive strategies in children’s future
review of past traumatic experiences. Alternatively, par-
ents may contribute to disruption of this process because
of their own anxious preoccupations or, at the extreme, by
misleading explanations or a conspiracy of silence. The
adjustment and recovery in adolescence may rely much
more critically on opportunities provided by parents and
society for constructive means to address their interven-
tion preoccupations, including career opportunities.
Proximal Psychopathology
Figure 1 includes a list of the range of child and adolescent
psychiatric disorders that have been reported after trau-
matic exposures and loss. ICD 10 includes an attachment
disorder secondary to intrafamilial abuse and violence
(World Health Organization 1990). There is a dose of
exposure association in which the severity of traumatic
exposure is strongly correlated with the risk for PTSD
(Foy et al 1996; Goenjian et al 1995), with preexisting
anxiety increasing the severity of PTSD within exposure
groups (La Greca et al 1998). Continuous ratings rather
than categorical diagnosis have proven to be more sensi-
tive to dose of exposure relationships and in identifying
mediating and moderating factors. Subjective appraisal of
threat to self and others, intensity of internal arousal, and
appropriateness of behavior of self and others further
contribute to risk. There is also evidence of an additive
effect of multiple and multimodal exposures to violence
among adolescents (Kilpatrick et al 1995). There is evi-
dence of an interplay of PTSD and grief in childhood,
leading to complicated bereavement, identified as a risk
factor among adults for psychiatric and physical morbidity
(Prigerson et al 1997). Bereavement carries its own
independent risks of subsequent depression and anxiety.
Multiple stress diatheses following traumatic experi-
ences are needed to understand the prevalence of psychi-
atric comorbidity. High rates of comorbid PTSD and
depression have been found among preadolescents and
adolescents after catastrophic natural or transportation
disasters and violence (Goenjian et al 1995; Yule and
Udwin 1991). Brent et al (1996) demonstrated that after
adolescent peer suicide, risk of depression among friends
is most associated with a family or personal history of
depression, while PTSD, the incidence of which increased
over the 3-year follow-up, is associated with features of
exposure to the suicide. Our studies after the earthquake in
Armenia found a dose of exposure-related chronic sepa-
ration anxiety disorder among a significant percentage
(7.4%) of early adolescent youth (Goenjian et al 1995), an
age group where this disorder is quite uncommon. Studies
of the contribution of trauma-specific features, prior ex-
periences, and anxiety sensitivity to the persistence of
separation anxiety or new-onset anxiety disorders, espe-
cially phobias, are needed.
Proximal Development
Proximal development encompasses the achievement of
proximal developmental tasks that contribute to the onto-
genesis of developmental competencies (Cicchetti 1989),
successful navigation of interpersonal and intrafamilial
developmental transitions (Rutter 1988), and normal bio-
logical maturation. Recently acquired developmental
achievements are particularly vulnerable to disruption
(Rutter 1988), including periods of relative neurobiologi-
cal cortical restructuring and neurophysiological consoli-
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7. dation (Pynoos et al 1997b). Selected aspects of proximal
development are highlighted below.
There can be general effects on allocation of attentional
resources and selective impact on age-related cognitive
developmental tasks. Selective attention can be skewed
toward trauma-related new information or incident-spe-
cific new fears (Yule et al 1992). Early childhood con-
frontations with violence can interfere with preschool
achievement of narrative coherence (Osofsky 1993). Sleep
disturbances may interfere with daytime learning (Pynoos
et al 1987) and potentially with sleep-related consolidation
of learning. Sleep disturbances associated with child
physical abuse appear to persist over many years (Clod et
al 1997). Specific interference with learning may have
quite different proximal developmental impact, with the
marginal student at greatest academic risk (Yule and
Udwin 1991) and school failure increasing the risk of
secondary psychiatric morbidity.
The generation of multiple intense negative emotions can
challenge maturing mechanisms of emotional regulation,
including the preschool task of increasing differentiation of
basic emotions, school-age elaboration on affective expres-
sion, and adolescent efforts to achieve a more sophisticated
understanding of the origins and consequences of negative
emotions (Saarni and Harris 1991). In adolescence, trauma-
related negative self-attributions and painful emotions may
contribute to excessive concerns about social evaluation and
social avoidance. Dysregulation of aggression and hostile
emotions, including revenge, can disrupt the maturing capac-
ity for restraint of aggression, appropriate use of instrumental
aggression, and assertiveness (Atkins et al 1993). Autono-
mous strivings may be subverted by trauma-related avoid-
ance, leading to lost developmental opportunities, or be
accelerated by trauma-generated adventuresome pursuits that
lie beyond the child or adolescent’s developmental capabili-
ties. The latter may increase risk of subsequent traumatic
exposures. Changes in future expectancies and perceived
narrowing of developmental opportunities can adversely
effect adolescent emerging ambition, initiative, and
motivation.
