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Neuropsychology Review, Vol. 14, No. 2, June 2004 (°

C 2004)

Clinical Perspectives on Neurobiological Effects

of Psychological Trauma1

Deborah A. Weber2 and Cecil R. Reynolds3

Physical trauma to the brain has always been known to affect brain functions and subsequent neu-
robiological development. Research primarily since the early 1990s has shown that psychological
trauma can have detrimental effects on brain function that are not only lasting but that may alter pat-
terns of subsequent neurodevelopment, particularly in children although developmental effects may
be seen in adults as well. Childhood trauma produces a diverse range of symptoms and defining the
brain’s response to trauma and the factors that mediate the body’s stress response systems is at the
forefront of scientific investigation. This paper reviews the current evidence relating psychological
trauma to anatomical and functional changes in the brain and discusses the need for accurate diagno-
sis and treatment to minimize such effects and to recognize their existence in developing treatment
programs.
KEY WORDS: trauma; neurobiology; PTSD.

In 2001, approximately 5 million children in the cal trauma run as high as 3–5 million children each year
United States were referred to state agencies for maltreat- (Perry, 1999; Perry and Azad, 1999; Schwarz and Perry,
ment (i.e. neglect, medical neglect, sexual abuse, physical 1994). Depending on the nature, pattern, and number of
abuse, and psychological maltreatment) (U.S. Department traumatic events, 27–100% of these children subsequently
of Health & Human Services, 2003). Approximately 67% develop physical, behavioral, social, psychological, cog-
of these children were subsequently screened in to Child nitive, and emotional problems (Schwarz and Perry, 1994).
Protective Services and approximately 33% were screened Emotional or physical trauma is believed to have dis-
out or referred to other agencies. Subsequent investiga- tinct neurobiological sequelae. Understanding the devel-
tions found over 28% of these children were maltreated or opmental issues involved in the response, process, and
at risk for maltreatment. According to the National Clear- adaptation to traumatic events is vital to understanding
ing House on Child Abuse and Neglect (2003), more than the neurobiological effects of childhood trauma. Children
half of these children (57%) suffered neglect, 19% were are particularly susceptible to developmental disorders re-
physically abused, 10% sexually abused, 7% psychologi- lated to trauma, however, the difficulty experienced by
cally maltreated, and 2% medically neglected. Since most young children reporting trauma and the differential man-
neglected and abused children never are reported to state ifestation of symptoms across development makes the
or local authorities, these government statistics are con- study of trauma’s effects on children particularly com-
sidered vast underestimates and do not denote actual rates plex. Stress and trauma are acknowledged as significant
of child neglect and abuse (Hopper, 2002). Indeed, esti- in precipitating psychiatric disorders, anxiety, and mood
mation rates of exposure to extreme emotional or physi- disorders (Yehuda, 2000) and the accommodation of child-
hood trauma often leads to psychopathology which can
1A portion of this paper was presented at the annual meeting of the include depression, dissociation, anxiety, conduct disor-
World Conference on Pediatric Neuropsychology and World Congress der (Miller, 1995), and even attention deficit hyperactiv-
of Pediatric Neurosciences III, April 2002, San Juan, Puerto Rico. ity disorder (ADHD) (Donnelly et al., 1999; Perry, 1994;
2 Department of Educational Psychology, Texas A&M University.
3 To whom correspondence should be addressed at Department of Educa- Weinstein et al., 2000). According to Perry (1994), child-
tional Psychology, MS 4225, Texas A&M University, College Station, hood PTSD can become a developmental disorder. Many
Texas 77843-4225; e-mail: [email protected]. of the developmental problems (motor delays, language,

115
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116 Weber and Reynolds

impulsivity, dysphoria, disorganized attachment, hyperac- Perry, 1994; 2002; Perry and Pollard, 1998). Prolonged
tivity, and attention) described in neglected children are and repeated stress results in altered neurochemical and
caused by abnormalities in the brain (Perry, 2002). Un- microarchitectural functioning. As van der Kolk (1993)
derstanding the sequelae of the neurobiological effects of noted, neurobiological abnormalities, including neuroen-
childhood psychological trauma is vital to early detec- docrine disturbances have been linked to severe childhood
tion, clinical phenomenology, and treatment. There may trauma. Specifically, these abnormalities have been asso-
be contributions to understanding normal and abnormal ciated with the catecholamine, serotonin, and endogenous
neural development as well. opiate systems.
It was only within the decade of the 1990s that the Stress is defined as any event that disrupts the home-
evolution and rapid discoveries of the neurosciences have ostasis or equilibrium of body systems. DeLongis et al.
enabled us to address questions that were not even imag- (1998) caution that relating a causal relationship between
ined a century before (Frank and Kupfer, 2000). Among stress and long-term health raises several theoretical and
these are the physical effects of psychological trauma on methodological questions. As such, it is important that
the developing brain. Childhood trauma produces a wide researchers realize stress in and of itself is not a uni-
and diverse range of symptoms and defining the brain’s tary variable but “a system of interdependent processes,
response to trauma and the factors that mediate the body’s including appraisal and coping, which mediate the fre-
stress response systems is at the forefront of scientific in- quency, intensity, duration, and type of psychological and
vestigation. somatic response” (p. 486). As such, the body’s stress re-
sponse mechanisms subsequently activate several systems
including the immune, neuroendocrine, peripheral auto-
BRAIN DEVELOPMENT nomic nervous system, and the hypothalamic-pituitary
axis with the release of cortisol, adrenocorticotropic hor-
The development of the human brain is dependent mone, and other neurochemicals designed to promote sur-
upon a complex interplay between environment and ge- vival (Schwarz and Perry, 1994). The initial stress-
netic potential. Cognitive, social, emotional, and physi- response reaction initiated by the body’s stress response
ological functioning are all mediated by the functional alters brain function and structure to enable survival. If the
capacity of our neural systems (Perry, 2002). Although stress response is of sufficient intensity, frequency, or du-
physical brain injury may well produce emotional distur- ration, the compensatory stress response mechanisms may
bances and abnormalities in the amygdala, hippocampal, become maladaptive (overactivated or fatigued) and the in-
and temporal lobe; similar effects may also result from dividual is unable to return to pre-event homeostasis. The
emotional trauma and neglect. Research has established physiologic system reorganizes and these inhibitory or
that extreme stress and trauma are associated with harmful facilitatory alterations may lead to common PTSD symp-
effects on the developing brain. Researchers have discov- toms (Perry and Pollard, 1998; Schwarz and Perry, 1994).
ered high levels of glucocorticoids resulting from stress While a child may experience a temporary change due to
are harmful to the hippocampal area of the brain (Bremner stress, the longer a child’s stress-response is activated, the
and Narayan, 1998). According to Joseph (1996) “emo- greater the likelihood of a “use-dependent” change in neu-
tional trauma is not just a psychological event but a phys- ral systems. A use-dependent change in neural systems oc-
iological experience” (p. 571). Psychological trauma and curs when an adaptive response to trauma persists beyond
neglect may result in neural degeneration, neurochemical the time needed to respond to the trauma and subsequently
abnormalities, cerebral dysfunction, and neuroanatomi- becomes maladaptive and the stress-response systems fail
cal disconnection. More importantly, repeated and severe to return to pre-event homeostasis. Limbic system hyper-
episodes of trauma and neglect can alter the functional arousal is the most common of such prolonged responses
and structural integrity of the brain. The immaturity of the (Fig. 1).
limbic system and the neocortex make children more sus- The more a neural system is activated the more a
ceptible than adults to the overwhelming effects of trauma use-dependent change will occur (Perry et al., 1995). It
and emotional events (Joseph, 1996; Perry, 2002). is the catecholamines and glucocorticoids that are the
Much of neurodevelopment is activity dependent. In first stage of defense to circumstances that threaten home-
the developing brain, critical windows of development ostasis (i.e. stress). Although it is imperative that an en-
are dependent upon microenvironmental and environmen- docrine response to stress is activated when faced with
tal cues in order for neural systems to properly organize provocative stimuli, exaggerated HPA activity or extended
from their immature, undifferentiated form (Lauder, 1988; exposure to high glucocorticoid levels is also harmful
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Neurobiological Effects of Psychological Trauma 117