Critical parent-child transitions can be accelerated or
impeded, as, for example, the chronic separation among
the Armenian adolescents is likely to interfere with their
age-appropriate adjustment in the balance of independence
and dependence. Posttrauma irritable, anxious, avoidant,
or withdrawn behavior, physical disability or disfigure-
ment, and preoccupation with trauma-related material may
profoundly affect current peer interactions. Peer rejection,
in part mediated by school milieu, carries its own inde-
pendent risk for disturbed social adjustment and subse-
quent psychopathology (Asher and Coie 1992).
A recent study of the dimension of moral development
illustrates the inherent opposition of constructive and
detrimental contributions of massive trauma in adoles-
cence. After the Armenia earthquake, adolescents mani-
fested an acceleration in their understanding of morality
and communal values, and increased empathic understand-
ing and depth of pride and remorse over moral behavior.
At the same time, these adolescents demonstrated pro-
found disturbances in conscience functioning, including
loss of moral willpower and negative moral expectancies
of self, other, and social institutions (Goenjian et al 1999).
The investigation of the developmental neurobiology of
traumatic stress is in its infancy, with only a few isolated
studies among children. The interpretation of findings will
need to placed in the context of three broad areas of
neurodevelopment: 1) maturation of brain structures, 2)
functional physiological correlates, and 3) associated ma-
turing cognition, emotional regulation, and behavioral
responses (Pynoos et al 1997b). Studies of early childhood
maltreatment, especially physical abuse and neglect
(Galvin et al 1997; Perry et al 1995; Teicher et al 1997)
have focused on early alterations in structure of brain
regions and modification of neurotransmitter systems,
such as catecholamine systems, that are functional early in
life and may have trophic effects on brain development.
Quantitative EEG findings of increased left hemispheric
coherence and MRI findings of volumetric reduction in the
corpus collosum (Teicher et al 1997) raise questions about
the effects of early abuse on cortical differentiation and
lateralization. Perry et al (1995) have proposed that
childhood trauma, by differentially effecting maturation of
brain subsystems, through use-dependent modifications,
sets these subsystems’ relative contributions to future
appraisal and response to danger.
Studies that have examined the effects of school-age
and preadolescent trauma have begun to document neuro-
hormonal and neurophysiological alterations. De Bellis et
al (1994) found low basal and CRF-stimulated ACTH
levels among sexually abused girls. Goenjian et al (1996)
reported low basal cortisols and hypersuppression after
dexamethasone among adolescent survivors of the Arme-
nian earthquake. Perry et al (1995) have reported post-
trauma bidirectional autonomic changes, primarily in heart
rate. Tachycardia appears to be most related to witnessing
and direct threat without physical violation, while lowered
heart rate is associated with sexual abuse, physical pene-
tration, and dissociative phenomena. Ornitz and Pynoos
(1989) found a significantly reduced level of normal
prepulse inhibition of startle response among school-aged
children exposed to catastrophic violence. We are cur-
rently evaluating the influence of trauma-related alter-
ations in startle modulation on information processing, an
investigation that needs to consider the complex develop-
mental course of endogenous event-related potentials (Py-
noos et al 1997b).
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8. These findings point to a number of critical questions in
the developmental neurobiology of traumatic stress. Do
danger-related changes in neurotransmitters have a neuro-
trophic influence on cortical development in infancy and
early childhood? How, when, and by what means do
phasic autonomic reactions become more tonic? Are
volumetric changes in brain regions attributable to a
stress-related “toxicity” or to diminishment in trophic
factors, such as stress-related changes in BDNF mRNA
activity (Rasmusson and Charney 1997)? To what extent
do neurohormonal alterations represent vulnerability to
adapation to danger, trauma, and other life stresses? Our
preliminary startle modulation studies raise the issue of
varying impacts of traumatic exposures during periods of
relative neural plasticity or consolidation, including the
possibility of neurophysiological regression, in addition to
lack of maturation. Furthermore, the slow developmental
progression in the acquisition of startle modulation under-
scores the prolonged neurodevelopmental maturation and
vulnerability of major inhibitory pathways that relate to
the human capacity to appraise and respond to danger.
Distal Development
Prospective longitudinal studies tracking the distal devel-
opmental outcome of child and adolescent traumatic ex-
periences have yet to appear. One important personality
axis affected by trauma is that of fear, courage, and
fearlessness (Rachman 1980). The child literature includes
reports of oscillations toward each of the extremes among
severely traumatized children (Gislason and Call 1982).
The incorporation of shifts on this axis into character can
result in enduring personality traits, including chronic
fearfulness, compulsive heroism, or under reactivity to
high-risk situations.
Traumatic experiences can skew expectancies about the
world, the safety and security of interpersonal life, and
forecasts about the future. Such expectancies conceptually
map onto a schema of risk, danger, injury, loss, safety,
security, protection, and intervention. Especially in child-
hood, these expectancies, once organized, tend to operate
outside of conscious awareness and resist dramatic change
(Cicchetti and Cohen 1995).
Negative self-attributions that arise out of the original
experience(s), may, if uncorrected, also become embedded
in character. Adult studies suggest that these negative
self-images are vulnerable to reactivation after future
traumatic exposure (Foa and Riggs 1994) and compromise
efforts at adjustment. These attributions may also influ-
ence the degree to which one is willing to rely on others
for danger appraisal, support with emotional regulation,
and protective intervention. Intervention themes can re-
main relatively fixed or evolve with maturity, new infor-
mation, and experience. They have the capacity to pow-
erfully influence future career choices, preferences for
geographical residence, and parenting behavior. Lack of
adequate schematization of protective intervention may
compromise self-preservative and self-caring functions in
children (Hartman and Burgess 1989) and interfere with
adult protective behavior (Wyatt et al 1992).
Distal Trauma Reminders and Secondary
Stresses
The influence of distal trauma reminders may depend on
the extent to which they are embedded in the circum-
stances of everyday life. The more they involve intricacies
of interpersonal interactions, bodily sensations, and inter-
nal affective states, the more difficult they are to identify
as sources of renewed arousal, anxiety, or avoidance.
Distal reminders may appear during parenthood, leading to
overly anxious, protective, or authoritarian behavior. Dis-
tal secondary stresses may be a continuation of stresses
that occurred in the immediate aftermath of the trauma or
may arise out of new developmental challenges or life
circumstances. They range from the need for future
medical treatment and accommodation to disability, con-
tact of an abusive parent or relative with children of the
next generation, or the challenge of self-revelation to
explain trauma-related behavior to intimate persons in
one’s later life.
Distal Pathology
A developmental psychopathology model of PTSD under-
scores the complex iterative impact on developmental
progression and distal pathology of repeated victimization
in childhood, a review of which is beyond the scope of this
paper. Nonetheless, even among heterogeneous outcomes,
there is a role for systematic review of trauma history and
determination of comorbid PTSD. A residential treatment
study, for example, showed that history of earlier trauma,
diagnosis of PTSD, and current reactivity to trauma
reminders explained otherwise unexplained aggressive
and avoidant behaviors among adolescents with mood and
disruptive behavioral disorders (Doyle and Bauer 1989). A
prospective study following adolescent Cambodian refu-
gees into young adulthood found a waxing and waning
course of PTSD, continuity of PTSD related to traumatic
exposure, and current depression associated with current
secondary stresses (Sack et al 1996). Clark and Kirisci
(1996) found significant detrimental effects of chronic
PTSD on the quality of life among adolescents, with
disturbances in health functioning, social competence, and
school performance. A recent HMO retrospective study
among adults suggests that witnessing family violence,
Child Development, PTSD, Child Trauma, Anxiety 1549BIOL PSYCHIATRY
1999;46:1542–1554

9. childhood victimization, and childhood exposure to severe
household dysfunction are risk factors for the leading
causes of death in adults (Felitti et al 1998).
Retrospective studies have suggested the importance
of a developmental path analysis in understanding the
association of child and adolescent traumatic experi-
ences, child and adolescent PTSD, and adult PTSD.
Findings include the association of childhood physical
abuse with increased risk of chronic PTSD after late-
adolescent or young-adulthood combat exposure (Zaidi
and Foy 1994), the chronicity of PTSD into adulthood
associated with sequential childhood physical abuse and
sexual abuse (Rodriguez et al 1998), and the greater risk
of developing PTSD in adulthood associated with a
history of multiple traumatic events (Robin et al 1997;
Yehuda et al 1995).
There is suggestive evidence of potential neurobio-
logical changes extending into adulthood. These include
tonic autonomic and catecholamine activity alterations
(Perry et al 1995); HPA axis alterations, including
increased glucocorticoid receptor numbers in adult
survivors of childhood sexual abuse (Stein et al 1997);
a pattern of low cortisol response to adult sexual trauma
after earlier sexual assault history (Resnick et al 1995);
and reduced left hippocampal volume in adults with
histories of childhood physical, sexual abuse, or both
(Bremner et al 1997; Stein et al 1997). It will be
important to prospectively study the effects of these
changes on the appraisal and response to danger and
future traumatic experiences.