Fig. 1. The psychobiological stress response. Stress activates the hypothalamus se-
cretion of CFR (corticotropin-releasing factor), dopamine, norepinephrine, serotonin,
acetylcholine, and other secretagogues into the hypophysical-pituitary portal circula-
tion which triggers the release of adrenocorticotropic hormone (ACTH) that activates
the adrenocortical synthesis and glucocorticoids that block all nonessential functions,
mobilizes energy, increases cardiovascular tone, and prepares the body for flight or fight.

(Meaney et al., 1996) to the developing brain. A pro- plasticity in the animal brain is a reflection of the ability
longed traumatic stress response often results in abnormal of the environment to adapt the efficiency and sensitivity
timing, intensity, and pattern of catecholamine activity in of neuroendocrine systems in mediating stress responses.
a child’s maturing brain (Perry, 1994, 2002). Sensitiza- Similarly, a child’s brain develops new synapses in re-
tion occurs when neurochemical systems that mediate the sponse to stimuli from the environment, which allows for
brain’s stress response become irreversible and change maximal learning but increases vulnerability for the devel-
(i.e., become more sensitive to future stress-induced oping brain. Sensitive periods exist in which trauma and
events). While sensitization may result from increased cat- stress affect brain development in particular ways; this
echolamine activity in the mature brain of an adult, in a vulnerability may lead to permanent changes or deficits in
child’s developing brain, neurotransmitters are a vital part cognitive abilities.
in the brain’s development, differentiation, synaptic pro- According to Perry (1997), the brain organizes from
liferation, and neuronal migration. Putnam and Trickett the bottom-up and inside-out as the more primitive and
(1997) also concur that understanding the effects of child- reactive (brainstem) functions of the brain are modulated
hood maltreatment requires an understanding of biolog- by the subcortical and cortical areas. The greater part of
ical mechanisms in conjunction with child development. the critical structural organization of the brain occurs dur-
Child development must be taken into account because ing childhood. In the use-dependent organization of the
maturation of neuroendocrine systems is dependent upon developing brain, a child’s developing brain experiences
windows of vulnerability that are known to exist in human repetitive sensory experiences and neural system organi-
development. zation respond accordingly. Critical periods of develop-
Sensitivity of the developing central nervous system ment exist where specific sensory experiences are neces-
(CNS) to traumatic stressors varies according to vulner- sary for optimal development and organization of brain
able periods of development. Early brain development is function. Studies have shown this use-dependent differ-
continually altered by environmental influences (Glaser, entiation also occurs throughout the CNS (Craigg, 1967;
2000). A child who is raised in an abusive, neglectful, or Cummins and Livesey, 1979). Brain development will
unpredictable environment may obtain a developing CNS be affected differently at different points in development
catecholaminergic system that is dysregulated and poorly and outcome may vary depending upon a child’s stage of
organized. Children are particularly vulnerable to stress CNS maturity at the time of trauma. While neural plas-
and trauma due to the prolonged period of plasticity in the ticity modulates a child’s brain in response to needs and
human brain’s development. Studies have also shown that environment, with aging, the brain becomes less plastic
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118 Weber and Reynolds

or less responsive to environmentally induced structural impact hemispheric integration which could lead to psy-
changes (assuming they remain external to the physio- chopathology (Teicher et al., 1997). Joseph (1996) noted
logic systems of the body). For example, the develop- that “three conditions—lateralized specialization, frontal
mental effects of trauma occurring before age 4 results lobe inhibitory activity, and incomplete myelination of the
in a much higher likelihood of psychotic and prepsy- callosum axons—can reduce the ability of the two hemi-
chotic symptomatology, while trauma occurring after age spheres to communicate among [otherwise] normal, intact
4 (on average) tends to result in more anxiety and affec- individuals” (p. 114). Lateral specialization of the brain
tive symptoms (Perry, 1994). According to Teicher et al. results in processing or recognition of certain types of
(1997), specific areas of a developing brain are particularly information more rapidly by the left or right half of the
vulnerable to trauma and stress. These areas are primar- brain. The inability of one brain half knowing what is oc-
ily parts of the limbic system and include the amygdala, curring in the other half serves a protective function for
corpus callosum, and hippocampus, and the prefrontal the linguistic consciousness and the brain by keeping it
cortex. from becoming overwhelmed, however, intrapsychic con-
flict (i.e. conflicting feelings, thoughts, and actions) is a
common side-effect (Joseph, 1996). Expression and per-
THE LIMBIC SYSTEM AND THE ception of emotion, especially negative emotion, appears
SYSTEM RESPONSE to be a specialization of the right hemisphere. Although
some researchers theorize that positive emotions such as
The limbic system stimulates the emotions that re- joy are in the left frontal lobe whereas the right frontal lobe
sult in behavior vital for self-preservation and survival is commonly associated with negative emotions such as
(van der Kolk, 1993). According to Teicher et al. (1996), sadness (Glaser, 2000), others suggest that all perception
“the prefrontal cortex, hippocampus, and amygdala are of emotion is a function of the right hemisphere (Teicher
among the most plastic brain regions” (p. 65). These re- et al., 1996). Ultimately, most researchers will agree that
gions of the brain are particularly late maturing, with under normal conditions the ability to evaluate, identify,
myelination really beginning to progress rapidly postpu- and communicate affect is dependent upon interaction be-
berty but not completing this process until into one’s 30s. tween both hemispheres of the brain. Since early brain
Regions of the limbic system impact behavior, memory, development is vulnerable to stress and trauma, left and
emotional states, and learning (Teicher et al., 1996). Indi- right hemispheric scrutiny is limited and subject to mis-
viduals exposed to severe trauma show abnormalities in interpretation and interpretation. A study by Teicher et al.
the arousal mechanisms of the sympathetic nervous sys- (1997) found evidence that abuse can affect hemispheric
tem, the endogenous opioid system, and the hypothalamic- laterality and is associated with a reversal in left/right
pituitary-adrenocortical track. According to Donnelly hemisphere asymmetry and left hemispheric abnormali-
et al. (1999), the dopamine (DA), epinephrine, and cat- ties. Teicher et al. (1996) also found EEG abnormalities
echolamines norepinephrine (NE) are involved in frontal localized to the anterior and frontotemporal regions were
lobe activation, anxiety, reward dependence, working three to four times more prevalent in patients with phys-
memory, thinking, perceiving, mood regulation, and ical/sexual abuse histories. Results of the study suggest
arousal. Many of the behavioral, affective, and cogni- that greater left-sided dysfunction may be associated with
tive symptoms associated with trauma are the result of childhood abuse. This, in turn, may result in a greater right
the release of norepinephrine in regions such as the cere- hemispheric dependence and an enhanced reaction and
bral cortex, hippocampus, and amygdala (Miller, perception to negative affect, in addition to unconscious
1995). storage of traumatic childhood memories.