Intersection of Childhood Traumatic Stress,
PTSD, and Other Anxiety Disorders
This developmental model suggest different avenues by
which dangerous circumstances, childhood traumatic
experiences, and PTSD can intersect with other anxiety
disorders over the life span. Recent adult studies have
begun to describe how difficult it is to ascertain the
impact of prior trauma and chronic PTSD among
patients presenting with predominant Panic, OCD, or
other primary anxiety profiles. Given the emerging
developmental epidemiology of child and adolescent
traumatic exposures and the prevalence of anxiety
disorders in childhood (Costello and Angold 1994), it is
important to begin to better characterize their potential
points of intersection. Last et al (1992) have suggested
that the age-of-onset data of childhood anxiety disor-
ders points to a developmental progression (simple
phobia followed by separation anxiety, overanxious or
general anxiety disorder, obsessive-compulsive disor-
der, social phobia, and panic, with or without agora-
phobia), which others have mapped against a normative
progression in fears and anxieties, age-related repetitive
behaviors, and play and mental activities (Carter et al
1995; Craske 1997). The field of childhood traumatic
stress would suggest that a more comprehensive model
would place the intersection of these two lines of
progression within the psychology and developmental
neurobiology of maturing capacities to appraise, emo-
tionally regulate, and respond to real dangers in the
world.
As more epidemiological information about age- and
gender-related traumatic exposures becomes available, it
would be fruitful to map the epidemiology of anxiety
disorders against a background of this information. Trau-
matic experiences and losses have been considered, among
nonshared environments, as being potentially salient in
explaining variance in childhood and adolescent psycho-
pathology (Pike and Plomin 1996). Family and twin
studies have suggested an important role for nonshared
environments in the etiology and course of anxiety disor-
ders (Kendler et al 1992a, 1992b). Prospective population
studies of child and adolescent anxiety disorders need to
incorporate ongoing systematic screening for traumatic
exposures, using typologies congruent with developmental
and environmental risks. For example, the peak incidences
(and surprisingly high prevalence) of serious near-drown-
ing, burns, and dog bites are between infancy and five
years of age, the latter two exposures having been reported
to be associated with PTSD and, over time, with childhood
phobic disorder (Gislason and Call 1982; Stoddard et al
1989). Consistent with our model, the report of traumatic
exposure should be complemented with information about
secondary adversities and the ecology of trauma
reminders.
As we incorporate more rigorous prospective informa-
tion about trauma exposures, it will become possible to
examine the concordance of specific traumatic features
and symptom profile of later anxiety disorder, as well as to
examine the mediating role of child-intrinsic factors in-
cluding different forms of anxiety sensitivity (Stein et al
1999). For example, Bouwer and Stein (1997) reported
that a significant subpopulation of adults with panic
disorder had a history of traumatic suffocation experi-
ences. These included school age and adolescent near-
drowning and political torture by suffocation. Fear and
symptom profiles included respiratory phenomena and
nocturnal panic. The severity of the exposures presented in
the case material would suggest the likelihood of acute
traumatic reactions, reactivity to reminders, and ongoing
interactions with proximal psychopathology and develop-
ment prior to the onset of young adult panic disorder
(Pynoos et al, in press). Such complex interactions may
contribute to the development and maintenance of an
increased alarm propensity.
1550 R.S. Pynoos et alBIOL PSYCHIATRY
1999;46:1542–1554

10. Adult anxiety disorder research has continued to sug-
gest the utility of a developmental psychopathology ap-
proach across the lifecycle. A significant subpopulation of
young and middle-age adults with panic disorder report a
history of childhood sexual abuse (Stein et al 1996) in
which the peak incidence is during preadolescence, for
example. This life-trajectory approach is especially rele-
vant in considering the findings of Prigerson et al (1996)
that childhood physical, sexual, and psychological abuse,
as well as parental loss, are risk factors for the onset of
late-life anxiety disorders, particularly after becoming a
caretaker of an ill spouse.
Child-parent interaction is a critical dimension of non-
shared environments (Pike and Plomin 1996). Many fea-
tures of parent-child interactions that have been described
as moderating the pathogenesis of anxiety disorders in
children are also evident in dangerous circumstances and
after children’s traumatic exposures. These features in-
clude reciprocation of avoidance responses; parental neg-
ative feedback, including being critical; and parental
restriction, which exacerbates children’s anxious and
avoidant behaviors (Barrett et al 1996; Dadds et al 1996;
Hirshfeld et al 1997). Costanzo et al (1995) have postu-
lated that outcome is mediated by mechanisms involved in
the acquisition of developmental competencies, including
disturbances in the child’s sense of control and self-
efficacy and overdependence on others to master stimuli,
leading to greater ambiguity in the child’s sense of agency
and effectiveness. These resulting child- or adolescent-
intrinsic factors may mediate responses to real danger and
represent an axis of vulnerability to PTSD after traumatic
experiences.
Fairbanks and McGuire (1993) have provided a power-
ful ethological demonstration of the nonshared environ-
mental impact on siblings of the introduction of real
danger into the group ecology, mediated by increases in
maternal protectiveness. Among vervet monkeys, all
mothers, across a spectrum of baseline laissez-faire to high
protectiveness, became more protective toward their in-
fants during years when a new male had been introduced
into the group (new males pose a threat of infanticide), as
compared with long-term resident males. Infants reared
from the new male groups were more fearful and cautious
when tested 1–3 years later, with longer latency to
approach a novel object or enter a novel environment.
Using principles of population genetics, these investiga-
tors are presently evaluating the relative contributions of
genetics and nonshared environment to cohort population
variance in behavioral inhibition. This ethological study
suggests that there can be an interplay of danger and
trauma and exaggerated parental protectiveness in the
developmental course of behaviorally inhibited children
and risk of anxiety disorder.
Research in childhood anxiety disorders is paralleling
that of childhood traumatic stress in addressing the
interplay among traumatic experiences, psychopathol-
ogy, child-parent interactions, and developmental dis-
turbance. For many children with anxiety disorders,
including PTSD, the relationship between disorder and
impairment is a reciprocal one, with impairment leading
to continued exacerbation of anxiety symptoms, which
in turn results in worse impairment. As an example,
social phobia is often triggered by a traumatic or
stressful event (Ost 1987) that can then lead to phobic
avoidance and deterioration in the child’s level of social
activity. Decreased peer performance may foster in-
creased social discomfort, leading to further withdrawal
and worsening impairment (Beidel and Morris 1994). A
developmental psychopathology model suggests the
mutual importance of lessening psychopathology and
habilitating developmental competencies, especially in
childhood, where lost developmental opportunities and
impaired acquisition of skills carry significant indepen-
dent risks for adverse life-trajectory outcomes.
This work was presented at the scientific satellite conference, “The Role
of Biological and Psychological Factors on Early Development and Their
Impact on Adult Life,” that preceded the Anxiety Disorders Association
of America (ADAA) annual meeting, San Diego, March 1999. The
conference was jointly sponsored by the ADAA and the National
Institute of Mental Health through an unrestricted educational grant
provided by Wyeth-Ayerst Laboratories.
References
Amorapanth P, Nader K, Repa JC, LeDoux JE (1999): The fear
arousing and motivational properties of aversive stimuli are
mediated by different systems within the amygdala (abstract).
Soc Neurosci.
Armony JL, LeDoux JE (1997): How the brain processes
emotional information. Ann N Y Acad Sci 821:259–270.
Asher SR, Coie JD (1992): Peer Rejection in Childhood. New
York: Cambridge University Press.
Atkins M, Stoff D, Osborne ML, Brown K (1993): Distinguish-
ing instrumental and hostile aggression: Does it make a
difference? J Abnorm Child Psychol 21:355–365.
Barrett PM, Rapee RM, Dadds MM, Ryan SM (1996): Family
enhancement of cognitive style in anxious and aggressive
children. J Abnorm Child Psychol 224:187–203.
Beidel DC, Morris TL (1995): Social phobia. In: March JS,
editor. Anxiety Disorders in Children and Adolescents. New
York: Guilford Press, 181–211.
Boney-McCoy S, Finkelhor D: (1995) Psychosocial sequelae of
violent victimization in a national youth sample. J Cons Clin
Psychol 63:726–736.
Bouwer C, Stein DJ (1997): Association of panic disorder with a
history of traumatic suffocation. Am J Psychiatry 154:1566–
1570.
Child Development, PTSD, Child Trauma, Anxiety 1551BIOL PSYCHIATRY
1999;46:1542–1554

11. Bremner JD, Randall P, Vermetten E, Staib L, Bronen RA,
Mazure C, et al (1997): MRI-based measurement of hip-
pocampal volume in posttraumatic stress disorder related to
childhood physical and sexual abuse: A preliminary report.
Biol Psychiatry 41:23–32.
Brent DA, Moritz G, Bridg, J, Perper J, Canobbio R (1996):
Long-term impact of exposure to suicide: A three-year
controlled follow-up. J Am Acad Child Adolesc Psychiatry
35:646–653.
Carter AS, Pauls DL, Leckman JF (1995): The development of
obsessionality: Continuities and discontinuities. In: Cic-
chetti D, Cohen DJ, editors. Developmental Psychopathol-
ogy: Theory and Models. New York: Wiley, 609–632.
Cicchetti D (1989): How research on child maltreatment has
informed the study of child development: Perspectives
from developmental psychopathology. In: Cicchetti D,
Carlson V, editors. Child Maltreatment: Theory and Re-
search on the Causes and Consequences of Child Abuse
and Neglect. New York: Cambridge University Press,
377–431.
Cicchetti D, Cohen DJ (1995): Manual of Developmental Psy-
chopathology. New York: Wiley.