Corpus Callosum Prefrontal Cortex

Information in the brain travels across hemispheres The prefrontal cortex is responsible for inhibitory
primarily but not exclusively via the corpus callosum behaviors and integrating motor and speech activity with
(Joseph, 1996). The ability of the two hemispheres of sensory information (Teicher et al., 1997). These executive
the brain to share information is impacted by the lack functions control attention, working memory, and relevant
of maturity of the corpus callosum in young children. information. The prefrontal cortex discriminates between
Research suggests brain laterality is influenced by ex- externally and internally employed models of the world
periential factors and it is speculated that stress could and impulsive behavior, inattention, lack of self-control,
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Neurobiological Effects of Psychological Trauma 119

and changes in personality can occur when the prefrontal ories is primarily the responsibility of the hippocampus
cortex is damaged. According to Bremner et al. (1999), (Joseph, 1996). This area of the brain is extremely sen-
“human subjects with lesions of the prefrontal cortex show sitive to neuronal excitability when recalling emotional
dysfunction of normal emotions and inability to relate in memories, especially in the absence of hippocampal par-
social situations that require correct interpretation of the ticipation. These early memories may be recalled through
emotional expressions of others” (p. 1788). This area of emotional disturbances and bodily sensations instead of
the brain is particularly susceptible to stress since it is the normal hippocampal retrieval mechanisms. The amyg-
not fully myelinated until the third decade of life (Teicher dala also plays a vital role in the development of condition
et al., 1997). According to Donnelly et al. (1999) exposure fear responses and autonomic reactions that may be stored
to stress is known to enhance dopamine turnover in areas in early memory (Joseph, 1996). The amygdala mediates
of the brain including the prefrontal cortex (which has fear response and is sensitive to inhibitory inputs from
a disproportionate number of dopamine receptor sites), the medial prefrontal dopaminergic system. This section
which can result in paranoia and hypervigilance. Altered of the brain is very sensitive, even to mild stressors and
dopaminergic functioning has been found in trauma vic- long-term potentiation of the amygdala may be related
tims and researchers speculate that common symptoms to learning abnormalities and the retrieval, storage, and
associated with PTSD may be a manifestation of dysreg- encoding of traumatic memories.
ulation of dopamine function. Exposure to high levels of emotional arousal may
One area of focus is the catecholaminergic system, negatively affect the hippocampus and the amygdala.
which plays a key role in the adaptation to stress and pro- Emotional stress, anxiety, and fear arouses the amyg-
duces common symptoms of PTSD. Studies have shown dala which releases large quantities of aminopeptide,
that elevations of plasma cortisol levels, which reduce im- corticotropin-releasing factor (CRF), which, in turn, po-
munosuppression, are present in trauma victims. Trauma tentiates autonomic and behavioral reaction to stress and
is believed to reduce NK cell activity (natural killer cells, fear. When stressed by restraint, cortisone levels dramati-
which target cells using antibody dependent cell-mediated cally increase and are released with the onset of stress to
cytotoxicity—they also use perforin to kill cells in the ab- activate key systems in the body’s stress-response mech-
sence of antibody), which may result in the symptoms of anisms. This CRF secretion activates the release of adreno-
PTSD. Exposure to stressful events may affect children corticotropic hormone (ACTH) from the pituitary.
biochemically by activating the release of norepinephrine State-dependent memories may result in trauma-induced
by the central noradrenegic neurons, resulting in patho- neurotransmitters, amygdala activation, and the develop-
physiology of PTSD (Miller, 1995). The hypothalamic- ment of abnormal neural pathways. Traumatic events may
pituitary-adrenal axis (HPA) is also vital in the physiolog- result in a diverse range of symptomology including harm-
ical reaction to trauma by stimulating the adrenal cortical ful alterations in behaviors, emotions, and neurobiology.
production of glucocorticoids. Additionally, aggression and inappropriate sexual activity
may be linked to prolonged traumatization and childhood
Amygdala sexual abuse.

The amygdala is the part of the limbic system that Hippocampus

provides emotional importance to the stimuli related to
affective states. Giving significance to experience and as- The hippocampus plays a crucial role in memory
sociating it with larger schemes in addition to control- function, spatial learning, and behavior inhibition. The
ling sexual and aggressive behaviors are all functions of hippocampus is also known to play a critical role in anxi-
the amygdala. The amygdala perceives fear and sets off ety and panic disorders (Teicher et al., 1997). Severe emo-
a response which might create a state of hyperarousal in tional trauma can result in the secretion of substances
children. More importantly, the amygdala plays a vital that overactivate the hippocampus. Hippocampal func-
role in the formation of emotional memory. According to tioning is hindered when the amygdala receives a high
Joseph (1996) the hippocampal’s relative immaturity at level of stimulation. According to Joseph (1996) “when
birth results in early memories (visual, tactile, gustatory, repetitively stressed and highly emotionally aroused, the
or emotional instead of cognitive or verbal) being cre- hippocampus appears to become so aroused that it is es-
ated and stored within the amygdala, which is functional sentially deactivated . . . [and] under conditions of extreme
after a child’s birth. The formation of emotional memo- stress the hippocampus may be damaged with subsequent
ries is primarily associated with the amygdala, whereas neural degeneration” (p. 586). While long-term exposure
the establishment of cognitive and nonemotional mem- to stress is associated with alterations in neurotransmitter
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120 Weber and Reynolds