Clark DB, Kirisci L (1996): Posttraumatic stress disorder, de-
pression, alcohol use disorders and quality of life in adoles-
cence. Anxiety 2:226–233.
Clod A, Teicher M, Hartman C, Harakal T (1997): Increased
nocturnal activity and impaired sleep maintenance in abused
children. J Am Acad Child Adolesc Psychiatry 36:1236–
1243.
Costanzo P, Miller-Johnson S, Wencel H (1995): Social devel-
opment. In: March JS, editor. Anxiety Disorders in Children
and Adolescents. New York: Guildford Press, 82–108.
Costello EJ, Angold A (1995): Epidemiology. In: March JS,
editor. Anxiety Disorders in Children and Adolescents. New
York: Guilford Press, 109–124.
Craske MG (1997): Fear and anxiety in children and adolescents.
Bull Menninger Clin 61(2): A4–A36.
Dadds MR, Barrett PM, Rapee RM (1996): Family process and
child anxiety and aggression. An observational analysis. J
Abnorm Child Psychol 24:715–734.
Davis M, Walker D, Lee Y (1997): Roles of the amygdala and
bed nucleus of the stria terminalis in fear and anxiety
measured with the acoustic startle reflex. Ann N Y Acad Sci
821:305–331.
De Bellis MD, Lefter L, Trickett P, Putnam FW (1994): Urinary
catecholamine excretion in sexually abused girls. J Am Acad
Child Adolesc Psychiatry 33:320–327.
Doyle JS, Bauer S (1989): Posttraumatic stress disorder in
children: Its identification and treatment in a residential
setting for emotionally disturbed youth. J Trauma Stress
2:275–288.
Fairbanks LA, McGuire MT (1993): Maternal protectiveness and
response to the unfamiliar in vervet monkeys. Am J Primatol
30:119–129.
Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM,
Edwards V, et al (1998): Relationship of childhood abuse and
household dysfunction to many of the leading causes of death
in adults: The Adverse Childhood Experiences Study. Am J
Prev Med 14:245–258.
Fivush R (1991): The social construction of personal narratives.
Merrill-Palmer Q 37:59–81.
Foa EB, Riggs DS (1994): Posttraumatic stress disorder in rape.
In: Pynoos R, editor. Posttraumatic Stress Disorder: A
Clinical Review. Lutherville, MD: Sidron Press, 133–163.
Foy D, Madvig B, Pynoos R, Camilleri A (1996): Etiological
factors in development of post-traumatic stress disorder in
children and adolescents. J Sch Psychol 34:133–145.
Galvin MR, Stilwell BM, Shekhar A, Kipta SM, Goldfarb SM
(1997): Maltreatment, conscience functioning and dopamine
beta hydroxylase in emotionally disturbed boys. Child Abuse
Negl 21:83–92.
Garcia J, Lasiter PS, Bermudez-Rattoni F, Deems A (1986): A
general theory of aversion learning. Ann N Y Acad Sci
43:8–21.
Gislason IL, Call J. (1982): Dog bite in infancy: Trauma and
personality development. J Am Acad Child Adolesc Psychia-
try 22:203–207.
Goenjian AK, Pynoos RS, Steinberg AM, Najarian LM, Asar-
now JR, Karayan I (1995): Psychiatric co-morbidity in
children after the 1988 earthquake in Armenia. J Am Acad
Child Adolesc Psychiatry 34:1174–1184.
Goenjian AK, Stilwell BM, Steinberg AM, Fairbanks LA, Galvin
M, Karayan I, Pynoos RS (1999): Moral development among
adolescents after trauma. J Am Acad Child Adolesc Psychia-
try 38:376–384.
Goenjian AK, Yehuda R, Pynoos RS, Steinberg AM, Tashjian
M, Yang RK, et al (1996): Basal cortisol, dexamethasone
suppression of cortisol, and MHPG in adolescents after the
1988 earthquake in Armenia. Am J Psychiatry 153:929–
934.
Hartman CR, Burgess A (1989): Sexual abuse of children:
Causes and consequences. In: Cicchetti D, Carlson V, editors.
Child Maltreatment: Theory and Research on the Causes and
Consequences of Child Abuse and Neglect. New York:
Cambridge University Press, 95–128.
Hirshfeld DR, Biederman J, Brody L, Faraone SV, Rosenbaum
JF (1997): Expressed emotion toward children with behav-
ioral inhibition: Associations with maternal anxiety disorder.
J Am Acad Child Adolesc Psychiatry 36:910–917.
Kendler KA, Neale MC, Kessler RC, Heath AC, Eaves LJ
(1992a): Generalized anxiety disorder in women: A popula-
tion-based twin study. Arch Gen Psychiatry 49:267–272.