systems and impairment in the hippocampal, according ative feedback loop to a positive feedback loop. The re-
to Southwick et al. (1992) there is also evidence that sulting HPA system change increases the hippocampal’s
“long-term potentiation has been found not only in the hip- exposure to cortisol toxicity and results in reduced hip-
pocampus but also in the lateral and basolateral nucleus of pocampal volume. High glucocorticoid levels decrease
the amygdala” (p. 350). In animals, long-lasting increases hippocampal glucocorticoid receptors and result in in-
in hippocampal synaptic responsivity impair behavioral creased feedback resistance and corticosterone secretion
learning and result in memory deficits. Hippocampal dys- (Southwick et al., 1992). Many studies now show stress
function affects the interpretation of incoming stimuli and produces hippocampal dysfunction, atrophy (smaller vol-
inhibits proper categorization and evaluation of experi- ume as seen on QMRI), and deficits in declarative mem-
ences. This can result in memories being experienced in a ory function (Bremner, 1998, Bremner et al., 1999; Nutt,
behavioral state or visual image (van der Kolk, 1993). 2000) due to the damaging effects of high levels of gluco-
According to van der Kolk (1993), memories are corticoids on the hippocampus. Glucocorticoids disrupt
fixed by myelinization. Until axons are myelinized the cellular metabolism and increase hippocampal neuronal
brain remains extremely plastic. Developmentally, this oc- vulnerability to a variety of agents. The De Bellis et al.
curs at different ages and is the cause of amnesia in in- (1994) study found a 7% smaller cerebral volume in chil-
fants since the hippocampus is not fully myelinated until dren suffering from PTSD (Glaser, 2000). Gurvitis et al.
later in life (Jacobs and Nadel, 1985; Schachter, 1990; (1996) found an average 26% reduction in the left hip-
van der Kolk, 1993). According to van der Kolk (1993) pocampus and 22% reduction in the right hippocampus in
“after the hippocampus is myelinized, the hippocampal Vietnam veterans with severe PTSD. Additionally, other
localization system, which allows memories to be placed studies (e.g. Ito et al., 1993, 1998; Teicher et al., 1993)
in their proper context in time and place, remains vulner- found left frontal and temporal abnormalities on an EEG
able to disruption by intense emotional states” (p. 227). in addition to limbic system dysfunction in individuals
With the maturing of the CNS, memory storage changes with significant abuse histories.
from primarily sensorimotor and perceptual to linguistic According to Perry and Pollard (1998),
and symbolic representations of mental experience. Auto-
nomic arousal results in access to memories that originated As with central neurobiologic systems, stress, distress,
under similar arousal conditions. This intense autonomic and trauma alter HPA regulation (i.e., a new homeosta-
sis has been induced by the stress). Abnormalities of the
arousal of memories influences interpretation of the trau- HPA axis have been noted in adults with PTSD. Chronic
matic event. activation of the HPA system in response to stress has
Stress produces deficits in memory resulting from negative consequences. The homeostatic state associated
damage to hippocampal neurons (Bremner et al., 1999). with chronic HPA activation wears the body out. Hip-
In addition to memory impairments, research has shown pocampal damage, impaired glucose utilization, and vul-
nerability to metabolic insults may result. Preliminary
that cognitive impairments, lack of coping responses, and studies in a sample of abused children suggest similar
dissociation are also associated with hippocampal dam- hippocampal and limbic abnormalities. (pp. 41–42)
age (Ratna and Mukergee, 1998). Deficits in short-term
memory are also associated with the reduction in right In animal studies a stress reaction produces increased
hippocampal volume. A study by Bremner and Narayan glucocorticoid secretion leading to loss of hippocampal
(1998) found an 8% reduction in right hippocampal vol- cells (Glaser, 2000). Studies also indicate a greater number
ume in PTSD patients. According to Joseph (1999), the of lymphocyte glucocorticoid receptors and a reduction
hippocampus also plays a major part in storing and con- in CRF which could account for the feedback inhibition
solidating long-term memory. Additionally, Joseph (1999) of the HPA. The greatest number of type II glucocorti-
postulates that, coid receptors is found in the hippocampus. During stress,
HPA activation is inhibited by the hippocampus. Neu-
Although these substances are normally released as part
of the “flight or fight” response, repeated or prolonged
ral death is also linked to increased glucocorticoids. Ac-
stress-induced secretory episodes of corticosteroids and cording to Sapolsky (1992), the CRF is released with
enkephalins can injury the dentate gyrus and Ammon’s the onset of stress to activate key systems in the body’s
horn and hyperactivate or kill hippocampal (as well as stress-response mechanisms. This CRF secretion activates
amygdala) pyramidal neurons–structures which normally the release of adrenocorticotropic hormone (ACTH) from
display synaptic growth and dendritic proliferation in re-
sponse to new learning. (p. 716)
the pituitary. The ACTH, in turn, triggers the release of
glucocorticoids and adrenocortical synthesis. Glucocorti-
According to Nutt (2000), when the hippocampus is coids quickly circulate, help mobilize energy from stor-
damaged, the HPA system is changed from a normal neg- age, block energy storage, increase cardiovascular tone,
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Neurobiological Effects of Psychological Trauma 121

and inhibit nonessential processes such as immunity, in terminating the body’s stress-response and is necessary
inflammation, reproduction, and growth. As stated by to shutdown reactions that damage the brain. According to
Sapolsky (1992), “there is a dose–response relationship Yehuda (1997) “the major function of cortisol is to manage
between the severity of the stressor and the magnitude of or contain the body’s biological stress-response by stimu-
the adrenocortical response” (p. 12). Adrenocortical ac- lating the termination of the neural defense reactions that
tivity is influenced by the amount of glucocorticoid con- have been activated by stress” (p. 58). Munck et al. (1984)
centrations in the bloodstream, which suggests that the also asserts that cortisol works in a reparative fashion and
adrenocortical axis has the ability to differentiate between actually shuts down other stress-related changes before
different magnitudes of stressors. The long-term effects more damage is caused. Originally, researchers thought
of chronic stress lead to excessive exposure to glucocorti- the release of cortisol was dependent on the level of stres-
coids. Studies involving rats have indicated neuronal loss sor experienced. Yet, according to Yehuda (2000),
in the hippocampal is connected with hypersecretion of
because of an increased number of glucocorticoid recep-
glucocorticoids. According to Sapolsky (1992), “a major tors on the pituitary, the normal stress response cascade is
pacemaker of hippocampal neuron loss appears to be the disrupted. Although ACTH stimulates the adrenal to re-
extent of glucocorticoid exposure over the lifetime; exces- lease cortisol, cortisol acts at the level of the pituitary to
sive glucocorticoids can be neurotoxic to the hippocam- shut off ACTH release from the pituitary, and ultimately
pus” (p. 113). In as little as 3 weeks, high glucocorticoid less cortisol is made and released from the adrenal glands.
(p. 267)
exposure will cause degeneration in neural dendrites. Ad-
ditionally, excessive glucocorticoids can be neurodegen- Although the damaging effects of high levels of cortisol
erative and disrupt normal development. are well documented, there is considerable debate over
Recent studies have indicated that “there is grow- the inconsistent levels of cortisol (i.e. high vs. low) that
ing evidence of hippocampal volume loss associated with have been found in victims of trauma. Yehuda (2000) pos-
chronic PTSD” (Bergherr et al., 1997, p. 39). Since this tulates that neuroendocrine alterations (low cortisol lev-
evidence suggests neuronal loss in the hippocampus is a els, increased sensitivity, and larger than normal basal of
consequence of acute stress and traumatization, it is im- glucocorticoid receptors) associated with PTSD are dis-
perative that clinicians identify children suffering from similar to other stress responses and hippocampal atrophy
long-term traumatizations as soon as possible. Accord- in PTSD victims may actually be a function of increased
ing to a study conducted by Teicher et al. (1993, 1996), glucocorticoid receptor sensitivity and not high levels of
increased limbic system dysfunction is associated with cortisol. According to Yehuda (2000), “the majority of
abuse occurring before the age of 18. The authors cau- the studies performed to date demonstrate that cortisol
tion however, that the study is correlational and does not levels in PTSD are lower compared to those of other psy-
establish a cause–effect relationship. Some authors even chiatric groups and normal controls” (p. 269). Of the six
propose that limbic dysfunction may be hereditary and studies of urinary cortisol levels done to date (1994), four
predispose a child to a greater risk of abuse (Table 1). found lower cortisol levels in psychiatric groups. Studies
(e.g. De Bellis et al., 1994; Golier and Yehuda, 1998; Hart
Cortisol Levels et al., 1995, 1996; Kaufman, 1991; Kaufman et al., 1997)
suggest that lower cortisol levels are found in some chil-
The stress-response of the developing brain results dren exposed to maltreatment, sexual abuse, neglect, and
in an increase in neurotransmitter and hormone activity, trauma. According to Glaser (2000), this is possibly due to
which affects neuronal migration, synaptic proliferation, an “enhanced negative feedback in the HPA axis” (p. 106).
differentiation, and total brain development. Immediate It is speculated that the HPA’s lack of response to situa-
response to stress includes the release of dopamine, nore- tions of stress may be related to the familiarity of the stress
pinephrine, serotonin, and acetylcholine in the brain. This, and a source of protection for the brains of vulnerable chil-
in turn, stimulates the hypothalamus, pituitary gland, and dren. However, a study by De Bellis et al. (1999) found
adrenal glands, which release cortisol. Increased cortisol increased cortisol levels in children suffering from sig-
levels have been linked to brain alterations including thy- nificant abuse and PTSD. Similar results were found in
mus gland shrinkage, cell death, and hippocampal atro- studies conducted by Pitman and Orr (1990) and Lemieux
phy. Other effects include a reduction in lymphocytes in and Coe (1995). These results contradict studies finding
the blood leading to a weaker immune system (Sapolsky, lower cortisol levels in individuals suffering from PTSD
1996) and neuronal death (Munck et al., 1984). While ac- (e.g. Mason et al., 1996; Yehuda et al., 1990, 1993, 1995).
knowledging the damaging effects of high cortisol levels, Yehuda et al. (1995) suggests these findings may be due
Yehuda (2000) cautions that cortisol also serves a vital role to the immaturity of the HPA in children.
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122 Weber and Reynolds

Table 1. Glossary of Neurostructural and Neurochemical Terms in Stress Response

Term Definition
Amygdala Located in front of the hippocampus, it is the part of the limbic system that provides emotional
importance to the stimuli related to affective states. Giving significance to experience and
associating it with larger schemes in addition to controlling sexual and aggressive behaviors are all
functions of the amygdala. More importantly, the amygdala plays a vital role in the formation of
emotional memory. The amygdala also plays a vital role in the development of condition fear
responses and autonomic reactions that may be stored in early memory.
Adrenocorticotropic hormone (ACTH) Triggers the release of glucocorticoids and adrenocortical synthesis. Glucocorticoids quickly
circulate, help mobilize energy from storage, block energy storage, increase cardiovascular tone,
and inhibit nonessential processes such as immunity, inflammation, reproduction, and growth.
Catecholamines The dopamine (DA), epinephrine, and norepinephrine (NE) are involved in frontal lobe activation,
anxiety, reward dependence, working memory, thinking, perceiving, mood regulation, and arousal.
They are major elements in the response to stress.
Corticotropin releasing factor (CRF) Released with the onset of stress to activate key systems in the body’s stress-response mechanisms.
This CRF secretion activates the release of adrenocorticotropic hormone (ACTH) from the
pituitary. Has an inhibitory effect of hippocampal functioning.
Cortisol Most potent of the naturally occurring glucocorticoids, works as an anti-inflammatory agent released
with the onset of stress and in addition to other neurochemicals, activates key systems in the body’s
stress-response mechanisms. Also serves a vital role in terminating the body’s stress-response and
is necessary to shutdown reactions that damages the brain. Has an inhibitory effect of hippocampal
functioning.
Cortisone A glucocorticoid that is likely a metabolite of hydrocortisone (s. cortisol). It influences the growth of
connective tissue.
Hippocampal Plays a crucial role in memory function, spatial learning, and behavior inhibition. Hippocampal
dysfunction affects the interpretation of incoming stimuli and inhibits proper categorization and
evaluation of experiences. This can result in memories being experienced in a behavioral state or
visual image.
Hypothalamic-pituitary axis (HPA) Vital in the physiological reaction to trauma by stimulating the adrenal cortical production of
glucocorticoids. Overwhelming stress and traumatization are linked with the activation of the HPA.
During stress HPA activation is inhibited by the hippocampal. Chronic activation has negative
consequences and can wear the body out.
Limbic system The limbic system governs the emotions vital for self-preservation, homeostasis, and basic needs.
These regions of the brain are particularly late maturing, with myelination completing until into
one’s 30s. Regions of the limbic system impact behavior, memory, emotional states, attention,
arousal, learning, and social and sexual behavior.
Neocortex The arousal of the neocortex activates the amygdala and in turn, the neocortex become more receptive
to processing sensory information which can lead to a state of attention, emotional arousal, or
vigilance.
Norepinephrine A neurotransmitter that plays a critical role in fight or flight reactions (automatic hyperarousal).
Norepinephrine is released by the CNS which results in a cardiovascular response that allows for
vigilance and focus on relevant stimuli, a total body mobilization that is necessary for survival.
This reaction activates the area of the brain involved in attention, concentration, and arousal. Many
of the behavioral, affective, and cognitive symptoms associated with trauma are the result of the
release of norepinephrine in regions such as the cerebral cortex, hippocampus, and amygdala
Sympathetic nervous system (SNS) Along with the HPA axis, the SNS is a major axis of stress response responsible for unconscious
emergency responses. The SNS increases blood pressure and accelerates the heart rate in response
to dangerous or stressful situations. This response serves a protective role and allows the body to
prepare for “fight or flight.” The long-term consequence is that the SNS becomes hyperreponsive in
many individuals with PTSD.
Temporal lobe Involved in complex visual, linguistic, auditory function, in addition to memory and emotional
functioning.

While studies have linked lower cortisol levels to cortisol levels. Overwhelming stress and traumatization
chronic PTSD, Yehuda cautions that assessing levels of are linked with the activation of the HPA. According to
cortisol before and after traumatic events is necessary in Bergherr et al. (1997), the long-term effect of PTSD in in-
order to establish that PTSD neuroendocrine alterations dividuals is associated with lower cortisol levels indicating
are due to the traumatic event and not pre-existing lower “that PTSD is associated with increased HPA sensitivity
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Neurobiological Effects of Psychological Trauma 123