Kendler KA, Neale MC, Kessler RC, Heath AC, Eaves LJ
(1992b): The genetic epidemiology of phobias in women:
The interrelationship of agoraphobia, social phobia, situa-
tional phobia and simple phobia. Arch Gen Psychiatry
49:273–281.
Kilpatrick DG, Saunders BE, Resnick HS, Smith DW (1995):
The National Survey of Adolescents: Preliminary Findings
on Lifetime Prevalence of Traumatic Events and Mental
Health Correlates. Charleston: Medical University of
South Carolina, National Crime Victims Research and
Treatment Center.
Klinnert MD, Campos J, Source JF, Emde RN, Svejda MJ
(1983): Social referencing. In: Plutchik P, Kellerman H,
editors. The Emotions in Early Development. New York:
Academic Press, 123–134.
Korn H, Faber D (1996): Escape behavior—brain stem and
1552 R.S. Pynoos et alBIOL PSYCHIATRY
1999;46:1542–1554

12. spinal cord circuitry and function. Curr Opinion Neurobiol
6:826–832.
La Greca AM, Silverman WK, Wasserstein SB (1998): Chil-
dren’s predisaster functioning as a predictor of posttraumatic
stress following Hurricane Andrew. J Cons Clin Psychol
66:883–892.
Last CG, Perrin S, Hersen M, Kazdin AE (1992): DSM-III-R
anxiety disorders in children: Sociodemographic and clin-
ical characteristics. J Am Acad Child Adolesc Psychiatry
31:1070–1076.
Lynch M, Cicchetti D (1998): An ecological-transactional
analysis of children and contents: The longitudinal inter-
play among child maltreatment, community violence, and
children’s symptomatology. Dev Psychopathol 10:235–
257.
Masten A, Best K, Garmezy N (1990): Resilience and develop-
ment: Contributions from the study of children who overcome
adversity. Dev Psychopathol 2:425–444.
Nader KO, Pynoos RS, Fairbanks LA, Al-Ajeel M, Al-Asfour A
(1993): A preliminary study of PTSD and grief among the
children of Kuwait following the Gulf crisis. Br J Clin
Psychol 32:407–416.
Ornitz EM, Pynoos RS (1989): Startle modulation in children
with posttraumatic stress disorder. Am J Psychiatry 146:866–
870.
Osofsky JD (1993): The New Orleans Violence & Children
Intervention Project. Ment Health 4:2.
Ost LG (1987): Age of onset in different phobias. J Abnorm
Psychol 96:223–229.
Perry BD, Pollard RA, Blakley TL, Baker WL, Vigilante D
(1995): Childhood trauma, the neurobiology of adaptation
and use-dependent development of the brain: How states
become traits. Infant Ment Health J 16:271–291.
Pfefferbaum B (1997): Posttraumatic stress disorder in children:
A review of the past ten years. J Am Acad Child Adolesc
Psychiatry 36:1503–1511.
Pike A, Plomin R (1996): Importance of nonshared environmen-
tal factors for childhood and adolescent psychopathology.
J Am Acad Child Adolesc Psychiatry 35:560–570.
Prigerson HG, Bierhals AJ, Kasl SV, Reynolds CF, Shear
MK, Day N, et al (1997): Traumatic grief as a risk factor
for mental and physical morbidity. Am J Psychiatry 154:
616–623.
Prigerson HG, Shear MK, Bierhals AJ, Zonarich DL, Reynolds
CF (1996): Childhood adversity, attachment and personality
styles as predictors of anxiety among elderly caregivers.
Anxiety 2:234–241.
Pynoos R, Frederick C, Nader KO, Arroyo W, Steinberg A,
Eth S, et al (1987): Life threat and posttraumatic stress in
school-age children. Arch Gen Psychiatry 44:1057–1063.
Pynoos RS, Goenjian A, Steinberg AM (1998): A public mental
health approach to the post-disaster treatment of children and
adolescents. Child Adolesc Psychiatr Clin North Am 7:195–
210.
Pynoos RS, Kinzie JD, Gordon M (in press): Children,
adolescents and families exposed to torture and related
trauma. In: Keane T, Gerrity E, Tuma F, editors. Mental
Health Consequences of Torture and Related Violence and
Trauma.
Rachman S (1980): Emotional processing. Behav Res Ther
18:51–60.
Pynoos RS, Ritzmann RF, Steinberg AM, Goenjian A, Prisecaru
I (1996): A behavioral animal model of PTSD featuring
repeated exposure to situational reminders. Biol Psychiatry
39:129–134.
Pynoos RS, Steinberg AM, Aronson L. (1997a): Traumatic
experiences: The early organization of memory in school-
age children and adolescents. In: Appelbaum P, Elin M,
Uyehara L, editors. Trauma and Memory: Clinical and
Legal Controversies. New York: Oxford University Press,
272–289.