to feedback suppression by cortisol” (p. 35). Studies have reactivity due to a basal homeostatic level of constant anx-
demonstrated PTSD veterans have a greater number of iety. Although sensitized to traumatic events, these chil-
glucocorticoid receptors, which is consistent with upreg- dren are at a greater risk for developing stress-induced
ulation and often a secondary reaction to low cortisol. This neuropsychiatric disorders when they get older as they ex-
is also associated with increased CRF hypersecretion. hibit maladaptive cognitive, behavioral, emotional, phys-
iologic, and social problems (Perry and Pollard, 1998).
TRAUMA AND CHILDREN Associated with a child’s response to trauma are gen-
der, developmental level, age, socioeconomic and fam-
According to Perry and Pollard (1998) neuropsy- ily factors, and proximity. Developmental level and age
chiatric disorders that are trauma related are affecting impact a child’s perception and comprehension of the
over 8 million children, approximately half of all chil- trauma. Parental support and response to trauma are also
dren exposed to traumatic events (Schwarz and Perry, predictive of a child’s response to trauma and severity
1994). Often, these children are misdiagnosed with atten- of trauma symptomology. Gender and locus of control
tion deficit disorder, oppositional defiant disorder, conduct can also affect a child’s response and coping mechanisms
disorder, anxiety, or a phobia (Perry and Azad, 1999). Life (Amaya-Jackson and March, 1995; Perry and Azad, 1999;
events that are stressful can also modify a wide array of im- Pfefferbaum, 1997; Schwarz and Perry, 1994).
munological actions. An increase in the risk of illness and A response that serves a protective role is one that
infectious disease is found in children where alterations in allows the body to prepare for “fight or flight.” When
the immune system are stress induced. When stress-related homeostasis is threatened, the adrenal glucocorticoids and
mechanisms are activated, the brain reacts by responding catecholamines serve as regulators of stress (Perry, 1994,
in a way that promotes survival. If a traumatic event is 2002). Stress in the developing brain causes an increase
prolonged or chronic, these protective mechanisms can in endogenous opiates and alters multiple neuroendocrine
become overactive causing a change in homeostasis. systems. Subsequently, the SNS increases blood pressure
The ability to regulate and modulate behavior in- and accelerates the heart rate in response to dangerous
creases as the brain develops (Perry et al., 1995) since the or stressful situations. Norepinephrine is released by the
neurobiologic systems respond to stress in an age-related CNS which results in a cardiovascular response that al-
fashion that parallels developmental life tasks. “Traumatic lows for vigilance and focus on relevant stimuli, a total
events modify an adult’s original state of organization or body mobilization that is necessary for survival. This re-
homeostasis but may be the original organizing experience action activates the area of the brain involved in attention,
for the child, thereby determining the foundational organi- concentration, and arousal.
zation and homeostasis of key neural systems” (Perry and Differing from the neurobiology of a hyperarousal re-
Pollard, 1998, p. 36). According to Pynoos et al. (1997) sponse, activating the autonomic nervous system leads to a
there are four periods in which the brain undergoes ma- slowing of the heart and lowering of blood pressure which
jor structural changes. Additionally, these periods (which results in a dissociative state. The likelihood of a dissocia-
range from 15 months to 4 years, 6–10 years, puberty, and tive response increases when a child is unable to escape
midadolescence) correspond with developmental growth a frightening experience and/or experiences physical in-
in cognitive and emotional functions. What is harmful jury, pain, or torture. Perry et al. (1995) found a parasym-
for a 2-year-old may not affect a 21-year-old and vice pathetic nervous system response (decreased heart rate
versa (Perry, 2002; Perry and Pollard, 1998). For exam- and blood pressure, increases in circulating epinephrine)
ple, not touching a newborn baby will result in severe in girls and young children when a dissociative response
traumatization but would have little effect on a 30-year- occurs. Dissociation is a common response to trauma and
old. Neglect and abuse experienced by children early in occurs when infants/children abandon initial alarm behav-
life deprives the brain of experience-expectant maturation. iors and become compliant, passive, or show restricted af-
For numerous children, abuse is not perceived as acutely fect. Common mental defense mechanisms such as avoid-
traumatic because of its very chronic and predictable na- ance, daydreaming, numbing, fantasy, fugue, catatonia, or
ture. Children who are commonly exposed to threatening fainting are often manifested (Perry and Pollard, 1998).
or chaotic caregiving develop a use-dependent neurobi- Essentially, dissociation involves a disengagement from
ological response which results in a sensitized and dys- the external world and focus on the internal world. Adap-
functional stress-response system. The sensitization of the tive styles of females and young children are more likely
stress-response systems may result in anxiety, hyperactiv- to involve dissociation, while males are more likely to
ity, impulsivity, hypertension, dysphoria, sleep problems, respond from a reactive stance or fight or flight response
and tachycardia. These children often exhibit exaggerated that prepares them to flee or fight the perceived threat
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124 Weber and Reynolds

(Perry et al., 1995). Additionally, females are more likely coeruleus neuron responsiveness, dopamine and endoge-
to internalize and males more likely to externalize symp- nous opiates release, elevated glucocorticoid levels, and
toms (e. g., see Reynolds and Kamphaus, 1992). Differ- decreased density of benzodiazepine receptors and opi-
ences in the adaptive stress response patterns of males and ate receptors are associated with the neurochemical sys-
females are clearly seen in the incidence of childhood neu- tem response to PTSD. These neurochemical reactions
ropsychiatric disorders. More males meet the criteria for produced by stress result in hypervigilance, anxiety, anal-
externalizing disorders (conduct disorder, ADHD, oppo- gesia, fear, hyperarousal, and behavioral responses that
sitional defiant disorder), while females experience more function together in an attempt to cope with imminent
internalizing disorders (anxiety, dissociative disorders, de- danger (Southwick et al., 1992). While these neurochem-
pression). Additionally, in adolescence, the ratio of neu- ical responses may be beneficial initially, the long-term
ropsychiatric disorders is three to one (male to female), yet consequences are associated with PTSD. In addition to
the prevalence rates change to two to one (female to male) alterations in the brain of persons experiencing PTSD,
in early adulthood (Perry et al., 1995). The risk of devel- including reduction in hippocampal volume, a study con-
oping PTSD is also three times greater in children exposed ducted by Canive et al. (1997) found gross structural ab-
to traumatic experiences before age 11 as opposed to later normalities in individuals with PTSD. Using MRI FLAIR
years (Amaya-Jackson and March, 1995). The long-term imaging sequences of patients with PTSD, Canive et al.
consequence of “fight or flight” is that the SNS becomes (1997) found focal white matter lesions in the brain of
hyperreponsive in many individuals with PTSD. the PTSD patients. The gross abnormalities of the PTSD
patients were higher than a comparative neurologically
POSTTRAUMATIC STRESS DISORDER normal group. The authors caution however, that the high
comorbidity of alcohol and depression associated with
PTSD was included as distinct psychiatric syndrome PTSD in adults makes the exact factors involved difficult
in the 1980 publication of the DSM-III. PTSD is usu- to assess. Similar research involving children with PTSD
ally seen as a psychological disorder by clinicians and may be beneficial in resolving the comorbidity problem of
yet recent research indicates that PTSD also should be alcohol and depression commonly found in adult patients.
viewed from a biological perspective (Southwick et al.,
1997). According to Pfefferbaum (1997), estimates for CHILDHOOD SEXUAL ABUSE
the prevalence of PTSD ranges from 1% to 14%. Perry
(1994) states a conservative estimate of PTSD in children The psychological impact of childhood sexual abuse
exceeds 15 million. Additionally, with the high number of is associated with various physiological and psychobio-
children exposed to trauma, abuse, neglect, maltreatment, logical changes. According to Joseph (1999) “a clear re-
and violence, the number of children developing PTSD lationship has been established between early childhood
continues to grow each year. According to Pfefferbaum abuse, and the development of severe social emotional dis-
(1997), PTSD comprises three essential features and in- turbances and limbic system injury, including child and
cludes: “1) persistent re-experiencing of the stressor, 2) adult onset psychopathology and dissociative abnormal-
persistent avoidance of reminders of the event and numb- ities and posttraumatic stress disorder” (p. 721). Ratna
ing of general responsiveness, and 3) persistent symp- and Mukergee (1998) noted in their research that 1 in 6
toms of arousal” (p. 1503). These key characteristics are women are victims of childhood sexual abuse. Addition-
sometimes referred to as the holy trinity of PTSD symp- ally, studies have shown 90% of 3–16 year olds who have
toms and simply summarized as avoidance, arousal, and been abused and 86% of adult survivors of sexual abuse to
re-experience. have PTSD symptoms or meet the PTSD diagnostic crite-
According to Southwick et al. (1997), recent studies ria (e.g. Mcleer et al., 1988; Rodriquez et al., 1996). Ac-
strongly support the idea that psychological trauma can cording to Weinstein et al. (2000), “considerable research
result in changes in the body’s neurobiological stress re- suggests the effects may be pervasive and long-lasting,
sponse years after the original event. According to a review leading to increased risk for adjustment difficulties and
of clinical literature by Southwick et al. (1997), studies mental health problems in adulthood” (p. 362). Addition-
indicate that hyperresponsiveness and alterations in the ally, the most common cause of PTSD is childhood sexual
SNS and HPA axis are provoked by original reminders abuse (Bremner et al., 1999).
of the trauma. The neurobiological dysfunction associ- Various studies (e.g. Bremner et al., 1997; Schacter
ated with PTSD includes the noradrenergic, dopaminer- et al., 1996; Stein et al., 1997) have also indicated a sta-
gic, opiate, benzodiazepine, and hypothalamic-pituitary- tistically significant decrease in hippocampal volume in
adrenal axis. Increases in regional norepinephrine, locus the left side of adult survivors of severe childhood sexual
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Neurobiological Effects of Psychological Trauma 125

abuse. The decreased hippocampal volume was associated ADHD

with the severity of PTSD. It is presumed that increased
cortisol levels resulting from the abuse lead to physical Research indicates symptoms of hyperarousal in vic-
hippocampal damage reflected in smaller hippocampal tims of trauma produces changes in the brain system that
volume. results in long-term hyperactivity. Trauma exposure may
According to Glaser (2000), catecholamine levels result in the failure to modulate aggression, impulsivity,
were higher in girls who were sexually abused. Greater and anger. This loss of drive regulation in externalizing
baseline (homeostasis) noradrenaline and dopamine lev- disorders is associated with ADHD, social and cognitive
els have been found in abused children with PTSD (e.g. impairments, and impulsive behavior which can lead to in-
De Bellis et al., 1999). Duration of abuse was significantly creased risk for trauma exposure and subsequently PTSD.
correlated with the levels of noradrenaline and dopamine The dysfunction of the prefrontal cortex is often what leads
found. to the diagnosis of Attention Deficit Hyperactivity Disor-
A recent study by Shin et al. (1999) looked at whether der (ADHD). Stress activates the catecholamines (nore-
childhood sexual abuse victims with and without PTSD pinephrine, epinephrine, and dopamine) and the sympa-
exhibited differences in the anterior limbic and paralim- thetic nervous system and the medulla receives messages
bic areas of the brain during imagery of the traumatic of stress and/or fear from the hippocampus and the amyg-
event. The study consisted of 16 women, who experienced dala. The adrenal gland also secretes noradrenaline and
penetrative sexual abuse before age 16, 8 of who meet adrenaline, which raises the heart rate, blood pressure,
the criteria for PTSD. Subjects underwent two PET scans and sweating. According to Glaser (2000), prefrontal cor-
during which they recalled traumatic and neutral stimuli tex dysfunction is linked to raised levels of dopamine and
scripts. The study found that during neutral conditions, noradrenaline. Studies show that the long-term effects of
both groups experienced increased cerebral blood flow chronic stress lead to excessive exposure to glucocorti-
(CBF) in the anterior temporal poles and the orbitofrontal coids. While glucocorticoids are a vital part of the survival
cortex, although the PTSD group exhibited the greatest stress-response, overexposure can result in a multitude of
increase. During the traumatic condition, the PTSD group disorders. According to Miller (1995), “symptoms associ-
had an increased heart rate and decreased CBF in the bilat- ated with traumatization, such as anxiety, startle response,
eral anterior frontal regions and left inferior frontal gyrus. hypervigilance, and avoidance of traumatization triggers
Both groups exhibited CBF decreases in the visual cortex. seem to directly or indirectly reflect a long-lasting problem
The results suggest that although the two groups differ of modulation alarm and arousal” (p. 9).
in patterns of activation among paralimbic regions, the ADHD is difficult to assess and diagnose distinctly
recollection and imagery of traumatic events is accompa- from several related disorders, yet numerous children are
nied by increased CBF to the anterior paralimbic region given the diagnosis. Comorbid conditions among children
in individuals exposed to trauma (with or without PTSD). with PTSD are more likely because critical developmen-
A study by Stein et al. (1997) found hippocampal tal windows and milestones are sensitive to changes in
volume was significantly reduced in 21 women who were neurobiological activation and maturation which can be
victims of childhood sexual abuse. The hippocampal vol- disrupted by trauma (Donnelly et al., 1999). According to
ume on the left side was 5% smaller for the sexually Weinstein et al. (2000), part of the misdiagnosis problem
abused group than sociodemographically similar women is that other behavioral disorders, PTSD, and ADHD all
with no histories of abuse. Additionally, “the left-sided have shared characteristics and symptoms between them
hippocampal volume correlated highly (rs = −0.73) with (Table 2). Given the complications resulting from misdi-
dissociative symptom severity” (Stein et al., 1997, p. 951). agnosis, the challenge is for clinicians to pay increased
Bremner et al. (1999) conducted a study in which women attention to differential diagnosis in PTSD and ADHD.
with PTSD who had also been victims of childhood sex- Donnelly et al. (1999) also notes that comorbidity be-
ual abuse “demonstrated increased activation in poste- tween PTSD and externalizing disorders may result in
rior cingulate, anterolateral prefrontal cortex (Brodmann’s the presentation of traditional features of ADHD includ-
areas 6 and 9), and motor cortex . . . as well as deacti- ing impulsivity, hyperactivity, irritability, restlessness, and
vation in right hippocampal, fusiform/inferior temporal distractibility. Oppositional Defiant Disorder (ODD), and
gyrus, supramarginal gyrus, and visual association cor- Conduct Disorder (CD) are also externalizing disorders
tex” (p. 1788). Features observed in PTSD including hip- that have become more prevalent with the increase in
pocampal damage, cognitive and memory impairment, PTSD. The hyperarousal characteristic of PTSD, includ-
and dissociation also frequently are observed in severe ing anger or irritability, sleeplessness, and hypervigilance,
sexual abuse (Ratna and Mukergee, 1998). makes it easy to misdiagnoses PTSD as ADHD or even
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126 Weber and Reynolds

Table 2. Comorbitity Symptoms

Posttraumatic Stress Disorder Attention-Deficit/Hyperactivity Disorder Oppositional Defiant Disorder Conduct Disorder
(PTSD) (ADHD) (ODD) (CD)
Anxiety
Avoidance
Social withdrawal Rejection by peer Social conflicts
Increased arousal Increased arousal
Sleeplessness Sleeplessness
Recurrent nightmares
Hyperviligance Hyperactivity/hyperviligance High motor activity
Feeling constantly threatened
Impaired relationships Poor relationships Poor relationships
Exaggerated startle response Exaggerated startle response High reactivity
Irritability Mood lability/irritability Mood lability
Impulsive behavior Impulsivity Impulsivity Impulsivity
Self-destructive behavior Disruptive Behavior Disruptive Behavior
Outbursts of anger Temper outbursts Losing temper
Hostility Oppositional behavior Hostile behavior
Difficulty completing tasks Difficulty completing tasks
Difficulty concentrating Difficulty concentrating
Feelings of guilt Poor self esteem Low/high self-esteem
Shame
Hopelessness
Despair
Dissociative symptoms Dysphoria
Feelings of ineffectiveness Demoralization
Somatic complaints
Auditory hallucinations
Paranoid ideation
Impaired affect modulation
Feelings permanently damaged
Loss of previous beliefs
Change in personality characteristics