Pynoos RS, Steinberg AM, Ornitz EM, Goenjian AK (1997b):
Issues in the developmental neurobiology of traumatic stress.
Ann N Y Acad Sci 821:176–193.
Pynoos RS, Steinberg AM, Wraith R (1995): A developmental
model of childhood traumatic stress. In: Cicchetti D, Cohen
DJ, editors. Manual of Developmental Psychopathology. New
York: Wiley, 72–95.
Rasmusson AM, Charney DS (1997): Animal models of rele-
vance to PTSD. Ann N Y Acad Sci 821:332–351.
Resnick HS, Yehuda R, Pitman RK, Foy DW (1995): Effect of
previous trauma on acute plasma cortisol level following
rape. Am J Psychiatry 152:1675–1677.
Robin RW, Chester B, Rasmussen JK, Jaranson JM, Goldman D
(1997): Prevalence and characteristics of trauma and posttrau-
matic stress disorder in a southwestern American Indian
community. Am J Psychiatry 154:1582–1588.
Rodriguez N, Van de Kemp H, Foy DW (1998): Posttraumatic
stress disorder in survivors of childhood sexual and physical
abuse: A critical review of the empirical research. J Child Sex
Abuse 7:45.
Rutter M (1985): Resilience in the face of adversity. Br J
Psychiatry 147:598–611.
Rutter M (1988): Epidemiological approaches to developmental
psychopathology. Arch Gen Psychiatry 45:486–495.
Saarni C, Harris PL (1991): Children’s Understanding of Emo-
tion. Cambridge, UK: Cambridge University Press.
Sack WH, Clarke GN, Seeley J (1996): Multiple forms of stress
in Cambodian adolescent refugees. Child Dev 67:107–116.
Stein MB, Jang KL, Livesley WJ (1999): Heritability of anxiety
sensitivity: A twin study. Am J Psychiatry 156:246–251.
Stein MB, Koverola C, Hanna C, Terce, MG, McClarity B
(1997): Hippocampal volume in women victimized by child-
hood sexual abuse. Psychol Med 27:951–959.
Stein MB, Walker JR, Anderson G, Hazen Al, Ross CA, Eldridge
G, et al (1996): Childhood physical and sexual abuse in
patients with anxiety disorders and in a community sample.
Am J Psychiatry 153:275–277.
Stein MB, Yehuda R, Doverola C, et al (1997): HPA axis
functioning in adult women who report experiencing severe
childhood sexual abuse. Biol Psychiatry 42:680–686.
Steinberg AM, Ritzmann RF (1990): A living systems approach
to understanding the concept of stress. Behav Sci 35:138–
146.
Stoddard FJ, Norman DK, Murphy JM, Beardslee, WR (1989):
Psychiatric outcome of burned children and adolescents. J Am
Acad Child Adolesc Psychiatry 28:589–594.
Child Development, PTSD, Child Trauma, Anxiety 1553BIOL PSYCHIATRY
1999;46:1542–1554

13. Teicher M, Ito Y, Glod CA, Andersen SL, Dumont N,
Ackerman E (1997): Preliminary evidence for abnormal
cortical development in physically and sexually abused
children using EEG coherence and MRI. Ann N Y Acad Sci
821:160–175.
Tiet QQ, Bird HR, Davies M, Hoven C, Cohen P, Jensen PS,
Goodman S (1998): Adverse life events and resilience. J Am
Acad Child Adolesc Psychiatry 37:1191–1200.
World Health Organization Division of Mental Health (1990):
ICD-10, Mental and Behavioral Disorders. Geneva: DCR
World Health Organization, Division of Mental Health.
Wyatt G, Guthrie D, Notgrass C (1992): The differential effects
of women’s child sexual abuse and subsequent sexual assault.
J Cons Clin Psychol 60:167–173.
Yehuda R, Kahana B, Schmeidler J, Southwick SM, Wilson S,
Giller EL (1995): Impact of cumulative lifetime trauma and
recent stress on current posttraumatic stress disorder symp-
toms in Holocaust survivors. Am J Psychiatry 152:1815–
1818.
Yule W, Bolton D, Udwin O (1992, June): Objective and
subjective predictors of PTSD in adolescence. Presented at
the World Conference of the International Society for Trau-
matic Stress Studies, Amsterdam.
Yule W, Udwin O (1991): Screening child survivors for post-
traumatic stress disorders: Experiences from the “Jupiter”
sinking. Br J Clin Psychol 30:131–138.
Zaidi LY, Foy D (1994): Childhood abuse experiences and
combat-related PTSD. J Trauma Stress 7:33–42.
1554 R.S. Pynoos et alBIOL PSYCHIATRY
1999;46:1542–1554