Bipolar Disorder if comprehensive history and trauma as- the pathway that connects the adrenal cortex and the brain.
sessments are not routine components of ADHD assess- The adrenal cortex secretes cortisol and long-term eleva-
ment. According to Weinstien et al. (2000), “in fact, some tion of cortisol levels may be harmful, especially early
literature suggests that sexually abused children may be in life. A study by Gunnar and Nelson (1994) found the
at heightened risk for the development of PTSD, though activity of the hippocampus was impeded by high corti-
they are more often diagnosed as ADHD than PTSD” sol levels. Sapolsky’s (1996) finding of a correlation be-
(p. 361). In one study (Mcleer et al., 1994), 54% of sex- tween hippocampus damage and excess cortisol, supports
ually abused children with PTSD also met the criteria for these conclusions. According to Donnelly et al. (1999), “in
ADHD diagnosis. younger children these may manifest as attachment dis-
orders, impaired social skills, aggressiveness, impulsivity,
ATTACHMENT and sexualized behaviors, depending upon the nature of
the trauma” (p. 206).
A securely attached child has the ability to regulate
distress and anxiety by using his/her caregiver as a se- Neuropsychological Assessment and Treatment
cure base. Gunnar et al. (1996) speculate that the negative
effects of elevated glucocorticoids in children are coun- The growing number of children in America exposed
tered by secure attachment relationships. Gunnar (1998) to trauma is resulting in a public health crisis. Children
hypothesized that the primary buffer of the HPA axis is a who have been traumatized often show symptoms of other
secure attachment. One adaptive response to stress is for disorders as well as PTSD (Amaya-Jackson and March,
the body to increase serum cortisol. Serum cortisol sup- 1995; Perry, 2002), thus, comorbidity often makes diagno-
presses the immune system and increases glucose in the sis difficult in traumatized children. Because PTSD symp-
body. The hypothalamic-pituitary-adrenal (HPA) axis is toms mimic many other child disorders, children are often
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Neurobiological Effects of Psychological Trauma 127

misdiagnosed and mistreated. According to Schwarz and be the order of the day when encountering traumatized
Perry (1994), or suspected-traumatized children, and purely traditional
psychological assessments of personality and emotion will
In general, because youngsters rarely attribute symptoms be insufficient to elucidate accurate, effective treatments
to trauma and may be reluctant patients or poor historians,
and to avoid actually designing treatment plans that violate
and because posttraumatic symptoms can be nonspecific,
superimposed on, or mimic other childhood disorders, it the prime directive of health care: first, do no harm.
is important to maintain a high level of suspicion regard-
ing the posttraumatic cause of any presenting symptoms CONCLUSIONS
and include the possibility of trauma in differential di-
agnoses of most childhood symptoms. Thus, even when
youngsters present without a history of trauma, it is nev-
The number of children exposed to traumatic events
ertheless useful to inquire routinely . . . . (p. 319) is continuing to increase. Last year alone, over 5 million
children in the United States were referred to state agencies
The authors go on to caution against suggestible questions (National Child Abuse and Neglect Data System, 2003) for
and instruct that inquiry should consist of nonbiased and suspected maltreatment. Trauma leaves a severe and last-
open-ended questions. ing impression on children (Amaya-Jackson and March,
Early assessment, detection, and treatment are vi- 1995) and society. Every day millions of children in the
tal to halting the devastating neurobiological sequela that United States are exposed to stressors such as violence,
occurs in many victims of childhood trauma. Many of neglect, abuse, deprivation, and acts of war. Contrary to
the treatments for children and adolescents suffering from what many would believe, the United States is character-
PTSD parallel interventions used with adult PTSD vic- ized as the most violent nation among the industrialized
tims (Putnam, 1996). However, differential diagnosis is world and child maltreatment in the United States is an
crucial since disorders that can mimic PTSD in children epidemic (Putnam, 1996; U.S. Advisory Board on Child
(e.g., ADHD, conduct disorder, and other externalizing Abuse and Neglect, 1995). The vulnerability of children
disorders; see Reynolds and Kamphaus, 2002, for a re- to trauma is more apparent now than ever before in our
view) require a different set of treatments than PTSD. history.
In fact, some of the treatments for the mimic disorders The epidemic of childhood trauma could have signifi-
such as stimulant medication for ADHD can be harmful cant implications for public policy (Bremmer and Narayan,
to children with PTSD and can aggravate their neuropsy- 1998). The numerous children suffering from childhood
chological symptoms. neglect and maltreatment, trauma, and PTSD could affect
Differential diagnosis requires at a minimum a de- educational, social, and health policies that will have far
tailed history of development, broad-band behavior rating reaching implications for society. Hippocampal toxicity
scales (e.g., Behavior Assessment System for Children; and its included deficits in scholastic performance will
Reynolds and Kamphaus, 1992), assessment of cogni- impair children throughout their lives. Early development
tive and academic status (as school failure is common of the brain is modified constantly by external stimuli and
among childhood PTSD victims and can also be misdiag- children are unusually sensitive to these deleterious effects
nosed as a learning disability), and specific neuropsycho- of stress due to the plasticity of the developing brain.
logical measures of arousal and attention. Assessment of According to Schwarz and Perry (1994), “PTSD may
brain function using a broad band of neuropsychological be preventable” and public education can help prevent
instruments is justified on the basis of the developmen- violence and children’s expose to trauma. Accurate and
tal neurobiological effects of trauma. As we have noted, comprehensive diagnostic studies of children referred for
chronically elevated cortisol levels can have detrimental ADHD and related symptoms must be the standard of
effects on several brain systems that are integral com- practice or many such individuals will be misdiagnosed
ponents of attentional and memory systems in particular. with ADHD instead of recognizing their status as individ-
Tests of memory and of new learning should be used to as- uals with PTSD. Mistreatment with stimulants may then
sess the functional impact of these potential alterations in exacerbate the symptoms and lead to more detrimental
brain development. The presence of memory and learning outcomes long-term (Schwarz and Perry, 1994). Unfor-
problems in such children will dictate additional treatment tunately, many managed care companies refuse to cer-
options such as cognitive remediation and the develop- tify comprehensive diagnostic services for such referrals.
ment and implementation of memory prostheses. With- Given the complexities of comorbidity generally and of the
out the proper diagnosis and prescription of these aids long-term consequences of undiagnosed and untreated—
by the neuropsychologist, children may be denied their or mistreated—PTSD, professionals engaged in diagnosis
use in the schools. Comprehensive assessment thus must where PTSD may be an issue will need to be acquainted
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128 Weber and Reynolds

with the empirical support for comprehensive diagnostic Glaser, D. (2000). Child abuse and neglect and the brain—a review.
services to substantiate the need for approval and provi- J. Child Psychol. Psychiatry 41(1): 97–116.
Golier, J., and Yehuda, R. (1998). Neuroendocrine activity and memory-
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The need to move beyond traditional psychological chopathol. 10(4): 857–869.
assessments for children exposed to trauma is crucial, Gunnar, M. R. (1998). Quality of early care and buffering of neuroen-
docrine stress reactions: Potential effects on the developing brain.
given the costs of misdiagnosis. Neuropsychologists must Prev. Med. 27(12): 208–211.
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logical impact of childhood trauma is dependent upon the Gunnar, M. R., and Nelson, C. A. (1994). Event-related potentials in
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ing effects of trauma. In addition to traditional psycholog- Dev. 65(1): 80–94.
Gurvitis, T., Shenton, M., Hokama, H., Ohta, H., Lasko, N., Gilbertson,
ical assessments, specific neuropsychological measures of M., Orr, S., Kikinis, R., Jolesz, F., McCarley, R., and Pitman, R.
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accurate treatment can occur. pal volume in chronic combat related posttraumatic stress disorder.
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